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+GitLab Docs Paper.code-workspace
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DISNET disease texts/100 Clean Disease Texts/Acute decompensated heart failure.txt

+Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), abnormal heart rhythms (such as atrial fibrillation), uncontrolled high blood pressure, or the person's failure to maintain a fluid restriction, diet, or medication. Other well recognized precipitating factors include anemia and hyperthyroidism which place additional strain on the heart muscle. Excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones, may also precipitate decompensation.
+Acute myocardial infarction can precipitate acute decompensated heart failure and will necessitate emergent revascularization with thrombolytics, percutaneous coronary intervention, or coronary artery bypass graft.
+A jugular venous distension is the most sensitive clinical sign for acute decompensation.
+Difficulty breathing, a cardinal symptom of left ventricular failure, may manifest with progressively increasing severity as the following:
+- Difficulty breathing with physical activity (exertional dyspnea)
+- Difficulty breathing while lying flat (orthopnea)
+- Episodes of waking up from sleep gasping for air (paroxysmal nocturnal dyspnea)
+- Acute pulmonary edem.
+Other cardiac symptoms of heart failure include chest pain/pressure and palpitations. Common noncardiac signs and symptoms of heart failure include loss of appetite, nausea, weight loss, bloating, fatigue, weakness, low urine output, waking up at night to urinate, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion.
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DISNET disease texts/100 Clean Disease Texts/Acute intermittent porphyria.txt

+Urine and serum show raised levels of porphobilinogen.
+Assay the red blood cells for the level of porphobilinogen deaminase.
+- Testing => Porphobilinogen
+- Porphobilinogen deaminase
+- Sodium
+- Potassium
+- Anti-nuclear antibody
+- Creatinine
+- Creatine kinase
+- White blood cell
+- Aspartate transaminase
+- Alanine transaminase
+- Epinephrine
+- Norepinephrine.
+Signs and symptoms of AIP can be variable. Severe and poorly localized abdominal pain is a very common symptom (found in 95% of those affected by AIP). Urinary signs and symptoms such as painful urination, urinary retention, urinary incontinence, or dark urine have also been known to occur. Psychiatric signs and symptoms of AIP may manifest as anxiety, paranoia, irritability, delusions, hallucinations, confusion, and depression. Signs that suggest increased activity of the sympathetic nervous system may be evident including tachycardia, hypertension, palpitations, orthostatic hypotension, sweating, restlessness, and tremor. Other neurologic signs and symptoms of AIP include seizures, peripheral neuropathy, abnormal sensations, chest pain, leg pain, back pain or headache, and coma. Nausea, vomiting, constipation, and diarrhea can also occur. Proximal muscle weakness typically beginning in the arms is characteristic; there can be muscle pain, tingling, numbness, weakness or paralysis; muscle weakness seen in AIP can progress to include the muscles of breathing causing respiratory failure and can be fatal.
+AIP patients have an increased risk of developing hepatocellular carcinoma, melanoma, lymphoma, chronic hypertension, chronic kidney disease, and chronic pain.
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DISNET disease texts/100 Clean Disease Texts/Anthrax.txt

+Bacillus anthracis is a rod-shaped, Gram-positive, aerobic bacterium about 1 by 9 μm in size. It was shown to cause disease by Robert Koch in 1876 when he took a blood sample from an infected cow, isolated the bacteria, and put them into a mouse. The bacterium normally rests in endospore form in the soil, and can survive for decades in this state. Herbivores are often infected whilst grazing, especially when eating rough, irritant, or spiky vegetation; the vegetation has been hypothesized to cause wounds within the gastrointestinal tract permitting entry of the bacterial endospores into the tissues, though this has not been proven. Once ingested or placed in an open wound, the bacteria begin multiplying inside the animal or human and typically kill the host within a few days or weeks. The endospores germinate at the site of entry into the tissues and then spread by the circulation to the lymphatics, where the bacteria multiply.
+The production of two powerful exotoxins and lethal toxin by the bacteria causes death. Veterinarians can often tell a possible anthrax-induced death by its sudden occurrence, and by the dark, nonclotting blood that oozes from the body orifices. Most anthrax bacteria inside the body after death are outcompeted and destroyed by anaerobic bacteria within minutes to hours post mortem. However, anthrax vegetative bacteria that escape the body via oozing blood or through the opening of the carcass may form hardy spores. These vegetative bacteria are not contagious. One spore forms per one vegetative bacterium. The triggers for spore formation are not yet known, though oxygen tension and lack of nutrients may play roles. Once formed, these spores are very hard to eradicate.
+The infection of herbivores (and occasionally humans) by the inhalational route normally proceeds as follows: Once the spores are inhaled, they are transported through the air passages into the tiny air sacs (alveoli) in the lungs. The spores are then picked up by scavenger cells (macrophages) in the lungs and are transported through small vessels (lymphatics) to the lymph nodes in the central chest cavity (mediastinum). Damage caused by the anthrax spores and bacilli to the central chest cavity can cause chest pain and difficulty in breathing. Once in the lymph nodes, the spores germinate into active bacilli that multiply and eventually burst the macrophages, releasing many more bacilli into the bloodstream to be transferred to the entire body. Once in the blood stream, these bacilli release three proteins named lethal factor, edema factor, and protective antigen. The three are not toxic by themselves, but their combination is incredibly lethal to humans. Protective antigen combines with these other two factors to form lethal toxin and edema toxin, respectively. These toxins are the primary agents of tissue destruction, bleeding, and death of the host. If antibiotics are administered too late, even if the antibiotics eradicate the bacteria, some hosts still die of toxemia because the toxins produced by the bacilli remain in their system at lethal dose levels.
+- Bacillus anthracis
+- Color-enhanced scanning electron micrograph shows splenic tissue from a monkey with inhalational anthrax; featured are rod-shaped bacilli (yellow) and an erythrocyte (red)
+- Gram-positive anthrax bacteria (purple rods) in cerebrospinal fluid: If present, a Gram-negative bacterial species would appear pink. (The other cells are white blood cells.
+Exposure => The spores are able to survive in harsh conditions for decades or even centuries. Such spores can be found on all continents, including Antarctica. Disturbed grave sites of infected animals have been known to cause infection after 70 years.
+Occupational exposure to infected animals or their products (such as skin, wool, and meat) is the usual pathway of exposure for humans. Workers who are exposed to dead animals and animal products are at the highest risk, especially in countries where anthrax is more common. Anthrax in livestock grazing on open range where they mix with wild animals still occasionally occurs in the United States and elsewhere. Many workers who deal with wool and animal hides are routinely exposed to low levels of anthrax spores, but most exposure levels are not sufficient to develop anthrax infections. A lethal infection is reported to result from inhalation of about 10,000–20,000 spores, though this dose varies among host species. Little documented evidence is available to verify the exact or average number of spores needed for infection.
+Historically, inhalational anthrax was called woolsorters' disease because it was an occupational hazard for people who sorted wool. Today, this form of infection is extremely rare in advanced nations, as almost no infected animals remain.
+Anthrax can enter the human body through the intestines (ingestion), lungs (inhalation), or skin (cutaneous) and causes distinct clinical symptoms based on its site of entry. In general, an infected human will be quarantined. However, anthrax does not usually spread from an infected human to a noninfected human. But, if the disease is fatal to the person's body, its mass of anthrax bacilli becomes a potential source of infection to others and special precautions should be used to prevent further contamination. Inhalational anthrax, if left untreated until obvious symptoms occur, is usually fatal.
+Anthrax can be contracted in laboratory accidents or by handling infected animals or their wool or hides. It has also been used in biological warfare agents and by terrorists to intentionally infect as exemplified by the 2001 anthrax attacks.
+Various techniques may be used for the direct identification of B. Anthracis in clinical material. Firstly, specimens may be Gram stained. Bacillus spp. Are quite large in size (3 to 4 μm long), they may grow in long chains, and they stain Gram-positive. To confirm the organism is B. Anthracis, rapid diagnostic techniques such as polymerase chain reaction-based assays and immunofluorescence microscopy may be used.
+All Bacillus species grow well on 5% sheep blood agar and other routine culture media. Polymyxin-lysozyme-EDTA-thallous acetate can be used to isolate B. Anthracis from contaminated specimens, and bicarbonate agar is used as an identification method to induce capsule formation. Bacillus spp. Usually grow within 24 hours of incubation at 35°C, in ambient air (room temperature) or in 5% CO2. If bicarbonate agar is used for identification, then the medium must be incubated in 5% CO2. B. Anthracis colonies are medium-large, gray, flat, and irregular with swirling projections, often referred to as having a "medusa head" appearance, and are not hemolytic on 5% sheep blood agar. The bacteria are not motile, susceptible to penicillin, and produce a wide zone of lecithinase on egg yolk agar. Confirmatory testing to identify B. Anthracis includes gamma bacteriophage testing, indirect hemagglutination, and enzyme-linked immunosorbent assay to detect antibodies. The best confirmatory precipitation test for anthrax is the Ascoli test.
+Cutaneous anthrax, also known as Hide porter's disease, is when anthrax occurs on the skin. It is the most common form (>90% of anthrax cases). Cutaneous anthrax is also the least dangerous form of anthrax (less than 1% mortality rate with treatment). Cutaneous anthrax presents as a boil-like skin lesion that eventually forms an ulcer with a black center (eschar). The black eschar often shows up as a large, painless, necrotic ulcer (beginning as an irritating and itchy skin lesion or blister that is dark and usually concentrated as a black dot, somewhat resembling bread mold) at the site of infection. In general, cutaneous infections form within the site of spore penetration between two and five days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections normally do not cause pain. Nearby lymph nodes may become infected, reddened, swollen, and painful. A scab forms over the lesion soon, and falls off in a few weeks. Complete recovery may take longer. Cutaneous anthrax is typically caused when B. Anthracis spores enter through cuts on the skin. This form is found most commonly when humans handle infected animals and/or animal products.
+Cutaneous anthrax is rarely fatal if treated, because the infection area is limited to the skin, preventing the lethal factor, edema factor, and protective antigen from entering and destroying a vital organ. Without treatment, about 20% of cutaneous skin infection cases progress to toxemia and death.
+Lungs => Respiratory infection in humans is relatively rare and presents as two stages. It infects the lymph nodes in the chest first, rather than the lungs themselves, a condition called hemorrhagic mediastinitis, causing bloody fluid to accumulate in the chest cavity, therefore causing shortness of breath. The first stage causes cold and flu-like symptoms. Symptoms include fever, shortness of breath, cough, fatigue, and chills. This can last hours to days. Often, many fatalities from inhalational anthrax are when the first stage is mistaken for the cold or flu and the victim does not seek treatment until the second stage, which is 90% fatal. The second (pneumonia) stage occurs when the infection spreads from the lymph nodes to the lungs. Symptoms of the second stage develop suddenly after hours or days of the first stage. Symptoms include high fever, extreme shortness of breath, shock, and rapid death within 48 hours in fatal cases. Historical mortality rates were over 85%, but when treated early (seen in the 2001 anthrax attacks), observed case fatality rate dropped to 45%. Distinguishing pulmonary anthrax from more common causes of respiratory illness is essential to avoiding delays in diagnosis and thereby improving outcomes. An algorithm for this purpose has been developed.
+Gastrointestinal => Gastrointestinal (GI) infection is most often caused by consuming anthrax-infected meat and is characterized by diarrhea, potentially with blood, abdominal pains, acute inflammation of the intestinal tract, and loss of appetite. Occasional vomiting of blood can occur. Lesions have been found in the intestines and in the mouth and throat. After the bacterium invades the gastrointestinal system, it spreads to the bloodstream and throughout the body, while continuing to make toxins. GI infections can be treated, but usually result in fatality rates of 25 to 60%, depending upon how soon treatment commences. This form of anthrax is the rarest form.
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DISNET disease texts/100 Clean Disease Texts/Arterial embolism.txt

+In addition to evaluating the symptoms above, the health care provider may find decreased or no blood pressure in the arm or leg.
+Tests to determine any underlying cause for thrombosis or embolism and to confirm presence of the obstruction may include:
+- Doppler ultrasound, especially duplex ultrasonography. It may also involve transcranial doppler exam of arteries to the brain
+- Echocardiography, sometimes involving more specialized techniques such as Transesophageal echocardiography (TEE) or myocardial contrast echocardiography (MCE) to diagnose myocardial infarction
+- Arteriography of the affected extremity or organ Digital subtraction angiography is useful in individuals where administration of radiopaque contrast material must be kept to a minimum.
+- Magnetic resonance imaging (MRI)
+- Blood tests for measuring elevated enzymes in the blood, including cardiac-specific troponin T and/or troponin I, myoglobins, and creatine kinase isoenzymes. These indicate embolisation to the heart that has caused myocardial infarction. Myoglobins and creatine kinase are also elevated in the blood in embolisation in other locations.
+- Blood cultures may be done to identify the organism responsible for any causative infection
+- Electrocardiography (ECG) for detecting myocardial infarction
+- Angioscopy using a flexible fiberoptic catheter inserted directly into an artery.
+Symptoms may begin quickly or slowly depending on the size of the embolus and how much it blocks the blood flow. Symptoms of embolisation in an organ vary with the organ involved but commonly include:
+- Pain in the involved body part
+- Temporarily decreased organ functio.
+Later symptoms are closely related to infarction of the affected tissue. This may cause permanently decreased organ function.
+For example, symptoms of myocardial infarction mainly include chest pain, dyspnea, diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations.
+Symptoms of limb infarction include coldness, decreased or no pulse beyond the site of blockage, pain, muscle spasm, numbness and tingling, pallor and muscle weakness, possibly to the grade of paralysis in the affected limb.
+Commonly occluded sites => Arterial emboli often occur in the legs and feet. Some may occur in the brain, causing a stroke, or in the heart, causing a heart attack. Less common sites include the kidneys, intestines, and eyes.
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DISNET disease texts/100 Clean Disease Texts/Arteriovenous malformation.txt

+AVMs are diagnosed primarily by the following methods:
+- Computerized tomography (CT) scan is a noninvasive X-ray to view the anatomical structures within the brain to detect blood in or around the brain. A newer technology called CT angiography involves the injection of contrast into the blood stream to view the arteries of the brain. This type of test provides the best pictures of blood vessels through angiography and soft tissues through CT.
+- Magnetic resonance imaging (MRI) scan is a noninvasive test, which uses a magnetic field and radio-frequency waves to give a detailed view of the soft tissues of the brain.
+- Magnetic resonance angiography (MRA) – scans created using magnetic resonance imaging to specifically image the blood vessels and structures of the brain. A magnetic resonance angiogram can be an invasive procedure, involving the introduction of contrast dyes (e. G., gadolinium MR contrast agents) into the vasculature of a patient using a catheter inserted into an artery and passed through the blood vessels to the brain. Once the catheter is in place, the contrast dye is injected into the bloodstream and the MR images are taken. Additionally or alternatively, flow-dependent or other contrast-free magnetic resonance imaging techniques can be used to determine the location and other properties of the vasculature.
+AVMs can occur in various parts of the body:
+- brain (cerebral AV malformation)
+- spleen
+- lung
+- kidney
+- spinal cord
+- liver
+- intercostal space
+- iris
+- spermatic cord
+- extremities – arm, shoulder, etc. AVMs may occur in isolation or as a part of another disease (for example, Von Hippel-Lindau disease or hereditary hemorrhagic telangiectasia).
+AVMs have been shown to be associated with aortic stenosis.
+Bleeding from an AVM can be relatively mild or devastating. It can cause severe and less often fatal strokes. If a cerebral AVM is detected before a stroke occurs, usually the arteries feeding blood into the nidus can be closed off to avert the danger. However, interventional therapy may also be relatively risky.
+Symptoms of AVM vary according to the location of the malformation. Roughly 88% of people with an AVM are asymptomatic; often the malformation is discovered as part of an autopsy or during treatment of an unrelated disorder (called in medicine an "incidental finding"); in rare cases, its expansion or a micro-bleed from an AVM in the brain can cause epilepsy, neurological deficit, or pain.
+The most general symptoms of a cerebral AVM include headaches and epileptic seizures, with more specific symptoms occurring that normally depend on the location of the malformation and the individual. Such possible symptoms include:
+- Difficulties with movement coordination, including muscle weakness and even paralysis;
+- Vertigo (dizziness);
+- Difficulties of speech (dysarthria) and communication, such as aphasia;
+- Difficulties with everyday activities, such as apraxia;
+- Abnormal sensations (numbness, tingling, or spontaneous pain);
+- Memory and thought-related problems, such as confusion, dementia or hallucinations.
+Cerebral AVMs may present themselves in a number of different ways:
+- Bleeding (45% of cases)
+- Acute onset of severe headache. May be described as the worst headache of the patient's life. Depending on the location of bleeding, may be associated with new fixed neurologic deficit. In unruptured brain AVMs, the risk of spontaneous bleeding may be as low as 1% per year. After a first rupture, the annual bleeding risk may increase to more than 5%.
+- Seizure or brain seizure (46%) Depending on the place of the AVM, it can cause loss of vision in one place.
+- Headache (34%)
+- Progressive neurologic deficit (21%) May be caused by mass effect or venous dilatations. Presence and nature of the deficit depend on location of lesion and the draining veins.
+- May be caused by mass effect or venous dilatations. Presence and nature of the deficit depend on location of lesion and the draining veins.
+- Pediatric patients Heart failure Macrocephaly Prominent scalp veins
+- Heart failure
+- Macrocephaly
+- Prominent scalp vein.
+Pulmonary arteriovenous malformations => In the lungs, pulmonary arteriovenous malformations have no symptoms in up to 29% of all cases.
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DISNET disease texts/100 Clean Disease Texts/Ascites.txt

+Causes of high serum-ascites albumin gradient (SAAG or transudate) are:
+- Cirrhosis – 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
+- Heart failure – 3%
+- Hepatic venous occlusion: Budd–Chiari syndrome or veno-occlusive disease
+- Constrictive pericarditis
+- Kwashiorkor (childhood protein-energy malnutrition.
+Causes of low SAAG ("exudate") are:
+- Cancer (metastasis and primary peritoneal carcinomatosis) – 10%
+- Infection: Tuberculosis – 2% or spontaneous bacterial peritonitis
+- Pancreatitis – 1%
+- Serositis
+- Nephrotic syndrome
+- Hereditary angioedema.
+Other rare causes:
+- Meigs syndrome
+- Vasculitis
+- Hypothyroidism
+- Renal dialysis
+- Peritoneum mesothelioma
+- Abdominal tuberculosis
+- Mastocytosi.
+Routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend a diagnostic paracentesis be performed if the ascites is new or if the patient with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as microbiological culture, Gram stain and cytopathology.
+The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites. A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive as a cause.
+Ultrasound investigation is often performed prior to attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detecting Budd-Chiari syndrome (thrombosis of the hepatic vein) and portal vein thrombosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. An abdominal CT scan is a more accurate alternate to reveal abdominal organ structure and morphology.
+Classification => Ascites exists in three grades:
+- Grade 1: mild, only visible on ultrasound and CT
+- Grade 2: detectable with flank bulging and shifting dullness
+- Grade 3: directly visible, confirmed with the fluid wave/thrill tes.
+Mild ascites is hard to notice, but severe ascites leads to abdominal distension. Patients with ascites generally will complain of progressive abdominal heaviness and pressure as well as shortness of breath due to mechanical impingement on the diaphragm.
+Ascites is detected on physical examination of the abdomen by visible bulging of the flanks in the reclining patient ("flank bulging"), "shifting dullness" (difference in percussion note in the flanks that shifts when the patient is turned on the side) or in massive ascites with a "fluid thrill" or "fluid wave" (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite side of the abdomen).
+Other signs of ascites may be present due to its underlying cause. For instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the liver) patients may also complain of leg swelling, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance.
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DISNET disease texts/100 Clean Disease Texts/Autonomic dysreflexia.txt

+The most common symptoms of autonomic hyperreflexia seen in people with spinal cord injury are loss of bowel and bladder function, resulting in impaction in the case of the bowels and distention in case of the bladder. These are generally found in patients with a spinal cord injury above the T6 (6th thoracic vertebral) level, but can occur in patients with a transection as low as T10 (10th thoracic vertebral) level.
+The risk is greatest with cervical spinal cord lesions and is rare with lesions below T6 thoracic vertebrae. It has rarely been reported in spinal cord lesions as low as T10. The first episode may occur weeks to years after spinal cord injury takes place, but most people at risk (80%) develop their first episode within the first year after injury. Once a person has their first episode of autonomic dysreflexia, the next 7–10 days are critical because there is a high incidence of recurrence within that time. Some people describe this predisposition as an easily excitable autonomic nervous system.
+Another causative factor may be an undetected urinary tract infection. The difficulty in assessing this may be complicated with the usage of indwelling or suprapubic catheters. When a painful stimulus occurs, as when voiding is interrupted or a bowel obstruction occurs, nerve impulses are sent to the brain via the spinal cord. However, in spinal cord transection, these impulses are unable to travel past the injury. This results in a spinal cord reflex to the autonomic nervous system in response to pain. In patients with spinal cord transection, types of stimulation that are tolerated by healthy people create an excessive response from the person's nervous system.
+Other causes include medication side effects and various disease processes. The use of stimulants such as cocaine and amphetamines which can result in urinary retention, and the use of CNS depressants and other psychoactive drugs can also lead to urinary retention and constipation thus leading to autonomic dysreflexia when in use over an extended period of time. Guillain–Barré syndrome is a demyelinating disease that can result in peripheral paralysis and can progress to encompass autonomic functions, leading to a loss of normal respiratory, bladder and bowel function resulting in autonomic dysreflexia. Severe head trauma and other brain injuries can instigate autonomic dysreflexia at the central nervous system by interfering with the reception of the signal that brings the urge to void the bladder and bowels and with the voluntary ability to micturate and defecate. Other causal theories for autonomic dysreflexia include noxious stimuli, or painful stimuli arising from the peripheral sensory neurons. These stimuli are interrupted in their journey to the brain due to a transection of the spine result in a paradoxical stimulation of autonomic pathways of the autonomic nervous system.
+Pain => Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. (Note: Not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli in normal people, e. G. Broken bones, will not result in AD, and may in fact even go unnoticed.) However, different studies have found that activation of pain receptors in muscle and skin below the lesion in spinal cord injured individuals did not trigger AD. These studies suggests that not all noxious stimuli are reliable triggers of AD, and because non-noxious stimuli can also trigger AD, attribution of an episode of AD to noxious stimuli may cause clinicians to overlook underlying non-noxious triggers. As a result, non-noxious trigger factors remain undetected, prolonging an episode of AD. They concluded that when deducing the potential causes of AD it is important to consider non-noxious sources of stimulation in addition to noxious triggers. Current assessment of autonomic dysreflexia in patients with known causative factors include palpation of the bladder and bowel and can also include bladder scan.
+The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance. In autonomic dysreflexia, patients will experience hypertension, sweating, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may suffer from headaches and blurred vision. Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe. Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms are usually experiencing essential hypertension, not autonomic dysreflexia. Aggressive treatment of these elderly patients with rapidly acting antihypertensive medications can have disastrous results.
+This condition is distinct and usually episodic, with the people experiencing remarkably high blood pressure (often with systolic readings over 200 mm. Hg), intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision. An elevation of 40 mm Hg over baseline systolic should be suspicious for dysreflexia.
+Complications => Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue ulcers or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers.
+Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes.
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DISNET disease texts/100 Clean Disease Texts/Benzodiazepine withdrawal syndrome.txt

+In severe cases, the withdrawal reaction or protracted withdrawal may exacerbate or resemble serious psychiatric and medical conditions, such as mania, schizophrenia, agitated depression, panic disorder, generalised anxiety disorder, and complex partial seizures and, especially at high doses, seizure disorders. Failure to recognize discontinuation symptoms can lead to false evidence for the need to take benzodiazepines, which in turn leads to withdrawal failure and reinstatement of benzodiazepines, often to higher doses. Pre-existing disorder or other causes typically do not improve, whereas symptoms of protracted withdrawal gradually improve over the ensuing months. For this reason at least six months should have elapsed after benzodiazepines cessation before re-evaluating the symptoms and updating a diagnosis.
+Symptoms may lack a psychological cause and can fluctuate in intensity with periods of good and bad days until eventual recovery.
+Withdrawal effects caused by sedative-hypnotics discontinuation, such as benzodiazepines, barbiturates, or alcohol, can cause serious medical complications. They are cited to be more hazardous to withdraw from than opioids. Users typically receive little advice and support for discontinuation. Some withdrawal symptoms are identical to the symptoms for which the medication was originally prescribed, and can be acute or protracted in duration. Onset of symptoms from long half-life benzodiazepines might be delayed for up to three weeks, although withdrawal symptoms from short-acting ones often present early, usually within 24–48 hours. There may be no fundamental differences in symptoms from either high or low dose discontinuation, but symptoms tend to be more severe from higher doses.
+Daytime reemergence and rebound withdrawal symptoms, sometimes confused with interdose withdrawal, may occur once dependence has set in. 'Reemergence' is the return of symptoms for which the drug was initially prescribed, in contrast, 'rebound' symptoms are a return of the symptoms for which the benzodiazepine was initially taken, but at a more intense level than before; whereas 'interdose withdrawal' is when a prior dosage of drug wears off and beginnings of an entirely new cycle of withdrawal sets in, the symptoms of which dissipate upon taking the next dosage but afterwhich yet another entirely new cycle of withdrawal begins when that dosage wears off, a new onset of withdrawal between each dosage thus called 'interdose withdrawal' and if not properly treated can recur indefinitely in a vicious circle (for which consider a benzo with a long half life (e. G. Valium) so the drug does not wear off between doses). Withdrawal symptoms may appear for the first time during dose reduction, and include insomnia, anxiety, distress, weight loss, dizziness, night sweats, shakes, muscle twitches, aphasia, panic attacks, depression, derealization, paranoia, etc., and are more commonly associated with short-acting benzodiazepines discontinuation, like triazolam. Daytime symptoms can occur after a few days to a few weeks of administration of nightly benzodiazepine use or z-drugs such as zopiclone; withdrawal-related insomnia rebounds worse than baseline even when benzodiazepines are used intermittently.
+The following symptoms may emerge during gradual or abrupt dosage reduction:
+- Akathisia
+- Agitation and Anxiety, possible terror and panic attacks
+- Blurred vision
+- Chest pain
+- Depersonalization
+- Depression (can be severe), possible suicidal ideation
+- Derealisation (feelings of unreality)
+- Dilated pupils
+- Dizziness
+- Dry mouth
+- Dysphoria
+- Elevation in blood pressure
+- Fatigue and weakness
+- Gastrointestinal disturbance (including nausea, diarrhea, vomiting)
+- Hearing disturbance
+- Headache
+- Hot and cold spells
+- Hyperosmia
+- Hypertension
+- Hypnagogic hallucinations
+- Hypochondriasis
+- Increased sensitivity to touch
+- Increased urinary frequency
+- Insomnia
+- Impaired memory and concentration
+- Loss of appetite and weight loss
+- Mild to moderate Aphasia
+- Mood swings
+- Muscular spasms, cramps, discomfort or fasciculations
+- Nightmares
+- Obsessive compulsive disorder
+- Paraesthesia
+- Paranoia
+- Perspiration
+- Photophobia
+- Postural hypotension
+- REM sleep rebound
+- Restless legs syndrome
+- Stiffness
+- Taste and smell disturbances
+- Tachycardia
+- Tinnitus
+- Tremor
+- Visual disturbances.
+Rapid discontinuation may result in a more serious syndrome.
+- Catatonia, which may result in death
+- Confusion
+- Convulsions, which may result in death
+- Coma (rare)
+- Delirium tremens
+- Hyperthermia
+- Mania
+- Neuroleptic malignant syndrome-like event (rare)
+- Organic brain syndrome
+- Post-traumatic stress disorder
+- Psychosis
+- Suicidal ideation or suicide
+- Violence and aggression.
+As withdrawal progresses, patients often find their physical and mental health improves with improved mood and improved cognition.
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DISNET disease texts/100 Clean Disease Texts/Blastomycosis.txt

+Blastomycosis is caused by the dimorphic microfungus Blastomyces dermatitidis, a member of the phylum Ascomycota in the family Ajellomycetaceae. It has been recognised as the asexual state of Ajellomyces dermatitidis. In endemic areas, the fungus lives in soil and rotten wood near lakes and rivers. Although it has never been directly observed growing in nature, it is thought to grow there as a cottony white mold, similar to the growth seen in artificial culture at 25 °C. The moist, acidic soil in the surrounding woodland harbors the fungus.
+Spectrum of disease => Blastomycosis manifests as a primary lung infection in about 70% of cases. The onset is relatively slow and symptoms are suggestive of pneumonia, often leading to initial treatment with antibacterials. Occasionally, if a lesion is seen on X-ray in a cigarette smoker, the disease may be misdiagnosed as carcinoma, leading to swift excision of the pulmonary lobe involved. Upper lung lobes are involved somewhat more frequently than lower lobes. If untreated, many cases progress over a period of months to years to become disseminated blastomycosis. In these cases, the large Blastomyces yeast cells translocate from the lungs and are trapped in capillary beds elsewhere in the body, where they cause lesions. The skin is the most common organ affected, being the site of lesions in approximately 60% of cases. The signature image of blastomycosis in textbooks is the indolent, verrucous or ulcerated dermal lesion seen in disseminated disease. Osteomyelitis is also common (12–60% of cases). Other recurring sites of dissemination are the genitourinary tract (kidney, prostate, epididymis; collectively ca. 25% of cases) and the brain (3–10% of cases).
+An uncommon but very dangerous type of primary blastomycosis manifests as acute respiratory distress syndrome (ARDS); for example, this was seen in 9 of 72 blastomycosis cases studied in northeast Tennessee. Such cases may follow massive exposure, e. G., during brush clearing operations. The fatality rate in the ARDS cases in the Tennessee study was 89%, while in non-ARDS cases of pulmonary blastomycosis, the fatality rate was 10%.
+Once suspected, the diagnosis of blastomycosis can usually be confirmed by demonstration of the characteristic broad based budding organisms in sputum or tissues by KOH prep, cytology, or histology. Tissue biopsy of skin or other organs may be required in order to diagnose extra-pulmonary disease. Blastomycosis is histologically associated with granulomatous nodules. Commercially available urine antigen testing appears to be quite sensitive in suggesting the diagnosis in cases where the organism is not readily detected. While culture of the organism remains the definitive diagnostic standard, its slow growing nature can lead to delays in treatment of up to several weeks. However, sometimes blood and sputum cultures may not detect blastomycosis.
+Blastomycosis can present in one of the following ways:
+- a flu-like illness with fever, chills, arthralgia (joint pain), myalgia (muscle pain), headache, and a nonproductive cough which resolves within days.
+- an acute illness resembling bacterial pneumonia, with symptoms of high fever, chills, a productive cough, and pleuritic chest pain.
+- a chronic illness that mimics tuberculosis or lung cancer, with symptoms of low-grade fever, a productive cough, night sweats, and weight loss.
+- a fast, progressive, and severe disease that manifests as ARDS, with fever, shortness of breath, tachypnea, hypoxemia, and diffuse pulmonary infiltrates.
+- skin lesions, usually asymptomatic, can be verrucous (wart-like) or ulcerated with small pustules at the margins.
+- bone lytic lesions can cause bone or joint pain.
+- prostatitis may be asymptomatic or may cause pain on urinating.
+- laryngeal involvement causes hoarseness.
+- 40% immunocompromised individuals have CNS involvement and present as brain abscess, epidural abscess or meningitis
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DISNET disease texts/100 Clean Disease Texts/Breast cancer.txt

+Most types of breast cancer are easy to diagnose by microscopic analysis of a sample—or biopsy—of the affected area of the breast. Also, there are types of breast cancer that require specialized lab exams.
+The two most commonly used screening methods, physical examination of the breasts by a healthcare provider and mammography, can offer an approximate likelihood that a lump is cancer, and may also detect some other lesions, such as a simple cyst. When these examinations are inconclusive, a healthcare provider can remove a sample of the fluid in the lump for microscopic analysis (a procedure known as fine needle aspiration, or fine needle aspiration and cytology—FNAC) to help establish the diagnosis. The needle aspiration may be performed in a healthcare provider's office or clinic using local anaesthetic if required. A finding of clear fluid makes the lump highly unlikely to be cancerous, but bloody fluid may be sent off for inspection under a microscope for cancerous cells. Together, physical examination of the breasts, mammography, and FNAC can be used to diagnose breast cancer with a good degree of accuracy.
+Other options for biopsy include a core biopsy or vacuum-assisted breast biopsy, which are procedures in which a section of the breast lump is removed; or an excisional biopsy, in which the entire lump is removed. Very often the results of physical examination by a healthcare provider, mammography, and additional tests that may be performed in special circumstances (such as imaging by ultrasound or MRI) are sufficient to warrant excisional biopsy as the definitive diagnostic and primary treatment method.
+- MRI showing breast cancer
+- Excised human breast tissue, showing an irregular, dense, white stellate area of cancer 2 cm in diameter, within yellow fatty tissue.
+- High-grade invasive ductal carcinoma, with minimal tubule formation, marked pleomorphism, and prominent mitoses, 40x field.
+- Micrograph showing a lymph node invaded by ductal breast carcinoma, with an extension of the tumor beyond the lymph node.
+- Neuropilin-2 expression in normal breast and breast carcinoma tissue.
+- F-18 FDG PET/CT: A breast cancer metastasis to the right scapula
+- Needle breast biopsy.
+- Elastography shows stiff cancer tissue on ultrasound imaging.
+- Ultrasound image shows irregularly shaped mass of breast cancer.
+- Infiltrating (Invasive) breast carcinoma.
+Breast cancers are classified by several grading systems. Each of these influences the prognosis and can affect treatment response. Description of a breast cancer optimally includes all of these factors.
+- Histopathology. Breast cancer is usually classified primarily by its histological appearance. Most breast cancers are derived from the epithelium lining the ducts or lobules, and these cancers are classified as ductal or lobular carcinoma. Carcinoma in situ is growth of low-grade cancerous or precancerous cells within a particular tissue compartment such as the mammary duct without invasion of the surrounding tissue. In contrast, invasive carcinoma does not confine itself to the initial tissue compartment.
+- Grade. Grading compares the appearance of the breast cancer cells to the appearance of normal breast tissue. Normal cells in an organ like the breast become differentiated, meaning that they take on specific shapes and forms that reflect their function as part of that organ. Cancerous cells lose that differentiation. In cancer, the cells that would normally line up in an orderly way to make up the milk ducts become disorganized. Cell division becomes uncontrolled. Cell nuclei become less uniform. Pathologists describe cells as well differentiated (low grade), moderately differentiated (intermediate grade), and poorly differentiated (high grade) as the cells progressively lose the features seen in normal breast cells. Poorly differentiated cancers (the ones whose tissue is least like normal breast tissue) have a worse prognosis.
+- Stage. Breast cancer staging using the TNM system is based on the size of the tumor (T), whether or not the tumor has spread to the lymph nodes (N) in the armpits, and whether the tumor has metastasized (M) (i.e. Spread to a more distant part of the body). Larger size, nodal spread, and metastasis have a larger stage number and a worse prognosis. The main stages are: Stage 0 is a pre-cancerous or marker condition, either ductal carcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS). Stages 1–3 are within the breast or regional lymph nodes. Stage 4 is 'metastatic' cancer that has a less favorable prognosis since it has spread beyond the breast and regional lymph nodes.
+- Stage 0 is a pre-cancerous or marker condition, either ductal carcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS).
+- Stages 1–3 are within the breast or regional lymph nodes.
+- Stage 4 is 'metastatic' cancer that has a less favorable prognosis since it has spread beyond the breast and regional lymph nodes.
+- Stage T1 breast cancer
+- Stage T2 breast cancer
+- Stage T3 breast cance.
+- Receptor status. Breast cancer cells have receptors on their surface and in their cytoplasm and nucleus. Chemical messengers such as hormones bind to receptors, and this causes changes in the cell. Breast cancer cells may or may not have three important receptors: estrogen receptor (ER), progesterone receptor (PR), and HER2. ER+ cancer cells (that is, cancer cells that have estrogen receptors) depend on estrogen for their growth, so they can be treated with drugs to block estrogen effects (e. G. Tamoxifen), and generally have a better prognosis. Untreated, HER2+ breast cancers are generally more aggressive than HER2-breast cancers, but HER2+ cancer cells respond to drugs such as the monoclonal antibody trastuzumab (in combination with conventional chemotherapy), and this has improved the prognosis significantly. Cells that do not have any of these three receptor types (estrogen receptors, progesterone receptors, or HER2) are called triple-negative, although they frequently do express receptors for other hormones, such as androgen receptor and prolactin receptor.
+- DNA assays. DNA testing of various types including DNA microarrays have compared normal cells to breast cancer cells. The specific changes in a particular breast cancer can be used to classify the cancer in several ways, and may assist in choosing the most effective treatment for that DNA type.
+- Stage 1A breast cancer
+- Stage 1B breast cancer
+- Stage 2A breast cancer
+- Stage 2A breast cancer
+- Stage 2B breast cancer
+- Stage 2B breast cancer
+- Stage 2B breast cancer
+- Stage 3A breast cancer
+- Stage 3A breast cancer
+- Stage 3A breast cancer
+- Stage 3B breast cancer
+- Stage 3B breast cancer
+- Stage 4 breast cance.
+The first noticeable symptom of breast cancer is typically a lump that feels different from the rest of the breast tissue. More than 80% of breast cancer cases are discovered when the woman feels a lump. The earliest breast cancers are detected by a mammogram. Lumps found in lymph nodes located in the armpits can also indicate breast cancer.
+Indications of breast cancer other than a lump may include thickening different from the other breast tissue, one breast becoming larger or lower, a nipple changing position or shape or becoming inverted, skin puckering or dimpling, a rash on or around a nipple, discharge from nipple/s, constant pain in part of the breast or armpit, and swelling beneath the armpit or around the collarbone. Pain ("mastodynia") is an unreliable tool in determining the presence or absence of breast cancer, but may be indicative of other breast health issues.
+Inflammatory breast cancer is a particular type of breast cancer which can pose a substantial diagnostic challenge. Symptoms may resemble a breast inflammation and may include itching, pain, swelling, nipple inversion, warmth and redness throughout the breast, as well as an orange-peel texture to the skin referred to as peau d'orange. As inflammatory breast cancer does not present as a lump there can sometimes be a delay in diagnosis.
+Another reported symptom complex of breast cancer is Paget's disease of the breast. This syndrome presents as skin changes resembling eczema, such as redness, discoloration, or mild flaking of the nipple skin. As Paget's disease of the breast advances, symptoms may include tingling, itching, increased sensitivity, burning, and pain. There may also be discharge from the nipple. Approximately half of women diagnosed with Paget's disease of the breast also have a lump in the breast.
+In rare cases, what initially appears as a fibroadenoma (hard, movable non-cancerous lump) could in fact be a phyllodes tumor. Phyllodes tumors are formed within the stroma (connective tissue) of the breast and contain glandular as well as stromal tissue. Phyllodes tumors are not staged in the usual sense; they are classified on the basis of their appearance under the microscope as benign, borderline, or malignant.
+Occasionally, breast cancer presents as metastatic disease—that is, cancer that has spread beyond the original organ. The symptoms caused by metastatic breast cancer will depend on the location of metastasis. Common sites of metastasis include bone, liver, lung and brain. Unexplained weight loss can occasionally signal breast cancer, as can symptoms of fevers or chills. Bone or joint pains can sometimes be manifestations of metastatic breast cancer, as can jaundice or neurological symptoms. These symptoms are called non-specific, meaning they could be manifestations of many other illnesses.
+Most symptoms of breast disorders, including most lumps, do not turn out to represent underlying breast cancer. Fewer than 20% of lumps, for example, are cancerous, and benign breast diseases such as mastitis and fibroadenoma of the breast are more common causes of breast disorder symptoms. Nevertheless, the appearance of a new symptom should be taken seriously by both patients and their doctors, because of the possibility of an underlying breast cancer at almost any age.
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DISNET disease texts/100 Clean Disease Texts/Campylobacteriosis.txt

+Campylobacteriosis is caused by Campylobacter bacteria (curved or spiral, motile, non–spore-forming, Gram-negative rods). The disease is usually caused by C. Jejuni, a spiral and comma shaped bacterium normally found in cattle, swine, and birds, where it is nonpathogenic, but the illness can also be caused by C. Coli (also found in cattle, swine, and birds), C. Upsaliensis (found in cats and dogs) and C. Lari (present in seabirds in particular).
+One effect of campylobacteriosis is tissue injury in the gut. The sites of tissue injury include the jejunum, the ileum, and the colon. C jejuni appears to achieve this by invading and destroying epithelial cells.
+C. Jejuni can also cause a latent autoimmune effect on the nerves of the legs, which is usually seen several weeks after a surgical procedure of the abdomen. The effect is known as an acute idiopathic demyelinating polyneuropathy (AIDP), i.e. Guillain–Barré syndrome, in which one sees symptoms of ascending paralysis, dysaesthesias usually below the waist, and, in the later stages, respiratory failure.
+Some strains of C jejuni produce a cholera-like enterotoxin, which is important in the watery diarrhea observed in infections. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism.
+Campylobacter organisms can be detected by performing a Gram stain of a stool sample with high specificity and a sensitivity of ~60%, but are most often diagnosed by stool culture. Fecal leukocytes should be present and indicate the diarrhea to be inflammatory in nature. Methods currently being developed to detect the presence of campylobacter organisms include antigen testing via an EIA or PCR.
+The prodromal symptoms are fever, headache, and myalgia, which can be severe, lasting as long as 24 hours. After 1–5 days, typically, these are followed by diarrhea (as many as 10 watery, frequently bloody, bowel movements per day) or dysentery, cramps, abdominal pain, and fever as high as 40 °C (104 °F). In most people, the illness lasts for 2–10 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery.
+There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking acute appendicitis. Furthermore, Helicobacter pylori is closely related to Campylobacter and causes peptic ulcer disease.
+Complications => Complications include toxic megacolon, dehydration and sepsis. Such complications generally occur in young children (< 1 year of age) and immunocompromised people. A chronic course of the disease is possible; this disease process is likely to develop without a distinct acute phase. Chronic campylobacteriosis features a long period of sub-febrile temperature and asthenia; eye damage, arthritis, endocarditis may develop if infection is untreated.
+Occasional deaths occur in young, previously healthy individuals because of blood volume depletion (due to dehydration), and in persons who are elderly or immunocompromised.
+Some individuals (1–2 in 100,000 cases) develop Guillain–Barré syndrome, in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently. This occurs only with infection of C. Jejuni and C. Upsaliensis.
+Other factors => In patients with HIV, infections may be more frequent, may cause prolonged bouts of dirty brown diarrhea, and may be more commonly associated with bacteremia and antibiotic resistance. In participants of unprotected anal intercourse, campylobacteriosis is more localized to the distal end of the colon and may be termed a proctocolitis. The severity and persistence of infection in patients with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection.
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DISNET disease texts/100 Clean Disease Texts/Carciac myxoma.txt

+Myxomas are the most common type of primary heart tumor.
+The tumor is derived from multipotential mesenchymal cells and may cause a ball valve-type obstruction.
+About 75% of myxomas occur in the left atrium of the heart, usually beginning in the wall that divides the two upper chambers of the heart. The rest are in the right atrium, rarely in the left ventricle. Right atrial myxomas are sometimes associated with tricuspid stenosis and atrial fibrillation.
+Myxomas are more common in women. About 10% of myxomas are passed down through families (inherited), as in Carney syndrome, where several other abnormalities are observed, such as skin myxomas, pigmentation, endocrine hyperactivity, schwannomas and epithelioid blue nevi. Such tumors are called familial myxomas. They tend to occur in more than one part of the heart at a time, and often cause symptoms at a younger age than other myxomas.
+A doctor will listen to the heart with stethoscope. A "tumor plop" (a sound related to movement of the tumor), abnormal heart sounds, or a murmur similar to the mid-diastolic rumble of mitral stenosis may be heard. These sounds may change when the patient changes position.
+Right atrial myxomas rarely produce symptoms until they have grown to be at least 13 cm (about 5 inches) wide.
+Tests may include:
+- Echocardiogram and Doppler study
+- Chest x-ray
+- CT scan of chest
+- Heart MRI
+- Left heart angiography
+- Right heart angiography
+- ECG—may show atrial fibrillatio.
+Blood tests: A FBC may show anemia and increased WBCs (white blood cells). The erythrocyte sedimentation rate (ESR) is usually increased.
+- Echocardiogram of atrial myxoma
+- Play media Echocardiogram showing atrial myxoma
+- Echocardiogram showing atrial myxoma.
+- Atrial myxoma and myocardium. H
+- E stain.
+- Atrial myxoma. H
+- E stain.
+- Atrial myxoma. H
+- E stain.
+- Atrial myxoma covered by endothelium. H
+- E stain.
+Symptoms may occur at any time, but most often they accompany a change of body position. Pedunculated myxomas can have a "wrecking ball effect", as they lead to stasis and may eventually embolize themselves. Symptoms may include:
+- Shortness of breath with activity
+- Platypnea – Difficulty breathing in the upright position with relief in the supine position
+- Paroxysmal nocturnal dyspnea – Breathing difficulty when asleep
+- Dizziness
+- Fainting
+- Palpitations – Sensation of feeling your heart beat
+- Chest pain or tightness
+- Sudden Death (In which case the disease is an autopsy finding.
+The symptoms and signs of left atrial myxomas often mimic mitral stenosis. General symptoms may also be present, such as:
+- Cough
+- Pulmonary edema, as blood backs up into the pulmonary artery, after increased pressures in the left atrium and atrial dilation
+- Hemoptysis
+- Fever
+- Cachexia – Involuntary weight loss
+- General discomfort (malaise)
+- Joint pain
+- Blue discoloration of the skin, especially the fingers (Raynaud's phenomenon)
+- Fingers that change color upon pressure or with cold or stress
+- Clubbing – Curvature of nails accompanied with soft tissue enlargement of the fingers
+- Swelling – any part of the body
+- Presystolic heart murmur.
+These general symptoms may also mimic those of infective endocarditis.
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DISNET disease texts/100 Clean Disease Texts/Carrion's disease.txt

+Carrion's disease is caused by Bartonella bacilliformis. Recent investigations show that Candidatus Bartonella ancashi may cause verruga peruana, although it may not meet all of Koch's postulates. There has been no experimental reproduction of the Peruvian wart in animals and there is little research on the disease's natural spread or impact in native animals.
+Diagnosis during the acute phase can be made by obtaining a peripheral blood smear with Giemsa stain, Columbia blood agar cultures, immunoblot, indirect immunofluorescence, and PCR. Diagnosis during the chronic phase can be made using a Warthin-Starry stain of wart biopsy, PCR, and immunoblot.
+The clinical symptoms of bartonellosis are pleomorphic and some patients from endemic areas may be asymptomatic. The two classical clinical presentations are the acute phase and the chronic phase, corresponding to the two different host cell types invaded by the bacterium (red blood cells and endothelial cells). An individual can be affected by either or both phases.
+Acute phase => It is also called the hematic phase. The most common findings are fever (usually sustained, but with temperature no greater than 102 °F (39 °C)), pale appearance, malaise, painless liver enlargement, jaundice, enlarged lymph nodes, and enlarged spleen. This phase is characterized by severe hemolytic anemia and transient immunosuppression. The case fatality ratios of untreated patients exceeded 40% but reach around 90% when opportunistic infection with Salmonella spp occurs. In a recent study, the attack rate was 13.8% (123 cases) and the case-fatality rate was 0.7%.
+Other symptoms include a headache, muscle aches, and general abdominal pain. Some studies have suggested a link between Carrion's disease and heart murmurs due to the disease's impact on the circulatory system. In children, symptoms of anorexia, nausea, and vomiting have been investigated as possible symptoms of the disease.
+Most of the mortality of Carrion's disease occurs during the acute phase. Studies vary in their estimates of mortality. In one study, mortality has been estimated as low as just 1% in studies of hospitalized patients, to as high as 88% in untreated, unhospitalized patients. In developed countries, where the disease rarely occurs, it is recommended to seek the advice of a specialist in infectious disease when diagnosed. Mortality is often thought to be due to subsequent infections due to the weakened immune symptoms and opportunistic pathogen invasion, or consequences of malnutrition due to weight loss in children. In a study focusing on pediatric and gestational effects of the disease, mortality rates for pregnant women with the acute phase were been estimated at 40% and rates of spontaneous abortion in another 40%.
+Chronic phase => It is also called the eruptive phase or tissue phase, in which the patients develop a cutaneous rash produced by a proliferation of endothelial cells and is known as "Peruvian warts" or "verruga peruana". Depending on the size and characteristics of the lesions, there are three types: miliary (1–4 mm), nodular or subdermic, and mular (>5mm). Miliary lesions are the most common. The lesions often ulcerate and bleed.
+The most common findings are bleeding of verrugas, fever, malaise, arthralgias (joint pain), anorexia, myalgias, pallor, lymphadenopathy, and liver and spleen enlargement.
+On microscopic examination, the chronic phase and its rash are produced by angioblastic hyperplasia, or the increased rates and volume of cell growth in the tissues that form blood vessels. This results in a loss of contact between cells and a loss of normal functioning.
+The chronic phase is the more common phase. Mortality during the chronic phase is very low.
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DISNET disease texts/100 Clean Disease Texts/Cerebral salt-wasting syndrome.txt

+Signs and symptoms of CSWS include large amounts of urination (at least 3 liters of urine output over a 24-hour period for adults) due to inadequate sodium retention in the body, high amounts of sodium in the urine, low blood sodium concentration, excessive thirst, extreme salt cravings, dysfunction of the autonomic nervous system, and dehydration. Patients often self-medicate by naturally gravitating toward a high-sodium diet and by dramatically increasing their water intake. Advanced symptoms include muscle cramps, lightheadedness, dizziness or vertigo, feelings of anxiety or panic (not mentally induced), increased heart rate or slowed heart rate, low blood pressure and orthostatic hypotension sometimes resulting in fainting. Other symptoms frequently associated with dysautonomia include: headaches, pallor, malaise, facial flushing, constipation or diarrhea, nausea, acid reflux, visual disturbances, numbness, nerve pain, trouble breathing, chest pains, loss of consciousness and seizures.
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DISNET disease texts/100 Clean Disease Texts/Cerebrovascular disease.txt

+Congenital => Congenital diseases are medical conditions that are present at birth that may be associated with inherited through genes. Examples of congenital cerebrovascular diseases include arteriovenous malformations, germinal matrix hemorrhage, and CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy). Arteriovenous malformations are abnormal tangles of blood vessels. Usually, a capillary bed separates arteries from veins, which protects the veins from the higher blood pressures that occur in arteries. In arteriovenous malformations, arteries are directly connected to veins, which increases the risk of venous rupture and hemorrhage. Arteriovenous malformations in the brain have a 2–4% chance of rupture each year. However, many arteriovenous malformations go unnoticed and are asymptomatic throughout a person's lifetime.
+A germinal matrix hemorrhage is bleeding into the brain of premature infants caused by the rupture of fragile blood vessels within the germinal matrix of premature babies. The germinal matrix is a highly vascularized area within an unborn infant's brain from which brain cells, including neurons and glial cells, originate. Infants are at most risk to germinal matrix hemorrhages when they are born prematurely, before 32 weeks. The stresses exposed after birth, along with the fragile blood vessels, increase the risk for hemorrhage. Signs and symptoms include flaccid weakness, seizures, abnormal posturing, or irregular respiration.
+CADASIL is an inherited disorder caused by mutations in the Notch 3 gene located on chromosome 19. The Notch 3 gene codes for a transmembrane protein whose function is not well-known. However, the mutation causes accumulation of this protein within small to medium-sized blood vessels. This disease often presents in early adulthood with migraines, stroke, mood disturbances, and cognitive deterioration. MRI shows white matter changes in the brain and also signs of repeated strokes. The diagnosis can be confirmed by gene testing.
+Acquired => Acquired cerebrovascular diseases are those that are obtained throughout a person's life that may be preventable by controlling risk factors. The incidence of cerebrovascular disease increases as an individual ages. Causes of acquired cerebrovascular disease include atherosclerosis, embolism, aneurysms, and arterial dissections. Atherosclerosis leads to narrowing of blood vessels and less perfusion to the brain, and it also increases the risk of thrombosis, or a blockage of an artery, within the brain. Major modifiable risk factors for atherosclerosis include:
+- Hypertension
+- Smoking
+- Obesity
+- Diabetes.
+Controlling these risk factors can reduce the incidence of atherosclerosis and stroke. Atrial fibrillation is also a major risk factor for strokes. Atrial fibrillation causes blood clots to form within the heart, which may travel to the arteries within the brain and cause an embolism. The embolism prevents blood flow to the brain, which leads to a stroke.
+An aneurysm is an abnormal bulging of small sections of arteries, which increases the risk of artery rupture. Intracranial aneurysms are a leading cause of subarachnoid hemorrhage, or bleeding around the brain within the subarachnoid space. There are various hereditary disorders associated with intracranial aneurysms, such as Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, and familial hyperaldosteronism type I. However, individuals without these disorders may also obtain aneurysms. The American Heart Association and American Stroke Association recommend controlling modifiable risk factors including smoking and hypertension.
+Arterial dissections are tears of the internal lining of arteries, often associated with trauma. Dissections within the carotid arteries or vertebral arteries may compromise blood flow to the brain due to thrombosis, and dissections increase the risk of vessel rupture.
+Idiopathic => Idiopathic diseases are those that occur spontaneously without a known cause. Moyamoya is an example of an idiopathic cerebrovascular disorder that results in narrowing and occlusion of intracranial blood vessels. The most common presentation is stroke or transient ischemic attack, but cognitive decline within children may also be a presenting symptom. The disease may begin to show symptoms beginning in adolescence, but some may not have symptoms until adulthood.
+The most common presentation of cerebrovascular diseases is an acute stroke, which occurs when blood supply to the brain is compromised. Symptoms of stroke are usually rapid in onset, and may include weakness of one side of the face or body, numbness on one side of the face or body, inability to produce or understand speech, vision changes, and balance difficulties. Hemorrhagic strokes can present with a very severe, sudden headache associated with vomiting, neck stiffness, and decreased consciousness. Symptoms vary depending on the location and the size of the area of involvement of the stroke. Edema, or swelling, of the brain may occur which increases intracranial pressure and may result in brain herniation. A stroke may result in coma or death if it involves key areas of the brain.
+Other symptoms of cerebrovascular disease include migraines, seizures, epilepsy, or cognitive decline. However, cerebrovascular disease may go undetected for years until an acute stroke occurs. In addition, patients with some rare congenital cerebrovascular diseases may begin to have these symptoms in childhood.
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DISNET disease texts/100 Clean Disease Texts/Chlamydia infection.txt

+The diagnosis of genital chlamydial infections evolved rapidly from the 1990s through 2006. Nucleic acid amplification tests (NAAT), such as polymerase chain reaction (PCR), transcription mediated amplification (TMA), and the DNA strand displacement amplification (SDA) now are the mainstays. NAAT for chlamydia may be performed on swab specimens sampled from the cervix (women) or urethra (men), on self-collected vaginal swabs, or on voided urine. NAAT has been estimated to have a sensitivity of approximately 90% and a specificity of approximately 99%, regardless of sampling from a cervical swab or by urine specimen. In women seeking an STI clinic and a urine test is negative, a subsequent cervical swab has been estimated to be positive in approximately 2% of the time.
+At present, the NAATs have regulatory approval only for testing urogenital specimens, although rapidly evolving research indicates that they may give reliable results on rectal specimens.
+Because of improved test accuracy, ease of specimen management, convenience in specimen management, and ease of screening sexually active men and women, the NAATs have largely replaced culture, the historic gold standard for chlamydia diagnosis, and the non-amplified probe tests. The latter test is relatively insensitive, successfully detecting only 60–80% of infections in asymptomatic women, and often giving falsely positive results. Culture remains useful in selected circumstances and is currently the only assay approved for testing non-genital specimens. Other method also exist including: ligase chain reaction (LCR), direct fluorescent antibody resting, enzyme immunoassay, and cell culture.
+Women => Chlamydial infection of the cervix (neck of the womb) is a sexually transmitted infection which has no symptoms for 50–70% of women infected. The infection can be passed through vaginal, anal, or oral sex. Of those who have an asymptomatic infection that is not detected by their doctor, approximately half will develop pelvic inflammatory disease (PID), a generic term for infection of the uterus, fallopian tubes, and/or ovaries. PID can cause scarring inside the reproductive organs, which can later cause serious complications, including chronic pelvic pain, difficulty becoming pregnant, ectopic (tubal) pregnancy, and other dangerous complications of pregnancy.
+Chlamydia is known as the "silent epidemic" as in women, it may not cause any symptoms in 70–80% of cases, and can linger for months or years before being discovered. Signs and symptoms may include abnormal vaginal bleeding or discharge, abdominal pain, painful sexual intercourse, fever, painful urination or the urge to urinate more often than usual (urinary urgency).
+For sexually active women who are not pregnant, screening is recommended in those under 25 and others at risk of infection. Risk factors include a history of chlamydial or other sexually transmitted infection, new or multiple sexual partners, and inconsistent condom use. Guidelines recommend all women attending for emergency contraceptive are offered Chlamydia testing, with studies showing up to 9% of women aged <25 years had Chlamydia.
+Men => In men, those with a chlamydial infection show symptoms of infectious inflammation of the urethra in about 50% of cases. Symptoms that may occur include: a painful or burning sensation when urinating, an unusual discharge from the penis, testicular pain or swelling, or fever. If left untreated, chlamydia in men can spread to the testicles causing epididymitis, which in rare cases can lead to sterility if not treated. Chlamydia is also a potential cause of prostatic inflammation in men, although the exact relevance in prostatitis is difficult to ascertain due to possible contamination from urethritis.
+Chlamydia conjunctivitis or trachoma was once the most important cause of blindness worldwide, but its role diminished from 15% of blindness cases by trachoma in 1995 to 3.6% in 2002. The infection can be spread from eye to eye by fingers, shared towels or cloths, coughing and sneezing and eye-seeking flies. Newborns can also develop chlamydia eye infection through childbirth (see below). Using the SAFE strategy (acronym for surgery for in-growing or in-turned lashes, antibiotics, facial cleanliness, and environmental improvements), the World Health Organization aims for the global elimination of trachoma by 2020 (GET 2020 initiative).
+Joints => Chlamydia may also cause reactive arthritis—the triad of arthritis, conjunctivitis and urethral inflammation—especially in young men. About 15,000 men develop reactive arthritis due to chlamydia infection each year in the U. S., and about 5,000 are permanently affected by it. It can occur in both sexes, though is more common in men.
+Infants => As many as half of all infants born to mothers with chlamydia will be born with the disease. Chlamydia can affect infants by causing spontaneous abortion; premature birth; conjunctivitis, which may lead to blindness; and pneumonia. Conjunctivitis due to chlamydia typically occurs one week after birth (compared with chemical causes (within hours) or gonorrhea (2–5 days)).
+Other conditions => A different serovar of Chlamydia trachomatis is also the cause of lymphogranuloma venereum, an infection of the lymph nodes and lymphatics. It usually presents with genital ulceration and swollen lymph nodes in the groin, but it may also manifest as rectal inflammation, fever or swollen lymph nodes in other regions of the body.
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DISNET disease texts/100 Clean Disease Texts/Cholesterol embolism.txt

+It is relatively unusual (25% of the total number of cases) for cholesterol emboli to occur spontaneously; this usually happens in people with severe atherosclerosis of the large arteries such as the aorta. In the other 75% it is a complication of medical procedures involving the blood vessels, such as vascular surgery or angiography. In coronary catheterization, for instance, the incidence is 1.4%. Furthermore, cholesterol embolism may develop after the commencement of anticoagulants or thrombolytic medication that decrease blood clotting or dissolve blood clots, respectively. They probably lead to cholesterol emboli by removing blood clots that cover up a damaged atherosclerotic plaque; cholesterol-rich debris can then enter the bloodsteam.
+Differential diagnosis => Findings on general investigations (such as blood tests) are not specific for cholesterol embolism, which makes diagnosis difficult. The main problem is the distinction between cholesterol embolism and vasculitis (inflammation of the small blood vessels), which may cause very similar symptoms-especially the skin findings and the kidney dysfunction. Worsening kidney function after an angiogram may also be attributed to kidney damage by substances used during the procedure (contrast nephropathy). Other causes that may lead to similar symptoms include ischemic renal failure (kidney dysfunction due to an interrupted blood supply), a group of diseases known as thrombotic microangiopathies and endocarditis (infection of the heart valves with small clumps of infected tissue embolizing through the body).
+Blood and urine => Tests for inflammation (C-reactive protein and the erythrocyte sedimentation rate) are typically elevated, and abnormal liver enzymes may be seen. If the kidneys are involved, tests of renal function (such as urea and creatinine) are elevated. The complete blood count may show particularly high numbers of a type of white blood cell known as eosinophils (more than 0.5 billion per liter); this occurs in only 60 – 80% of cases, so normal eosinophil counts do not rule out the diagnosis. Examination of the urine may show red blood cells (occasionally in casts as seen under the microscope) and increased levels of protein; in a third of the cases with kidney involvement, eosinophils can also be detected in the urine. If vasculitis is suspected, complement levels may be determined as reduced levels are often encountered in vasculitis; complement is a group of proteins that forms part of the innate immune system. Complement levels are frequently reduced in cholesterol embolism, limiting the use of this test in the distinction between vasculitis and cholesterol embolism.
+Tissue diagnosis => The microscopic examination of tissue (histology) gives the definitive diagnosis. The diagnostic histopathologic finding is intravascular cholesterol crystals, which are seen as cholesterol clefts in routinely processed tissue (embedded in paraffin wax). The cholesterol crystals may be associated with macrophages, including giant cells, and eosinophils.
+The sensitivity of small core biopsies is modest, due to sampling error, as the process is often patchy. Affected organs show the characteristic histologic changes in 50 – 75% of the clinically diagnosed cases. Non-specific tissue findings suggestive of a cholesterol embolization include ischemic changes, necrosis and unstable-appearing complex atherosclerotic plaques (that are cholesterol-laden and have a thin fibrous cap). While biopsy findings may not be diagnostic, they have significant value, as they help exclude alternate diagnoses, e. G. Vasculitis, that often cannot be made confidently based on clinical criteria.
+The symptoms experienced in cholesterol embolism depend largely on the organ involved. Non-specific symptoms often described are fever, muscle ache and weight loss. Embolism to the legs causes a mottled appearance and purple discoloration of the toes, small infarcts and areas of gangrene due to tissue death that usually appear black, and areas of the skin that assume a marbled pattern known as livedo reticularis. The pain is usually severe and requires opiates. If the ulcerated plaque is below the renal arteries the manifestations appear in both lower extremities. Very rarely the ulcerated plaque is below the aortic bifurcation and those cases the changes occur only in one lower extremity.
+Kidney involvement leads to the symptoms of renal failure, which are non-specific but usually cause nausea, reduced appetite (anorexia), raised blood pressure (hypertension), and occasionally the various symptoms of electrolyte disturbance such as an irregular heartbeat. Some patients report hematuria (bloody urine) but this may only be detectable on microscopic examination of the urine. Increased amounts of protein in the urine may cause edema (swelling) of the skin (a combination of symptoms known as nephrotic syndrome).
+If emboli have spread to the digestive tract, reduced appetite, nausea and vomiting may occur, as well as nonspecific abdominal pain, gastrointestinal hemorrhage (vomiting blood, or admixture of blood in the stool), and occasionally acute pancreatitis (inflammation of the pancreas).
+Both the central nervous system (brain and spinal cord) and the peripheral nervous system may be involved. Emboli to the brain may cause stroke-like episodes, headache and episodes of loss of vision in one eye (known as amaurosis fugax). Emboli to the eye can be seen by ophthalmoscopy and are known as plaques of Hollenhorst. Emboli to the spinal cord may cause paraparesis (decreased power in the legs) or cauda equina syndrome, a group of symptoms due to loss of function of the distal part of the spinal cord-loss of control over the bladder, rectum and skin sensation around the anus. If the blood supply to a single nerve is interrupted by an embolus, the result is loss of function in the muscles supplied by that nerve; this phenomenon is called a mononeuropathy.
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DISNET disease texts/100 Clean Disease Texts/Coccidioidomycosis.txt

+It must rain first to start the cycle of initial growth of the fungus underneath the soil. In soil (and in agar media), Coccidioides exist in filament form. It forms hyphae in both horizontal and vertical directions. Over a prolonged dry period, cells within hyphae degenerate to form alternating barrel-shaped cells (arthroconidia). Arthroconidia are light-weight and carried by air currents. This happens when the soil is disturbed often by clearing trees, construction and farming. As the population grows, so have all these industries, causing a potential cascade effect. The more land that is cleared, the more arid the soil, the riper the environment for Coccidioides. These spores can be easily inhaled without the person knowing. On arriving in alveoli, they enlarge in size to become spherules, and internal septations develop. This division of cells is made possible by the optimal temperature inside the body. Septations develop and form endospores within the spherule. Rupture of spherules release these endospores, which in turn repeat the cycle and spread the infection to adjacent tissues within the body of the infected individual. Nodules can form in lungs surrounding these spherules. When they rupture, they release their contents into bronchi, forming thin-walled cavities. These cavities can result in symptoms like characteristic chest pain, coughing up blood, and persistent cough. In individuals with a weakened immune system, the infection can spread through the blood. On rare occasion it can enter the body through a break in the skin, causing infection.
+Coccidioidomycosis diagnosis relies on a combination of an infected person's signs and symptoms, findings on radiographic imaging, and laboratory results. The disease is commonly misdiagnosed as bacterial community-acquired pneumonia. The fungal infection can be demonstrated by microscopic detection of diagnostic cells in body fluids, exudates, sputum and biopsy tissue by methods of Papanicolaou or Grocott's methenamine silver staining. These stains can demonstrate spherules and surrounding inflammation.
+With specific nucleotide primers, C. Immitis DNA can be amplified by polymerase chain reaction (PCR). It can also be detected in culture by morphological identification or by using molecular probes that hybridize with C. Immitis RNA. C. Immitis and C. Posadasii cannot be distinguished on cytology or by symptoms, but only by DNA PCR.
+An indirect demonstration of fungal infection can be achieved also by serologic analysis detecting fungal antigen or host IgM or IgG antibody produced against the fungus. The available tests include the tube-precipitin (TP) assays, complement fixation assays, and enzyme immunoassays. TP antibody is not found in cerebrospinal fluid (CSF). TP antibody is specific and is used as a confirmatory test, whereas ELISA is sensitive and thus used for initial testing.
+If the meninges are affected, CSF will show abnormally low glucose levels in CSF, an increased level of protein in the CSF, and lymphocytic pleocytosis. Rarely, CSF eosinophilia is present.
+Imaging => Chest x-rays rarely demonstrate nodules or cavities in the lungs, but these images commonly demonstrate lung opacification, pleural effusions, or enlargement of lymph nodes associated with the lungs. Computed tomography scans of the chest are better able to detect these changes than chest x-rays.
+An estimated 60% of people infected with the fungi responsible for coccidioidomycosis have minimal to no symptoms, while 40% will have a range of possible clinical symptoms. Of those who do develop symptoms, the primary infection is most often respiratory, with symptoms resembling bronchitis or pneumonia that resolve over a matter of a few weeks. In endemic regions, coccidioidomycosis is responsible for 20% of cases of community-acquired pneumonia. Notable coccidioidomycosis signs and symptoms include a profound feeling of tiredness, fever, cough, headaches, rash, muscle pain, and joint pain. Fatigue can persist for many months after initial infection. The classic triad of coccidioidomycosis known as "desert rheumatism" includes the combination of fever, joint pains, and erythema nodosum.
+Nearly 3% to 5% of infected individuals do not recover from the initial acute infection and develop a chronic infection. This can take the form of chronic lung infection or widespread disseminated infection (affecting the tissues lining the brain, soft tissues, joints, and bone). Chronic infection is responsible for most of the morbidity and mortality. Chronic fibrocavitary disease is manifested by cough, sputum, fevers, night sweats and weight loss. Osteomyelitis, including involvement of the spine, and meningitis which may occur months to years after initial infection. Severe lung disease may develop in HIV-infected persons.
+Types => After Coccidioides infection, coccidioidomycosis begins with Valley fever, which is its initial acute form. Valley fever may progress to the chronic form and then to disseminated coccidioidomycosis. Therefore, Coccidioidomycosis may be divided into the following types:
+Complications => Serious complications may occur in patients who have weakened immune systems, including severe pneumonia with respiratory failure and bronchopleural fistulas requiring resection, lung nodules, and possible disseminated form, where the infection spreads throughout the body. The disseminated form of coccidioidomycosis can devastate the body, causing skin ulcers, abscesses, bone lesions, swollen joints with severe pain, heart inflammation, urinary tract problems, and inflammation of the brain's lining, which can lead to death.
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DISNET disease texts/100 Clean Disease Texts/Conversion disorder.txt

+Exclusion of neurological disease => Conversion disorder presents with symptoms that typically resemble a neurological disorder such as stroke, multiple sclerosis, epilepsy or hypokalemic periodic paralysis. The neurologist must carefully exclude neurological disease, through examination and appropriate investigations. However, it is not uncommon for patients with neurological disease to also have conversion disorder.
+In excluding neurological disease, the neurologist has traditionally relied partly on the presence of positive signs of conversion disorder, i.e. Certain aspects of the presentation that were thought to be rare in neurological disease but common in conversion. The validity of many of these signs has been questioned, however, by a study showing that they also occur in neurological disease. One such symptom, for example, is la belle indifférence, described in DSM-IV as "a relative lack of concern about the nature or implications of the symptoms". In a later study, no evidence was found that patients with functional symptoms are any more likely to exhibit this than patients with a confirmed organic disease. In DSM-V, la belle indifférence was removed as a diagnostic criteria.
+Another feature thought to be important was that symptoms tended to be more severe on the non-dominant (usually left) side of the body. There have been a number of theories about this, such as the relative involvement of cerebral hemispheres in emotional processing, or more simply, that it was "easier" to live with a functional deficit on the non-dominant side. However, a literature review of 121 studies established that this was not true, with publication bias the most likely explanation for this commonly held view. Although agitation is often assumed to be a positive sign of conversion disorder, release of epinephrine is a well-demonstrated cause of paralysis from hypokalemic periodic paralysis.
+Misdiagnosis does sometimes occur. In a highly influential study from the 1960s, Eliot Slater demonstrated that misdiagnoses had occurred in one third of his 112 patients with conversion disorder. Later authors have argued that the paper was flawed, however, and a meta-analysis has shown that misdiagnosis rates since that paper was published are around 4%, the same as for other neurological diseases.
+Exclusion of feigning => Conversion disorder is unique in ICD-10 in explicitly requiring the exclusion of deliberate feigning. Unfortunately, this is likely to be demonstrable only where the patient confesses, or is "caught out" in a broader deception, such as a false identity. One neuroimaging study suggested that feigning may be distinguished from conversion by the pattern of frontal lobe activation; however, this was a piece of research, rather than a clinical technique. True rates of feigning in medicine remain unknown. However, it is believed that feigning of conversion disorder is no more likely than of other medical conditions.
+Psychological mechanism => The psychological mechanism of conversion can be the most difficult aspect of a conversion diagnosis. Even if there is a clear antecedent trauma or other possible psychological trigger, it is still not clear exactly how this gives rise to the symptoms observed. Patients with medically unexplained neurological symptoms may not have any psychological stressor, hence the use of the term "functional neurological symptom disorder" in DSM-V as opposed to "conversion disorder", and DSM-V's removal of the need for a psychological trigger.
+Conversion disorder begins with some stressor, trauma, or psychological distress. Usually the physical symptoms of the syndrome affect the senses or movement. Common symptoms include blindness, partial or total paralysis, inability to speak, deafness, numbness, difficulty swallowing, incontinence, balance problems, seizures, tremors, and difficulty walking. These symptoms are attributed to conversion disorder when a medical explanation for the afflictions cannot be found. Symptoms of conversion disorder usually occur suddenly. Conversion disorder is typically seen in individuals aged 10 to 35, and affects between 0.011% and 0.5% of the general population.
+Conversion disorder can present with motor or sensory symptoms including any of the following:
+Motor symptoms or deficits:
+- Impaired coordination or balance
+- Weakness/paralysis of a limb or the entire body (hysterical paralysis or motor conversion disorders)
+- Impairment or loss of speech (hysterical aphonia)
+- Difficulty swallowing (dysphagia) or a sensation of a lump in the throat
+- Urinary retention
+- Psychogenic non-epileptic seizures or convulsions
+- Persistent dystonia
+- Tremor, myoclonus or other movement disorders
+- Gait problems (astasia-abasia)
+- Loss of consciousness (fainting.
+Sensory symptoms or deficits:
+- Impaired vision (hysterical blindness), double vision
+- Impaired hearing (deafness)
+- Loss or disturbance of touch or pain sensatio.
+Conversion symptoms typically do not conform to known anatomical pathways and physiological mechanisms. It has sometimes been stated that the presenting symptoms tend to reflect the patient's own understanding of anatomy and that the less medical knowledge a person has, the more implausible are the presenting symptoms. However, no systematic studies have yet been performed to substantiate this statement.
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DISNET disease texts/100 Clean Disease Texts/Cryoglobulinemia.txt

+Cryoglobulinemia and cryoglobulinemic disease must be distinguished from cryofibrinogenemia or cryofibrinogenemic disease, conditions which involve the cold-induced intravascular deposition of circulating native fibrinogens. The cryoglobulins in plasma or serum precipitate at lower temperatures (e. G. 4°C). Since cryofibrinogens are present in plasma but greatly depleted in serum, precipitation tests for them are positive in plasma but negative in serum. Cryofibrinogenemia is occasionally found in cases of cryoglobulinemic disease. Cryoglobulinemic disease must also be distinguished from frostbite as well as numerous other conditions that have a clinical (particularly cutaneous) presentation similar to cryoglobulinemic disease but are not exacerbated by cold temperature, e. G. Dysfibrinogenemia and dysfibrinogenemic disease (conditions involving the intravascular deposition of genetically abnormal circulating fibrinogens), purpura fulminans, cholesterol emboli, warfarin necrosis, ecthyma gangrenosum, and various hypercoagulable states.
+Rheumatoid factor is a sensitive test for cryoglobulinemia. The precipitated cryoglobulins are examined by immunoelectrophoresis and immunofixation to detect and quantify the presence of monoclonal IgG, IgM, IgA, κ light chain, or λ light chain immunoglobins. Other routine tests include measuring blood levels of rheumatoid factor activity, complement C4, other complement components, and hepatitic C antigen. Biopsies of skin lesions and, where indicated, kidney or other tissues can help in determining the nature of the vascular disease (immunoglobulin deposition, cryoglobulinemic vasculitis, or, in cases showing the presence of cryfibrinogenemia, fibrinogen deposition. In all events, further studies to determine the presence of hematological, infections, and autoimmune disorders are conducted on the basis of these findings as well as each cases clinical findings.
+The clinical features of cryoglobulinemic disease can reflect those due not only to the circulation of cryoglobulins but also to any underlying hematological premalignant or malignant disorder, infectious disease, or autoimmune syndrome. The following sections of clinical features focuses on those attributed to the cryoglobulins. Cryoglobulins cause tissue damage by three mechanisms; they can: a) increase blood viscosity thereby reducing blood flow to tissues to cause the hyperviscosity syndrome (i.e. Headache, confusion, blurry or loss of vision, hearing loss, and epistaxis; b) deposit in small arteries and capillaries thereby plugging these blood vessels and causing infarction and necrosis of tissues including in particular skin, distal extremities, and kidneys; and c) in type II and type III disease, deposit on the epithelium of blood vessels and activate the blood complement system to form pro-inflammatory elements such as C5a thereby initiating the systemic vascular inflammatory reaction termed cryoglobulinemic vasculitis.
+Essential cryoglobulinemic disease => The signs and symptoms in the increasingly rare cases of cryoglobulinemic disease that cannot be attributed to an underlying disease generally resemble those of patients suffering Type II and III (i.e. Mixed) cryoglobulinemic disease.
+Type I cryoglobulinemic disease => Signs and symptoms due to the cryoglobulins of type I disease reflect the hyperviscosity and deposition of cryoglobulins within the blood vessels which reduce or stop blood perfusion to tissues. These events occur particularly in cases where blood cryoglobulin levels of monoclonal IgM are high in patients with IgM MGUS, smoldering Waldenström's macroglobulinemia, or Waldenström's macroglobulinemia and in uncommon cases where the levels of monoclonal IgA, IgG, free κ light chains, or free λ light chains are extremely high in patients with non-IgM MGUS, non-IgM smoldering multiple myeloma, or multiple myeloma. The interruption of blood flow to neurological tissues can cause symptoms of confusion, headache, hearing loss, and peripheral neuropathy. Interruption of blood flow to other tissues in type I disease can cause cutaneous manifestations of purpura, acrocyanosis, necrosis, ulcers, and livedo reticularis; spontaneous nose bleeds, joint pain, membranoproliferative glomerulonephritis; and cardiovascular disturbances such as shortness of breath, hypoxemia, and congestive heart failure.
+Types II and III cryoglobulinemic disease => Types II and III (or mixed or variant) cryoglobulinemic disease may also present with symptoms and signs of blood hyperviscosity and intravascular cryoglobulin deposition but also include those attributable to cryoglobulinemic vasculitis. "Meltzer's triad" of palpable purpura, joint pain, and generalized weakness occurs in ~33% of patients presenting with type II or type III disease. One or more skin lesions including palpable purpura, ulcers, digital gangrene, and areas of necrosis occur in 69 – 89% of these mixed disease cases (see attached photograph); less common findings include painful peripheral neuropathy (19 – 44% of cases), kidney disease (primarily membranoproliferative glomerulonephritis (30%), joint pain (28%), and, less commonly, dry eye syndrome, Raynaud phenomenon (i.e. Episodic painful reductions in blood flow to the fingers and toes). While the glomerulonephritis occurring in mixed disease appears to be due to inflammatory vasculitis, the glomerulonephritis occurring in type I disease appears due to the interruption of blood flow. The hematological, infectious, and autoimmune diseases underlying type II cryoglobulinemic disease and the infectious and autoimmune diseases underlying type III cryoglobulinemic disease are also critical parts of the disease's clinical findings.
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DISNET disease texts/100 Clean Disease Texts/Diphtheria.txt

+The current clinical case definition of diphtheria used by the United States' Centers for Disease Control and Prevention is based on both laboratory and clinical criteria.
+- Laboratory criteria => Isolation of C. Diphtheriae from a Gram stain or throat culture from a clinical specimen,
+- Histopathologic diagnosis of diphtheria by Albert's stai.
+- Clinical criteria => Upper respiratory tract illness with sore throat
+- Low-grade fever (above 39 °C (102 °F) is rare)
+- An adherent, dense, grey pseudomembrane covering the posterior aspect of the pharynx: in severe cases, it can extend to cover the entire tracheobronchial tree.
+- Case classification => Probable: a clinically compatible case that is not laboratory-confirmed and is not epidemiologically linked to a laboratory-confirmed case
+- Confirmed: a clinically compatible case that is either laboratory-confirmed or epidemiologically linked to a laboratory-confirmed cas.
+Empirical treatment should generally be started in a patient in whom suspicion of diphtheria is high.
+The symptoms of diphtheria usually begin two to seven days after infection. Symptoms of diphtheria include fever of 38 °C (100.4 °F) or above, chills, fatigue, bluish skin coloration (cyanosis), sore throat, hoarseness, cough, headache, difficulty swallowing, painful swallowing, difficulty breathing, rapid breathing, foul-smelling and bloodstained nasal discharge, and lymphadenopathy. Within two to three days, diphtheria may destroy healthy tissues in the respiratory system. The dead tissue forms a thick, gray coating that can build up in the throat or nose. This thick gray coating is called a “pseudomembrane. ” It can cover tissues in the nose, tonsils, voice box, and throat, making it very hard to breathe and swallow. Symptoms can also include cardiac arrhythmias, myocarditis, and cranial and peripheral nerve palsies.
+Diphtheritic croup => Laryngeal diphtheria can lead to a characteristic swollen neck and throat, or "bull neck". The swollen throat is often accompanied by a serious respiratory condition, characterized by a brassy or "barking" cough, stridor, hoarseness, and difficulty breathing, and historically referred to variously as "diphtheritic croup", "true croup", or sometimes simply as "croup". Diphtheritic croup is extremely rare in countries where diphtheria vaccination is customary. As a result, the term "croup" nowadays most often refers to an unrelated viral illness that produces similar but milder respiratory symptoms.
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DISNET disease texts/100 Clean Disease Texts/Erysipelas.txt

+Most cases of erysipelas are due to Streptococcus pyogenes (also known as beta-hemolytic group A streptococci), although non-group A streptococci can also be the causative agent. Beta-hemolytic, non-group A streptococci include Streptococcus agalactiae, also known as group B strep or GBS. Historically, the face was most affected; today, the legs are affected most often. The rash is due to an exotoxin, not the Streptococcus bacteria, and is found in areas where no symptoms are present; e. G., the infection may be in the nasopharynx, but the rash is found usually on the upper dermis and superficial lymphatics.
+Erysipelas infections can enter the skin through minor trauma, insect bites, dog bites, eczema, athlete's foot, surgical incisions and ulcers and often originate from streptococci bacteria in the subject's own nasal passages. Infection sets in after a small scratch or abrasion spreads, resulting in toxaemia.
+Erysipelas does not affect subcutaneous tissue. It does not release pus, only serum or serous fluid. Subcutaneous edema may lead the physician to misdiagnose it as cellulitis, but the style of the rash is much more well circumscribed and sharply marginated than the rash of cellulitis.
+Risk factors => This disease is most common among the elderly, infants, and children. People with immune deficiency, diabetes, alcoholism, skin ulceration, fungal infections, and impaired lymphatic drainage (e. G., after mastectomy, pelvic surgery, bypass grafting) are also at increased risk.
+This disease is diagnosed mainly by the appearance of well-demarcated rash and inflammation. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erysipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast.
+Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titer occurs after around 10 days of illness.
+Affected individuals typically develop symptoms including high fevers, shaking, chills, fatigue, headaches, vomiting, and general illness within 48 hours of the initial infection. The erythematous skin lesion enlarges rapidly and has a sharply demarcated, raised edge. It appears as a red, swollen, warm, and painful rash, similar in consistency to an orange peel. More severe infections can result in vesicles (pox or insect bite-like marks), blisters, and petechiae (small purple or red spots), with possible skin necrosis (death). Lymph nodes may be swollen, and lymphedema may occur. Occasionally, a red streak extending to the lymph node can be seen.
+The infection may occur on any part of the skin, including the face, arms, fingers, legs, and toes; it tends to favour the extremities. Fat tissue and facial areas, typically around the eyes, ears, and cheeks, are most susceptible to infection. Repeated infection of the extremities can lead to chronic swelling (lymphangitis).
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DISNET disease texts/100 Clean Disease Texts/Erythema nodosum.txt

+EN is associated with a wide variety of conditions, including:
+In about 30–50% of cases, the cause of EN is unknown.
+- Streptococcal infection which, in children, is by far the most common precipitant,
+- Primary infection of Tuberculosis
+- Mycoplasma pneumoniae
+- Histoplasma capsulatum
+- Yersinia
+- Epstein-Barr virus
+- Coccidioides immitis (Valley fever)
+- Cat scratch diseas.
+- Inflammatory bowel disease (IBD)
+- Behçet's disease
+- Sarcoidosi.
+- Sulfonamides
+- Penicillins
+- Oral contraceptives
+- Bromides
+- Hepatitis B vaccination.
+- Non-Hodgkins lymphoma (NHL)
+- Carcinoid tumours
+- Pancreatic cance.
+EN may also be due to excessive antibody production in lepromatous leprosy leading to deposition of immune complexes.
+There is an association with the HLA-B27 histocompatibility antigen, which is present in 65% of patients with erythema nodosum.
+A useful mnemonic for causes is SORE SHINS (Streptococci, OCP, Rickettsia, Eponymous (Behçet), Sulfonamides, Hansen's Disease (Leprosy), IBD, NHL, Sarcoidosis.
+Erythema nodosum is diagnosed clinically. A biopsy can be taken and examined microscopically to confirm an uncertain diagnosis. Microscopic examination usually reveals a neutrophilic infiltrate surrounding capillaries that results in septal thickening, with fibrotic changes in the fat around blood vessels. A characteristic microscopic finding is radial granulomas, well-defined nodular aggregates of histiocytes surrounding a stellate cleft.
+Additional evaluation should be performed to determine the underlying cause of erythema nodosum. This may include a full blood count, erythrocyte sedimentation rate (ESR), antistreptolysin-O (ASO) titer and throat culture, urinalysis, intradermal tuberculin test, and a chest x-ray. The ESR is typically high, the C-reactive protein elevated, and the blood showing an increase in white blood cells.
+The ESR is initially very high, and falls as the nodules of erythema nodosum. The ASO titer is high in cases associated with a streptococcal throat infection. A chest X-ray should be performed to rule out pulmonary diseases, in particular sarcoidosis and Löfgren syndrome.
+Pre-eruptive phase => The first signs of erythema nodosum are often flu-like symptoms such as a fever, cough, malaise, and aching joints. Some people also experience stiffness or swelling in the joints and weight loss.
+Eruptive stage => Erythema nodosum is characterised by 1–2-inch (25–51 mm) nodules (rounded lumps) below the skin surface, usually on the shins. These subcutaneous nodules can appear anywhere on the body, but the most common sites are the shins, arms, thighs, and torso. Each nodule typically disappears after around two weeks, though new one may continue to form for up to six or eight weeks. A new nodule usually appears red and is hot and firm to touch. The redness starts to fade and it gradually becomes softer and smaller until it disappears. Each nodule usually heals completely without scarring over the course of about two weeks. Joint pain and inflammation sometimes continues for several weeks or months after the nodules appear.
+Less common variants of erythema nodosum include:
+- Ulcerating forms, seen in Crohn's disease
+- Erythema contusiforme, when a subcutaneous hemorrhage (bleeding under the skin) occurs with a erythema nodosum lesion, causing the lesion to look like a contusion (bruise)
+- Erythema nodosum migrans (also known as subacute nodular migratory panniculitis), a rare form of chronic erythema nodosum characterized by asymmetrical nodules that are mildly tender and migrate over time.
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DISNET disease texts/100 Clean Disease Texts/Ethylene glycol poisoning.txt

+As many of the clinical signs and symptoms of ethylene glycol poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult. It is most reliably diagnosed by the measurement of the blood ethylene glycol concentration. Ethylene glycol in biological fluids can be determined by gas chromatography. Many hospital laboratories do not have the ability to perform this blood test and in the absence of this test the diagnosis must be made based on the clinical presentation of the patient. In this situation a helpful test to diagnose poisoning is the measurement of the osmolal gap. The patients' serum osmolality is measured by freezing point depression and then compared with the predicted osmolality based on the patients' measured sodium, glucose, blood urea nitrogen, and any ethanol that may have been ingested. The presence of a large osmolal gap supports a diagnosis of ethylene glycol poisoning. However, a normal osmolar gap does not rule out ethylene glycol exposure because of wide individual variability.
+The increased osmolal gap is caused by the ethylene glycol itself. As the metabolism of ethylene glycol progresses there will be less ethylene glycol and this will decrease the blood ethylene glycol concentration and the osmolal gap making this test less useful. Additionally, the presence of other alcohols such as ethanol, isopropanol, or methanol or conditions such as alcoholic or diabetic ketoacidosis, lactic acidosis, or kidney failure may also produce an elevated osmolal gap leading to a false diagnosis.
+Other laboratory abnormalities may suggest poisoning, especially the presence of a metabolic acidosis, particularly if it is characterized by a large anion gap. Large anion gap acidosis is usually present during the initial stage of poisoning. However, acidosis has a large number of differential diagnosis, including poisoning from methanol, salicylates, iron, isoniazid, paracetamol, theophylline, or from conditions such as uremia or diabetic and alcoholic ketoacidosis. The diagnosis of ethylene glycol poisoning should be considered in any patient with a severe acidosis. Urine microscopy can reveal needle or envelope-shaped calcium oxalate crystals in the urine which can suggest poisoning; although these crystals may not be present until the late stages of poisoning. Finally, many commercial radiator antifreeze products have fluorescein added to enable radiator leaks to be detected using a Wood's lamp. Following ingestion of antifreeze products containing ethylene glycol and fluorescein, a Wood's lamp may reveal fluorescence of a patient’s mouth area, clothing, vomitus, or urine which can help to diagnose poisoning.
+Signs of ethylene glycol poisoning depend upon the time after ingestion. Symptoms usually follow a three-step progression, although poisoned individuals will not always develop each stage.
+- Stage 1 (30 minutes to 12 hours) consists of neurological and gastrointestinal symptoms and looks similar to alcohol poisoning. Poisoned individuals may appear to be intoxicated, dizzy, lacking coordination of muscle movements, drooling, depressed, and have slurred speech, seizuring, abnormal eye movements, headaches, and confusion. Irritation to the stomach may cause nausea and vomiting. Also seen are excessive thirst and urination. Over time, the body metabolizes ethylene glycol into other toxins.
+- Stage 2 (12 to 36 hours) where signs of "alcohol" poisoning appear to resolve, underlying severe internal damage is still occurring. An elevated heart rate, hyperventilation or increased breathing effort, and dehydration may start to develop, along with high blood pressure and metabolic acidosis. These symptoms are a result of accumulation of organic acids formed by the metabolism of ethylene glycol. Additionally low calcium concentrations in the blood, overactive muscle reflexes, muscle spasms, QT interval prolongation, and congestive heart failure may occur. If untreated, death most commonly occurs during this period.
+- Stage 3 (24 to 72 hours) kidney failure is the result of ethylene glycol poisoning. In cats, this stage occurs 12–24 hours after getting into antifreeze; in dogs, at 36–72 hours after getting into antifreeze. During this stage, severe kidney failure is developing secondary to calcium oxalate crystals forming in the kidneys. Severe lethargy, coma, depression, vomiting, seizures, drooling, and inappetance may be seen. Other symptoms include acute tubular necrosis, red blood cells in the urine, excess proteins in the urine, lower back pain, decreased or absent production of urine, elevated blood concentration of potassium, and acute kidney failure. If kidney failure occurs it is typically reversible, although weeks or months of supportive care including hemodialysis may be required before kidney function returns.
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DISNET disease texts/100 Clean Disease Texts/Felty's syndrome.txt

+The cause of Felty's syndrome is unknown, but it has been found to be more common in those with chronic rheumatoid arthritis. Some patients have Human Leukocytic Antigen (HLA-DR4) in their serum. This syndrome is mostly present in people having extra articular manifestations of rheumatoid arthritis. People with this syndrome are at risk of infection because they have a low white blood cell count.
+This condition affects less than 1% of patients with rheumatoid arthritis. The presence of three conditions: rheumatoid arthritis, an enlarged spleen (splenomegaly), and an abnormally low white blood cell count are indications that Felty's syndrome is possibly occurring. This condition as a whole is difficult to diagnose due to its complexity given a combination of disorders. It is commonly overlooked or misdiagnosed as other conditions (e. G., leukemia, systemic lupus erythrematosus) because of the rarity and lack of good understanding about it. An acronym can be used to make recognizing this disease somewhat easier:
+S: Splenomegaly.
+A: Anemia.
+N: Neutropenia.
+T: Thrombocytopenia.
+A: Arthritis (rheumatoid).
+Conditions of the Blood => A complete blood count (CBC) can be done to diagnose anemia (normochromic, normocytic), thrombocytopenia, and neutropenia. Abnormal liver function tests are commonly used to help in diagnosis as the spleen and liver are strongly affected by one another.
+Splenomegaly => If rheumatoid arthritis is present and other symptoms occur that are not commonly found within RA itself, such as a palpable spleen, further testing should be done. A palpable spleen is not always a clinical significance, therefore CT scan, MRI, or ultrasound can be administered in order to help diagnose the condition. According to Poulin et al, dimensional guidelines for diagnosing splenomegaly are as follows:
+- Moderate if the largest dimension is 11 – 20 cm
+- Severe if the largest dimension is greater than 20 c.
+Rheumatoid Arthritis => RA in patients with Felty's syndrome is chronic (after 10 – 15 years), and presents with increased severity along with extra articular manifestations. RA can be mistaken for other conditions such as gout if not clinically diagnosed. Diagnosis can be confirmed by use of X-rays or synovial fluid analysis.
+The symptoms of Felty's syndrome are similar to those of rheumatoid arthritis. Patients suffer from painful, stiff, and swollen joints, most commonly in the joints of the hands, feet, and arms. In some affected individuals, Felty's syndrome may develop during a period when the symptoms and physical findings associated with rheumatoid arthritis have subsided or are not present; in this case, Felty's syndrome may remain undiagnosed. In more rare instances, the development of Felty's syndrome may precede the development of the symptoms and physical findings associated with rheumatoid arthritis.
+Felty's syndrome is also characterized by an abnormally enlarged spleen (splenomegaly) and abnormally low levels of certain white blood cells (neutropenia). As a result of neutropenia, affected individuals are increasingly susceptible to certain infections. Keratoconjunctivitis sicca may occur due to secondary Sjorgen's syndrome. Individuals with Felty's syndrome may also experience fever, weight loss, and/or fatigue. In some cases, affected individuals may have discoloration (abnormal brown pigmentation) of the skin, particularly of the leg, sores (ulcers) on the lower leg, and/or an abnormally large liver (hepatomegaly). In addition, affected individuals may have abnormally low levels of circulating red blood cells (anemia), a decrease in circulating blood platelets that assist in blood clotting functions (thrombocytopenia), abnormal liver function tests and/or inflammation of the blood vessels (vasculitis).
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DISNET disease texts/100 Clean Disease Texts/Food intolerance.txt

+Reactions to chemical components of the diet are more common than true food allergies. Although, there is no evidence to support this. They are caused by various organic chemicals occurring naturally in a wide variety of foods, both of animal and vegetable origin more often than to food additives, preservatives, colourings and flavourings, such as sulfites or dyes. Both natural and artificial ingredients may cause adverse reactions in sensitive people if consumed in sufficient amount, the degree of sensitivity varying between individuals.
+Pharmacological responses to naturally occurring compounds in food, or chemical intolerance, can occur in individuals from both allergic and non-allergic family backgrounds. Symptoms may begin at any age, and may develop quickly or slowly. Triggers may range from a viral infection or illness to environmental chemical exposure. It occurs more commonly in women, which may be because of hormone differences, as many food chemicals mimic hormones.
+A deficiency in digestive enzymes can also cause some types of food intolerances. Lactose intolerance is a result of the body not producing sufficient lactase to digest the lactose in milk; dairy foods which are lower in lactose, such as cheese, are less likely to trigger a reaction in this case. Another carbohydrate intolerance caused by enzyme deficiency is hereditary fructose intolerance.
+Celiac disease, an autoimmune disorder caused by an immune response to the protein gluten, results in gluten intolerance and can lead to temporary lactose intolerance.
+The most widely distributed naturally occurring food chemical capable of provoking reactions is salicylate, although tartrazine and benzoic acid are well recognised in susceptible individuals. Benzoates and salicylates occur naturally in many foods, including fruits, juices, vegetables, spices, herbs, nuts, tea, wines, and coffee. Salicylate sensitivity causes reactions to not only aspirin and NSAIDs but also foods in which salicylates naturally occur, such as cherries.
+Other natural chemicals which commonly cause reactions and cross reactivity include amines, nitrates, sulphites and some antioxidants. Chemicals involved in aroma and flavour are often suspect.
+The classification or avoidance of foods based on botanical families bears no relationship to their chemical content and is not relevant in the management of food intolerance.
+Salicylate-containing foods include apples, citrus fruits, strawberries, tomatoes, and wine, while reactions to chocolate, cheese, bananas, avocado, tomato or wine point to amines as the likely food chemical. Thus, exclusion of single foods does not necessarily identify the chemical responsible as several chemicals can be present in a food, the patient may be sensitive to multiple food chemicals and reaction more likely to occur when foods containing the triggering substance are eaten in a combined quantity that exceeds the patient's sensitivity thresholds. People with food sensitivities have different sensitivity thresholds, and so more sensitive people will react to much smaller amounts of the substance.
+Diagnosis of food intolerance can include hydrogen breath testing for lactose intolerance and fructose malabsorption, professionally supervised elimination diets, and ELISA testing for IgG-mediated immune responses to specific foods. It is important to be able to distinguish between food allergy, food intolerance, and autoimmune disease in the management of these disorders. Non-IgE-mediated intolerance is more chronic, less acute, less obvious in its clinical presentation, and often more difficult to diagnose than allergy, as skin tests and standard immunological studies are not helpful. Elimination diets must remove all poorly tolerated foods, or all foods containing offending compounds. Clinical investigation is generally undertaken only for more serious cases, as for minor complaints which do not significantly limit the person's lifestyle the cure may be more inconvenient than the problem.
+IgG4 tests are invalid; IgG4 presence indicates that the person has been repeatedly exposed to food proteins recognized as foreign by the immune system which is a normal physiological response of the immune system after exposure to food components. Although elimination of foods based on IgG-4 testing in IBS patients resulted in an improvement in symptoms, the positive effects of food elimination were more likely due to wheat and milk elimination than IgG-4 test-determined factors. The IgG-4 test specificity is questionable as healthy individuals with no symptoms of food intolerance also test positive for IgG-4 to several foods.
+Diagnosis is made using medical history and cutaneous and serological tests to exclude other causes, but to obtain final confirmation a Double Blind Controlled Food Challenge must be performed. Treatment can involve long-term avoidance, or if possible re-establishing a level of tolerance.
+Today there are many methods available such as Cytotoxic testing, MRT testing, Elisa Testing and Microarray Elisa Testing. Allergy US reviewed these methods and Microarray technology appears to be the most reliable among them. Http: //allergyus. Com/food-intolerance-tests-in-usa/.
+Food intolerance is more chronic, less acute, less obvious in its presentation, and often more difficult to diagnose than a food allergy. Symptoms of food intolerance vary greatly, and can be mistaken for the symptoms of a food allergy. While true allergies are associated with fast-acting immunoglobulin IgE responses, it can be difficult to determine the offending food causing a food intolerance because the response generally takes place over a prolonged period of time. Thus, the causative agent and the response are separated in time, and may not be obviously related. Food intolerance symptoms usually begin about half an hour after eating or drinking the food in question, but sometimes symptoms may be delayed by up to 48 hours.
+Food intolerance can present with symptoms affecting the skin, respiratory tract, gastrointestinal tract (GIT) either individually or in combination. On the skin may include skin rashes, urticaria (hives), angioedema, dermatitis, and eczema. Respiratory tract symptoms can include nasal congestion, sinusitis, pharyngeal irritations, asthma and an unproductive cough. GIT symptoms include mouth ulcers, abdominal cramp, nausea, gas, intermittent diarrhea, constipation, irritable bowel syndrome (IBS), and may include anaphylaxis.
+Food intolerance has been found associated with irritable bowel syndrome and inflammatory bowel disease, chronic constipation, chronic hepatitis C infection, eczema, NSAID intolerance, respiratory complaints, including asthma, rhinitis and headache, functional dyspepsia, eosinophilic esophagitis and ENT illnesses.
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DISNET disease texts/100 Clean Disease Texts/GM1 gangliosidoses.txt

+Types => GM1 has three forms: early infantile, late infantile, and adult.
+Early infantile GM1 => Symptoms of early infantile GM1 (the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver enlargement (hepatomegaly), spleen enlargement (splenomegaly), coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response to sound, and problems with gait.
+About half of affected patients develop cherry-red spots in the eye.
+Children may be deaf and blind by age 1 and often die by age 3 from cardiac complications or pneumonia.
+- Autosomal recessive disorder; beta-galactosidase deficiency; neuronal storage of GM1 ganglioside and visceral storage of galactosyl oligosaccharides and keratan sulfate.
+- Early psychomotor deterioration: decreased activity and lethargy in the first weeks; never sit; feeding problems-failure to thrive; visual failure (nystagmus noted) by 6 months; initial hypotonia; later spasticity with pyramidal signs; secondary microcephaly develops; decerebrate rigidity by 1 year and death by age 1–2 years (due to pneumonia and respiratory failure); some have hyperacusis.
+- Macular cherry-red spots in 50% by 6–10 months; corneal opacities in some
+- Facial dysmorphology: frontal bossing, wide nasal bridge, facial edema (puffy eyelids); peripheral edema, epicanthus, long upper lip, microretrognathia, gingival hypertrophy (thick alveolar ridges), macroglossia
+- Hepatomegaly by 6 months and splenomegaly later; some have cardiac failure
+- Skeletal deformities: flexion contractures noted by 3 months; early subperiosteal bone formation (may be present at birth); diaphyseal widening later; demineralization; thoracolumbar vertebral hypoplasia and beaking at age 3–6 months; kyphoscoliosis. *Dysostosis multiplex (as in the mucopolysaccharidoses)
+- 10–80% of peripheral lymphocytes are vacuolated; foamy histiocytes in bone marrow; visceral mucopolysaccharide storage similar to that in Hurler disease; GM1 storage in cerebral gray matter is 10-fold elevated (20–50-fold increased in viscera)
+- Galactose-containing oligosacchariduria and moderate keratan sulfaturia
+- Morquio disease Type B: Mutations with higher residual beta-galactosidase activity for the GM1 substrate than for keratan sulfate and other galactose-containing oligosaccharides have minimal neurologic involvement but severe dysostosis resembling Morquio disease type A (Mucopolysaccharidosis type 4).
+
+Late infantile GM1 => Onset of late infantile GM1 is typically between ages 1 and 3 years.
+Neurological symptoms include ataxia, seizures, dementia, and difficulties with speech.
+Adult GM1 => Onset of adult GM1 is between ages 3 and 30.
+Symptoms include muscle atrophy, neurological complications that are less severe and progress at a slower rate than in other forms of the disorder, corneal clouding in some patients, and dystonia (sustained muscle contractions that cause twisting and repetitive movements or abnormal postures). Angiokeratomas may develop on the lower part of the trunk of the body. Most patients have a normal size liver and spleen.
+Prenatal diagnosis is possible by measurement of Acid Beta Galactosidase in cultured amniotic cells.
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DISNET disease texts/100 Clean Disease Texts/Gastroparesis.txt

+Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.
+It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves. The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease. It may also occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis.
+Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery. Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.
+Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.
+Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men. A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.
+Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCl) in order to properly empty itself of a meal.
+Gastroparesis can be diagnosed with tests such as x-rays, manometry, and gastric emptying scans. The clinical definition for gastroparesis is based solely on the emptying time of the stomach (and not on other symptoms), and severity of symptoms does not necessarily correlate with the severity of gastroparesis. Therefore, some patients may have marked gastroparesis with few, if any, serious complications.
+The most common symptoms of gastroparesis are the following:
+- Chronic nausea (93%)
+- Vomiting (especially of undigested food) (68–84%)
+- Abdominal pain (46–90%)
+- A feeling of fullness after eating just a few bites (60–86%.
+Other symptoms include the following:
+- Abdominal bloating
+- Body aches (myalgia)
+- Erratic blood glucose levels
+- Gastroesophageal reflux (GERD)
+- Heartburn
+- Lack of appetite
+- Morning nausea
+- Muscle weakness
+- Night sweats
+- Palpitations
+- Spasms of the stomach wall
+- Constipation or infrequent bowel movements
+- Weight loss, malnutrition
+- Weight gain.
+Morning nausea may also indicate gastroparesis. Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.
+Primary complications of gastroparesis include:
+- Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)
+- General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it
+- Severe fatigue and weight loss due to calorie deficit
+- Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)
+- Bacterial infection due to overgrowth in undigested food
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DISNET disease texts/100 Clean Disease Texts/Generalized anxiety disorder.txt

+Genetics => Genes are attributed about a third of general anxiety disorder's variance. Individuals with a genetic predisposition for GAD are more likely to develop GAD, especially in response to a life stressor.
+Substance-induced => Long-term use of benzodiazepines can worsen underlying anxiety, with evidence that reduction of benzodiazepines can lead to a lessening of anxiety symptoms. Similarly, long-term alcohol use is associated with anxiety disorders, with evidence that prolonged abstinence can result in a disappearance of anxiety symptoms. However, it can take up to two years for anxiety symptoms to return to baseline in about a quarter of people recovering from alcoholism.
+In one study in 1988–90, illness in approximately half of patients attending mental health services at British hospital psychiatric clinic, for conditions including anxiety disorders such as panic disorder or social phobia, was determined to be the result of alcohol or benzodiazepine dependence. In these patients, anxiety symptoms, while worsening initially during the withdrawal phase, disappeared with abstinence from benzodiazepines or alcohol. Sometimes anxiety pre-existed alcohol or benzodiazepine dependence, but the dependence was acting to keep the anxiety disorders going and often progressively making them worse. Recovery from benzodiazepines tends to take a lot longer than recovery from alcohol, but people can regain their previous good health.
+Tobacco smoking has been established as a risk factor for developing anxiety disorders. Excessive caffeine usage has been linked to anxiety.
+DSM-5 criteria => The diagnostic criteria for GAD as defined by the Diagnostic and Statistical Manual of Mental Disorders DSM-5 (2013), published by the American Psychiatric Association, are paraphrased as follows:
+- Too much anxiety or worry over more than six months. This is present most of the time in regards to many activities.
+- Inability to manage these symptoms
+- At least three of the following occur: Note: Only one item is required in children. Restlessness Tires easily Problems concentrating Irritability Muscle tension. Problems with sleep
+- Restlessness
+- Tires easily
+- Problems concentrating
+- Irritability
+- Muscle tension.
+- Problems with sleep
+- Symptoms result in problems with functioning.
+- Symptoms are not due to medications, drugs, other physical health problems
+- Symptoms do not fit better with another psychiatric problem such as panic disorde.
+No major changes to GAD have occurred since publication of the Diagnostic and Statistical Manual of Mental Disorders (2004); minor changes include wording of diagnostic criteria.
+ICD-10 criteria => ICD-10 Generalized anxiety disorder "F41.1" Note: For children different criteria may be applied (see F93.80).
+- A period of at least six months with prominent tension, worry, and feelings of apprehension, about everyday events and problems.
+- At least four symptoms out of the following list of items must be present, of which at least one from items (1) to (4). Autonomic arousal symptoms (1) Palpitations or pounding heart, or accelerated heart rate. (2) Sweating. (3) Trembling or shaking. (4) Dry mouth (not due to medication or dehydration). Symptoms concerning chest and abdomen (5) Difficulty breathing. (6) Feeling of choking. (7) Chest pain or discomfort. (8) Nausea or abdominal distress (e. G. Churning in the stomach). Symptoms concerning brain and mind (9) Feeling dizzy, unsteady, faint or light-headed. (10) Feelings that objects are unreal (derealization), or that one's self is distant or "not really here" (depersonalization). (11) Fear of losing control, going crazy, or passing out. (12) Fear of dying. General symptoms (13) Hot flashes or cold chills. (14) Numbness or tingling sensations. Symptoms of tension (15) Muscle tension or aches and pains. (16) Restlessness and inability to relax. (17) Feeling keyed up, or on edge, or of mental tension. (18) A sensation of a lump in the throat or difficulty with swallowing. Other non-specific symptoms (19) Exaggerated response to minor surprises or being startled. (20) Difficulty in concentrating or mind going blank, because of worrying or anxiety. (21) Persistent irritability. (22) Difficulty getting to sleep because of worrying.
+- The disorder does not meet the criteria for panic disorder (F41.0), phobic anxiety disorders (F40.-), obsessive-compulsive disorder (F42.-) or hypochondriacal disorder (F45.2).
+- Most commonly used exclusion criteria: not sustained by a physical disorder, such as hyperthyroidism, an organic mental disorder (F0) or psychoactive substance-related disorder (F1), such as excess consumption of amphetamine-like substances, or withdrawal from benzodiazepines.
+History of diagnosis => The American Psychiatric Association introduced GAD as a diagnosis in the DSM-III in 1980, when anxiety neurosis was split into GAD and panic disorder. The definition in the DSM-III required uncontrollable and diffuse anxiety or worry that is excessive and unrealistic and persists for 1 month or longer. High rates in comorbidity of GAD and major depression led many commentators to suggest that GAD would be better conceptualized as an aspect of major depression instead of an independent disorder. Many critics stated that the diagnostic features of this disorder were not well established until the DSM-III-R. Since comorbidity of GAD and other disorders decreased with time, the DSM-III-R changed the time requirement for a GAD diagnosis to 6 months or longer. The DSM-IV changed the definition of excessive worry and the number of associated psychophysiological symptoms required for a diagnosis. Another aspect of the diagnosis the DSM-IV clarified was what constitutes a symptom as occurring "often". The DSM-IV also required difficulty controlling the worry to be diagnosed with GAD. The DSM-5 emphasized that excessive worrying had to occur more days than not and on a number of different topics. It has been stated that the constant changes in the diagnostic features of the disorder have made assessing epidemiological statistics such as prevalence and incidence difficult, as well as increasing the difficulty for researchers in identifying the biological and psychological underpinnings of the disorder. Consequently, making specialized medications for the disorder is more difficult as well. This has led to the continuation of GAD being medicated heavily with SSRIs.
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DISNET disease texts/100 Clean Disease Texts/Helicobacter pylori.txt

+Colonization with H. Pylori is not a disease in and of itself, but a condition associated with a number of disorders of the upper gastrointestinal tract. Testing for H. Pylori is recommended if peptic ulcer disease or low-grade gastric MALT lymphoma is present, after endoscopic resection of early gastric cancer, first-degree relatives with gastric cancer, and in certain cases of dyspepsia, not routinely. Several ways of testing exist. One can test noninvasively for H. Pylori infection with a blood antibody test, stool antigen test, or with the carbon urea breath test (in which the patient drinks 14°C—or 13°C-labelled urea, which the bacterium metabolizes, producing labelled carbon dioxide that can be detected in the breath). Also, a urine ELISA test with a 96% sensitivity and 79% specificity is available. None of the test methods is completely failsafe. Even biopsy is dependent on the location of the biopsy. Blood antibody tests, for example, range from 76% to 84% sensitivity. Some drugs can affect H. Pylori urease activity and give false negatives with the urea-based tests. The most accurate method for detecting H. Pylori infection is with a histological examination from two sites after endoscopic biopsy, combined with either a rapid urease test or microbial culture.
+Up to 85% of people infected with H. Pylori never experience symptoms or complications. Acute infection may appear as an acute gastritis with abdominal pain (stomach ache) or nausea. Where this develops into chronic gastritis, the symptoms, if present, are often those of non-ulcer dyspepsia: stomach pains, nausea, bloating, belching, and sometimes vomiting or black stool.
+Individuals infected with H. Pylori have a 10 to 20% lifetime risk of developing peptic ulcers and a 1 to 2% risk of acquiring stomach cancer. Inflammation of the pyloric antrum is more likely to lead to duodenal ulcers, while inflammation of the corpus (body of the stomach) is more likely to lead to gastric ulcers and gastric carcinoma. However, H. Pylori possibly plays a role only in the first stage that leads to common chronic inflammation, but not in further stages leading to carcinogenesis. A meta-analysis conducted in 2009 concluded the eradication of H. Pylori reduces gastric cancer risk in previously infected individuals, suggesting the continued presence of H. Pylori constitutes a relative risk factor of 65% for gastric cancers; in terms of absolute risk, the increase was from 1.1% to 1.7%.
+H. Pylori has been associated with colorectal polyps and colorectal cancer. It may also be associated with eye disease.
+Pain typically occurs when the stomach is empty, between meals and in the early morning hours, but it can also occur at other times. Less common ulcer symptoms include nausea, vomiting, and loss of appetite. Bleeding can also occur; prolonged bleeding may cause anemia leading to weakness and fatigue. If bleeding is heavy, hematemesis, hematochezia, or melena may occur.
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DISNET disease texts/100 Clean Disease Texts/Hemolytic-uremic syndrome.txt

+The similarities between HUS, aHUS, and TTP make differential diagnosis essential. All three of these systemic TMA-causing diseases are characterized by thrombocytopenia and microangiopathic hemolysis, plus one or more of the following: neurological symptoms (e. G., confusion, cerebral convulsions, seizures); renal impairment (e. G., elevated creatinine, decreased estimated glomerular filtration rate, abnormal urinalysis); and gastrointestinal (GI) symptoms (e. G., diarrhea, nausea/vomiting, abdominal pain, gastroenteritis). The presence of diarrhea does not exclude aHUS as the cause of TMA, as 28% of patients with aHUS present with diarrhea and/or gastroenteritis. First diagnosis of aHUS is often made in the context of an initial, complement-triggering infection, and Shiga-toxin has also been implicated as a trigger that identifies patients with aHUS. Additionally, in one study, mutations of genes encoding several complement regulatory proteins were detected in 8 of 36 (22%) patients diagnosed with STEC-HUS. However, the absence of an identified complement regulatory gene mutation does not preclude aHUS as the cause of the TMA, as approximately 50% of patients with aHUS lack an identifiable mutation in complement regulatory genes.
+Diagnostic work-up supports the differential diagnosis of TMA-causing diseases. A positive Shiga-toxin/EHEC test confirms a cause for STEC-HUS, and severe ADAMTS13 deficiency (i.e. , ≤5% of normal ADAMTS13 levels) confirms a diagnosis of TTP.
+STEC-HUS occurs after ingestion of a strain of bacteria expressing Shiga toxin(s), usually types of E. Coli, that expresses verotoxin (also called Shiga-like toxin). E. Coli can produce stx1 and/or stx2 Shiga toxins, the latter being more dangerous. A combination of both toxins in certain ratios is usually associated with HUS. These Shiga toxins bind GB3 receptors, globotriaosylceramide, which are present in renal tissue more than any other tissue and are also found in central nervous system neurons and other tissue. Children have more GB3 receptors than adults which may be why children are more susceptible to HUS. Cattle, swine, deer, and other mammals do not have GB3 receptors, but can be asymptomatic carriers of Shiga toxin-producing bacteria. Some humans can also be asymptomatic carriers. Once the bacteria colonizes, diarrhea followed by bloody diarrhea, hemorrhagic colitis, typically follows. HUS develops about 5–10 days after onset of diarrhea, with decreased urine output (oliguria), blood in the urine (hematuria), kidney failure, thrombocytopenia (low levels of platelets) and destruction of red blood cells (microangiopathic hemolytic anemia). Hypertension is common. In some cases, there are prominent neurologic changes.
+Patients with HUS commonly exhibit the signs and symptoms of thrombotic microangiopathy (TMA), which can include abdominal pain, low platelet count, elevated lactate dehydrogenase LDH, a chemical released from damaged cells, and which is therefore a marker of cellular damage) decreased haptoglobin (indicative of the breakdown of red blood cells) anemia (low red blood cell count)/schistocytes (damaged red blood cells), elevated creatinine (a protein waste product generated by muscle metabolism and eliminated renally, proteinuria (indicative of kidney injury), confusion, fatigue, edema (swelling), nausea/vomiting, and diarrhea. Additionally, patients with aHUS typically present with an abrupt onset of systemic signs and symptoms such as acute kidney failure, hypertension (high blood pressure), myocardial infarction (heart attack), stroke, lung complications, pancreatitis (inflammation of the pancreas), liver necrosis (death of liver cells or tissue), encephalopathy (brain dysfunction), seizure, and coma. Failure of neurologic, cardiac, renal, and gastrointestinal (GI) organs, as well as death, can occur unpredictably at any time, either very quickly or following prolonged symptomatic or asymptomatic disease progression.
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DISNET disease texts/100 Clean Disease Texts/Herpes labialis.txt

+Herpes labialis infection occurs when the herpes simplex virus comes into contact with oral mucosal tissue or abraded skin of the mouth. Infection by the type 1 strain of herpes simplex virus (HSV-1) is most common; however, cases of oral infection by the type 2 strain are increasing. Specifically, type 2 has been implicated as causing 10–15% of oral infections.
+Cold sores are the result of the virus reactivating in the body. Once HSV-1 has entered the body, it never leaves. The virus moves from the mouth to remain latent in the central nervous system. In approximately one-third of people, the virus can "wake up" or reactivate to cause disease. When reactivation occurs, the virus travels down the nerves to the skin where it may cause blisters (cold sores) around the lips, in the mouth or, in about 10% of cases, on the nose, chin, or cheeks.
+Cold sore outbreaks may be influenced by stress, menstruation, sunlight, sunburn, fever, dehydration, or local skin trauma. Surgical procedures such as dental or neural surgery, lip tattooing, or dermabrasion are also common triggers. HSV-1 can in rare cases be transmitted to newborn babies by family members or hospital staff who have cold sores; this can cause a severe disease called neonatal herpes simplex.
+The colloquial term for this condition, "cold sore" comes from the fact that herpes labialis is often triggered by fever, for example, as may occur during an upper respiratory tract infection (i.e. A cold).
+People can transfer the virus from their cold sores to other areas of the body, such as the eye, skin, or fingers; this is called autoinoculation. Eye infection, in the form of conjunctivitis or keratitis, can happen when the eyes are rubbed after touching the lesion. Finger infection (herpetic whitlow) can occur when a child with cold sores or primary HSV-1 infection sucks his fingers.
+Blood tests for herpes may differentiate between type 1 and type 2. When a person is not experiencing any symptoms, a blood test alone does not reveal the site of infection. Genital herpes infections occurred with almost equal frequency as type 1 or 2 in younger adults when samples were taken from genital lesions. Herpes in the mouth is more likely to be caused by type 1, but (see above) also can be type 2. The only way to know for certain if a positive blood test for herpes is due to infection of the mouth, genitals, or elsewhere, is to sample from lesions. This is not possible if the afflicted individual is asymptomatic.
+Herpes infections usually show no symptoms; when symptoms do appear they typically resolve within two weeks. The main symptom of oral infection is inflammation of the mucosa of the cheek and gums—known as acute herpetic gingivostomatitis—which occurs within 5–10 days of infection. Other symptoms may also develop, including headache, nausea, dizziness and painful ulcers—sometimes confused with canker sores—fever, and sore throat.
+Primary HSV infection in adolescents frequently manifests as severe pharyngitis with lesions developing on the cheek and gums. Some individuals develop difficulty in swallowing (dysphagia) and swollen lymph nodes (lymphadenopathy). Primary HSV infections in adults often results in pharyngitis similar to that observed in glandular fever (infectious mononucleosis), but gingivostomatitis is less likely.
+Recurrent oral infection is more common with HSV-1 infections than with HSV-2. Symptoms typically progress in a series of eight stages:
+- Latent (weeks to months incident-free): The remission period; After initial infection, the viruses move to sensory nerve ganglia (trigeminal ganglion), where they reside as lifelong, latent viruses. Asymptomatic shedding of contagious virus particles can occur during this stage.
+- Prodromal (day 0–1): Symptoms often precede a recurrence. Symptoms typically begin with tingling (itching) and reddening of the skin around the infected site. This stage can last from a few days to a few hours preceding the physical manifestation of an infection and is the best time to start treatment.
+- Inflammation (day 1): Virus begins reproducing and infecting cells at the end of the nerve. The healthy cells react to the invasion with swelling and redness displayed as symptoms of infection.
+- Pre-sore (day 2–3): This stage is defined by the appearance of tiny, hard, inflamed papules and vesicles that may itch and are painfully sensitive to touch. In time, these fluid-filled blisters form a cluster on the lip (labial) tissue, the area between the lip and skin (vermilion border), and can occur on the nose, chin, and cheeks.
+- Open lesion (day 4): This is the most painful and contagious of the stages. All the tiny vesicles break open and merge to create one big, open, weeping ulcer. Fluids are slowly discharged from blood vessels and inflamed tissue. This watery discharge is teeming with active viral particles and is highly contagious. Depending on the severity, one may develop a fever and swollen lymph glands under the jaw.
+- Crusting (day 5–8): A honey/golden crust starts to form from the syrupy exudate. This yellowish or brown crust or scab is not made of active virus but from blood serum containing useful proteins such as immunoglobulins. This appears as the healing process begins. The sore is still painful at this stage, but, more painful, however, is the constant cracking of the scab as one moves or stretches their lips, as in smiling or eating. Virus-filled fluid will still ooze out of the sore through any cracks.
+- Healing (day 9–14): New skin begins to form underneath the scab as the virus retreats into latency. A series of scabs will form over the sore (called Meier Complex), each one smaller than the last. During this phase irritation, itching, and some pain are common.
+- Post-scab (12–14 days): A reddish area may linger at the site of viral infection as the destroyed cells are regenerated. Virus shedding can still occur during this stage.
+The recurrent infection is thus often called herpes simplex labialis. Rare reinfections occur inside the mouth (intraoral HSV stomatitis) affecting the gums, alveolar ridge, hard palate, and the back of the tongue, possibly accompanied by herpes labialis.
+A lesion caused by herpes simplex can occur in the corner of the mouth and be mistaken for angular cheilitis of another cause. Sometimes termed "angular herpes simplex". A cold sore at the corner of the mouth behaves similarly to elsewhere on the lips. Rather than utilizing antifungal creams, angular herpes simplex is treated in the same way as a cold sore, with topical antiviral drugs.
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DISNET disease texts/100 Clean Disease Texts/Hypercalcaemia.txt

+Primary hyperparathyroidism and malignancy account for about 90% of cases of hypercalcaemia.
+- Parathyroid function => Primary hyperparathyroidism Solitary parathyroid adenoma Primary parathyroid hyperplasia Parathyroid carcinoma Multiple endocrine neoplasia (MEN1
+- MEN2A) Familial isolated hyperparathyroidism
+- Solitary parathyroid adenoma
+- Primary parathyroid hyperplasia
+- Parathyroid carcinoma
+- Multiple endocrine neoplasia (MEN1
+- MEN2A)
+- Familial isolated hyperparathyroidism
+- Lithium use
+- Familial hypocalciuric hypercalcemia/familial benign hypercalcemia.
+- Solid tumour with metastasis (e. G. Breast cancer or classically squamous cell carcinoma, which can be PTHrP-mediated)
+- Solid tumour with humoral mediation of hypercalcaemia (e. G. Lung cancer, most commonly non-small cell lung cancer or kidney cancer, phaeochromocytoma)
+- Haematologic cancers (multiple myeloma, lymphoma, leukaemia)
+- Ovarian small cell carcinoma of the hypercalcemic typ.
+- Vitamin-D disorders => Hypervitaminosis D (vitamin D intoxication)
+- Elevated 1,25(OH)2D (see calcitriol under Vitamin D) levels (e. G. Sarcoidosis and other granulomatous diseases such as tuberculosis)
+- Idiopathic hypercalcaemia of infancy
+- rebound hypercalcaemia after rhabdomyolysi.
+- High bone-turnover rates => Hyperthyroidism
+- Multiple myeloma
+- Prolonged immobilization
+- Paget's disease
+- Thiazide use
+- Vitamin A intoxicatio.
+- Kidney failure => Severe secondary hyperparathyroidism
+- Tertiary hyperparathyroidism
+- Aluminium intoxication
+- Milk-alkali syndrom.
+- Other => Adrenal insufficiency
+- Zollinger Ellison syndrom.
+Abnormal heart rhythms can also result, and ECG findings of a short QT interval suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction. Hypercalcaemia has also been known to cause an ECG finding mimicking hypothermia, known as an Osborn wave.
+The neuromuscular symptoms of hypercalcemia are caused by a negative bathmotropic effect due to the increased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, increased calcium raises the threshold for depolarization. This results in diminished deep tendon reflexes (hyporeflexia), and skeletal muscle weakness. There is a general mnemonic for remembering the effects of hypercalcaemia: "Stones, Bones, Groans, Thrones and Psychiatric Overtones".
+- Stones (renal or biliary) (see calculus)
+- Bones (bone pain)
+- Groans (abdominal pain, nausea and vomiting)
+- Thrones (polyuria) resulting in dehydration
+- Psychiatric overtones (Depression 30–40%, anxiety, cognitive dysfunction, insomnia, coma.
+- Other symptoms include cardiac arrhythmias (especially in those taking digoxin), fatigue, nausea, vomiting (emesis), anorexia, abdominal pain, constipation,
+- paralytic ileus. If renal impairment occurs as a result, manifestations can include polyuria, nocturia, and polydipsia. Psychiatric manifestation can include emotional instability, confusion, delirium, psychosis,
+- stupor. Limbus sign seen in eye due to hypercalcemia.
+Hypercalcemia can result in an increase in heart rate and a positive inotropic effect (increase in contractility).
+Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/l). Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result. The high levels of calcium ions decrease the neuron membrane permeability to sodium ions, thus decreasing excitability, which leads to hypotonicity of smooth and striated muscle. This explains the fatigue, muscle weakness, low tone and sluggish reflexes in muscle groups. The sluggish nerves also explain drowsiness, confusion, hallucinations, stupor and / or coma. In the gut this causes constipation. Hypocalcaemia causes the opposite by the same mechanism.
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DISNET disease texts/100 Clean Disease Texts/Hyperosmolar hyperglycemic state.txt

+The main risk factor is a history of diabetes mellitus type 2. Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1. Triggers include infections, stroke, trauma, certain medications, and heart attacks.
+Other risk factors:
+- Lack of sufficient insulin (but enough to prevent ketosis)
+- Poor kidney function
+- Poor fluid intake (dehydration)
+- Older age (50–70 years)
+- Certain medical conditions (cerebral vascular injury, myocardial infarction, sepsis)
+- Some medications (glucocorticoids, beta-blockers, thiazide diuretics, calcium channel blockers, phenytoin).
+Criteria => According to the American Diabetes Association, diagnostic features include:
+- Plasma glucose level >30 mmol/L (>600 mg/dL)
+- Serum osmolality >320 mOsm/kg
+- Profound dehydration, up to an average of 9L (and therefore substantial thirst (polydipsia))
+- Serum pH >7.40
+- Bicarbonate >15 mEq/L
+- Small ketonuria (~+ on dipstick) and absent-to-low ketonemia (<3 mmol/L)
+- Some alteration in consciousness
+- BUN > 30 md/dL (increased)
+- Creatinine > 1.5 mg/dL (increased).
+Imaging => Cranial imaging is not used for diagnosis of this condition. However, if MRI is performed, it may show cortical restricted diffusion with unusual characteristics of reversible T2 hypointensity in the subcortical white matter.
+Differential diagnosis => The major differential diagnosis is diabetic ketoacidosis (DKA). In contrast to DKA, serum glucose levels in HHS are extremely high, usually greater than 40 – 50 mmol/L (600 mg/dL). Metabolic acidosis is absent or mild. A temporary state of confusion (delirium) is also more common in HHS than DKA. HHS also tends to affect older people more. DKA may have fruity breath, and rapid and deep breathing.
+DKA often has serum glucose level greater than 300 mg/dL (HHS is >600 mg/dL). DKA usually occurs in type 1 diabetics whereas HHS is more common in type 2 diabetics. DKA is characterized by a rapid onset, and HHS occurs gradually over a few days. DKA also is characterized by ketosis due to the breakdown of fat for energy.
+Both DKA and HHS may show symptoms of dehydration, increased thirst, increased urination, increased hunger, weight loss, nausea, vomiting, abdominal pain, blurred vision, headaches, weakness, and low blood pressure with standing.
+Symptoms of high blood sugar including increased thirst (polydipsia), increased volume of urination (polyurea), and increase hunger (polyphagia).
+Symptoms of HHS include:
+- Altered level of consciousness
+- Neurologic signs including: blurred vision, headaches, focal seizures, myoclonic jerking, reversible paralysis
+- Motor abnormalities including flaccidity, depressed reflexes, tremors or fasiciculations
+- Hyperviscosity and increased risk of blood clot formation
+- Dehydration
+- Weight loss
+- Nausea, vomiting, and abdominal pain
+- Weakness
+- Low blood pressure with standing
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DISNET disease texts/100 Clean Disease Texts/Hypervitaminosis A.txt

+Hypervitaminosis A results from excessive intake of preformed vitamin A. A genetic variance in tolerance to vitamin A intake may occur. Children are particularly sensitive to vitamin A, with daily intakes of 1500 IU/kg body weight reportedly leading to toxicity.
+- Types of vitamin A => Provitamin carotenoids-such as beta carotene-are “largely impossible” to cause toxicity, as their conversion to retinol is highly regulated. No vitamin A toxicity has ever been reported from ingestion of excessive amounts. Overconsumption of beta carotene can only cause carotenosis, a harmless and reversible cosmetic condition in which the skin turns orange.
+- Preformed vitamin A absorption and storage in the liver occur very efficiently until a pathologic condition develops. When ingested, 70 – 90% of preformed vitamin A is absorbed and used.
+- Sources of toxicity => Diet-liver is high in vitamin A. The liver of certain animals — including the polar bear, bearded seal, walrus, moose, — are particularly toxic.
+- Supplements-usually when taken above recommended dosages-can be toxic. Cod liver oil is particularly high in vitamin A.
+- Medications-at high doses of vitamin A-are often used on long-term basis in numerous preventive and therapeutic medical applications, which may lead to hypervitaminosis A.
+- Types of toxicity => Acute toxicity occurs over a period of hours or a few days, and is less of a problem than chronic toxicity.
+- Chronic toxicity-ingestion of high amounts of preformed vitamin A for months or years-results from daily intakes greater than 25,000 IU for 6 years or longer and more than 100,000 IU for 6 months or longer-are considered toxic.
+Tests => Tests may include:
+- bone X-rays
+- blood calcium test
+- cholesterol test
+- liver function test
+- blood test for vitamin.
+Retinol concentrations are nonsensitive indicators => Assessing vitamin A status in persons with subtoxicity or toxicity is complicated because serum retinol concentrations are not sensitive indicators in this range of liver vitamin A reserves. The range of serum retinol concentrations under normal conditions is 1–3 μmol/l and, because of homeostatic regulation, that range varies little with widely disparate vitamin A intakes.
+Retinol esters have been used as markers => Retinyl esters can be distinguished from retinol in serum and other tissues and quantified with the use of methods such as high-performance liquid chromatography.
+Elevated amounts of retinyl ester (i.e. , > 10% of total circulating vitamin A) in the fasting state have been used as markers for chronic hypervitaminosis A in humans and monkeys. This increased retinyl ester may be due to decreased hepatic uptake of vitamin A and the leaking of esters into the bloodstream from saturated hepatic stellate cells.
+Symptoms may include:
+- Abnormal softening of the skull bone (craniotabes—infants and children)
+- Blurred vision
+- Bone pain or swelling
+- Bulging fontanelle (infants)
+- Changes in consciousness
+- Decreased appetite
+- Dizziness
+- Double vision (young children)
+- Drowsiness
+- Headache
+- Gastric mucosal calcinosis
+- Heart valve calcification
+- Hypercalcemia
+- Increased intracranial pressure manifesting as cerebral edema, papilledema, and headache (may be referred to as Idiopathic intracranial hypertension)
+- Irritability
+- Liver damage
+- Nausea
+- Poor weight gain (infants and children)
+- Skin and hair changes
+- Cracking at corners of the mouth
+- Hair loss
+- Higher sensitivity to sunlight
+- Oily skin and hair (seborrhea)
+- Premature epiphyseal closure
+- Skin peeling, itching
+- Spontaneous fracture
+- Yellow discoloration of the skin (aurantiasis cutis)
+- Uremic pruritus
+- Vision changes
+- Vomitin
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DISNET disease texts/100 Clean Disease Texts/Hypocalcaemia.txt

+Hypoparathyroidism is a common cause of hypocalcemia. Calcium is tightly regulated by the parathyroid hormone (PTH). In response to low calcium levels, PTH induces the kidneys to reabsorb calcium, the kidneys to increase production of calcitriol (the active form of vitamin D) thereby increasing intestinal absorption of calcium, and the bones to release calcium. These actions lead to a re-balance in the blood calcium levels. However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the parathyroid glands via parathyroidectomy or neck dissection for head and neck cancers. Hypoparathyroidism may also be due to autoimmune destruction of the glands.
+- Eating disorders
+- Prolonged vomiting (e. G. With a viral illness)
+- Exposure to mercury, including infantile acrodynia
+- Excessive dietary magnesium, as with supplementation.
+- Excessive dietary zinc, as with supplementation (causes rapid hypocalcemia).
+- Prolonged use of medications/laxatives containing magnesium
+- Chelation therapy for metal exposure, particularly EDTA
+- Osteoporosis treatment or preventive agents, such as bisphosphonates and denosumab.
+- Agents for the treatment of hypercalcemia, such as Calcitonin.
+- Chronic kidney failure
+- Absent active vitamin D Decreased dietary intake Decreased sun exposure Defective Vitamin D metabolism Anticonvulsant therapy Vitamin-D dependent rickets, type I
+- Decreased dietary intake
+- Decreased sun exposure
+- Defective Vitamin D metabolism Anticonvulsant therapy Vitamin-D dependent rickets, type I
+- Anticonvulsant therapy
+- Vitamin-D dependent rickets, type I
+- Ineffective active vitamin D Intestinal malabsorption Vitamin-D dependent rickets, type II
+- Intestinal malabsorption
+- Vitamin-D dependent rickets, type II
+- Pseudohypoparathyroidism
+- Severe acute hyperphosphataemia
+- Tumour lysis syndrome
+- Acute kidney failure Rhabdomyolysis (initial stage)
+- Rhabdomyolysis (initial stage)
+- Exposure to hydrofluoric acid which can be fatal if 2.5% of skin is exposed
+- As a complication of pancreatitis
+- Alkalosis, often caused by hyperventilation As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation. Tetany may also be seen with this condition.
+- As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation.
+- Tetany may also be seen with this condition.
+- Neonatal hypocalcemia Very low birth weight (less than 1500 grams) Gestational age less than 32 weeks
+- Very low birth weight (less than 1500 grams)
+- Gestational age less than 32 week.
+Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the measured level of calcium. A corrected calcium level based on the albumin level is: Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0-serum albumin g/dL).
+The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, reduced calcium lowers the threshold for depolarization. The symptoms can be recalled by the mnemonic "CATs go numb"-convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth.
+- Petechiae which appear as on-off spots, then later become confluent, and appear as purpura (larger bruised areas, usually in dependent regions of the body).
+- Oral, perioral and acral paresthesias, tingling or 'pins and needles' sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.
+- Carpopedal and generalized tetany (unrelieved and strong contractions of the hands, and in the large muscles of the rest of the body) are seen.
+- Latent tetany Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic) Chvostek's sign (tapping of the inferior portion of the cheekbone will produce facial spasms)
+- Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic)
+- Chvostek's sign (tapping of the inferior portion of the cheekbone will produce facial spasms)
+- Tendon reflexes are hyperactive
+- Life-threatening complications Laryngospasm Cardiac arrhythmias
+- Laryngospasm
+- Cardiac arrhythmias
+- Effects on cardiac output Negative chronotropic effect, or a decrease in heart rate. Negative inotropic effect, or a decrease in contractility
+- Negative chronotropic effect, or a decrease in heart rate.
+- Negative inotropic effect, or a decrease in contractility
+- - ECG changes include the following: Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the patient at high risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death, unless the patient can be medically or electrically cardioverted and returned to a normal cardiac rhythm.)
+- Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the patient at high risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death, unless the patient can be medically or electrically cardioverted and returned to a normal cardiac rhythm.
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DISNET disease texts/100 Clean Disease Texts/Hypomagnesemia.txt

+Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium (hypermagnesemia), however, are nearly always caused by a medical treatment. Up to 12 percent of all people admitted to hospital and as high as 60–65% of people in the intensive care unit (ICU) have hypomagnesemia. Hypomagnesemia is probably underdiagnosed, as testing for serum magnesium levels is not routine.
+Low levels of magnesium in blood may mean that there is not enough magnesium in the diet, the intestines are not absorbing enough magnesium, or the kidneys are excreting too much magnesium. Deficiencies may be due to the following conditions:
+Drugs => Alcoholism. Hypomagnesemia occurs in 30% of alcohol abusers and in 85% of delirium tremens inpatients, due to malnutrition and chronic diarrhea. Alcohol stimulates the kidneys' excretion of magnesium, which is also increased because of alcoholic and diabetic ketoacidosis, low blood phosphate levels, and hyperaldosteronism resulting from liver disease. Also, hypomagnesemia is related to thiamine deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate.
+- Medications => Loop and thiazide diuretic use (the most common cause of hypomagnesemia)
+- Antibiotics (i.e. Aminoglycoside, amphotericin, pentamidine, gentamicin, tobramycin, viomycin) block resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia.
+- Long term use of proton-pump inhibitors such as omeprazole.
+- Other drugs. Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect. Adrenergics, displace magnesium into the cell Cisplatin, stimulates kidney excretion Ciclosporin, stimulates kidney excretion Mycophenolate mofetil
+- Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect.
+- Adrenergics, displace magnesium into the cell
+- Cisplatin, stimulates kidney excretion
+- Ciclosporin, stimulates kidney excretion
+- Mycophenolate mofeti.
+- Genetic causes => Gitelman-like diseases, which include the syndromes caused by genetic mutations in SLC12A3, CLNCKB, BSND, KCNJ10, FXYD2, HNF1B or PCBD1. In these diseases, the hypomagnesemia is accompanied by other defects in electrolyte handling such as hypocalciuria and hypokalemia. The genes involved in this group of diseases all encode proteins that are involved in reabsorbing electrolytes (including magnesium) in the distal convoluted tubule of the kidney.
+- Hypercalciuric hypomagnesemic syndromes, which encompass the syndromes caused by mutations in CLDN16, CLDN19, CASR or CLCNKB. In these diseases, reabsorption of divalent cations (such as magnesium and calcium) in the thick ascending limb of Henle's loop of the kidney is impaired. This results in loss of magnesium and calcium in the urine.
+- Mitochondriopathies, such as caused by mutations in SARS2, MT-TI or as seen with Kearns-Sayre syndrome.
+- Other genetic causes of hypomagnesemia, such as mutations in TRPM6, CNNM2, EGF, EGFR, KCNA1 or FAM111A. Many of the proteins encoded by these genes play a role in the transcellular absorption of magnesium in the distal convoluted tubule.
+- Metabolic abnormalities => Insufficient selenium, vitamin D, sunlight exposure or vitamin B6.
+- Gastrointestinal causes: the distal tractus digestivus secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohn's disease, ulcerative colitis, Whipple's disease and celiac sprue can all cause hypomagnesemia.
+- Postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant. Citation needed.
+- Other => Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines.
+- Malabsorption
+- Acute pancreatitis
+- Fluoride poisoning
+- Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications.
+The diagnosis can be made by finding a plasma magnesium concentration of less than 0.6 mmol/L (1.46 mg/dl). Since most magnesium is intracellular, a body deficit can be present with a normal plasma concentration.
+The ECG may show a tachycardia with a prolonged QT interval, which has been noted in proton pump inhibitor-associated hypomagnesemia.
+Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, hypokalemia, hypoparathyroidism which might result in hypocalcemia, chondrocalcinosis, spasticity and tetany, epileptic seizures, basal ganglia calcifications and in extreme and prolonged cases coma, intellectual disability or death. Other symptoms that have been suggested to be associated with hypomagnesemia are athetosis, jerking, nystagmus, and an extensor plantar reflex, confusion, disorientation, hallucinations, depression, hypertension and fast heart rate.
+People being treated on an intensive care unit who have a low magnesium level may have a higher risk of requiring mechanical ventilation, and death.
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DISNET disease texts/100 Clean Disease Texts/Hypovolemia.txt

+Common causes of hypovolemia are.
+- Loss of blood (external or internal bleeding or blood donation)
+- Loss of plasma (severe burns and lesions discharging fluid)
+- Loss of body sodium and consequent intravascular water; e. G. Diarrhea or vomitin.
+Excessive sweating is not a cause of hypovolemia, because the body eliminates significantly more water than sodium.
+Clinical symptoms may not be present until 10–20% of total whole-blood volume is lost.
+Hypovolemia can be recognized by tachycardia, diminished blood pressure, and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.
+Note that in children compensation can result in an artificially high blood pressure despite hypovolemia. Children will typically compensate (maintain blood pressure despite loss of blood volume) for a longer period than adults, but will deteriorate rapidly and severely once they do begin to decompensate. This is another reason (aside from initial lower blood volume) that even the possibility of internal bleeding in children should almost always be treated aggressively.
+Obvious signs of external bleeding should be noted while remembering that people can bleed to death internally without any external blood loss. ("Blood on the floor, plus 4 more" = intrathoracic, intraperitoneal, retroperitoneal, pelvis/thigh).
+There should be considered possible mechanisms of injury that may have caused internal bleeding, such as ruptured or bruised internal organs. If trained to do so and if the situation permits, there should be conducted a secondary survey and checked the chest and abdomen for pain, deformity, guarding, discoloration or swelling. Bleeding into the abdominal cavity can cause the classical bruising patterns of Grey Turner's sign or Cullen's sign.
+Usually referred to as a "class" of shock. Most sources state that there are 4 stages of hypovolemic shock; however, a number of other systems exist with as many as 6 stages.
+The 4 stages are sometimes known as the "Tennis" staging of hypovolemic shock, as the stages of blood loss (under 15% of volume, 15–30% of volume, 30–40% of volume and above 40% of volume) mimic the scores in a game of tennis: 15,15–30,30–40 and 40. It is basically the same as used in classifying bleeding by blood loss.
+The signs and symptoms of the major stages of hypovolemic shock include:
+Stage 1 Stage 2 Stage 3 Stage 4 headingBody Blood loss Up to 15% (750 mL) 15–30% (750–1500 mL) 30–40% (1500–2000 mL) Over 40% (over 2000 mL) Blood pressure Normal (Maintained by vasoconstriction) Increased diastolic BP Systolic BP < 100 Systolic BP < 70 Heart rate Normal Slight tachycardia (> 100 bpm) Tachycardia (> 120 bpm) Extreme tachycardia (> 140 bpm) with weak pulse Respiratory rate Normal Increased (> 20) Tachypneic (> 30) Extreme tachypnea Mental status Normal Slight anxiety, restless Altered, confused Decreased LOC, lethargy, coma Skin Pallor Pale, cool, clammy Increased diaphoresis Extreme diaphoresis; mottling possible Capillary refill Normal Delayed Delayed Absent Urine output Normal 20–30 mL/h 20 mL/h Negligible
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DISNET disease texts/100 Clean Disease Texts/Inborn error of metabolism.txt

+Dozens of congenital metabolic diseases are now detectable by newborn screening tests, especially the expanded testing using mass spectrometry. This is an increasingly common way for the diagnosis to be made and sometimes results in earlier treatment and a better outcome. There is a revolutionary Gas chromatography–mass spectrometry-based technology with an integrated analytics system, which has now made it possible to test a newborn for over 100 mm genetic metabolic disorders.
+Because of the multiplicity of conditions, many different diagnostic tests are used for screening. An abnormal result is often followed by a subsequent "definitive test" to confirm the suspected diagnosis.
+Common screening tests used in the last sixty years:
+- Ferric chloride test (turned colors in reaction to various abnormal metabolites in urine)
+- Ninhydrin paper chromatography (detected abnormal amino acid patterns)
+- Guthrie bacterial inhibition assay (detected a few amino acids in excessive amounts in blood) The dried blood spot can be used for multianalyte testing using Tandem Mass Spectrometry (MS/MS). This given an indication for a disorder. The same has to be further confirmed by enzyme assays, IEX-Ninhydrin, GC/MS or DNA Testing.
+- Quantitative measurement of amino acids in plasma and urine
+- IEX-Ninhydrin post column derivitization liquid ion-exchange chromatography (detected abnormal amino acid patterns and quantitative analysis)
+- Urine organic acid analysis by gas chromatography–mass spectrometry
+- Plasma acylcarnitines analysis by mass spectrometry
+- Urine purines and pyrimidines analysis by gas chromatography-mass spectrometr.
+Specific diagnostic tests (or focused screening for a small set of disorders):
+- Tissue biopsy or necropsy: liver, muscle, brain, bone marrow
+- Skin biopsy and fibroblast cultivation for specific enzyme testing
+- Specific DNA testin.
+A 2015 review reported that even with all these diagnostic tests, there are cases when "biochemical testing, gene sequencing, and enzymatic testing can neither confirm nor rule out an IEM, resulting in the need to rely on the patient's clinical course. ".
+Because of the enormous number of these diseases and wide range of systems affected, nearly every "presenting complaint" to a doctor may have a congenital metabolic disease as a possible cause, especially in childhood. The following are examples of potential manifestations affecting each of the major organ systems.
+- Growth failure, failure to thrive, weight loss
+- Ambiguous genitalia, delayed puberty, precocious puberty
+- Developmental delay, seizures, dementia, encephalopathy, stroke
+- Deafness, blindness, pain agnosia
+- Skin rash, abnormal pigmentation, lack of pigmentation, excessive hair growth, lumps and bumps
+- Dental abnormalities
+- Immunodeficiency, low platelet count, low red blood cell count, enlarged spleen, enlarged lymph nodes
+- Many forms of cancer
+- Recurrent vomiting, diarrhea, abdominal pain
+- Excessive urination, kidney failure, dehydration, edema
+- Low blood pressure, heart failure, enlarged heart, hypertension, myocardial infarction
+- Liver enlargement, jaundice, liver failure
+- Unusual facial features, congenital malformations
+- Excessive breathing (hyperventilation), respiratory failure
+- Abnormal behavior, depression, psychosis
+- Joint pain, muscle weakness, cramps
+- Hypothyroidism, adrenal insufficiency, hypogonadism, diabetes mellitu
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DISNET disease texts/100 Clean Disease Texts/Influenza.txt

+Symptom: sensitivity specificity Fever Cough Nasal congestion headingBody 68–86% 25–73% 84–98% 7–29% 68–91% 19–41% All three findings, especially fever, were less sensitive in people over 60 years of age.
+Approximately 33% of people with influenza are asymptomatic.
+Symptoms of influenza can start quite suddenly one to two days after infection. Usually the first symptoms are chills or a chilly sensation, but fever is also common early in the infection, with body temperatures ranging from 38 to 39 °C (approximately 100 to 103 °F). Many people are so ill that they are confined to bed for several days, with aches and pains throughout their bodies, which are worse in their backs and legs. Symptoms of influenza may include:
+- Fever and chills
+- Cough
+- Nasal congestion
+- Runny nose
+- Sneezing
+- Sore throat
+- Hoarseness
+- Ear pressure
+- Earache
+- Muscle aches
+- Fatigue
+- Headache
+- Irritated, watering eyes
+- Reddened eyes, skin (especially face), mouth, throat and nose
+- Petechial rash
+- In children, gastrointestinal symptoms such as diarrhea, vomiting, and abdominal pain, (may be severe in children with influenza B).
+It can be difficult to distinguish between the common cold and influenza in the early stages of these infections. Influenza is a mixture of symptoms of common cold and pneumonia, body ache, headache, and fatigue. Diarrhea is not normally a symptom of influenza in adults, although it has been seen in some human cases of the H5N1 "bird flu" and can be a symptom in children. The symptoms most reliably seen in influenza are shown in the adjacent table.
+Since antiviral drugs are effective in treating influenza if given early (see treatment section, below), it can be important to identify cases early. Of the symptoms listed above, the combinations of fever with cough, sore throat and/or nasal congestion can improve diagnostic accuracy. Two decision analysis studies suggest that during local outbreaks of influenza, the prevalence will be over 70%, and thus patients with any of these combinations of symptoms may be treated with neuraminidase inhibitors without testing. Even in the absence of a local outbreak, treatment may be justified in the elderly during the influenza season as long as the prevalence is over 15%.
+The available laboratory tests for influenza continue to improve. The United States Centers for Disease Control and Prevention (CDC) maintains an up-to-date summary of available laboratory tests. According to the CDC, rapid diagnostic tests have a sensitivity of 50–75% and specificity of 90–95% when compared with viral culture. These tests may be especially useful during the influenza season (prevalence = 25%) but in the absence of a local outbreak, or peri-influenza season (prevalence = 10%).
+Occasionally, influenza can cause severe illness including primary viral pneumonia or secondary bacterial pneumonia. The obvious symptom is trouble breathing. In addition, if a child (or presumably an adult) seems to be getting better and then relapses with a high fever, that is a danger sign since this relapse can be bacterial pneumonia.
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DISNET disease texts/100 Clean Disease Texts/Intention tremor.txt

+Intention tremors are common among individuals with multiple sclerosis (MS). One common symptom of multiple sclerosis is ataxia, a lack of coordinated muscle movement caused by cerebellar lesions characteristic of multiple sclerosis. The disease often destroys physical and cognitive function of individuals.
+Intention tremors can be a first sign of multiple sclerosis, since loss or deterioration of motor function and sensitivity are often one of the first symptoms of cerebellar lesions.
+Intention tremors have a variety of other recorded causes as well. These include a variety of neurological disorders, such as stroke, alcoholism, alcohol withdrawal, peripheral neuropathy, Wilson's disease, Creutzfeldt–Jakob disease, Guillain–Barré syndrome and fragile X syndrome, as well as brain tumors, low blood sugar, hyperthyroidism, hypoparathyroidism, insulinoma, normal aging, and traumatic brain injury. Holmes tremor, a rubral or midbrain tremor, is another form of tremor that includes intention tremors, among other symptoms. This disease affects the proximal muscles of the head, shoulders, and neck. Tremors of this disease occur at frequencies of 2–4 Hz or more.
+Intention tremor is also known to be associated with infections, West Nile virus, rubella, H. Influenza, rabies, and varicella. A variety of poisons have been shown to cause intention tremor, including mercury, methyl bromide, and phosphine. In addition, vitamin deficiencies have been linked to intention tremor, especially deficiency in vitamin E. Pharmacological agents such as anti-arrhythmic drugs, anti-epileptic agents, benzodiazepine, cyclosporine, lithium, neuroleptics, and stimulants have been known to cause intention tremor. Some ordinary activities including ingesting too much caffeine, cigarettes, and alcohol, along with stress, anxiety, fear, anger and fatigue have also been shown to cause intention tremor by negatively affecting the cerebellum, brainstem, or thalamus, as discussed in mechanisms.
+A working diagnosis is made from a neurological examination and evaluation. Parts of a complete examination include a physical examination, MRI, patient history, and electrophysiological and accelerometric studies. A diagnosis of solely intention tremor can only be made if the tremor is of low frequency (below 5 Hz) and without the presence of any resting tremors. Electrophysiological studies can be useful in determining frequency of the tremor, and accelerometric studies quantify tremor amplitude. MRI is used to locate damage to and degradation of the cerebellum that may be causing the intention tremor. Focal lesions such as neoplasms, tumors, hemorrhages, demyelination, or other damage may be causing dysfunction of the cerebellum and correspondingly the intention tremor.
+Physical tests are an easy way to determine the severity of the intention tremor and impairment of physical activity. Common tests that are used to assess intention tremor are the finger-to-nose and heel-to-shin tests. In a finger-to-nose test, a physician has the individual touch their nose with their finger while monitoring for irregularity in timing and control of the movement. An individual with intention tremors will have coarse side-to-side movements that increase in severity as the finger approaches the nose. Similarly, the heel-to-shin test evaluates intention tremors of the lower extremities. In such a test, the individual, in a supine position, places one heel on top of the opposite knee and is then instructed to slide the heel down the shin to the ankle while being monitored for coarse and irregular side-to-side movement as the heel approaches the ankle. Important historical elements to the diagnosis of intention tremor are:
+- age at onset
+- mode of onset (sudden or gradual)
+- anatomical affected sites
+- rate of progression
+- exacerbating and remitting factors
+- alcohol abuse
+- family history of tremor
+- current medications.
+Secondary symptoms commonly observed are dysarthria (a speech disorder characterized by poor articulation and slurred speech), nystagmus (rapid involuntary eye movement, especially rolling of the eyes), gait problems (abnormality in walking), and postural tremor or titubation (to-and-fro movements of the neck and trunk). A postural tremor may also accompany intention tremors.
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DISNET disease texts/100 Clean Disease Texts/Intraparenchymal hemorrhage.txt

+Hypertension
+- Arteriovenous malformation
+- Aneurysm rupture
+- Cerebral amyloid angiopathy
+- Intracranial neoplasm
+- Coagulopathy
+- Hemorrhagic transformation of an ischemic infarct
+- Cerebral venous thrombosis
+- Sympathomimetic drug abuse
+- Moyamoya
+- Sickle cell disease
+- Eclampsia or postpartum vasculopathy
+- Infection
+- Vasculitis
+- Neonatal intraventricular hemorrhage
+- Traum.
+In younger patients, vascular malformations, specifically AVMs and cavernous angiomas are more common causes for hemorrhage. In addition, venous malformations are associated with hemorrhage.
+In the elderly population, amyloid angiopathy is associated with cerebral infarcts as well as hemorrhage in superficial locations, rather than deep white matter or basal ganglia. These are usually described as "lobar". These bleedings are not associated with systemic amyloidosis.
+Hemorrhagic neoplasms are more complex, heterogeneous bleeds often with associated edema. These hemorrhages are related to tumor necrosis, vascular invasion and neovascularity. Glioblastomas are the most common primary malignancies to hemorrhage while thyroid, renal cell carcinoma, melanoma, and lung cancer are the most common causes of hemorrhage from metastatic disease.
+Other causes of intraparenchymal hemorrhage include hemorrhagic transformation of infarction which is usually in a classic vascular distribution and is seen in approximately 24 to 48 hours following the ischemic event. This hemorrhage rarely extends into the ventricular system.
+Computed tomography (CT scan): A CT scan may be normal if it is done soon after the onset of symptoms. A CT scan is the best test to look for bleeding in or around your brain. In some hospitals, a perfusion CT scan may be done to see where the blood is flowing and not flowing in your brain.
+Magnetic resonance imaging (MRI scan): A special MRI technique (diffusion MRI) may show evidence of an ischemic stroke within minutes of symptom onset. In some hospitals, a perfusion MRI scan may be done to see where the blood is flowing and not flowing in your brain.
+Angiogram: a test that looks at the blood vessels that feed the brain. An angiogram will show whether the blood vessel is blocked by a clot, the blood vessel is narrowed, or if there is an abnormality of a blood vessel known as an aneurysm.
+Carotid duplex: A carotid duplex is an ultrasound study that assesses whether or not you have atherosclerosis (narrowing) of the carotid arteries. These arteries are the large blood vessels in your neck that feed your brain.
+Transcranial Doppler (TCD): Transcranial Doppler is an ultrasound study that assesses whether or not you have atherosclerosis (narrowing) of the blood vessels inside of your brain. It can also be used to see if you have emboli (blood clots) in your blood vessels.
+Clinical manifestations of intraparenchymal hemorrhage are determined by the size and location of hemorrhage, but may include the following:
+- Hypertension, fever, or cardiac arrhythmias
+- Nuchal rigidity
+- Subhyaloid retinal hemorrhages
+- Altered level of consciousness
+- Anisocoria, Nystagmus
+- Focal neurological deficits
+- Putamen-Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia, neglect, or apraxia
+- Thalamus-Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion
+- Lobar-Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia
+- Caudate nucleus-Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion
+- Brain stem-Tetraparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability
+- Cerebellum-Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousnes
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DISNET disease texts/100 Clean Disease Texts/Itch.txt

+Infections => Allergic reaction to contact with specific chemicals, such as urushiol, derived from poison ivy or poison oak, or Balsam of Peru, found in many foods and fragrances. Certain allergens may be diagnosed in a patch test.
+- Body louse, found in substandard living conditions
+- Cutaneous larva migrans, a skin disease
+- Head lice, if limited to the neck and scalp
+- Herpes, a viral disease
+- Insect bites, such as those from mosquitos or chiggers
+- Photodermatitis – sunlight reacts with chemicals in the skin, leading to the formation of irritant metabolites
+- Pubic lice, if limited to the genital area
+- Scabies, especially when several other persons in close contact also itch
+- Shaving, which may irritate the skin
+- Swimmer's itch, a short-term immune reaction
+- Varicella – i.e. Chickenpox, prevalent among young children and highly contagiou.
+- Environmental and allergic => Foreign objects on the skin are the most common cause of non-pathological itching.
+- Urticaria (also called hives) usually causes itchin.
+- Skin disorders => Dandruff – an unusually large amount of flaking is associated with this sensation
+- Punctate palmoplantar keratoderma, a group of disorders characterized by abnormal thickening of the palms and soles
+- Skin conditions (such as psoriasis, eczema, sunburn, athlete's foot, and hidradenitis suppurativa). Most are of an inflammatory nature.
+- Scab healing, scar growth, and the development or emergence of moles, pimples, and ingrown hairs from below the epidermis
+- Xerosis – dry skin, the most common cause, frequently seen in the winter and also associated with older age, frequent bathing in hot showers or baths, and high-temperature and low-humidity environment.
+- Medical disorders => Diabetes mellitus, a group of metabolic diseases in which a person has high blood sugar
+- Hyperparathyroidism, overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH)
+- Iron deficiency anemia, a common anemia (low red blood cell or hemoglobin levels)
+- Jaundice and cholestasis – bilirubin is a skin irritant at high concentrations
+- Malignancy or internal cancer, such as lymphoma or Hodgkin's disease
+- Polycythemia, which can cause generalized itching due to increased histamines
+- Psychiatric disease ("psychogenic itch", as may be seen in delusional parasitosis)
+- Thyroid illness
+- Uraemia – the itching sensation this causes is known as uremic pruritu.
+- Medication => Drugs (such as opioids) that activate histamine (H1) receptors or trigger histamine release
+- Chloroquine, a dru.
+- Related to pregnancy => Gestational pemphigoid, a dermatosis of pregnancy
+- Intrahepatic cholestasis of pregnancy, a medical condition in which cholestasis occurs
+- Pruritic urticarial papules and plaques of pregnancy (PUPPP), a chronic hives-like ras.
+Other => Menopause, or changes in hormonal balances associated with agin.
+Pain and itch have very different behavioral response patterns. Pain evokes a withdrawal reflex, which leads to retraction and therefore a reaction trying to protect an endangered part of the body. Itch in contrast creates a scratch reflex, which draws one to the affected skin site. Itch generates stimulus of a foreign object underneath or upon the skin and also the urge to remove it. For example, responding to a local itch sensation is an effective way to remove insects from one's skin.
+Scratching has traditionally been regarded as a way to relieve oneself by reducing the annoying itch sensation. However, there are hedonic aspects of scratching, as one would find noxious scratching highly pleasurable. This can be problematic with chronic itch patients, such as ones with atopic dermatitis, who may scratch affected spots until they no longer produce a pleasant or painful sensation, instead of when the itch sensation disappears. It has been hypothesized that motivational aspects of scratching include the frontal brain areas of reward and decision making. These aspects might therefore contribute to the compulsive nature of itch and scratching.
+Contagious itch => Events of "contagious itch" are very common occurrences. Even a discussion on the topic of itch can give one the desire to scratch. Itch is likely to be more than a localized phenomenon in the place we scratch. Results from a study showed that itching and scratching were induced purely by visual stimuli in a public lecture on itching. The sensation of pain can also be induced in a similar fashion, often by listening to a description of an injury, or viewing an injury itself.
+There is little detailed data on central activation for contagious itching, but it is hypothesized that a human mirror neuron system exists in which we imitate certain motor actions when we view others performing the same action. A similar phenomenon in which mirror neurons are used to explain the cause is contagious yawning.
+Pain inhibition by itching => The sensation of itch can be reduced by many painful sensations. Studies done in the last decade have shown that itch can be inhibited by many other forms of painful stimuli, such as noxious heat, physical rubbing/scratching, noxious chemicals, and electric shock.
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DISNET disease texts/100 Clean Disease Texts/Juvenile dermatomyositis.txt

+The underlying cause of JDM is unknown. It most likely has a genetic component, as other autoimmune disease tend to run in the families of patients. The disease is usually triggered by a condition that causes immune system activity that does not stop as it should, but the trigger is almost certainly not the cause in most cases. Common triggers include immunizations, infections, injuries, and sunburn.
+Proximal muscle weakness, characteristic skin rash and elevated muscle enzymes are routinely used to identify JDM. Typical magnetic resonance imaging and muscle biopsy changes are considered the next most useful diagnostic criteria, followed by myopathic changes on electromyogram, calcinosis, dysphonia and nailfold capillaroscopy. Other useful criteria include myositis-specific or-related antibodies, nailfold capillaroscopy, factor VIII-related antigen, muscle ultrasound, calcinosis and neopterin.
+The vasculitis caused by JDMS manifests itself predominantly in two ways:
+One is a distinctive rash. The rash often affects the face, eyelids, and hands, and sometimes the skin above joints, including the knuckles, knees, elbows, etc. The color of the rash is a pinkish purple, and is called heliotrope (after a flower of the same name with approximately this color). On the hands and face, the rash very closely resembles allergies, eczema, fifth disease, or other more common skin condition, but the heliotrope color is unique to the inflammatory process of JDMS. Some children develop calcinosis, which are calcium deposits under the skin. The rash is the source of the "dermato-" part of the name of the disease.
+The second symptom caused by vasculitis is muscle inflammation. This symptom is the source of the "-myositis" part of the name of the disease ("myo" = muscle, "-itis" = inflammation of). Muscle Inflammation causes muscle weakness, which can cause fatigue, clumsiness, not keeping up physically with peers, and eventually inability to perform tasks like climbing stairs, lifting objects, and performing other manual tasks. Other signs may include falling, dysphonia, or dysphagia. The muscle weakness often causes a medical misdiagnosis of muscular dystrophy or other muscle disease. Some patients develop contractures, when the muscle shortens and causes joints to stay bent; exercise, occupational therapy, and physical therapy can prevent this. The muscles first affected tend to be proximal (i.e. , neck, shoulders, back, and abdominal). About half of children with JDMS also have pain in their muscles.
+Other symptoms may include irritability, weight loss, and mouth ulcers. When a child becomes irritable, fatigued, reluctant to socialize, and the face becomes flushed easily, physicians refer to this constellation of symptoms as "misery. ".
+Progression => The speed of the progression of JDMS is highly variable. Nearly all JDM patients have some skin involvement. The JDMS rash usually occurs as the initial symptom. Sometimes it is so slight as not to be recognized for what it is until muscle symptoms appear. Sometimes muscle symptoms never appear at all or occur very gradually over the course of months, and sometimes going from normal strength to being unable to walk within days. Usually, muscle symptoms appear weeks to months after the onset of the rash.
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DISNET disease texts/100 Clean Disease Texts/Kaposi's sarcoma.txt

+Kaposi's sarcoma-associated herpesvirus (KSHV), also called HHV-8 is present in almost 100% of Kaposi sarcoma lesions, whether HIV-related, classic, endemic, or iatrogenic.
+Transmission => In Europe and North America, KSHV is transmitted through saliva. Thus, kissing is a theoretical risk factor for transmission. Higher rates of transmission among gay and bisexual men have been attributed to "deep kissing" sexual partners with KSHV. Another alternative theory suggests that use of saliva as a sexual lubricant might be a major mode for transmission. Prudent advice is to use commercial lubricants when needed and avoid deep kissing with partners with KSHV infection or whose status is unknown.
+KSHV is also transmissible via organ transplantation and blood transfusion. Testing for the virus before these procedures is likely to effectively limit iatrogenic transmission.
+Classification => HHV-8, is responsible for all varieties of KS. Since Moritz Kaposi first described this cancer, the disease has been reported in five separate clinical settings, with different presentations, epidemiology, and prognoses.:599 All of these forms are infected with KSHV and are different manifestations of the same disease but have differences in clinical aggressiveness, prognosis and treatment.
+- Classic Kaposi sarcoma most commonly appears early on the toes and soles as reddish, violaceous, or bluish-black macules and patches that spread and coalesce to form nodules or plaques.:599 A small percentage of these patients may have visceral lesions. In most cases the treatment involves surgical removal of the lesion. The condition tends to be indolent and chronic, affecting elderly men from the Mediterranean region, Arabian countries or of Eastern European descent. Countries bordering the Mediterranean basin have higher rates of KSHV/HHV-8 infection than the remainder of Europe.
+- Endemic KS, which has two types. Although this may be present worldwide, it has been originally described later in young African people, mainly from sub-Saharan Africa. This variant is not related to HIV infection and is a more aggressive disease that infiltrates the skin extensively. African lymphadenopathic Kaposi sarcoma is aggressive, occurring in children under 10 years of age, presenting with lymph node involvement, with or without skin lesions.:599 African cutaneous Kaposi sarcoma presents with nodular, infiltrative, vascular masses on the extremities, mostly in men between the ages of 20 and 50, and is endemic in tropical Africa.:599
+- African lymphadenopathic Kaposi sarcoma is aggressive, occurring in children under 10 years of age, presenting with lymph node involvement, with or without skin lesions.:599
+- African cutaneous Kaposi sarcoma presents with nodular, infiltrative, vascular masses on the extremities, mostly in men between the ages of 20 and 50, and is endemic in tropical Africa.:599
+- Immunosuppression-associated Kaposi sarcoma had been described, but only rarely until the advent of calcineurin inhibitors (such as ciclosporines, which are inhibitors of T-cell function) for transplant patients in the 1980s, when its incidence grew rapidly. The tumor arises either when an HHV 8-infected organ is transplanted into someone who has not been exposed to the virus or when the transplant recipient already harbors pre-existing HHV 8 infection. Unlike classic Kaposi sarcoma, the site of presentation is more variable.:60.
+AIDS-associated Kaposi sarcoma typically presents with cutaneous lesions that begin as one or several red to purple-red macules, rapidly progressing to papules, nodules, and plaques, with a predilection for the head, back, neck, trunk, and mucous membranes. In more advanced cases, they can be found in the stomach and intestines, the lymph nodes, and the lungs.:599 KS-AIDS stimulated the greatest interest as one of the first illnesses associated with AIDS, and was first described in 1981. It is over 300 times more common in AIDS patients than in renal transplant recipients. In this case, HHV 8 is sexually transmitted among people also at risk for sexually transmitted HIV infection.
+Although KS may be suspected from the appearance of lesions and the patient's risk factors, definite diagnosis can be made only by biopsy and microscopic examination. Detection of the KSHV protein LANA in tumor cells confirms the diagnosis.
+In differential diagnosis, arteriovenous malformations, pyogenic granuloma and other vascular proliferations can be microscopically confused with KS.
+KS lesions are nodules or blotches that may be red, purple, brown, or black, and are usually papular.
+They are typically found on the skin, but spread elsewhere is common, especially the mouth, gastrointestinal tract and respiratory tract. Growth can range from very slow to explosively fast, and is associated with significant mortality and morbidity.
+Commonly affected areas include the lower limbs, back, face, mouth, and genitalia. The lesions are usually as described above, but may occasionally be plaque-like (often on the soles of the feet) or even involved in skin breakdown with resulting fungating lesions. Associated swelling may be from either local inflammation or lymphoedema (obstruction of local lymphatic vessels by the lesion). Skin lesions may be quite disfiguring for the sufferer, and a cause of much psychosocial pathology.
+The mouth is involved in about 30% of cases, and is the initial site in 15% of AIDS-related KS. In the mouth, the hard palate is most frequently affected, followed by the gums. Lesions in the mouth may be easily damaged by chewing and bleed or suffer secondary infection, and even interfere with eating or speaking.
+Gastrointestinal tract => Involvement can be common in those with transplant-related or AIDS-related KS, and it may occur in the absence of skin involvement. The gastrointestinal lesions may be silent or cause weight loss, pain, nausea/vomiting, diarrhea, bleeding (either vomiting blood or passing it with bowel motions), malabsorption, or intestinal obstruction.
+Respiratory tract => Involvement of the airway can present with shortness of breath, fever, cough, hemoptysis (coughing up blood), or chest pain, or as an incidental finding on chest x-ray. The diagnosis is usually confirmed by bronchoscopy when the lesions are directly seen, and often biopsied.
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DISNET disease texts/100 Clean Disease Texts/Lambert–Eaton myasthenic syndrome.txt

+LEMS is often associated with lung cancer (50–70%), specifically small-cell carcinoma, making LEMS a paraneoplastic syndrome. Of the people with small-cell lung cancer, 1–3% have LEMS. In most of these cases, LEMS is the first symptom of the lung cancer, and it is otherwise asymptomatic.
+LEMS may also be associated with autoimmune diseases, such as hypothyroidism (an underactive thyroid gland) or diabetes mellitus type 1. Myasthenia gravis, too, may happen in the presence of tumors (thymoma, a tumor of the thymus in the chest); people with MG without a tumor and people with LEMS without a tumor have similar genetic variations that seem to predispose them to these diseases. HLA-DR3-B8 (an HLA subtype), in particular, seems to predispose to LEMS.
+The diagnosis is usually made on electromyography (EMG), which is one of the standard tests in the investigation of otherwise unexplained muscle weakness. This involves the insertion of small needles into the nerves supplying several muscles, administering small electrical impulses through these needles, and measuring the electrical response of the muscle in question. Two EMG investigations can be characteristic in LEMS: compound motor action potentials (CMAPs) and single-fiber examination.
+CMAPs show small amplitudes but normal latency and conduction velocities. If repeated impulses are administered (2 per second or 2 Hz), it is normal for CMAP amplitudes to become smaller as the acetylcholine in the motor end plate is depleted. In LEMS, this decrease is larger than observed normally. Eventually, stored acetylcholine is made available, and the amplitudes increase again. In LEMS, this remains insufficient to reach a level sufficient for transmission of an impulse from nerve to muscle; all can be attributed to insufficient calcium in the nerve terminal. A similar pattern is witnessed in myasthenia gravis. In LEMS, in response to exercising the muscle, the CMAP amplitude increases greatly (over 200%, often much more). This also occurs on the administration of a rapid burst of electrical stimuli (20 impulses per second for 10 seconds). This is attributed to the influx of calcium in response to these stimuli. On single-fiber examination, features may include increased jitter (seen in other diseases of neuromuscular transmission) and blocking.
+Blood tests may be performed to exclude other causes of muscle disease (elevated creatine kinase may indicate a myositis, and abnormal thyroid function tests may indicate thyrotoxic myopathy). Antibodies against voltage-gated calcium channels can be identified in 85% of people with EMG-confirmed LEMS. Once LEMS is diagnosed, investigations such as a CT scan of the chest are usually performed to identify any possible underlying lung tumors. Around 50–60% of these are discovered immediately after the diagnosis of LEMS. The remainder is diagnosed later, but usually within two years and typically within four years. As a result, scans are typically repeated every six months for the first two years after diagnosis. While CT of the lungs is usually adequate, a positron emission tomography scan of the body may also be performed to search for an occult tumour, particularly of the lung.
+The weakness from LEMS typically involves the muscles of the proximal arms and legs (the muscles closer to the trunk). In contrast to myasthenia gravis, the weakness affects the legs more than the arms. This leads to difficulties climbing stairs and rising from a sitting position. Weakness is often relieved temporarily after exertion or physical exercise. High temperatures can worsen the symptoms. Weakness of the bulbar muscles (muscles of the mouth and throat) is occasionally encountered. Weakness of the eye muscles is uncommon. Some may have double vision, drooping of the eyelids and difficulty swallowing, but generally only together with leg weakness; this too distinguishes LEMS from myasthenia gravis, in which eye signs are much more common. In the advanced stages of the disease, weakness of the respiratory muscles may occur. Some may also experience problems with coordination (ataxia).
+Three-quarters of people with LEMS also have disruption of the autonomic nervous system. This may be experienced as a dry mouth, constipation, blurred vision, impaired sweating, and orthostatic hypotension (falls in blood pressure on standing, potentially leading to blackouts). Some report a metallic taste in the mouth.
+On neurological examination, the weakness demonstrated with normal testing of power is often less severe than would be expected on the basis of the symptoms. Strength improves further with repeated testing, e. G. Improvement of power on repeated hand grip (a phenomenon known as "Lambert's sign"). At rest, reflexes are typically reduced; with muscle use, reflex strength increases. This is a characteristic feature of LEMS. The pupillary light reflex may be sluggish.
+In LEMS associated with lung cancer, most have no suggestive symptoms of cancer at the time, such as cough, coughing blood, and unintentional weight loss. LEMS associated with lung cancer may be more severe.
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DISNET disease texts/100 Clean Disease Texts/Laryngitis.txt

+Laryngitis can be infectious as well as noninfectious in origin. The resulting inflammation of the vocal folds results in a distortion of the sound produced there. It normally develops in response to either an infection, trauma to the vocal folds, or allergies. Chronic laryngitis may also be caused by more severe problems, such as nerve damage, sores, polyps, or hard and thick lumps (nodules) on the vocal cords.
+Viral => Most acute cases of laryngitis are caused by viral infections, the most common of which tend to be rhinovirus, influenza virus, parainfluenza virus, adenovirus, coronavirus, and RSV. In patients who have a compromised immune system, other viruses such as herpes, HIV and coxsackievirus may also be potential causes.
+Bacterial => This is another major cause of acute laryngitis, and may develop in conjunction with or due to a viral infection. Common bacterial strains are; group A streptococcus, Streptococcus pneumoniae, C. Diphtheriae, M. Catarrhalis, Haemophilus influenzae, Bordetella pertussis, Bacillus anthracis, and M. Tuberculosis. In developing countries, more unusual bacterial causes may occur such as mycobacterial and syphilitic, though these may occur in developed nations as well.
+Fungal => Laryngitis caused by fungal infection is common but not frequently diagnosed according to a review by BMJ and can account for up to 10% of acute laryngitis cases. Patients with both functioning and impaired immune systems can develop fungal laryngitis, which may develop as a result of recent antibiotic or inhaled corticosteroids use. Certain strains of fungi that may cause laryngitis include; Histoplasma, Blastomyces, Candida (especially in immunocompromised persons), and Cryptococcus and Coccidioides.
+Trauma => Often due to excessive use of the vocal folds such as excessive yelling, screaming, singing. Though this often results in damage to the outer layers of the vocal folds, the subsequent healing may lead to changes in the physiology of the folds. Another potential cause of inflammation may be overuse of the vocal cords. Laryngeal trauma, including iatrogenic (caused by endotracheal intubation), can also result in inflammation of the vocal cords.
+Allergies => Findings are unclear as to whether asthma may cause symptoms commonly associated with laryngitis. Some researchers have posited that allergic causes of laryngitis are often misdiagnosed as being the result of acid reflux.
+Reflux => One possible explanation of chronic laryngitis is that inflammation is caused by gastro-oesophageal reflux which causes subsequent irritation of the vocal folds.
+- Autoimmune disorders => Approximately between 30 – 75% of persons with rheumatoid arthritis report symptoms of laryngitis.
+- Symptoms of laryngitis are present in only 0.5 – 5% of people that have sarcoidosis. According to a meta-analysis by Silva et al. (2007), this disease is often an uncommon cause of laryngeal symptoms and is frequently misdiagnosed as another voice disorder.
+- Acute laryngitis
+- Chronic laryngitis Granulomatous laryngitis Pseudomyxomatous laryngitis
+- Granulomatous laryngitis
+- Pseudomyxomatous laryngiti.
+Visual diagnosis => The larynx itself will often show erythema (reddening) and edema (swelling). This can be seen with laryngoscopy or stroboscopy (method depends on the type of laryngitis).:108 Other features of the laryngeal tissues may include.
+- Redness of the laryngeal tissues (acute)
+- Dilated blood vessels (acute)
+- Thick, yet dry laryngal tissue (chronic)
+- Stiff vocal folds
+- Sticky secretions between the vocal folds and nearby structures (the interarytenoid region.
+Referral => Some signs and symptoms indicate the need for early referral. These include.
+- Difficulty swallowing
+- Vocal stridor
+- Ear pain
+- Recent weight loss
+- History of smoking
+- Current or recent radiotherapy treatment (in the neck region)
+- Recent neck surgery or surgery involving endotracheal tubing
+- Person is a professional voice user (teacher, singer, actor, call center worker, and so on.
+The primary symptom of laryngitis is a hoarse voice.:108 Because laryngitis can have various causes, other signs and symptoms may vary. They can include.
+- Dry or sore throat
+- Coughing (both a causal factor and a symptom of laryngitis)
+- Frequent throat clearing
+- Increased saliva production
+- Dysphagia (difficulty swallowing)
+- Sensation of swelling in the area of the larynx (discomfort in the front of the neck)
+- Globus pharyngeus (feeling like there is a lump in the throat)
+- Cold or flu-like symptoms (which, like a cough, may also be a causal factor for laryngitis)
+- Swollen lymph nodes in the throat, chest, or face
+- Fever
+- General muscle pain (myalgia)
+- Shortness of breath, predominantly in childre.
+Voice quality => Aside from a hoarse-sounding voice, changes to pitch and volume may occur with laryngitis. Speakers may experience a lower or higher pitch than normal, depending on whether their vocal folds are swollen or stiff. They may also have breathier voices, as more air flows through the space between the vocal folds (the glottis), quieter volume and a reduced range.
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DISNET disease texts/100 Clean Disease Texts/Lateral medullary syndrome.txt

+It is the clinical manifestation resulting from occlusion of the posterior inferior cerebellar artery (PICA) or one of its branches or of the vertebral artery, in which the lateral part of the medulla oblongata infarcts, resulting in a typical pattern. The most commonly affected artery is the vertebral artery, followed by the PICA, superior middle and inferior medullary arteries.
+Since lateral medullary syndrome is often caused by a stroke, diagnosis is time dependent. Diagnosis is usually done by assessing vestibular-related symptoms in order to determine where in the medulla that the infarction has occurred. Head Impulsive Nystagmus Test of Skew (HINTS) examination of oculomotor function is often performed, along with computed tomography (CT) or magnetic resonance imaging (MRI) to assist in stroke detection. Standard stroke assessment must be done to rule out a concussion or other head trauma.
+This syndrome is characterized by sensory deficits that affect the trunk and extremities contralaterally (opposite to the lesion), and sensory deficits of the face and cranial nerves ipsilaterally (same side as the lesion). Specifically a loss of pain and temperature sensation if the lateral spinothalamic tract is involved. The cross body finding is the chief symptom from which a diagnosis can be made.
+Patients often have difficulty walking or maintaining balance (ataxia), or difference in temperature of an object based on which side of the body the object of varying temperature is touching. Some patients may walk with a slant or suffer from skew deviation and illusions of room tilt. The nystagmus is commonly associated with vertigo spells. These vertigo spells can result in falling, caused from the involvement of the region of Deiters’ nucleus.
+Common symptoms with lateral medullary syndrome may include difficulty swallowing, or dysphagia. This can be caused by the involvement of the nucleus ambiguous, as it supplies the vagus and glossopharyngeal nerves. Slurred speech (dysarthria), and disordered vocal quality (dysphonia) are also common. The damage to the cerebellum or the inferior cerebellar peduncle can cause ataxia. Damage to the hypothalamospinal fibers disrupts sympathetic nervous system relay and gives symptoms that are similar to the symptoms caused by Horner syndrome – such as miosis, anhidrosis and partial ptosis.
+Palatal myoclonus, the twitching of the muscles of the mouth, may be observed due to disruption of the central tegmental tract. Other symptoms include: hoarseness, nausea, vomiting, a decrease in sweating, problems with body temperature sensation, dizziness, difficulty walking, and difficulty maintaining balance. Lateral medullary syndrome can also cause bradycardia, a slow heart rate, and increases or decreases in the patients average blood pressure. 
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DISNET disease texts/100 Clean Disease Texts/MERRF syndrome.txt

+The cause of MERRF disorder is due to the mitochondrial genomes mutation. This means that its a pathogenic variants in mtDNA and is transmitted by maternal inheritance. A four points mutations in the genome can be identified which are associated with MERRF: A8344G, T8356°C, G8361A, and G8363A. The point mutation A8344G is mostly associated with MERRF, in a study published by Paul Jose Lorenzoni from the Department of neurology at University of Panama stated that 80% of the patients with MERRF disease exhibited this point mutation. This point mutation disrupts the mitochondrial gene for tRNA-Lys and so disrupts synthesis of proteins essential for oxidative phosphorylation. The remaining mutations only account for 10% of cases, and the remaining 10% of he patients with MERRF did not have an identifiable mutation in the mitochondrial DNA.
+Many genes are involved. These genes include:
+- MT-TK
+- MT-TL1
+- MT-TH
+- MT-TS1
+- MT-TS2
+- MT-TF.
+It involves the following characteristics:
+- progressive myoclonic epilepsy
+- "Ragged Red Fibers"-clumps of diseased mitochondria accumulate in the subsarcolemmal region of the muscle fiber and appear as "Ragged Red Fibers" when muscle is stained with modified Gömöri trichrome stain.
+There is currently no cure for MERRF.
+The diagnosis varies from individual to individual, each is evaluated and diagnosed according to their age, clinical phenotype and pressed inheritance pattern. If the Individual has been experiencing myoclonus the doctor will run a series of genetic studies to determine if its a mitochondrial disorder.
+The molecular genetic studies are run to identify the reason of for the mutations underlying the mitochondrial dysfunction. This approach will avoid the need for a muscle biopsy or an exhaustive metabolic evaluation. After the sequencing the mitochondrial genomes, four points mutations in the genome can be identified which are associated with MERRF: A8344G, T8356°C, G8361A, and G8363A. The point mutation A8344G is mostly associated with MERRF, in a study published by Paul Jose Lorenzoni from the Department of neurology at University of Panama stated that 80% of the patients with MERRF disease exhibited this point mutation. The remaining mutations only account for 10% of cases, and the remaining 10% of the patients with MERRF did not have an identifiable mutation in the mitochondrial DNA.
+If a patient does not exhibit mitochondrial DNA mutations, there are other ways that they can be diagnosed with MERRF. They can go through computed tomography (CT) or magnetic resonance imaging (MRI). The classification for the severity of MERRF syndrome is difficult to distinguish since most individuals will exhibit multi-symptoms. For children with complex neurologic or multi-system involvement, as the one described below, is often necessary.
+History and Physical Examination of the patient => A detailed family history should be obtained from at least three generations. In particularly a history to determine if there has been any neonatal and childhood deaths: Also a way to determine if any one of the family members exhibit any of the features of the multi-system disease. Specifically if there has been a maternal inheritance, when the disease is transmitted to females only, or if there is a family member who experienced a multi system involvement such as: Brain condition that a family member has been record to have such as seizures, dystonia, ataxia, or stroke like episodes. The eyes with optic atrophy, the skeletal muscle where there has been a history of myalgia, weakness or ptosis. Also in the family history look for neuropathy and dysautonomia, or observe heart conditions such ascardiomyopathy. The patients history might also exhibit a problem in their kidney, such as proximal nephron dysfunction. An endocrine condition, for example diabetes and hypoparathyroidism. The patient might have also had gastrointestinal condition which could have been due to liver disease, episodes of nausea or vomiting. Multiple lipomas in the skin, sideroblastic anemia and pancytopenia in the metabolic system or short stature might all be examples of patients with possible symptoms of MERRF disease.
+An individual displaying MERRFs syndrome will manifest not only a single symptom, but regularly patients display more than one affected body part at a time. It has been observed that patients with MERRF syndrome will primarily display Myoclonus as a first symptom, along with it they can also manifest seizures, cerebellar ataxia and myopathy. Secondary features include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity or multiple lipomata. Additional symptoms include dementia, optic atrophy, bilateral deafness and peripheral neuropathy, spasticity, lipomatosis, and/or cardiomyopathy with wolff parkinson-white syndrome. Most patients will not exhibit all of these symptoms, however more than one of these symptoms will be present in a patient who has been diagnosed with MERRFS disease. Due to the multi-symptoms presented by the individual, the severity of the syndrome is very difficult to evaluate. Mitochondrial disorders may present at any age, and this holds truth for MERRS, since it forms part of them. Therefore, if a patient is presenting some of these symptoms, the doctor is able to narrow it down to MEERF mitochondrial disorder.
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DISNET disease texts/100 Clean Disease Texts/Metal fume fever.txt

+Metal fume fever is due to the inhalation of certain metals, either as fine dust or most commonly as fumes. Simple metal compounds such as oxides are equally capable of causing it. The effects of particularly toxic compounds, such as nickel carbonyl, are not considered merely metal fume fever.
+Exposure usually arises through hot metalworking processes, such as smelting and casting of zinc alloys, welding of galvanized metals, brazing, or soldering. If the metal concerned is particularly high-risk, the residue from cold sanding processes may also cause fume fever, even if the dose is lower. It may also be caused by electroplated surfaces or metal-rich anti-corrosion paint, such as cadmium passivated steel or zinc chromate primer on aluminium aircraft parts. Exposure has also been reported in use of lead-free ammunition, by the harder steel core stripping excess metal from the jacket of the bullet and barrel of the rifle.
+The most plausible metabolic source of the symptoms is a dose-dependent release of certain cytokines, an event which occurs by inhaling metal oxide fumes that injure the lung cells. This is not an allergic reaction, though allergic reactions to metal fumes can occur.
+Diagnosis is primarily anecdotal, that is, it depends upon a good occupational history. Diagnosis of metal fume fever can be easily missed because the complaints are non-specific, resemble a number of other common illnesses, and presentation occurs typically 2–4 hours after the exposure. When respiratory symptoms are prominent, metal fume fever may be confused with acute bronchitis or pneumonia. The diagnosis is based primarily upon a history of exposure to metal oxide fumes. Cain and Fletcher (2010) report a case of metal fume fever that was diagnosed only by taking a full occupational history and by close collaboration between primary and secondary health care personnel.
+Physical symptoms vary among persons exposed, depending largely upon the stage in the course of the syndrome during which examination occurs. Patients may present with wheezing or crackles in the lungs. They typically have an increased white blood cell count, and urine, blood plasma and skin zinc levels may (unsurprisingly) be elevated. Chest X-ray abnormalities may also be present.
+An interesting feature of metal fume fever involves rapid adaptation to the development of the syndrome following repeated metal oxide exposure. Workers with a history of recurrent metal fume fever often develop a tolerance to the fumes. This tolerance, however, is transient, and only persists through the work week. After a weekend hiatus, the tolerance has usually disappeared. This phenomenon of tolerance is what led to the name "Monday Fever".
+In 2006, approximately 700 metal fume exposures were reported to the United States Poison control center. The American Welding Society estimated that 2500 employees in the steel industry develop metal fume fever in the US each year and that the majority of the cases are not reported.
+The signs and symptoms are generally flu-like. They include fever, chills, nausea, headache, fatigue, muscle aches, joint pains, lack of appetite, shortness of breath, pneumonia, chest pain, change in blood pressure, and coughing. A sweet or metallic taste in the mouth may also be reported, along with a dry or irritated throat which may lead to hoarseness. Symptoms of a more severe metal toxicity may also include a burning sensation in the body, shock, no urine output, collapse, convulsions, shortness of breath, yellow eyes or yellow skin, rash, vomiting, watery or bloody diarrhea or low or high blood pressure, which require prompt medical attention. Flu-like symptoms normally disappear within 24 to 48 hours. Full recovery often requires one to three weeks.
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DISNET disease texts/100 Clean Disease Texts/Morvan's syndrome.txt

+General symptoms => In one of the few reported cases, the subject presented with muscle weakness and fatigue, muscle twitching, excessive sweating and salivation, small joint pain, itching and weight loss. The subject also developed confusional episodes with spatial and temporal disorientation, visual and auditory hallucinations, complex behavior during sleep and progressive nocturnal insomnia associated with diurnal drowsiness. There was also severe constipation, urinary incontinence, and excessive lacrimation. When left alone, the subject would slowly lapse into a stuporous state with dreamlike episodes characterized by complex and quasi-purposeful gestures and movements (enacted dreams). Marked hyperhidrosis and excessive salivation were evident. Neurological examination disclosed diffuse muscle twitching and spontaneous and reflex myoclonus, slight muscle atrophy in the limbs, absence of tendon reflexes in the lower limbs and diffuse erythema especially on the trunk with scratching lesions of the skin. Compulsive behaviours, stereotypies and reduplicative paramnesias can be part of the CNS spectrum.
+Insomnia => In all of the reported cases, the need for sleep was severely reduced and in some cases not necessary. The duration of sleep in one case decreased to about 2–4 hours per 24-hour period. Clinical features pertaining to insomnia include daytime drowsiness associated with a loss of ability to sleep, intermingled with confusional oneiric status, and the emergence of atypical REM sleep from wakefulness. The Polysomnogram (PSG) picture of this disease is characterized by an inability to generate physiological sleep (key features are the suppression of the hallmarks of stage 2 non-REM sleep: spindles and K complexes) and by the emergence of REM sleep without atonia. The involvement of the thalamus and connected limbic structures in the pathology indicate the prominent role that the limbic thalamus plays in the pathophysiology of sleep. In a case documented in 1974, PSG findings documented the sustained absence of all sleep rhythms for up to a period of 4 months.
+Electroencephalography (EEG) in one case was dominated by "wakefulness" and “subwakefulness” states alternating or intermingled with short (< 1 min) atypical REM sleep phases, characterized by a loss of muscle atonia. The “subwakefulness” state was characterized by 4–6 Hz theta activity intermingled with fast activity and desynchronized lower voltage theta activity, behaviourally associated with sleep-like somatic and autonomic behavior. The subject was said to suffer from “agrypnia excitata”, which consists of severe total insomnia of long duration associated with decreased vigilance, mental confusion, hallucinations, motor agitation, and complex motor behavior mimicking dreams, and autonomic activation. CNS and autonomic symptoms were caused by impaired corticolimbic control of the subcortical structures regulating the sleep-wake and autonomic functions.
+Neuromyotonia => Neuromyotonia refers to muscle twitching and cramping at rest that is exacerbated with exercise. It is caused by sustained or repetitive spontaneous muscle activity of peripheral nerve origin. Myokymia, or spontaneous rippling and twitching movements of muscles, is a visible component of neuromyotonia. Electromyography (EMG) discloses spontaneous, repetitive motor unit or single fiber discharges firing in irregular rhythmic bursts at high intraburst frequencies. Some of the muscles exhibiting twitching include the bilateral gastrocnemii, quadriceps femoris, biceps brachii, and right masseter. In vivo electrophysiological studies suggest at least some dysfunction of the muscle cell membrane. In the examined muscles, no abnormal insertional activity or fibrillation potentials were noted. Nerve conduction studies were normal.
+Other symptoms => Breathing difficulties can occur, resulting from neuromyotonic activity of the laryngeal muscles. Laryngeal spasm possibly resulting from neuromyotonia has been described previously, and this highlights that, in patients with unexplained laryngospasm, neuromytonia should be added to the list of differential diagnoses.
+Studies have shown subtly decreased metabolism on positron emission tomography (PET) and single photon emission computed tomography (SPECT) in the left inferior frontal and left temporal lobes. And or basal ganglia hypermetabolism. Ancillary laboratory tests including MRI and brain biopsy have confirmed temporal lobe involvement. Cranial MRI shows increased signal in the hippocampus.
+Cerebral spinal fluid (CSF) shows normal protein, glucose, white blood cell, and IgG index but there are weak oligoclonal bands, absent in the blood. Marked changes in circadian serum levels of neurohormones and increased levels of peripheral neurotransmitters were also observed. The absence of morphological alterations of the brain pathology, the suggestion of diffusion of IgG into the thalamus and striatum, more marked than in the cortex (consistent with effects on the thalamolimbic system) the oligoclonal bands in the CSF and the amelioration after PE all strongly support an antibody-mediated basis for the condition. Raised CSF IgG concentrations and oligoclonal bands have been reported in patients with psychosis. Anti-acetylcholine receptors (anti-AChR) antibodies have also been detected in patients with thymoma, but without clinical manifestations of myasthenia gravis. There have also been reports of non-paraneoplastic limbic encephalitis associated with raised serum VGKC suggesting that these antibodies may give rise to a spectrum of neurological disease presenting with symptoms arising peripherally, centrally, or both. Yet, in two cases, oligoclonal bands were absent in the CSF and serum, and CSF immunoglobulin profiles were unremarkable.
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DISNET disease texts/100 Clean Disease Texts/Myocarditis.txt

+A large number of causes of myocarditis have been identified, but often a cause cannot be found. In Europe and North America, viruses are common culprits. Worldwide, however, the most common cause is Chagas' disease, an illness endemic to Central and South America that is due to infection by the protozoan Trypanosoma cruzi. Many of the causes listed below, particularly those involving protozoa, fungi, parasites, allergy, autoimmune disorders, and drugs are also causes of eosinophilic myocarditis.
+- Infections => Viral (adenovirus, parvovirus B19, coxsackie virus, HIV, enterovirus, rubella virus, polio virus, cytomegalovirus, human herpesvirus 6 and possibly hepatitis C)
+- Protozoan (Trypanosoma cruzi causing Chagas disease and Toxoplasma gondii)
+- Bacterial (Brucella, Corynebacterium diphtheriae, gonococcus, Haemophilus influenzae, Actinomyces, Tropheryma whipplei, Vibrio cholerae, Borrelia burgdorferi, leptospirosis, and Rickettsia, Mycoplasma pneumoniae)
+- Fungal (Aspergillus)
+- Parasitic (ascaris, Echinococcus granulosus, Paragonimus westermani, schistosoma, Taenia solium, Trichinella spiralis, visceral larva migrans, and Wuchereria bancrofti.
+Bacterial myocarditis is rare in patients without immunodeficiency.
+Toxins => Drugs, including alcohol, anthracyclines and some other forms of chemotherapy, and antipsychotics, e. G. Clozapine, also some designer drugs such as mephedrone.
+- Immunologic => Allergic (acetazolamide, amitriptyline)
+- Rejection after a heart transplant
+- Autoantigens (scleroderma, systemic lupus erythematosus, sarcoidosis, systemic vasculitis such as eosinophilic granulomatosis with polyangiitis, and granulomatosis with polyangiitis, Kawasaki disease)
+- Toxins (arsenic, toxic shock syndrome toxin, carbon monoxide, or snake venom)
+- Heavy metals (copper or iron.
+Physical agents => Electric shock, hyperpyrexia, and radiatio.
+Myocarditis refers to an underlying process that causes inflammation and injury of the heart. It does not refer to inflammation of the heart as a consequence of some other insult. Many secondary causes, such as a heart attack, can lead to inflammation of the myocardium and therefore the diagnosis of myocarditis cannot be made by evidence of inflammation of the myocardium alone.
+Myocardial inflammation can be suspected on the basis of electrocardiographic (ECG) results, elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.
+The ECG findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis).
+The gold standard is still biopsy of the myocardium, in general done in the setting of angiography. A small tissue sample of the endocardium and myocardium is taken, and investigated by a pathologist by light microscopy and—if necessary—immunochemistry and special staining methods. Histopathological features are myocardial interstitium with abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure.
+Cardiac magnetic resonance imaging (cMRI or CMR) has been shown to be very useful in diagnosing myocarditis by visualizing markers for inflammation of the myocardium. Recently, consensus criteria for the diagnosis of myocarditis by CMR have been published.
+- Play media Ultrasound showing cardiogenic shock due to myocarditis
+- Play media Ultrasound showing cardiogenic shock due to myocarditis
+- Play media Ultrasound showing cardiogenic shock due to myocarditis.
+The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium or to the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include the following:
+- Chest pain (often described as "stabbing" in character)
+- Congestive heart failure (leading to swelling, shortness of breath and liver congestion)
+- Palpitations (due to abnormal heart rhythms)
+- Sudden death (in young adults, myocarditis causes up to 20% of all cases of sudden death)
+- Fever (especially when infectious, e. G. In rheumatic fever)
+- Symptoms in young children tend to be more nonspecific, with generalized malaise, poor appetite, abdominal pain, and chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing, and is often mistaken for asthma.
+Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, rash, diarrhea, joint pains, and easily becoming tired.
+Myocarditis is often associated with pericarditis, and many people with myocarditis present with signs and symptoms that suggest myocarditis and pericarditis at the same time.
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DISNET disease texts/100 Clean Disease Texts/Necatoriasis.txt

+Necatoriasis is caused by N. Americanus. N. Americanus can be divided into two areas – larvae and adult stage. The third stage larvae are guided to human skin by following thermal gradients. Typically, the larvae enter through the hands and feet following contact with contaminated soil. A papular, pruritic, itchy rash will develop around the site of entry into the human host. This is also known as "ground itch". Generally, migration through the lungs is asymptomatic but a mild cough and pharyngeal irritation may occur during larval migration in the airways. Once larvae break through the alveoli and are swallowed, they enter the gastrointestinal tract and attach to the intestinal mucosa where they mature into adult worms. The hookworms attach to the mucosal lining using their cutting plates which allows them to penetrate blood vessels and feed on the host's blood supply. Each worm consumes 30μl of blood per day. The major issue results from this intestinal blood loss which can lead to iron-deficiency anemia in moderate to heavy infections. Other common symptoms include epigastric pain and tenderness, nausea, exertional dyspnea, pain in lower extremities and in joints, sternal pain, headache, fatigue, and impotence. Death is rare in humans.
+The standard method for diagnosing necatoriasis is through identification of N. Americanus eggs in a fecal sample using a microscope. Eggs can be difficult to visualize in a lightly infected sample so a concentration method is generally used such as flotation or sedimentation. However, the eggs of A. Duodenale and N. Americanus cannot be distinguished; thus, the larvae must be examined to identify these hookworms. Larvae cannot be found in stool specimens unless the specimen was left at ambient temperature for a day or more.
+The most common technique used to diagnose a hookworm infection is to take a stool sample, fix it in 10% formalin, concentrate it using the formalin-ethyl acetate sedimentation technique, and then create a wet mount of the sediment for viewing under a microscope.
+When adult worms attach to the villi of the small intestine, they suck on the host's blood, which may cause abdominal pain, diarrhea, cramps, and weight loss that can lead to anorexia. Heavy infections can lead to the development of iron deficiency and hypochromic microcytic anemia. This form of anemia in children can give rise to physical and mental retardation. Infection caused by cutaneous larvae migrans, a skin disease in humans, is characterized by skin ruptures and severe itching.
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DISNET disease texts/100 Clean Disease Texts/Nicotine poisoning.txt

+Increased nicotine or cotinine (the nicotine metabolite) is detected in urine or blood, or serum nicotine concentrations increase.
+Nicotine poisoning tends to produce symptoms that follow a biphasic pattern. The initial symptoms are mainly due to stimulatory effects and include nausea and vomiting, excessive salivation, abdominal pain, pallor, sweating, hypertension, tachycardia, ataxia, tremor, headache, dizziness, muscle fasciculations, and seizures. After the initial stimulatory phase, a later period of depressor effects can occur and may include symptoms of hypotension and bradycardia, central nervous system depression, coma, muscular weakness and/or paralysis, with difficulty breathing or respiratory failure.
+From September 1,2010 to December 31,2014, there were at least 21,106 traditional cigarette calls to US poison control centers. During the same period, the ten most frequent adverse effects to traditional cigarettes reported to US poison control centers were vomiting (80.0%), nausea (9.2%), drowsiness (7.8%), cough (7.2%), agitation (6.6%), pallor (3.0%), tachycardia (2.5%), diaphoresis (1.5%), dizziness (1.5%), and diarrhea (1.4%). 95% of traditional cigarette calls were related to children 5 years old or less. Most of the traditional cigarette calls were a minor effect.
+Calls to US poison control centers related to e-cigarette exposures involved inhalations, eye exposures, skin exposures, and ingestion, in both adults and young children. Minor, moderate, and serious adverse effects involved adults and young children. Minor effects correlated with e-cigarette liquid poisoning were tachycardia, tremor, chest pain and hypertension. More serious effects were bradycardia, hypotension, nausea, respiratory paralysis, atrial fibrillation and dyspnea. The exact correlation is not fully known between these effects and e-cigarettes. 58% of e-cigarette calls to US poison control centers were related to children 5 years old or less. E-cigarette calls had a greater chance to report an adverse effect and a greater chance to report a moderate or major adverse effect than traditional cigarette calls. Most of the e-cigarette calls were a minor effect.
+From September 1,2010 to December 31,2014, there were at least 5,970 e-cigarette calls to US poison control centers. During the same period, the ten most frequent adverse effects to e-cigarettes and e-liquid reported to US poison control centers were vomiting (40.4%), eye irritation or pain (20.3%), nausea (16.8%), red eye or conjunctivitis (10.5%), dizziness (7.5%), tachycardia (7.1%), drowsiness (7.1%), agitation (6.3%), headache (4.8%), and cough (4.5%).
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DISNET disease texts/100 Clean Disease Texts/Non-alcoholic fatty liver disease.txt

+Diet => Soft drinks have been linked to NAFLD due to high concentrations of fructose, which may be present either in high-fructose corn syrup or, in similar quantities, as a metabolite of sucrose. The quantity of fructose delivered by soft drinks may cause increased deposition of fat in the abdomen.
+Genetics => Native American men have a high prevalence of non-alcoholic fatty liver disease. Two genetic mutations for this susceptibility have been identified, and these mutations provided clues to the mechanism of NASH and related diseases.
+Polymorphisms (genetic variations) in the single-nucleotide polymorphisms (SNPs) T455°C and C482T in APOC3 are associated with fatty liver disease, insulin resistance, and possibly hypertriglyceridemia. 95 healthy Asian Indian men and 163 healthy non-Asian Indian men around New Haven, Connecticut were genotyped for polymorphisms in those SNPs. 20% homogeneous wild both loci. Carriers of T-455°C, C-482T, or both (not additive) had a 30% increase in fasting plasma apolipoprotein C3,60% increase in fasting plasma triglyceride and retinal fatty acid ester, and 46% reduction in plasma triglyceride clearance. Prevalence of non-alcoholic fatty liver disease was 38% in carriers, 0% wild (normal). Subjects with fatty liver disease had marked insulin resistance.
+Drugs => NAFLD can also be caused by some medications (drug-induced illness):
+- Amiodarone
+- Antiviral drugs (nucleoside analogues)
+- Aspirin rarely as part of Reye's syndrome in children
+- Corticosteroids
+- Methotrexate
+- Tamoxifen
+- Tetracyclin.
+Common findings are elevated liver enzymes and a liver ultrasound showing steatosis. An ultrasound may also be used to exclude gallstone problems (cholelithiasis). A liver biopsy (tissue examination) is the only test widely accepted as definitively distinguishing NASH from other forms of liver disease and can be used to assess the severity of the inflammation and resultant fibrosis.
+Non-invasive diagnostic tests have been developed, such as FibroTest, that estimates liver fibrosis, and SteatoTest, that estimates steatosis, however their use has not been widely adopted. Apoptosis has been indicated as a potential mechanism of hepatocyte injury as caspase-cleaved cytokeratin 18 (M30-Apoptosense ELISA) in serum/plasma is often elevated in patients with NASH and tests based on these parameters have been developed; however, as the role of oncotic necrosis has yet to be examined it is unknown to what degree apoptosis acts as the predominant form of injury.
+Other diagnostic tests are available. Relevant blood tests include erythrocyte sedimentation rate, glucose, albumin, and kidney function. Because the liver is important for making proteins used in coagulation some coagulation related studies are often carried out especially the INR (international normalized ratio). In people with fatty liver with associated inflammatory injury (steatohepatitis) blood tests are usually used to rule out viral hepatitis (hepatitis A, B, C and herpes viruses like EBV or CMV), rubella, and autoimmune related diseases. Hypothyroidism is more prevalent in NASH patients which would be detected by determining the TSH.
+It has been suggested that in cases involving overweight patients whose blood tests do not improve on losing weight and exercising that a further search of other underlying causes is undertaken. This would also apply to those with fatty liver who are very young or not overweight or insulin-resistant. In addition those whose physical appearance indicates the possibility of a congenital syndrome, have a family history of liver disease, have abnormalities in other organs, and those that present with moderate to advanced fibrosis or cirrhosis.
+Most people with NAFLD have few or no symptoms. Patients may complain of fatigue, malaise, and dull right-upper-quadrant abdominal discomfort. Mild jaundice may be noticed, although this is rare. More commonly NAFLD is diagnosed following abnormal liver function tests during routine blood tests. By definition, alcohol consumption of over 20 g/day (about 25 ml/day of net ethanol) excludes the condition.
+NAFLD is associated with insulin resistance and metabolic syndrome (obesity, combined hyperlipidemia, diabetes mellitus (type II), and high blood pressure). Recent research has shown that NAFLD increases the risk of cardiovascular diseases, such as cardiac arrhythmias.
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DISNET disease texts/100 Clean Disease Texts/Non-small-cell lung carcinoma.txt

+Smoking is by far the leading risk factor for lung cancer. Cigarette smoke contains more than 6,000 components, many of which lead to DNA damage (see table of tobacco-related DNA damages in Tobacco smoking).
+Other causes include radon, exposure to secondhand smoke, exposure to substances such as asbestos, chromium, nickel, beryllium, soot, or tar, family history of lung cancer, and air pollution.
+In general, DNA damage appears to be the primary underlying cause of cancer. Though most DNA damages are repairable, leftover un-repaired DNA damages from cigarette smoke are the likely cause of NSCLC.
+DNA replication past an un-repaired damage can give rise to a mutation because of inaccurate translesion synthesis. In addition, during repair of DNA double-strand breaks, or repair of other DNA damages, incompletely cleared sites of repair can lead to epigenetic gene silencing.
+Many of the symptoms of NSCLC can be signs of other diseases, but having chronic or overlapping symptoms may be a signal of the presence of the disease. Some symptoms are indicators of less advanced cases while some may signal that the cancer has spread. Some of the symptoms of less advanced cancer include chronic cough, coughing up blood, chest pain, hoarseness, shortness of breath, wheezing, chest pain, weight loss, and loss of appetite. A few more symptoms associated with the early progression of the disease are feeling weak, being very tired, having trouble swallowing, swelling in the face or neck, and continuous or recurring infections like bronchitis or pneumonia. Signs of more advanced cases include bone pain, nervous system changes (headache, weakness, dizziness, balance problems, seizures), jaundice, lumps near the surface of the body, numbness of extremities due to Pancoast Syndrome, and nausea, vomiting and constipation brought on by hypercalcemia. Some more of the symptoms that indicate further progression of the cancer include shortness of breath, superior vena cava syndrome, trouble swallowing, large amounts of mucus, weakness, fatigue, and hoarseness.
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DISNET disease texts/100 Clean Disease Texts/Normal pressure hydrocephalus.txt

+Diagnosis of NPH is usually first led by brain imaging, either CT or MRI, to rule out any mass lesions in the brain. This is then followed by lumbar puncture and evaluation of clinical response to removal of CSF. This can be followed by continuous external lumbar CSF drainage during 3 or 4 days.
+- CT scan may show enlarged ventricles without convolutional atrophy.
+- MRI may show some degree of transependymal migration of CSF surrounding the ventricles on T2/FLAIR sequence. Imaging however cannot differentiate between pathologies with similar clinical picture like Alzheimer's dementia, vascular dementia or Parkinson's disease.
+- Following imaging, lumbar puncture is usually the first step in diagnosis and the CSF opening pressure is measured carefully. In most cases, CSF pressure is usually above 155 mmH2O. Clinical improvement after removal of CSF (30 mL or more) has a high predictive value for subsequent success with shunting. This is called the "lumbar tap test" or Miller Fisher test. On the contrary, a "negative" test has a very low predictive accuracy, as many patients may improve after a shunt in spite of lack of improvement after CSF removal.
+- Infusion test is a test that may have higher sensitivity and specificity than a lumbar puncture, but is not performed in most centers. The outflow conductance (Cout) of the cerebrospinal fluid (CSF) system is a parameter considered by some centers to be predictive in selection for hydrocephalus surgery. Cout can be determined through an infusion test. This is not a test that is normally performed prior to shunting, but may become more accepted.
+- In some centers, External lumbar drainage has been shown to have the highest sensitivity and specificity with regards to predicting a successful outcome following surgery.
+Types => There are two types of normal pressure hydrocephalus: idiopathic and secondary. The secondary type of NPH can be due to a subarachnoid hemorrhage, head trauma, tumor, infection in the central nervous system, or a complication of cranial surgery.
+NPH may exhibit a classic triad of clinical findings (known as the Adams triad or Hakim's triad) of urinary incontinence, gait disturbance, and dementia (commonly referred to as "wet, wacky and wobbly" or "weird walking water").
+- Gait disturbance is typically the initial and most prominent symptom of the triad and may be progressive, due to expansion of the ventricular system, particularly at the level of the lateral ventricles, leading to traction on the corticospinal tract motor fibers descending to the lumbosacral spinal cord. The gait disturbance can be classified as mild (cautious gait or difficulty with tandem gait), marked (evident difficulty walking or considerable unstable gait) or severe (unaided gait not possible) In the early stages, most often this gait disturbance occurs in the form of unsteadiness and impaired balance, especially when encountering stairs and curbs. Weakness and tiredness of the legs may also be part of the complaint, although examination discloses no paresis or ataxia. Often a mobility aid is used for added stability, once the patient has reached the mild to marked stage. Such aids may include a quad cane or wheeled walker. The patient's gait at the marked stage will often show a decrease in step height and foot-floor clearance, as well as a decrease in walking speed. This style is often referred to as a magnetic gait, in which the feet appear to be stuck to the walking surface, and is considered the characteristic gait disturbance of NPH. The gait may begin to mimic a Parkinsonian gait, with short shuffling steps and stooped, forward-leaning posture, but there is no rigidity or tremor. An increased tendency to fall backwards is also seen, and a broad-based gait may be employed by the patient in order to increase their base of support and thereby their stability. In the very late stages, the patient can progress from an inability to walk, to an inability to stand, sit, rise from a chair or turn over in bed; this advanced stage is referred to as "hydrocephalic astasia-abasia".
+- Dementia is predominantly frontal lobe in nature and of the subcortical type of dementia. It presents in the form of abulia, forgetfulness, inertia, inattention, decreased speed of complex information procession (also described as a dullness in thinking and actions), and disturbed manipulation of acquired knowledge, which is reflective of the loss of integrity of the frontal lobes. Memory problems are usually a component of the overall problem and have been predominant in some cases, which can lead to the misdiagnosis of Alzheimer's disease. However, in NPH there may be an obvious discrepancy between (often severely) impaired recall and intact or much less impaired recognition. The dementia is thought to result from traction on frontal and limbic fibers that also run in the periventricular region.
+- Urinary incontinence appears late in the illness, and is found to be of the spastic hyperreflexic, increased-urgency type associated with decreased inhibition of bladder contractions and detrusor instability. In the most severe cases, bladder hyperreflexia is associated with a lack of concern for micturition due to the severe frontal lobe cognitive impairment. This is also known as "frontal lobe incontinence", where the patient becomes indifferent to their recurrent urinary symptoms
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DISNET disease texts/100 Clean Disease Texts/Obesity hypoventilation syndrome.txt

+Formal criteria for diagnosis of OHS are:
+- Body mass index over 30 kg/m2 (a measure of obesity, obtained by taking one's weight in kilograms and dividing it by one's height in meters squared)
+- Arterial carbon dioxide level over 45 mmHg or 6.0 kPa as determined by arterial blood gas measurement
+- No alternative explanation for hypoventilation, such as use of narcotics, severe obstructive or interstitial lung disease, severe chest wall disorders such as kyphoscoliosis, severe hypothyroidism (underactive thyroid), neuromuscular disease or congenital central hypoventilation syndrom.
+If OHS is suspected, various tests are required for its confirmation. The most important initial test is the demonstration of elevated carbon dioxide in the blood. This requires an arterial blood gas determination, which involves taking a blood sample from an artery, usually the radial artery. Given that it would be complicated to perform this test on every patient with sleep-related breathing problems, some suggest that measuring bicarbonate levels in normal (venous) blood would be a reasonable screening test. If this is elevated (27 mmol/l or higher), blood gasses should be measured.
+To distinguish various subtypes, polysomnography is required. This usually requires brief admission to a hospital with a specialized sleep medicine department where a number of different measurements are conducted while the subject is asleep; this includes electroencephalography (electronic registration of electrical activity in the brain), electrocardiography (same for electrical activity in the heart), pulse oximetry (measurement of oxygen levels) and often other modalities. Blood tests are also recommended for the identification of hypothyroidism and polycythemia.
+To distinguish between OHS and various other lung diseases that can cause similar symptoms, medical imaging of the lungs (such as a chest X-ray or CT/CAT scan), spirometry, electrocardiography and echocardiography may be performed. Echo-and electrocardiography may also show strain on the right side of the heart caused by OHS, and spirometry may show a restrictive pattern related to obesity.
+Most people with obesity hypoventilation syndrome have concurrent obstructive sleep apnea, a condition characterized by snoring, brief episodes of apnea (cessation of breathing) during the night, interrupted sleep and excessive daytime sleepiness. In OHS, sleepiness may be worsened by elevated blood levels of carbon dioxide, which causes drowsiness ("CO2 narcosis"). Other symptoms present in both conditions are depression, and hypertension (high blood pressure) that is difficult to control with medication. The high carbon dioxide can also cause headaches, which tend to be worsening in the morning.
+The low oxygen level leads to physiologic constriction of the pulmonary arteries to correct ventilation-perfusion mismatching, which puts excessive strain on the right side of the heart. When this leads to right sided heart failure, it is known as cor pulmonale. Symptoms of this disorder occur because the heart has difficulty pumping blood from the body through the lungs. Fluid may, therefore, accumulate in the skin of the legs in the form of edema (swelling), and in the abdominal cavity in the form of ascites; decreased exercise tolerance and exertional chest pain may occur. On physical examination, characteristic findings are the presence of a raised jugular venous pressure, a palpable parasternal heave, a heart murmur due to blood leaking through the tricuspid valve, hepatomegaly (an enlarged liver), ascites and leg edema. Cor pulmonale occurs in about a third of all people with OHS.
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DISNET disease texts/100 Clean Disease Texts/Opioid use disorder.txt

+Opioid use disorder can develop as a result of self-medication, though this is controversial. Scoring systems have been derived to assess the likelihood of opiate addiction in chronic pain patients.
+According to position papers on the treatment of opioid dependence published by the United Nations Office on Drugs and Crime and the World Health Organization, care providers should not treat opioid use disorder as the result of a weak character or will. Additionally, detoxification alone does not constitute adequate treatment.
+The DSM-5 guidelines for diagnosis of opioid use disorder require that the individual has significant impairment or distress related to opioid uses. In order to make the diagnosed two or more of eleven criteria must be present in a given year:
+- More opioids are taken than intended
+- The individual is unable to decrease the amount of opioids used
+- Large amounts of time are spent trying to obtain opioids, use opioids, or recover from taking them
+- The individual has cravings for opioids
+- Difficulty fulfilling professional duties at work or school
+- Continued use of opioids leading to social and interpersonal consequences
+- Decreased social or recreational activities
+- Using opioids despite it being physically dangerous settings
+- Continued use despite opioids worsening physical or psychological health (i.e. Depression, constipation)
+- Tolerance
+- Withdrawa.
+Signs and symptoms include:
+- Drug seeking behavior
+- Multiple prescriptions from different providers
+- Increased use over time
+- Opioid cravings
+- Multiple medical complications from drug use (HIV/AIDS, hospitalizations, abscesses)
+- Legal or social ramifications secondary to drug use
+- Withdrawal symptom.
+Withdrawal => Symptoms of withdrawal from opioids include:
+- Early symptoms => Altered perception of temperature (hot/cold flashes)
+- Agitation
+- Anxiety
+- Change in libido (abnormally high or low)
+- Dehydration
+- Fatigue
+- Muscle aches
+- Mental fog or confusion
+- Lack of motivation
+- Increased tearing
+- Insomnia
+- Restless legs
+- Runny nose
+- Sweating
+- Yawning
+- Skin-crawlin.
+- Late symptoms => Abdominal cramping
+- Sneezing
+- Diarrhea
+- Dilated pupils
+- Goose bumps
+- Nausea
+- Vomitin.
+Opioid intoxication => Signs and symptoms of opioid intoxication include:
+- Decreased perception of pain
+- Euphoria
+- Confusion
+- Desire to sleep
+- Nausea
+- Constipation
+- Miosi.
+Signs and symptoms of opioid overdose include, but are not limited to:
+- Pin-point pupils may occur. Patient presenting with dilated pupils may still be suffering an opioid overdose.
+- Decreased heart rate
+- Decreased body temperature
+- Decreased breathing
+- Altered level of consciousness. People may be unresponsive or unconscious.
+- Pulmonary edema (fluid accumulation in the lungs)
+- Shock
+- Deat
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DISNET disease texts/100 Clean Disease Texts/Optic neuritis.txt

+The optic nerve comprises axons that emerge from the retina of the eye and carry visual information to the primary visual nuclei, most of which is relayed to the occipital cortex of the brain to be processed into vision. Inflammation of the optic nerve causes loss of vision, usually because of the swelling and destruction of the myelin sheath covering the optic nerve.
+The most common cause is multiple sclerosis or ischemic optic neuropathy (Blood Clot). Blood Clot that supplies the optic nerve. Up to 50% of patients with MS will develop an episode of optic neuritis, and 20 – 30% of the time optic neuritis is the presenting sign of MS. The presence of demyelinating white matter lesions on brain MRI at the time of presentation of optic neuritis is the strongest predictor for developing clinically definite MS. Almost half of the patients with optic neuritis have white matter lesions consistent with multiple sclerosis.
+Some other common causes of optic neuritis include infection (e. G. Tooth Abscess in upper jaw, syphilis, Lyme disease, herpes zoster), autoimmune disorders (e. G. Lupus, neurosarcoidosis, neuromyelitis optica), Pinch in Optic Nerve, Methanol poisoning, B12 deficiency and diabetes. Injury to the eye, which usually does not heal by itself.
+Less common causes are: papilledema, brain tumor or abscess in occipitalregion, Cerebral trauma or hemorrhage, Meningitis Arachnoidal adhesions, sinus thrombosis, Liver Dysfunction or, Late Stage Kidney.
+Cause and Rank based on Deaths Annual Num Cases TOTAL (US) (2011) Annual Cases leading to Optic Neuritis Percent Prognosis and Treatment headingBody Multiple Sclerosis (Rank 33) 400,042 146,232 45% Most Common cause, Almost all patients will experience some form of vision dysfunction. Partial vision loss can occur through the duration of the disease, Total vision loss occurs in severe cases and late stages Blood Clot (Rank 29) (Optic ONLY) 17,000 16,777 5% Reversible if early and before reduced Blood flow causes permanent damage. Nerve Pinch, (0) NOT REPORTED 4% Usually heals itself, Treatment Not needed Injury to Optic Nerve (Including Poisoning, i.e. Methanol) (0) 23,827 20,121 <1% Depends on Severity, Usually Treatable Liver Dysfunction (Rank 19) If untreated can lead to Failure (Rank 8) 141,211 11,982 7% Poor Outcomes and Progresses and can lead to total vision loss Reduced Kidney Function (Treatable with diet change) (Rank 67-If untreated, can progress to Late Stage with much greater mortality rates. 509,898 16,281 9% Good Outcomes if Early, and can usually be treated with diet changes, Progresses and can lead to total vision loss Late Stage Kidney Failure (Rank 7) 33,212 1,112 2% Poor Outcomes-Usually permanent nerve damage at this stage Papilledema, (Brain tumor or abscess) (Rank 10) 45,888 9,231 3% Depends on Severity Meningitis (Rank 61) 2,521 189 <1% Depends on Severity Other Infections (Not from Abscess) 5,561 <1% Good Outcomes, Treatable with Antibiotics or other Microbial drugs Diabetes (early Stage Treatable) Late Stage has worse prognosis (Rank 6) 49,562 21,112 15% Type 1 carries poor prognosis, Type 2 can be treated and vision returned Unknown n/a 2%.
+Demyelinating recurrent optic neuritis and non-demyelinating (CRION) => The repetition of an idiopathic optic neuritis is considered a distinct clinical condition, and when it shows demyelination, it has been found to be associated to anti-MOG and AQP4-negative neuromyelitis optica.
+When an inflammatory recurrent optic neuritis is not demyelinating, it is called "Chronic relapsing inflammatory optic neuropathy" (CRION).
+When it is anti-MOG related, it is demyelinating and it is considered inside the anti-MOG associated inflammatory demyelinating diseases.
+Major symptoms are sudden loss of vision (partial or complete), sudden blurred or "foggy" vision, and pain on movement of the affected eye. Early symptoms that require investigation include symptoms from multiple sclerosis (twitching, lack of coordination, slurred speech, frequent episodes of partial vision loss or blurred vision), episodes of "disturbed/blackened" rather than blurry indicate moderate stage and require immediate medical attention to prevent further loss of vision. Other early symptoms are reduced night vision, photophobia and red eyes. Many patients with optic neuritis may lose some of their color vision in the affected eye (especially red), with colors appearing subtly washed out compared to the other eye. Patients may also experience difficulties judging movement in depth which can be particular troublesome during driving or sport (Pulfrich effect). Likewise transient worsening of vision with increase of body temperature (Uhthoff's phenomenon) and glare disability are a frequent complaint. However, several case studies in children have demonstrated the absence of pain in more than half of cases (approximately 60%) in their pediatric study population, with the most common symptom reported simply as "blurriness. " Other remarkable differences between the presentation of adult optic neuritis as compared to pediatric cases include more often unilateral optic neuritis in adults, while children much predominantly present with bilateral involvement.
+On medical examination the head of the optic nerve can easily be visualized by a slit lamp with high plus or by using direct ophthalmoscopy; however, frequently there is no abnormal appearance of the nerve head in optic neuritis (in cases of retrobulbar optic neuritis), though it may be swollen in some patients (anterior papillitis or more extensive optic neuritis). In many cases, only one eye is affected and patients may not be aware of the loss of color vision until they are asked to close or cover the healthy eye.
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DISNET disease texts/100 Clean Disease Texts/Orofacial granulomatosis.txt

+The cause of the condition is unknown. The disease is characterized by non-caseating granulomatous inflammation. That is, the granulomas do not undergo the caseating ("cheese-like") necrosis typical of the granulomas of tuberculosis.
+There is disagreement as to whether OFG represents an early form of Crohn's disease or sarcoidosis, or whether it is a distinct, but similar clinical entity. Crohn's disease can affect any part of gastrointestinal tract, from mouth to anus. When it involves the mouth alone, some authors refer to this as "oral Crohn's disease", distinguishing it from OFG, and others suggest that OFG is the same condition as Crohn's disease when it presents in the oral cavity.
+OFG may represent a delayed hypersensitivity reaction, but the causative antigen(s) is not identified or varies form one individual to the next. Suspected sources of antigens include metals, e. G. Cobalt, or additives and preservatives in foods, including benzoates, benzoic acid, cinnamaldehyde, metabisulfates, butylated hydroxyanisole, dodecyl gallate, tartrazine, or menthol, Examples of foods which may contain these substances include margarine, cinnamon, eggs, chocolate or peppermint oil.
+Some suggest that infection with atypical mycobacteria could be involved, (paratuberculosis), and that OFG is a reaction to mycobacterial stress protein mSP65 acting as an antigen.
+In response to an antigen, a chronic, submucosal, T cell mediated inflammatory response occurs, which involves cytokines (e. G. Tumor necrosis factor alpha), protease-activated receptors, matrix metalloproteinases and cyclooxygenases. The granulomas in OFG form in the lamina propria, and may form adjacent to or within lymphatic vessels. This is thought to cause obstruction of lymphatic drainage and lymphedema which is manifest as swelling clinically.
+There may be a genetic predisposition to the condition. People who develop OFG often have a history of atopy, such as childhood asthma or eczema.
+The diagnosis is usually made by tissue biopsy, however this cannot reliably distinguish between the granulomas of OFG and those of Crohn's disease or sarcoidosis. Other causes of granulomatous inflammation are ruled out, such as sarcoidosis, Crohn's disease, allergic or foreign body reactions and mycobacterial infections.
+Signs and symptoms may include:
+- Persistent or recurrent enlargement of the lips, causing them to protrude. If recurrent, the interval during which the lips are enlarged may be weeks or months. The enlargement can cause midline fissuring of the lip ("median cheilitis") or angular cheilitis (sores at the corner of the mouth). The swelling is non-pitting (c. F. Pitting edema) and feels soft or rubbery on palpation. The mucous membrane of the lip may be erythemaous (red) and granular. One or both lips may be affected.
+- Oral ulceration (mouth ulcers) which may be aphthous like, or be more chronic and deep with raised margins. Alternatively, lesions similar to pyostomatitis vegetans may occur in OFG, but this is uncommon.
+- "Full width" gingivitis (compare with marginal gingivitis).
+- Gingival enlargement (swelling of the gums).
+- Fissured tongue (grooves in the tongue).
+- Enlargement of the mucous membrane of the mouth, which may be associated with cobblestoning and mucosal tags (similar lesions often occur on the intestinal mucosa in Crohn's disease).
+- Enlargement of the perioral and periorbital soft tissues (the tissues of the face around the mouth and the eyes). The facial skin may be dry, exfoliative (flaking) or erythematous.
+- Cervical lymphadenopathy (enlarged lymph nodes in the neck).
+- Facial palsy (weakness and altered sensation of the face).
+The enlargement of the tissues of the mouth, lips and face seen in OFG is painless. Melkersson-Rosenthal syndrome is where OFG occurs with fissured tongue and paralysis of the facial nerve. The cause of the facial paralysis is thought to be caused by the formation of granulomas in the facial nerve, which supplies the muscles of facial expression.
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DISNET disease texts/100 Clean Disease Texts/Orthostatic hypotension.txt

+Orthostatic hypotension is caused primarily by gravity-induced blood pooling in the lower extremities, which in turn compromises venous return, resulting in decreased cardiac output and subsequent lowering of arterial pressure. For example, changing from a lying position to standing loses about 700 ml of blood from the thorax, with a decrease in systolic and diastolic blood pressures. The overall effect is an insufficient blood perfusion in the upper part of the body.
+Still, the blood pressure does not normally fall very much, because it immediately triggers a vasoconstriction (baroreceptor reflex), pressing the blood up into the body again. (Often, this mechanism is exaggerated and is why diastolic blood pressure is a bit higher when a person is standing up, compared to a person in the horizontal position.) Therefore, a secondary factor that causes a greater than normal fall in blood pressure is often required. Such factors include low blood volume, diseases, and medications.
+Hypovolemia => Orthostatic hypotension may be caused by low blood volume, bleeding, the excessive use of diuretics, vasodilators, or other types of drugs, dehydration, or prolonged bed rest(immobility); as well as occurring in people with anemia.
+Diseases => The disorder may be associated with Addison's disease, atherosclerosis (build-up of fatty deposits in the arteries), diabetes, pheochromocytoma, porphyria, and certain neurological disorders, including multiple system atrophy and other forms of dysautonomia. It is also associated with Ehlers–Danlos syndrome and anorexia nervosa. It is also present in many patients with Parkinson's disease resulting from sympathetic denervation of the heart or as a side-effect of dopaminomimetic therapy. This rarely leads to fainting unless the person has developed true autonomic failure or has an unrelated heart problem.
+Another disease, dopamine beta hydroxylase deficiency, also thought to be underdiagnosed, causes loss of sympathetic noradrenergic function and is characterized by a low or extremely low levels of norepinephrine, but an excess of dopamine.
+Quadriplegics and paraplegics also might experience these symptoms due to multiple systems' inability to maintain a normal blood pressure and blood flow to the upper part of the body.
+Orthostatic hypotension can be a side-effect of certain antidepressants, such as tricyclics or monoamine oxidase inhibitors (MAOIs). Marijuana and tetrahydrocannabinol can on occasion produce marked orthostatic hypotension. Alcohol can also potentiate orthostatic hypotension to the point of syncope. Orthostatic hypotension can also be a side effect of alpha-1 blockers (alpha1 adrenergic blocking agents). Alpha1 blockers inhibit vasoconstriction normally initiated by the baroreceptor reflex upon postural change and the subsequent drop in pressure.
+Other factors => Patients prone to orthostatic hypotension are the elderly, post partum mothers, and those having been on bedrest. People suffering from anorexia nervosa and bulimia nervosa often suffer from orthostatic hypotension as a common side-effect. Consuming alcohol may also lead to orthostatic hypotension due to its dehydrating effects.
+Orthostatic hypotension can be confirmed by measuring a person's blood pressure after lying flat for 5 minutes, then 1 minute after standing, and 3 minutes after standing. Orthostatic hypotension is defined as a fall in systolic blood pressure of at least 20 mmHg and/or in the diastolic blood pressure of at least 10 mmHg between the supine reading and the upright reading. In addition, the heart rate should also be measured for both positions. A significant increase in heart rate from supine to standing may indicate a compensatory effort by the heart to maintain cardiac output or postural orthostatic tachycardia syndrome (POTS). A tilt table test may also be performed.
+Orthostatic hypotension is characterised by symptoms that occur after standing (from lying or sitting), particularly when this is done rapidly. Many report lightheadedness (a feeling that one might be about to faint), sometimes severe. Generalized weakness or tiredness may also occur. Some also report difficulty concentrating, blurred vision, tremulousness, vertigo, anxiety, palpitations (awareness of the heartbeat), feeling sweaty or clammy, and sometimes nausea. A person may look pale.
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DISNET disease texts/100 Clean Disease Texts/Pancreatic cancer.txt

+The symptoms of pancreatic adenocarcinoma do not usually appear in the disease's early stages, and are individually not distinctive to the disease. The symptoms at diagnosis vary according to the location of the cancer in the pancreas, which anatomists divide (from left to right on most diagrams) into the thick head, the neck, and the tapering body, ending in the tail.
+Regardless of a tumor's location, the most common symptom is unexplained weight loss, which may be considerable. A large minority (between 35% and 47%) of people diagnosed with the disease will have had nausea, vomiting or a feeling of weakness. Tumors in the head of the pancreas typically also cause jaundice, pain, loss of appetite, dark urine, and light-colored stools. Tumors in the body and tail typically also cause pain.
+People sometimes have recent onset of atypical type 2 diabetes that is difficult to control, a history of recent but unexplained blood vessel inflammation caused by blood clots (thrombophlebitis) known as Trousseau sign, or a previous attack of pancreatitis. A doctor may suspect pancreatic cancer when the onset of diabetes in someone over 50 years old is accompanied by typical symptoms such as unexplained weight loss, persistent abdominal or back pain, indigestion, vomiting, or fatty feces. Jaundice accompanied by a painlessly swollen gallbladder (known as Courvoisier's sign) may also raise suspicion, and can help differentiate pancreatic cancer from gallstones.
+Medical imaging techniques, such as computed tomography (CT scan) and endoscopic ultrasound (EUS) are used both to confirm the diagnosis and to help decide whether the tumor can be surgically removed (its "resectability"). On contrast CT scan, pancreatic cancer typically shows a gradually increasing radiocontrast uptake, rather than a fast washout as seen in a normal pancreas or a delayed washout as seen in chronic pancreatitis. Magnetic resonance imaging and positron emission tomography may also be used, and magnetic resonance cholangiopancreatography may be useful in some cases. Abdominal ultrasound is less sensitive and will miss small tumors, but can identify cancers that have spread to the liver and build-up of fluid in the peritoneal cavity (ascites). It may be used for a quick and cheap first examination before other techniques.
+A biopsy by fine needle aspiration, often guided by endoscopic ultrasound, may be used where there is uncertainty over the diagnosis, but a histologic diagnosis is not usually required for removal of the tumor by surgery to go ahead.
+Liver function tests can show a combination of results indicative of bile duct obstruction (raised conjugated bilirubin, γ-glutamyl transpeptidase and alkaline phosphatase levels). CA19 – 9 (carbohydrate antigen 19.9) is a tumor marker that is frequently elevated in pancreatic cancer. However, it lacks sensitivity and specificity, not least because 5% of people lack the Lewis (a) antigen and cannot produce CA19 – 9. It has a sensitivity of 80% and specificity of 73% in detecting pancreatic adenocarcinoma, and is used for following known cases rather than diagnosis.
+The most common form of pancreatic cancer (adenocarcinoma) is typically characterized by moderately to poorly differentiated glandular structures on microscopic examination. There is typically considerable desmoplasia or formation of a dense fibrous stroma or structural tissue consisting of a range of cell types (including myofibroblasts, macrophages, lymphocytes and mast cells) and deposited material (such as type I collagen and hyaluronic acid). This creates a tumor microenvironment that is short of blood vessels (hypovascular) and so of oxygen (tumor hypoxia). It is thought that this prevents many chemotherapy drugs from reaching the tumor, as one factor making the cancer especially hard to treat.
+Since pancreatic cancer usually does not cause recognizable symptoms in its early stages, the disease is typically not diagnosed until it has spread beyond the pancreas itself. This is one of the main reasons for the generally poor survival rates. Exceptions to this are the functioning PanNETs, where over-production of various active hormones can give rise to symptoms (which depend on the type of hormone).
+Bearing in mind that the disease is rarely diagnosed before the age of 40, common symptoms of pancreatic adenocarcinoma occurring before diagnosis include:
+- Pain in the upper abdomen or back, often spreading from around the stomach to the back. The location of the pain can indicate the part of the pancreas where a tumor is located. The pain may be worse at night and may increase over time to become severe and unremitting. It may be slightly relieved by bending forward. In the UK, about half of new cases of pancreatic cancer are diagnosed following a visit to a hospital emergency department for pain or jaundice. In up to two-thirds of people abdominal pain is the main symptom, for 46% of the total accompanied by jaundice, with 13% having jaundice without pain.
+- Jaundice, a yellow tint to the whites of the eyes or skin, with or without pain, and possibly in combination with darkened urine. This results when a cancer in the head of the pancreas obstructs the common bile duct as it runs through the pancreas.
+- Unexplained weight loss, either from loss of appetite, or loss of exocrine function resulting in poor digestion.
+- The tumor may compress neighboring organs, disrupting digestive processes and making it difficult for the stomach to empty, which may cause nausea and a feeling of fullness. The undigested fat leads to foul-smelling, fatty feces that are difficult to flush away. Constipation is common.
+- At least 50% of people with pancreatic adenocarcinoma have diabetes at the time of diagnosis. While long-standing diabetes is a known risk factor for pancreatic cancer (see Risk factors), the cancer can itself cause diabetes, in which case recent onset of diabetes could be considered an early sign of the disease. People over 50 who develop diabetes have eight times the usual risk of developing pancreatic adenocarcinoma within three years, after which the relative risk declines.
+- Other findings => Trousseau's syndrome, in which blood clots form spontaneously in the portal blood vessels, the deep veins of the extremities, or the superficial veins anywhere on the body, may be associated with pancreatic cancer, and is found in about 10% of cases.
+- Clinical depression has been reported in association with pancreatic cancer in some 10–20% of cases, and can be a hindrance to optimal management. The depression sometimes appears before the diagnosis of cancer, suggesting that it may be brought on by the biology of the disease.
+Other common manifestations of the disease include: weakness and tiring easily; dry mouth; sleep problems; and a palpable abdominal mass. ".
+The spread of pancreatic cancer to other organs (metastasis) may also cause symptoms. Typically, pancreatic adenocarcinoma first spreads to nearby lymph nodes, and later to the liver or to the peritoneal cavity, large intestine or lungs. It is uncommon for it to spread to the bones or brain.
+Cancers in the pancreas may also be secondary cancers that have spread from other parts of the body. This is uncommon, found in only about 2% of cases of pancreatic cancer. Kidney cancer is by far the most common cancer to spread to the pancreas, followed by colorectal cancer, and then cancers of the skin, breast, and lung. Surgery may be performed on the pancreas in such cases, whether in hope of a cure or to alleviate symptoms.
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DISNET disease texts/100 Clean Disease Texts/Panic attack.txt

+Long-term, predisposing causes – The onset of panic disorder usually occurs in early adulthood, although it may appear at any age. It occurs more frequently in women and more often in people with above-average intelligence. Various twin studies where one identical twin has an anxiety disorder have reported a 31–88% incidence of the other twin also having an anxiety disorder diagnosis. Environmental factors such as an overcautious view of the world expressed by parents and cumulative stress over time have been found to be correlated with panic attacks.
+- Biological causes – obsessive compulsive disorder, Postural Orthostatic Tachycardia Syndrome, post traumatic stress disorder, hypoglycemia, hyperthyroidism, Wilson's disease, mitral valve prolapse, pheochromocytoma, and inner ear disturbances (labyrinthitis). Dysregulation of the norepinephrine system in the locus ceruleus, an area of the brain stem, has been linked to panic attacks.
+- Marijuana – According to the Harvard Mental Health Letter, "the most commonly reported side effects of smoking marijuana are anxiety and panic attacks. Studies report that about 20% to 30% of recreational users experience such problems after smoking marijuana. "
+- Phobias – People will often experience panic attacks as a direct result of exposure to a phobic object or situation.
+- Short-term triggering causes – Significant personal loss, including an emotional attachment to a romantic partner, life transitions, significant life change.
+- Maintaining causes – Avoidance of panic-provoking situations or environments, anxious/negative self-talk ("what-if" thinking), mistaken beliefs ("these symptoms are harmful and/or dangerous"), withheld feelings.
+- Hyperventilation syndrome – Breathing from the chest may cause overbreathing, exhaling excessive carbon dioxide in relation to the amount of oxygen in one's bloodstream. Hyperventilation syndrome can cause respiratory alkalosis and hypocapnia. This syndrome often involves prominent mouth breathing as well. This causes a cluster of symptoms, including rapid heart beat, dizziness, and lightheadedness, which can trigger panic attacks.
+- Situationally bound panic attacks – Associating certain situations with panic attacks, due to experiencing one in that particular situation, can create a cognitive or behavioral predisposition to having panic attacks in certain situations (situationally bound panic attacks).
+- Discontinuation or marked reduction in the dose of a substance such as a drug (drug withdrawal), for example an antidepressant (antidepressant discontinuation syndrome), can cause a panic attack.
+In adolescents it may in part be due to the social transitions.
+People who have repeated, persistent attacks or feel severe anxiety about having another attack are said to have panic disorder. Panic disorder is strikingly different from other types of anxiety disorders in that panic attacks are often sudden and unprovoked. However, panic attacks experienced by those with panic disorder may also be linked to or heightened by certain places or situations, making daily life difficult.
+Agoraphobia is an anxiety disorder which primarily consists of the fear of experiencing a difficult or embarrassing situation from which the sufferer cannot escape. Panic attacks are commonly linked to agoraphobia and the fear of not being able to escape a bad situation. As the result, severe sufferers of agoraphobia may become confined to their homes, experiencing difficulty traveling from this "safe place". The word "agoraphobia" is an English adoption of the Greek words agora (αγορά) and phobos (φόβος). The term "agora" refers to the place where ancient Greeks used to gather and talk about issues of the city, so it basically applies to any or all public places; however the essence of agoraphobia is a fear of panic attacks especially if they occur in public as the victim may feel like he or she has no escape. In the case of agoraphobia caused by social phobia or social anxiety, sufferers may be very embarrassed by having a panic attack publicly in the first place. This translation is the reason for the common misconception that agoraphobia is a fear of open spaces, and is not clinically accurate. Agoraphobia, as described in this manner, is actually a symptom professionals check for when making a diagnosis of panic disorder. Other syndromes like obsessive compulsive disorder or post traumatic stress disorder and social anxiety disorder can also cause agoraphobia; basically any irrational fear that keeps one from going outside can cause the syndrome.
+People who have had a panic attack in certain situations may develop irrational fears, called phobias, of these situations and begin to avoid them. Eventually, the pattern of avoidance and level of anxiety about another attack may reach the point where individuals with panic disorder are unable to drive or even step out of the house. At this stage, the person is said to have panic disorder with agoraphobia. This can be one of the most harmful side-effects of panic disorder as it can prevent sufferers from seeking treatment in the first place.
+Experimentally induced => Panic attack symptoms can be experimentally induced in the laboratory by various means. Among them, for research purposes, by administering a bolus injection of the neuropeptide cholecystokinin-tetrapeptide (CCK-4). Various animal models of panic attacks have been experimentally studied.
+DSM-5 diagnostic criteria for a panic attack include a discrete period of intense fear or discomfort, in which four (or more) of the following symptoms developed abruptly and reached a peak within minutes:
+In DSM-5, culture-specific symptoms (e. G., tinnitus, neck soreness, headache, and uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms.
+Some or all of these symptoms can be found in the presence of a pheochromocytoma.
+Screening tools such as the Panic Disorder Severity Scale can be used to detect possible cases of disorder and suggest the need for a formal diagnostic assessment.
+People with panic attacks often report a fear of dying or heart attack, flashing vision, faintness or nausea, numbness throughout the body, heavy breathing and hyperventilation, or loss of body control. Some people also suffer from tunnel vision, mostly due to blood flow leaving the head to more critical parts of the body in defense. These feelings may provoke a strong urge to escape or flee the place where the attack began (a consequence of the "fight-or-flight response", in which the hormone causing this response is released in significant amounts). This response floods the body with hormones, particularly epinephrine (adrenaline), which aid it in defending against harm.
+A panic attack is a response of the sympathetic nervous system (SNS). The most common symptoms include trembling, dyspnea (shortness of breath), heart palpitations, chest pain (or chest tightness), hot flashes, cold flashes, burning sensations (particularly in the facial or neck area), sweating, nausea, dizziness (or slight vertigo), light-headedness, hyperventilation, paresthesias (tingling sensations), sensations of choking or smothering, difficulty moving, and derealization. These physical symptoms are interpreted with alarm in people prone to panic attacks. This results in increased anxiety and forms a positive feedback loop.
+Often, the onset of shortness of breath and chest pain are the predominant symptoms. People with a panic attack may incorrectly attribute them to a heart attack and thus trigger seeking treatment in an emergency room. However, since chest pain and shortness of breath are indeed hallmark symptoms of cardiovascular illnesses, including unstable angina and myocardial infarction (heart attack), especially in a person whose mental health status and heart health status are not known, attributing these pains to simple anxiety and not (also) a physical condition is a diagnosis of exclusion (other conditions must be ruled out first) until an electrocardiogram and a mental health assessment have been carried out.
+Panic attacks are distinguished from other forms of anxiety by their intensity and their sudden, episodic nature. They are often experienced in conjunction with anxiety disorders and other psychological conditions, although panic attacks are not generally indicative of a mental disorder.
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DISNET disease texts/100 Clean Disease Texts/Paratyphoid fever.txt

+Paratyphoid fever is caused by any of three strains of Salmonella paratyphoid: S. Paratyphi A; S. Schottmuelleri (also called S. Paratyphi B); or S. Hirschfeldii (also called S. Paratyphi C).
+Transmission => They are usually spread by eating or drinking food or water contaminated with the feces of an infected person. They may occur when a person who prepares food is infected. Risk factors include poor sanitation as is found among poor crowded populations. Occasionally they may be transmitted by sex. Humans are the only animal infected.
+Paratyphoid B => Paratyphoid B is more frequent in Europe. It can present as a typhoid-like illness, as a severe gastroenteritis or with features of both. Herpes labialis, rare in true typhoid fever, is frequently seen in paratyphoid B. Diagnosis is with isolation of the agent in blood or stool and demonstration of antibodies antiBH in the Widal test. The disease responds well to chloramphenicol or co-trimoxazole.
+Paratyphoid C => Paratyphoid C is a rare infection, generally seen in the Far East. It presents as a septicaemia with metastatic abscesses. Cholecystitis is possible in the course of the disease. Antibodies to paratyphoid C are not usually tested and the diagnosis is made with blood cultures. Chloramphenicol therapy is generally effective.
+Carriers => Humans and, occasionally, domestic animals are the carriers of paratyphoid fever. Members of the same family can be transient or permanent carriers. In most parts of the world, short-term fecal carriers are more common than urinary carriers. The chronic urinary carrier state occurs in those who have schistosomiasis (parasitic blood fluke).
+It is possible to continue to shed Salmonella Paratyphi for up to one year and, during this phase, a person is considered to be a carrier. The chronic carrier state may follow acute illness, mild or even subclinical infections. Chronic carriers are most often women who were infected in their middle age.
+Paratyphoid fever resembles typhoid fever. Infection is characterized by a sustained fever, headache, abdominal pain, malaise, anorexia, a nonproductive cough (in early stage of illness), a relative bradycardia (slow heart rate), and hepatosplenomegaly (an enlargement of the liver and spleen). About 30% of Caucasians develop rosy spots on the central body. In adults, constipation is more common than diarrhea.
+Only 20% to 40% of people initially have abdominal pain. Nonspecific symptoms such as chills, sweating, headache, loss of appetite, cough, weakness, sore throat, dizziness, and muscle pains are frequently present before the onset of fever. Some very rare symptoms are psychosis (mental disorder), confusion, and seizures.
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DISNET disease texts/100 Clean Disease Texts/Parry–Romberg syndrome.txt

+The fact that some people affected with this disease have circulating antinuclear antibodies in their serum supports the theory that Parry–Romberg syndrome may be an autoimmune disease, specifically a variant of localized scleroderma. Several instances have been reported where more than one member of a family has been affected, prompting speculation of an autosomal dominant inheritance pattern. However, there has also been at least one report of monozygotic twins in which only one of the twins was affected, casting doubt on this theory. Various other theories about the cause and pathogenesis have been suggested, including alterations in the peripheral sympathetic nervous system (perhaps as a result of trauma or infection involving the cervical plexus or the sympathetic trunk), as the literature reported it following sympathectomy, disorders in migration of cranial neural crest cells, or chronic cell-mediated inflammatory process of the blood vessels. It is likely that the disease results from different mechanisms in different people, with all of these factors potentially being involved.
+Diagnosis can be made solely on the basis of history and physical examination in people who present with only facial asymmetry. For those who report neurological symptoms such as migraine or seizures, MRI scan of the brain is the imaging modality of choice. A diagnostic lumbar puncture and serum test for autoantibodies may also be indicated in people who present with a seizure disorder of recent onset.
+- A 3D, soft tissue reconstruction of a CT scan of a 17-year-old girl with Parry Romberg syndrome.
+- CT scan3D bone reconstruction of a 17-year-old girl with Parry Romberg syndrome.
+Initial facial changes usually involve the area of the face covered by the temporal or buccinator muscles. The disease progressively spreads from the initial location, resulting in atrophy of the skin and its adnexa, as well as underlying subcutaneous structures such as connective tissue, (fat, fascia, cartilage, bones) and/or muscles of one side of the face. The mouth and nose are typically deviated towards the affected side of the face.
+The process may eventually extend to involve tissues between the nose and the upper corner of the lip, the upper jaw, the angle of the mouth, the area around the eye and brow, the ear, and/or the neck. The syndrome often begins with a circumscribed patch of scleroderma in the frontal region of the scalp which is associated with a loss of hair and the appearance of a depressed linear scar extending down through the midface on the affected side. This scar is referred to as a "coup de sabre" lesion because it resembles the scar of a wound made by a sabre, and is indistinguishable from the scar observed in frontal linear scleroderma.
+In 20% of cases, the hair and skin overlying affected areas may become hyperpigmented or hypopigmented with patches of unpigmented skin. In up to 20% of cases the disease may involve the ipsilateral (on the same side) or contralateral (on the opposite side) neck, trunk, arm, or leg. The cartilage of the nose, ear and larynx can be involved. The disease has been reported to affect both sides of the face in 5 – 10% of the cases.
+Symptoms and physical findings usually become apparent during the first or early during the second decade of life. The average age of onset is nine years of age, and the majority of individuals experience symptoms before 20 years of age. The disease may progress for several years before eventually going into remission (abruptly ceasing).
+Neurological => Neurological abnormalities are common. Roughly 45% of people with Parry–Romberg syndrome are also afflicted with trigeminal neuralgia (severe pain in the tissues supplied by the ipsilateral trigeminal nerve, including the forehead, eye, cheek, nose, mouth and jaw) and/or migraine (severe headaches that may be accompanied by visual abnormalities, nausea and vomiting).
+10% of affected individuals develop a seizure disorder as part of the disease. The seizures are typically Jacksonian in nature (characterized by rapid spasms of a muscle group that subsequently spread to adjacent muscles) and occur on the side contralateral to the affected side of the face. Half of these cases are associated with abnormalities in both the gray and white matter of the brain—usually ipsilateral but sometimes contralateral—that are detectable on magnetic resonance imaging (MRI) scan.
+Ocular => Enophthalmos (recession of the eyeball within the orbit) is the most common eye abnormality observed in Parry–Romberg syndrome. It is caused by a loss of subcutaneous tissue around the orbit. Other common findings include drooping of the eyelid (ptosis), constriction of the pupil (miosis), redness of the conjunctiva, and decreased sweating (anhidrosis) of the affected side of the face. Collectively, these signs are referred to as Horner's syndrome. Other ocular abnormalities include ophthalmoplegia (paralysis of one or more of the extraocular muscles) and other types of strabismus, uveitis, and heterochromia of the iris.
+Oral => The tissues of the mouth, including the tongue, gingiva, teeth and soft palate are commonly involved in Parry–Romberg syndrome. 50% of affected individuals develop dental abnormalities such as delayed eruption, dental root exposure, or resorption of the dental roots on the affected side. 35% have difficulty or inability to normally open the mouth or other jaw symptoms, including temporomandibular joint disorder and spasm of the muscles of mastication on the affected side. 25% experience atrophy of one side of the upper lip and tongue.
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DISNET disease texts/100 Clean Disease Texts/Pituitary apoplexy.txt

+Almost all cases of pituitary apoplexy arise from a pituitary adenoma, a benign tumor of the pituitary gland. In 80%, the patient has been previously unaware of this (although some will retrospectively report associated symptoms). It was previously thought that particular types of pituitary tumors were more prone to apoplexy than others, but this has not been confirmed. In absolute terms, only a very small proportion of pituitary tumors eventually undergoes apoplexy. In an analysis of incidentally found pituitary tumors, apoplexy occurred in 0.2% annually, but the risk was higher in tumors larger than 10 mm ("macroadenomas") and tumors that were growing more rapidly; in a meta-analysis, not all these associations achieved statistical significance.
+The majority of cases (60–80%) are not precipitated by a particular cause. A quarter has a history of high blood pressure, but this is a common problem in the general population, and it is not clear whether it significantly increase the risk of apoplexy. A number of cases has been reported in association with particular conditions and situations; it is uncertain whether these were in fact causative. Amongst reported associations are surgery (especially coronary artery bypass graft, where there are significant fluctuations in the blood pressure), disturbances in blood coagulation or medication that inhibits coagulation, radiation therapy to the pituitary, traumatic brain injury, pregnancy (during which the pituitary enlarges) and treatment with estrogens. Hormonal stimulation tests of the pituitary have been reported to provoke episodes. Treatment of prolactinomas (pituitary adenomas that secrete prolactin) with dopamine agonist drugs, as well as withdrawal of such treatment, has been reported to precipitate apoplexy.
+Hemorrhage from a Rathke's cleft cyst, a remnant of Rathke's pouch that normally regresses after embryological development, may cause symptoms that are indistinguishable from pituitary apoplexy. Pituitary apoplexy is regarded by some as distinct from Sheehan's syndrome, where the pituitary undergoes infarction as a result of prolonged very low blood pressure, particularly when caused by bleeding after childbirth. This condition usually occurs in the absence of a tumor. Others regard Sheehan's syndrome as a form of pituitary apoplexy.
+It is recommended that magnetic resonance imaging (MRI) scan of the pituitary gland is performed if the diagnosis is suspected; this has a sensitivity of over 90% for detecting pituitary apoplexy; it may demonstrate infarction (tissue damage due to a decreased blood supply) or hemorrhage. Different MRI sequences can be used to establish when the apoplexy occurred, and the predominant form of damage (hemorrhage or infarction). If MRI is not suitable (e. G. Due to claustrophobia or the presence of metal-containing implants), a computed tomography (CT) scan may demonstrate abnormalities in the pituitary gland, although it is less reliable. Many pituitary tumors (25%) are found to have areas of hemorrhagic infarction on MRI scans, but apoplexy is not said to exist unless it is accompanied by symptoms.
+In some instances, lumbar puncture may be required if there is a suspicion that the symptoms might be caused by other problems (meningitis or subarachnoid hemorrhage). This is the examination of the cerebrospinal fluid that envelops the brain and the spinal cord; the sample is obtained with a needle that is passed under local anesthetic into the spine. In pituitary apoplexy the results are typically normal, although abnormalities may be detected if blood from the pituitary has entered the subarachnoid space. If there is remaining doubt about the possibility of subarachnoid hemorrhage (SAH), a magnetic resonance angiogram (MRI with a contrast agent) may be required to identify aneurysms of the brain blood vessels, the most common cause of SAH.
+Professional guidelines recommend that if pituitary apoplexy is suspected or confirmed, the minimal blood tests performed should include a complete blood count, urea (a measure of renal function, usually performed together with creatinine), electrolytes (sodium and potassium), liver function tests, routine coagulation testing, and a hormonal panel including IGF-1, growth hormone, prolactin, luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, thyroid hormone, and either testosterone in men or estradiol in women.
+Visual field testing is recommended as soon as possible after diagnosis, as it quantifies the severity of any optic nerve involvement, and may be required to decide on surgical treatment.
+Acute symptoms => The initial symptoms of pituitary apoplexy are related to the increased pressure in and around the pituitary gland. The most common symptom, in over 95% of cases, is a sudden-onset headache located behind the eyes or around the temples. It is often associated with nausea and vomiting. Occasionally, the presence of blood leads to irritation of the lining of the brain, which may cause neck rigidity and intolerance to bright light, as well as a decreased level of consciousness. This occurs in 24% of cases.
+Pressure on the part of the optic nerve known as the chiasm, which is located above the gland, leads to loss of vision on the outer side of the visual field on both sides, as this corresponds to areas on the retinas supplied by these parts of the optic nerve; it is encountered in 75% of cases. Visual acuity is reduced in half, and over 60% have a visual field defect. The visual loss depends on which part of the nerve is affected. If the part of the nerve between the eye and the chiasm is compressed, the result is vision loss in one eye. If the part after the chiasm is affected, visual loss on one side of the visual field occurs.
+Adjacent to the pituitary lies a part of the skull base known as the cavernous sinus. This contains a number of nerves that control the eye muscles. 70% of people with pituitary apoplexy experience double vision due to compression of one of the nerves. In half of these cases, the oculomotor nerve (the third cranial nerve), which controls a number of eye muscles, is affected. This leads to diagonal double vision and a dilated pupil. The fourth (trochlear) and sixth (abducens) cranial nerves are located in the same compartment and can cause diagonal or horizontal double vision, respectively. The oculomotor nerve is predominantly affected as it lies closest to the pituitary. The cavernous sinus also contains the carotid artery, which supplies blood to the brain; occasionally, compression of the artery can lead to one-sided weakness and other symptoms of stroke.
+The pituitary gland consists of two parts, the anterior (front) and posterior (back) pituitary. Both parts release hormones that control numerous other organs. In pituitary apoplexy, the main initial problem is a lack of secretion of adrenocorticotropic hormone (ACTH, corticotropin), which stimulates the secretion of cortisol by the adrenal gland. This occurs in 70% of those with pituitary apoplexy. A sudden lack of cortisol in the body leads to a constellation of symptoms called "adrenal crisis" or "Addisonian crisis" (after a complication of Addison's disease, the main cause of adrenal dysfunction and low cortisol levels). The main problems are low blood pressure (particularly on standing), low blood sugars (which can lead to coma) and abdominal pain; the low blood pressure can be life-threatening and requires immediate medical attention.
+Hyponatremia, an unusually low level of sodium in the blood that may cause confusion and seizures, is found in 40% of cases. This may be caused by low cortisol levels or by inappropriate release of antidiuretic hormone (ADH) from the posterior pituitary. Several other hormonal deficiencies may develop in the subacute phase. 50% have a deficiency in thyroid-stimulating hormone (TSH), leading to undersecretion of thyroid hormone by the thyroid gland and characteristic symptoms such as fatigue, weight gain, and cold intolerance. 75% develop a deficiency to gonadotropins (LH and FSH), which control the reproductive hormone glands. This leads to a disrupted menstrual cycle, infertility and decreased libido.
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DISNET disease texts/100 Clean Disease Texts/Polyarteritis nodosa.txt

+There is no association with ANCA, but about 30% of people with PAN have chronic hepatitis B and deposits containing HBsAg-HBsAb complexes in affected vessels, indicating an immune complex–mediated cause in that subset. The cause remains unknown in the remaining cases; there may be causal and clinical distinctions between classic idiopathic PAN, the cutaneous forms of PAN, and the PAN associated with chronic hepatitis. In the pediatric population, cutaneous PAN is frequently associated to streptococcal infections, and positive streptococcal serology is included in the diagnostic criteria.
+No specific lab tests exist for diagnosing polyarteritis nodosa. Diagnosis is generally based on the physical examination and a few laboratory studies that help confirm the diagnosis:
+A patient is said to have polyarteritis nodosa if he or she has three of the 10 signs known as the 1990 American College of Rheumatology (ACR) criteria, when a radiographic or pathological diagnosis of vasculitis is made:
+In polyarteritis nodosa, small aneurysms are strung like the beads of a rosary, therefore making "rosary sign" an important diagnostic feature of the vasculitis. The 1990 ACR criteria were designed for classification purposes only. Nevertheless, their good discriminatory performances, indicated by the initial ACR analysis, suggested their potential usefulness for diagnostic purposes as well. Subsequent studies did not confirm their diagnostic utility, demonstrating a significant dependence of their discriminative abilities on the prevalence of the various vasculitides in the analyzed populations. Recently, an original study, combining the analysis of more than 100 items used to describe patients' characteristics in a large sample of vasculitides with a computer simulation technique designed to test the potential diagnostic utility of the various criteria, proposed a set of eight positively or negatively discriminating items to be used as a screening tool for diagnosis in patients suspected of systemic vasculitis.
+In this disease, symptoms result from ischemic damage to affected organs, often the skin, heart, kidneys, and nervous system. Generalised symptoms include fever, fatigue, weakness, loss of appetite, and weight loss. Muscle and joint aches are common. The skin may show rashes, swelling, ulcers, and lumps. Palpable purpura and livedo reticularis can occur in some patients.
+Nerve involvement may cause sensory changes with numbness, pain, burning, and weakness (peripheral neuropathy). Central nervous system involvement may cause strokes or seizures. Kidney involvement can produce varying degrees of kidney failure, such as hypertension, edema, oliguria, and uremia. Involvement of the arteries of the heart may cause a heart attack, heart failure, and inflammation of the sac around the heart (pericarditis).
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DISNET disease texts/100 Clean Disease Texts/Porencephaly.txt

+Porencephaly is a rare disorder. The exact prevalence of porencephaly is not known; however, it has been reported that 6.8% of patients with cerebral palsy or 68% of patients with epilepsy and congenital vascular hemiparesis have porencephaly. Porencephaly has a number of different, often unknown, causes including absence of brain development and destruction of brain tissue. With limited research, the most commonly regarded cause of porencephaly is disturbances in blood circulation, ultimately leading to brain damage. However, a number of different and multiple factors such as abnormal brain development or damage to the brain tissue can also affect the development of porencephaly.
+The following text lists out potential risk factors of developing porencephaly and porencephalic cysts and cavities along with brief description of certain terminologies.
+- Lack of oxygen and blood supply to the brain leading to internal bleeding
+- Cerebral degeneration – loss of neuron structure and function
+- Maternal cardiac arrest
+- Trauma during pregnancy
+- Abdominal trauma
+- Pathogenic infection
+- Accidents
+- Abnormal brain development during birth
+- Vascular thrombosis – blood clot formation within blood vessels
+- Hemorrhage – loss of blood outside of the circulatory system
+- Brain contusion or injury
+- Multifocal cerebrovascular insufficiency
+- Placental bleeding – prevention of oxygen and blood supply to infant brain
+- Maternal toxemia – toxin within circulatory system of mother that is transferred to fetus, causing brain damage
+- Cerebral hypoxia – reduced oxygen concentration within blood system
+- Vascular occlusion – blood clotting of vessels
+- Cystic periventricular leukomalacia
+- Cerebral atrophy – decrease in neuron number and size and loss of brain mass
+- Chronic lung disease
+- Male gender
+- Endotoxins
+- Prenatal and postnatal encephalitis and meningitis
+- Drug abuse of mothe.
+Cysts or cavities can occur anywhere within the brain and the locations of these cysts depend highly on the patient. Cysts can develop in the frontal lobe, parietal lobe, forebrain, hindbrain, temporal lobe, or virtually anywhere in the cerebral hemisphere.
+Genetics => From recent studies, de novo and inherited mutations in the gene COL4A1, suggesting genetic predisposition within the family, that encodes type IV collagen α1 chain has shown to be associated with and present in patients with porencephaly. COL4A1 mutation causes a variety of phenotypes, including porencephaly, infantile hemiplegia, and cerebral small vessel diseases involving both stroke and infarction. Abnormal gene expression of COL4A1 can contribute to the development of porencephaly. COL4A1 gene expresses a type IV collagen (basement protein) that is present in all tissue and blood vessels and is extremely important for the structural stability of vascular basement membranes. The COL4A1 protein provides a strong layer around blood vessels. The mutation can weaken the blood vessels within the brain, elevating the probability of a hemorrhage, and eventually promoting internal bleeding then leading to porencephaly during neurodevelopment of infantile stage. Therefore, the formation of cavities can be a result of hemorrhages which promote cerebral degeneration. In a mouse model, mouse with COL4A1 mutations displayed cerebral hemorrhage, porencephaly, and abnormal development of vascular basement membranes, such as uneven edges, inconsistent shapes, and highly variable thickness. Purposely causing a mutation in the COL4A1 gene caused several mouse to develop cerebral hemorrhage and porencephaly-like diseases. Though, there is no direct correlation between mutations of the COL4A1 gene, it appears that it has an influential effect on the development of porencephaly.
+Another genetic mutation, factor V G1691A mutation, has been reported to show possible association to the development of porencephaly. A mutation in factor V G1691A increases the risk of thrombosis, blood clots, in neonates, infants, and children. Therefore, 76 porencephalic and 76 healthy infants were investigated for factor V G1691A mutation along with other different prothrombotic risk factors. The results indicated that there was higher prevalence of the factor V G1691A mutation in the porencephalic patient group. The prediction that childhood porencephaly is caused by hypercoagulable state, a condition where one has a higher chance of developing blood clots, was supported by the significance of the factor V G1691A mutation. Also, pregnant women in hypercoagulable state can cause the fetus to have the same risks, therefore possibly causing fetal loss, brain damage, lesions, and infections that lead to porencephaly. However, other different prothrombotic risk factors individually did not reach statistical significance to link it to the development of porencephaly, but a combination of multiple prothrombotic risk factors in the porencephaly group was significant. Overall, factor V G1691A mutation has been linked to the development of porencephaly. However, this one mutation is not the cause of porencephaly, and whether further prothrombiotic risk factors are associated with porencephaly still remains unknown.
+Cocaine and other street drugs => In utero exposure to cocaine and other street drugs can lead to porencephaly.
+Patients diagnosed with porencephaly display a variety of symptoms, from mild to severe effects on the patient. Patients with severe cases of porencephaly suffer epileptic seizures and developmental delays, whereas patients with a mild case of porencephaly display little to no seizures and healthy neurodevelopment. Infants with extensive defects show symptoms of the disorder shortly after birth, and the diagnosis is usually made before the age of 1.
+The following text lists out common signs and symptoms of porencephaly in affected individuals along with a short description of certain terminologies.
+- Degenerative or non-degenerative cavities or cysts
+- Delayed growth and development
+- Spastic paresis – weakness or loss in voluntary movement
+- Contractures – painful shortening of muscles affecting motion
+- Hypotonia – reduced muscle strength
+- Epileptic seizures and epilepsy – multiple symptoms that involve sudden muscle spasms and loss of consciousness
+- Macrocephaly – condition where head circumference is larger compared to other children of a certain age
+- Microcephaly – condition where head circumference is smaller compared to other children of a certain age
+- Hemiplegia – paralysis of appendages
+- Tetraplegia – paralysis of limb leading to loss of function
+- Intellectual and cognitive disability
+- Poor or absent speech development
+- Hydrocephalus – accumulation of cerebrospinal fluid in the brain
+- Mental retardation
+- Poor motor control, abnormal movements of appendages
+- Cerebral palsy – a motor condition causing movement disabilities
+- Blood vascular diseases such as intracerebral hemorrhage and cerebral infarction.
+- Cerebral white-matter lesion
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DISNET disease texts/100 Clean Disease Texts/Prediabetes.txt

+Family history of diabetes
+- Cardiovascular disease
+- Increased triglycerides levels
+- Low levels of good cholesterol (HDL)
+- Overweight or obesity
+- Elevated blood pressure
+- Elevated fasting plasma glucose
+- Women who have had gestational diabetes, had high birth weight babies (greater than 9 lbs.), and/or have polycystic ovarian syndrome (PCOS).
+These are associated with insulin resistance and are risk factors for the development of type 2 diabetes mellitus. Those in this stratum (IGT or IFG) are at increased risk of cardiovascular disease. Of the two, impaired glucose tolerance better predicts cardiovascular disease and mortality.
+In a way, prediabetes is a misnomer since it is an early stage of diabetes. It now is known that the health complications associated with type 2 diabetes often occur before the medical diagnosis of diabetes is made.
+Genetics => Type 2 DM, which is the condition for which prediabetes is a precursor, has 90–100% concordance in twins; there is no HLA association. Genetics play a relatively small role, however, in the widespread occurrence of type 2 diabetes. This may be deduced logically from the huge increase in the occurrence of type 2 diabetes that has correlated with the significant change in western lifestyle and diet. As the human genome is further explored, it is possible that multiple genetic anomalies at different loci will be found that confer varying degrees of predisposition to type 2 diabetes.
+Usually, prediabetes is diagnosed with a blood test:
+- Fasting blood sugar (glucose) level of: 110 to 125 mg/dL (6.1 mM/L to 6.9 mM/L) – WHO criteria 100 to 125 mg/dL (5.6 mM/L to 6.9 mM/L) – ADA criteria
+- 110 to 125 mg/dL (6.1 mM/L to 6.9 mM/L) – WHO criteria
+- 100 to 125 mg/dL (5.6 mM/L to 6.9 mM/L) – ADA criteria
+- Two hour glucose tolerance test after ingesting the standardized 75 Gm glucose solution the blood sugar level of 140 to 199 mg/dL (7.8 to 11.0 mM)
+- Glycated haemoglobin between 5.7 and 6.4 percent.
+Glycated hemoglobin is; however, of questionable accuracy and while fasting glucose can indicate the diagnosis when positive if it is negative it is not very accurate. A 2016 review found worse outcomes when blood sugar levels were over 100 mg/dL and glycated haemoglobin over 5.7%.
+Levels above these limits would justify a diagnosis for diabetes.
+Screening => Fasting plasma glucose screening should begin at age 30–45 and be repeated at least every three years. Earlier and more frequent screening should be conducted in at-risk individuals. The risk factors for which are listed below:
+- Family history (parent or sibling)
+- Dyslipidemia (triglycerides > 200 or HDL < 35)
+- Overweight or obesity (body mass index > 25)
+- History of gestational diabetes or infant born with birth weight greater than 9 lb (4 kg)
+- High risk ethnic group
+- Hypertension (systolic blood pressure >140 mmHg or diastolic blood pressure > 90 mmHg)
+- Prior fasting blood glucose > 99
+- Known vascular disease
+- Markers of insulin resistance (PCOS, acanthosis nigricans).
+Prediabetes typically has no distinct signs or symptoms except the sole sign of high blood sugar. Patients should monitor for signs and symptoms of type 2 diabetes mellitus. These include the following:
+- Constant hunger
+- Unexplained weight loss
+- Weight gain
+- Flu-like symptoms, including weakness and fatigue
+- Blurred vision
+- Slow healing of cuts or bruises
+- Tingling or loss of feeling in hands or feet
+- Recurring gum or skin infections
+- Recurring vaginal or bladder infections
+- A high BMI (Body Mass Index) result
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DISNET disease texts/100 Clean Disease Texts/Pregnancy.txt

+The beginning of pregnancy may be detected either based on symptoms by the woman herself, or by using pregnancy tests. However, an important condition with serious health implications that is quite common is the denial of pregnancy by the pregnant woman. About one in 475 denials will last until around the 20th week of pregnancy. The proportion of cases of denial, persisting until delivery is about 1 in 2500. Conversely, some non-pregnant women have a very strong belief that they are pregnant along with some of the physical changes. This condition is known as a false pregnancy.
+Most pregnant women experience a number of symptoms, which can signify pregnancy. A number of early medical signs are associated with pregnancy. These signs include:
+- the presence of human chorionic gonadotropin (hCG) in the blood and urine
+- missed menstrual period
+- implantation bleeding that occurs at implantation of the embryo in the uterus during the third or fourth week after last menstrual period
+- increased basal body temperature sustained for over 2 weeks after ovulation
+- Chadwick's sign (darkening of the cervix, vagina, and vulva)
+- Goodell's sign (softening of the vaginal portion of the cervix)
+- Hegar's sign (softening of the uterus isthmus)
+- Pigmentation of the linea alba – linea nigra, (darkening of the skin in a midline of the abdomen, caused by hyperpigmentation resulting from hormonal changes, usually appearing around the middle of pregnancy).
+- Darkening of the nipples and areolas due to an increase in hormones.
+Pregnancy detection can be accomplished using one or more various pregnancy tests, which detect hormones generated by the newly formed placenta, serving as biomarkers of pregnancy. Blood and urine tests can detect pregnancy 12 days after implantation. Blood pregnancy tests are more sensitive than urine tests (giving fewer false negatives). Home pregnancy tests are urine tests, and normally detect a pregnancy 12 to 15 days after fertilization. A quantitative blood test can determine approximately the date the embryo was conceived because HCG doubles every 36 to 48 hours. A single test of progesterone levels can also help determine how likely a fetus will survive in those with a threatened miscarriage (bleeding in early pregnancy).
+Obstetric ultrasonography can detect fetal abnormalities, detect multiple pregnancies, and improve gestational dating at 24 weeks. The resultant estimated gestational age and due date of the fetus are slightly more accurate than methods based on last menstrual period. Ultrasound is used to measure the nuchal fold in order to screen for Downs syndrome.
+The symptoms and discomforts of pregnancy are those presentations and conditions that result from pregnancy but do not significantly interfere with activities of daily living or pose a threat to the health of the mother or baby. This is in contrast to pregnancy complications. Sometimes a symptom that is considered a discomfort can be considered a complication when it is more severe. For example, nausea (morning sickness) can be a discomfort, but if, in combination with significant vomiting it causes a water-electrolyte imbalance, it is a complication known as hyperemesis gravidarum.
+Common symptoms and discomforts of pregnancy include:
+- Tiredness.
+- Constipation
+- Pelvic girdle pain
+- Back pain
+- Braxton Hicks contractions. Occasional, irregular, and often painless contractions that occur several times per day.
+- Edema (swelling). Common complaint in advancing pregnancy. Caused by compression of the inferior vena cava and pelvic veins by the uterus leads to increased hydrostatic pressure in lower extremities.
+- Increased urinary frequency. A common complaint, caused by increased intravascular volume, elevated glomerular filtration rate, and compression of the bladder by the expanding uterus.
+- Urinary tract infection
+- Varicose veins. Common complaint caused by relaxation of the venous smooth muscle and increased intravascular pressure.
+- Haemorrhoids (piles). Swollen veins at or inside the anal area. Caused by impaired venous return, straining associated with constipation, or increased intra-abdominal pressure in later pregnancy.
+- Regurgitation, heartburn, and nausea.
+- Stretch marks
+- Breast tenderness is common during the first trimester, and is more common in women who are pregnant at a young age.
+In addition, pregnancy may result in pregnancy complication such as deep vein thrombosis or worsening of an intercurrent disease in pregnancy.
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DISNET disease texts/100 Clean Disease Texts/Premenstrual syndrome.txt

+While PMS is linked to the luteal phase, the causes of PMS are not clear, but several factors may be involved. Changes in hormones during the menstrual cycle seem to be an important factor; changing hormone levels affect some women more than others. Chemical changes in the brain, stress, and emotional problems, such as depression, do not seem to cause PMS but they may make it worse. Low levels of vitamins and minerals, high sodium, alcohol, and/or caffeine can exacerbate symptoms such as water retention and bloating. PMS occurs more often in women who are between their late 20s and early 40s; have at least 1 child; have a family history of depression; and have a past medical history of either postpartum depression or a mood disorder.
+There are no laboratory tests or unique physical findings to verify the diagnosis of PMS. The three key features are:
+- The woman's chief complaint is one or more of the emotional symptoms associated with PMS (most typically irritability, tension, or unhappiness). The woman does not have PMS if she only has physical symptoms, such as cramps or bloating.
+- Symptoms appear predictably during the luteal (premenstrual) phase, reduce or disappear predictably shortly before or during menstruation, and remain absent during the follicular (preovulatory) phase.
+- The symptoms must be severe enough to interfere with the woman's everyday life.
+Mild PMS is common, and more severe symptoms would qualify as PMDD. PMS is not listed in the DSM-IV, unlike PMDD. To establish a pattern and determine if it is PMDD, a woman's physician may ask her to keep a prospective record of her symptoms on a calendar for at least two menstrual cycles. This will help to establish if the symptoms are, indeed, limited to the premenstrual time, predictably recurring, and disruptive to normal functioning. A number of standardized instruments have been developed to describe PMS, including the Calendar of Premenstrual syndrome Experiences (COPE), the Prospective Record of the Impact and Severity of Menstruation (PRISM), and the Visual Analogue Scales (VAS).
+Other conditions that may better explain symptoms must be excluded. A number of medical conditions are subject to exacerbation at menstruation, a process called menstrual magnification. These conditions may lead the woman to believe that she has PMS, when the underlying disorder may be some other problem, such as anemia, hypothyroidism, eating disorders and substance abuse. A key feature is that these conditions may also be present outside of the luteal phase. Conditions that can be magnified perimenstrually include depression or other affective disorders, migraine, seizure disorders, fatigue, irritable bowel syndrome, asthma, and allergies. Problems with other aspects of the female reproductive system must be excluded, including dysmenorrhea (pain during the menstrual period, rather than before it), endometriosis, perimenopause, and adverse effects produced by oral contraceptive pills.
+The National Institute of Mental Health research definition compares the intensity of symptoms from cycle days 5 to 10 to the six-day interval before the onset of the menstrual period. To qualify as PMS, symptom intensity must increase at least 30% in the six days before menstruation. Additionally, this pattern must be documented for at least two consecutive cycles.
+More than 200 different symptoms have been associated with PMS. Common emotional and non-specific symptoms include stress, anxiety, difficulty with sleep, headache, feeling tired, mood swings, increased emotional sensitivity, and changes in interest in sex.
+Physical symptoms associated with the menstrual cycle include bloating, lower back pain, abdominal cramps, constipation/diarrhea, swelling or tenderness in the breasts, cyclic acne, and joint or muscle pain, and food cravings. The exact symptoms and their intensity vary significantly from woman to woman, and even somewhat from cycle to cycle and over time. Most women with premenstrual syndrome experience only a few of the possible symptoms, in a relatively predictable pattern.
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DISNET disease texts/100 Clean Disease Texts/Primary hyperparathyroidism.txt

+The most common cause of primary hyperparathyroidism is a sporadic, single parathyroid adenoma resulting from a clonal mutation (~97%). Less common are parathyroid hyperplasia (~2.5%), parathyroid carcinoma (malignant tumor), and adenomas in more than one gland (together ~0.5%).
+Primary hyperparathyroidism is also a feature of several familial endocrine disorders: Multiple endocrine neoplasia type 1 and type 2A (MEN type 1 and MEN type 2A), and familial hyperparathyroidism.
+Genetic associations include:
+OMIM Name Gene headingBody 145000 HRPT1 MEN1, HRPT2 145001 HRPT2 HRPT2 610071 HRPT3 unknown at 2p13.3 – 14.
+In all cases, the disease is idiopathic, but is thought to involve inactivation of tumor suppressor genes (Menin gene in MEN1), or involve gain of function mutations (RET proto-oncogene MEN 2a).
+Recently, it was demonstrated that liquidators of the Chernobyl power plant are faced with a substantial risk of primary hyperparathyroidism, possibly caused by radioactive strontium isotopes.
+Primary hyperparathyroidism can also result from pregnancy. It is apparently very rare, with only about 110 cases have so far been reported in world literature, but this is probably a considerable underestimate of its actual prevalence in pregnant women.
+The diagnosis of primary hyperparathyroidism is made by blood tests.
+Serum calcium levels are elevated, and the parathyroid hormone level is abnormally high compared with an expected low level in response to the high calcium. A relatively elevated parathyroid hormone has been estimated to have a sensitivity of 60%-80% and a specificity of approximately 90% for primary hyperparathyroidism.
+A more powerful variant of comparing the balance between calcium and parathyroid hormone is to perform a 3-hour calcium infusion. After infusion, a parathyroid hormone level above a cutoff of 14 ng/l has a sensitivity of 100% and a specificity of 93% in detecting primary hyperparathyroidism, with a confidence interval of 80% to 100%.
+Urinary cAMP is occasionally measured; this is generally elevated.
+Biochemical confirmation of primary hyperparathyroidism is following by investigations to localize the culprit lesion. Primary hyperparathyroidism is most commonly due to solitary parathyroid adenoma. Less commonly it may be due to double parathyroid adenomas or parathyroid hyperplasia. Tc99 sestamibi scan of head, neck and upper thorax is the most commonly used test for localizing parathyroid adenomas having a sensitivity and specificity of 70 – 80%. Sensitivity falls down to 30% in case of double/multiple parathyroid adenomas or in case of parathyroid hyperplasia. Ultrasonography is also a useful test in localizing suspicious parathyroid lesions.
+The signs and symptoms of primary hyperparathyroidism are those of hypercalcemia. They are classically summarized by "stones, bones, abdominal groans, thrones and psychiatric overtones".
+- "Stones" refers to kidney stones, nephrocalcinosis, and diabetes insipidus (polyuria and polydipsia). These can ultimately lead to renal failure.
+- "Bones" refers to bone-related complications. The classic bone disease in hyperparathyroidism is osteitis fibrosa cystica, which results in pain and sometimes pathological fractures. Other bone diseases associated with hyperparathyroidism are osteoporosis, osteomalacia, and arthritis.
+- "Abdominal groans" refers to gastrointestinal symptoms of constipation, indigestion, nausea and vomiting. Hypercalcemia can lead to peptic ulcers and acute pancreatitis. The peptic ulcers can be an effect of increased gastric acid secretion by hypercalcemia.
+- "Thrones" refers to polyuria and constipation
+- "Psychiatric overtones" refers to effects on the central nervous system. Symptoms include lethargy, fatigue, depression, memory loss, psychosis, ataxia, delirium, and coma.
+Left ventricular hypertrophy may also be seen.
+Other signs include proximal muscle weakness, itching, and band keratopathy of the eyes.
+When subjected to formal research, symptoms of depression, pain, and gastric dysfunction seem to correlate with mild cases of hypercalcemia.
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DISNET disease texts/100 Clean Disease Texts/Primary sclerosing cholangitis.txt

+The exact cause of primary sclerosing cholangitis is unknown and its pathogenesis is poorly understood. Although PSC is thought to be an autoimmune disease, it does not demonstrate a clear response to immunosuppressants. Thus, many experts believe it to be a complex, multifactorial (including immune-mediated) disorder and perhaps one that encompasses several different hepatobiliary diseases.
+Data have provided novel insights suggesting:
+- an important association between the intestinal microbiota and PSC and
+- a process referred to as cellular senescence and the senescence-associated secretory phenotype (SASP) in the pathogenesis of PSC.
+In addition, there are longstanding, well-recognized associations between PSC and human leukocyte antigen (HLA) alleles (A1, B8, and DR3).
+PSC is generally diagnosed on the basis of having at least two of three clinical criteria after secondary causes of sclerosing cholangitis have been ruled out:
+- serum alkaline phosphatase (ALP) > 1.5x the upper limit of normal for longer than 6 months;
+- cholangiography demonstrating biliary strictures or irregularity consistent with PSC; and,
+- liver biopsy consistent with PSC (if available).
+Historically, a cholangiogram would be obtained via endoscopic retrograde cholangiopancreatography (ERCP), which typically reveals "beading" (alternating strictures and dilation) of the bile ducts inside and/or outside the liver. Currently, the preferred option for diagnostic cholangiography, given its non-invasive yet highly accurate nature, is magnetic resonance cholangiopancreatography (MRCP), a magnetic resonance imaging technique. MRCP has unique strengths, including high spatial resolution, and can even be used to visualize the biliary tract of small animal models of PSC.
+Most people with PSC have evidence of autoantibodies and abnormal immunoglobulin levels. For example, approximately 80% of people with PSC have perinuclear anti-neutrophil cytoplasmic antibodies; however, this and other immunoglobulin findings are not specific to those with PSC and are of unclear clinical significance/consequence. Antinuclear antibodies and anti-smooth muscle antibody are found in 20%-50% of PSC patients and, likewise, are not specific for the disease but may identify a subgroup of PSC patients who also have autoimmune hepatitis (i.e. PSC-AIH overlap syndrome).
+Other markers which may be measured and monitored are a complete blood count, serum liver enzymes, bilirubin levels (usually grossly elevated), kidney function, and electrolytes. Fecal fat measurement is occasionally ordered when symptoms of malabsorption (e. G., gross steatorrhea) are prominent.
+The differential diagnosis can include primary biliary cholangitis (formerly referred to as primary biliary cirrhosis), drug-induced cholestasis, cholangiocarcinoma, IgG4-related disease, post-liver transplantation non-anastomotic biliary strictures, and HIV-associated cholangiopathy. Primary sclerosing cholangitis and primary biliary cholangitis are distinct entities and exhibit important differences, including the site of tissue damage within the liver, associations with inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease, response to treatment, and risks of disease progression.
+Nearly half of people with PSC do not have symptoms and are often incidentally discovered to have PSC due to abnormal liver function tests, but a substantial proportion will have debilitating signs and symptoms of the disease. Signs and symptoms of PSC may include severe itching and non-specific fatigue. Yellowing of the skin and white portion of the eyes may also be seen. Enlargement of the liver and spleen are seen in approximately 40% of affected individuals. Abdominal pain affects about 20% of people with PSC.
+Multiple episodes of life-threatening acute cholangitis (infection within the bile ducts) can be seen due to impaired drainage of the bile ducts, which increases the risk of infection.
+- Dark urine due to excess conjugated bilirubin, which is water-soluble and excreted by the kidneys (i.e. Choluria)
+- Malabsorption, especially of fat, and steatorrhea (fatty stool), due to an inadequate amount of bile reaching the small intestine, leading to decreased levels of the fat-soluble vitamins, A, D, E, and K.
+Portal hypertension, a complication of cirrhosis, which can manifest with esophageal and parastomal varices as well as hepatic encephalopathy (mental status alteration/disturbance caused by liver dysfunction and shunting of blood away from the scarred liver; such that ammonia detoxification is reduced with concomitant encephalopathy)
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DISNET disease texts/100 Clean Disease Texts/Reactive hypoglycemia.txt

+The NIH states: "The causes of most cases of reactive hypoglycemia are still open to debate. Some researchers suggest that certain people may be more sensitive to the body’s normal release of the hormone epinephrine, which causes many of the symptoms of hypoglycemia. Others believe deficiencies in glucagon secretion might lead to reactive hypoglycemia.
+Stomach surgery or hereditary fructose intolerance are believed to be causes, albeit uncommon, of reactive hypoglycemia. Myo-Inositol or D-chiro-inositol withdrawal can cause temporary reactive hypoglycemia.
+There are different kinds of reactive hypoglycemia:
+- Alimentary hypoglycemia (consequence of dumping syndrome; it occurs in about 15% of people who have had stomach surgery)
+- Hormonal hypoglycemia (e. G., hypothyroidism)
+- Helicobacter pylori-induced gastritis (some reports suggest this bacteria may contribute to the occurrence of reactive hypoglycemia)
+- Congenital enzyme deficiencies (hereditary fructose intolerance, galactosemia, and leucine sensitivity of childhood)
+- Late hypoglycemia (occult diabetes; characterized by a delay in early insulin release from pancreatic β-cells, resulting in initial exaggeration of hyperglycemia during a glucose tolerance test).
+"Idiopathic reactive hypoglycemia" is a term no longer used because researchers now know the underlying causes of reactive hypoglycemia and have the tools to perform the diagnosis and the pathophysiological data explaining the mechanisms.
+To check if there is real hypoglycemia when symptoms occur, neither an oral glucose tolerance test nor a breakfast test is effective; instead, a hyperglucidic breakfast test or ambulatory glucose testing is the current standard.
+The body requires a relatively constant input of glucose, a sugar produced upon digestion of carbohydrates, for normal functioning. Glucagon and insulin are among the hormones that ensure a normal range of glucose in the human body. Upon consumption of a meal, blood sugar normally rises, which triggers pancreatic cells to produce insulin. This hormone initiates the absorption of the just-digested blood glucose as glycogen into the liver for metabolism or storage, thereby lowering glucose levels in the blood. In contrast, the hormone glucagon is released by the pancreas as a response to lower than normal blood sugar levels. Glucagon initiates uptake of the stored glycogen in the liver into the bloodstream so as to increase glucose levels in the blood. Sporadic, high-carbohydrate snacks and meals are deemed the specific causes of sugar crashes. The “crash” one feels is due to the rapid increase and subsequent decline of blood sugar in the body system as one begins and ceases consumption of high-sugar foods. More insulin than is actually needed is produced in response to the large, rapid ingestion of sugary foods.
+Symptoms vary according to individuals' hydration level and sensitivity to the rate and/or magnitude of decline of their blood glucose concentration. A crash is usually felt within four hours or less of heavy carbohydrate consumption. Symptoms of reactive hypoglycemia include:
+- double vision or blurry vision
+- unclear thinking
+- insomnia
+- heart palpitation or fibrillation
+- fatigue
+- dizziness
+- light-headedness
+- sweating
+- headaches
+- depression
+- nervousness
+- muscle twitches
+- irritability
+- tremors
+- flushing
+- craving sweets
+- increased appetite
+- rhinitis
+- nausea, vomiting
+- panic attack
+- numbness/coldness in the extremities
+- confusion
+- irrationality
+- bad temper
+- paleness
+- cold hands
+- disorientation
+- the need to sleep or 'crash'
+- coma can be a result in severe untreated episode.
+The majority of these symptoms, often correlated with feelings of hunger, mimic the effect of inadequate sugar intake as the biology of a crash is similar in itself to the body’s response to low blood sugar levels following periods of glucose deficiency.
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DISNET disease texts/100 Clean Disease Texts/Reflex syncope.txt

+Reflex syncope occurs in response to a trigger due to dysfunction of the heart rate and blood pressure regulating mechanism. When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting.
+Vasovagal syncope => Typical triggers include:
+- Prolonged standing
+- Emotional stress
+- Pain
+- The sight of blood
+- Time varying magnetic field (i.e. Transcranial magnetic stimulation.
+- Situational syncope => After or during urination (micturition syncope)
+- Straining, such as to have a bowel movement
+- Coughing
+- Swallowing
+- Lifting a heavy weight.
+Carotid sinus syncope => Pressing upon a certain spot in the neck. This may happen when wearing a tight collar, shaving, or turning the head.
+In addition to the mechanism described above, a number of other medical conditions may cause syncope. Making the correct diagnosis for loss of consciousness is difficult. The core of the diagnosis of vasovagal syncope rests upon a clear description of a typical pattern of triggers, symptoms, and time course.
+It is pertinent to differentiate lightheadedness, seizures, vertigo, and low blood sugar as other causes.
+In people with recurrent vasovagal syncope, diagnostic accuracy can often be improved with one of the following diagnostic tests:
+- A tilt table test (results should be interpreted in the context of patients' clinical presentations and with an understanding of the sensitivity and specificity of the test)
+- Implantation of an insertable loop recorder
+- A Holter monitor or event monitor
+- An echocardiogram
+- An electrophysiology stud.
+Episodes of vasovagal syncope are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger. Before losing consciousness, the individual frequently experiences early signs or symptoms such as lightheadedness, nausea, the feeling of being extremely hot or cold (accompanied by sweating), ringing in the ears, an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak or form words (sometimes combined with mild stuttering), weakness and visual disturbances such as lights seeming too bright, fuzzy or tunnel vision, black cloud-like spots in vision, and a feeling of nervousness can occur as well. The symptoms may become more intense over several seconds to several minutes before the loss of consciousness (if it is lost). Onset usually occurs when a person is sitting up or standing.
+When people lose consciousness, they fall down (unless prevented from doing so) and, when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness. If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a seizure may result from the blood's inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense. Fainting occurs with a loss of oxygen to the brain.
+The autonomic nervous system's physiological state (see below) leading to loss of consciousness may persist for several minutes, so.
+- If sufferers try to sit or stand when they wake up, they may pass out again
+- The person may be nauseated, pale, and sweaty for several minutes or hour
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DISNET disease texts/100 Clean Disease Texts/Ross River fever.txt

+A blood test is the only way to confirm a case of Ross River Fever. Several types of blood tests may be used to examine antibody levels in the blood. Tests may either look for simply elevated antibodies (which indicate some sort of infection), or specific antibodies to the virus.
+Symptoms of the disease may vary widely in severity, but major indicators are arthralgia, arthritis, fever, and rash. The incubation period is 7–9 days. About a third of infections are asymptomatic, particularly in children.
+Acute illness => About 95% of symptomatic cases report joint pain. This is typically symmetrical and with acute onset, affecting the fingers, toes, ankles, wrists, back, knees and elbows. Fatigue occurs in 90% and fever, myalgia and headache occur in 50–60%.
+A rash occurs in 50% of patients and is widespread and maculopapular. Lymphadenopathy occurs commonly; sore throat and coryza less frequently. Diarrhea is rare. About 50% of people report needing time off work with the acute illness. If the rash is unnoticed, these symptoms are quite easily mistaken for more common illnesses like influenza or the common cold. Recovery from the flu symptoms is expected within a month, but, because the virus currently cannot be removed once infection has occurred secondary symptoms of joint and muscle inflammation, pain and stiffness can last for many years.
+Less common manifestations include splenomegaly, hematuria and glomerulonephritis. Headache, neck stiffness, and photophobia may occur. There have been three case reports suggesting meningitis or encephalitis.
+Chronic illness => Reports from the 1980s and 1990s suggested RRV infection was associated with arthralgia, fatigue and depression lasting for years. More recent prospective studies have reported a steady improvement in symptoms over the first few months, with 15–66% of patients having ongoing arthralgia at 3 months. Arthralgias have resolved in the majority by 5–7 months. The incidence of chronic fatigue is 12% at 6 months and 9% at 12 months, similar to Epstein-Barr virus and Q fever. The only significant predictor of the likelihood of developing chronic symptoms is the severity of the acute illness itself. No other aspects of the patient's medical or psychiatric history have been found to be predictive. However, in those with the most persisting symptoms (12 months or more), comorbid rheumatologic conditions and/or depression are frequently observed.
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DISNET disease texts/100 Clean Disease Texts/Rubella.txt

+The disease is caused by rubella virus, a togavirus that is enveloped and has a single-stranded RNA genome. The virus is transmitted by the respiratory route and replicates in the nasopharynx and lymph nodes. The virus is found in the blood 5 to 7 days after infection and spreads throughout the body. The virus has teratogenic properties and is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them. During this incubation period, the patient is contagious typically for about one week before he/she develops a rash and for about one week thereafter.
+Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are involved in virus infection or non-resolution of the disease.
+Rubella virus specific IgM antibodies are present in people recently infected by rubella virus, but these antibodies can persist for over a year, and a positive test result needs to be interpreted with caution. The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.
+Rubella has symptoms that are similar to those of flu. However, the primary symptom of rubella virus infection is the appearance of a rash (exanthem) on the face which spreads to the trunk and limbs and usually fades after three days (that is why it is often referred to as three-day measles). The facial rash usually clears as it spreads to other parts of the body. Other symptoms include low grade fever, swollen glands (sub-occipital and posterior cervical lymphadenopathy), joint pains, headache, and conjunctivitis.
+The swollen glands or lymph nodes can persist for up to a week and the fever rarely rises above 38 °C (100.4 °F). The rash of German measles is typically pink or light red. The rash causes itching and often lasts for about three days. The rash disappears after a few days with no staining or peeling of the skin. When the rash clears up, the skin might shed in very small flakes where the rash covered it. Forchheimer's sign occurs in 20% of cases, and is characterized by small, red papules on the area of the soft palate.
+Rubella can affect anyone of any age and is generally a mild disease, rare in infants or those over the age of 40. The older the person is the more severe the symptoms are likely to be. Up to 60% of older girls or women experience joint pain or arthritic type symptoms with rubella.
+In children rubella normally causes symptoms which last two days and include:
+- Rash beginning on the face which spreads to the rest of the body.
+- Low fever of less than 38.3 °C (101 °F).
+- Posterior cervical lymphadenopathy.
+In older children and adults additional symptoms may be present including:
+- Swollen glands
+- Coryza (cold-like symptoms)
+- Aching joints (especially in young women.
+Rare problems can occur including the following:
+- Brain inflammation
+- Ear infection.
+Coryza in rubella may convert to pneumonia, either direct viral pneumonia or secondary bacterial pneumonia, and bronchitis (either viral bronchitis or secondary bacterial bronchitis).
+Rubella can cause congenital rubella syndrome in the newborn. The syndrome (CRS) follows intrauterine infection by the rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects. It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anemia and hepatitis. The risk of major defects or organogenesis is highest for infection in the first trimester. CRS is the main reason a vaccine for rubella was developed.
+Many mothers who contract rubella within the first critical trimester either have a miscarriage or a stillborn baby. If the fetus survives the infection, it can be born with severe heart disorders (patent ductus arteriosus being the most common), blindness, deafness, or other life-threatening organ disorders. The skin manifestations are called "blueberry muffin lesions". For these reasons, rubella is included on the TORCH complex of perinatal infections.
+About 100,000 cases of this condition occur each year.
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DISNET disease texts/100 Clean Disease Texts/Scarlet fever.txt

+Spread of strep throat occurs by close contact, via respiratory droplets (for example, saliva or nasal discharge). A person in close contact with another person infected with Group A streptococcal pharyngitis has a 35% chance of becoming infected. One in ten children who are infected with Group A streptococcal pharyngitis will develop scarlet fever.
+Although the presentation of scarlet fever can be clinically diagnosed, further testing may be required to distinguish it from other illnesses. Also, history of a recent exposure to someone with strep throat can be useful. There are two methods used to confirm suspicion of scarlet fever rapid antigen detection test and throat culture.
+The rapid antigen detection test is a very specific test but not very sensitive. This means that if the result is positive (indicating that the Group A Strep Antigen was detected and therefore confirming that the patient has a Group A Strep Pharyngitis) then it is appropriate to treat them with antibiotics. However, if the Rapid Antigen Detection Test is negative (indicating that they do not have Group A Strep Pharyngitis), then a throat culture is required to confirm since it could be a false negative result. The throat culture is the current gold standard for diagnosis.
+Serologic testing looks for the antibodies that the body produces against the streptococcal infection including antistreptolysin-O and antideoxyribonuclease B. It takes the body 2–3 weeks to make these antibodies so this type of testing is not useful for diagnosing a current infection. However, it is useful when assessing a patient who may have one of the complications from a previous streptococcal infection.
+Throat cultures done after antibiotic therapy can tell you if the infection has been removed. These throat swabs however are not indicated because up to 25% of properly treated individuals can continue to carry the streptococcal infection while asymptomatic.
+- Differential diagnosis => Viral exanthem: Viral infections are often accompanied by a rash which can be described as morbilliform or maculopapular. This type of rash is accompanied by a prodromal period of cough and runny nose in addition to a fever, indicative of a viral process.
+- Allergic or contact dermatitis: The erythematous appearance of the skin will be in a more localized distribution rather than the diffuse and generalized rash seen in Scarlet Fever.
+- Drug eruption: These are potential side effects of taking certain drugs such as Penicillin. The reddened maculopapular rash which results can be itchy and be accompanied by a fever.
+- Kawasaki disease Children with this disease also present with a strawberry tongue and undergo a desquamative process on their palms and soles. However these children tend to be younger than 5 years old, their fever lasts longer (at least five days) and they have additional clinical criteria (including signs such as conjunctival redness and cracked lips) which can help distinguish this from Scarlet Fever.
+- Toxic shock syndrome: Both Streptococcal and Staphylococcal bacteria can cause this syndrome. Clinical manifestations include diffuse rash and desquamation of the palms and soles. Can be distinguished from Scarlet Fever by low blood pressure, the rash will lack sandpaper texture, and multi-organ system involvement.
+- Staphylococcal scalded skin syndrome: This is a disease which occurs primarily in young children due to a toxin producing strain of the bacteria Staphylococcus Aureus. The abrupt start of the fever and diffused sunburned appearance of the rash can resemble Scarlet Fever. However, this rash is associated with tenderness and large blister formation. These blisters easily pop and then cause the skin to peel.
+- Staphylococcal Scarlet Fever: The rash is identical to the streptococcal scarlet fever in distribution and texture however the skin affected by the rash will be tender.
+Rash which has a characteristic appearance, spreading pattern, and desquamating process "Strawberry tongue".
+- The tongue starts out by having a white coating on it while the papillae of the tongue are swollen and reddened. The protrusion of the red papillae through the white coating gives the tongue a "white strawberry" appearance.
+- Then a few days later (following the desquamating process, or the shedding of the tissue which created the white coating) the whiteness disappears while the red and enlarged papillae give it the "red strawberry" appearance.
+- Note that this involvement of the tongue is a part of the rash which is characteristic of scarlet fever.
+Pastia's lines.
+Lines of petechiae which appear as pink/red areas located in arm pits and elbow pit.
+Vomiting and abdominal pain.
+Strep throat => Typical symptoms of streptococcal pharyngitis (also known as strep throat):
+- Sore throat, painful swallowing
+- Fever-typically over 39 °C (102.2 °F)
+- Fatigue
+- Enlarged and reddened tonsils with yellow or white exudates present (this is typically an exudative pharyngitis)
+- Enlarged and tender lymph nodes usually located on the front of the neck.
+The following symptoms will usually be absent: cough, hoarseness, runny nose, diarrhea, and conjunctivitis. Their presence indicates it is more likely a viral infection.
+Rash => The rash begins 1–2 days following the onset of symptoms caused by the strep pharyngitis (sore throat, fever, fatigue). This characteristic rash has been denoted as "scarlatiniform" and it appears as a diffuse redness of the skin with small papules, or bumps, which resemble goose pimples. These bumps are what give the characteristic sand paper texture to the rash. The reddened skin will blanch when you apply pressure to it. It is possible for the skin to be itchy however it will not be painful. It usually first appears on the trunk and then gradually spreads out to the arms and legs. The palms, soles and face are usually left uninvolved by the rash. The face is however is usually flushed, most prominent in cheeks, with a ring of paleness around the mouth. After the rash spreads, it becomes more pronounced in creases in the skin, such as the skin folds in the inguinal and axillary regions of the body. Also in those areas it is possible for there to be Pastia’s Lines which are petechiae arranged in a linear pattern. Within 1 week of onset the rash begins to fade followed by a longer process of desquamation, or shedding of the outer layer of skin, which lasts several weeks. The desquamation process usually begins on the face and progresses downward on the body. After the desquamation the skin will be left with a sunburned appearance.
+The streptococcal pharyngitis which is the usual presentation of scarlet fever in combination with the characteristic rash commonly involves the tonsils. The tonsils will appear swollen and reddened. The palate and uvula are also commonly affected by the infection. The involvement of the soft palate can be seen as tiny red and round spots known as Forscheimer spots.
+Variable presentations => The features of scarlet fever can differ depending on the age and race of the person. Children less than 5 years old can have atypical presentations. Children less than 3 years old can present with nasal congestion and a lower grade fever. Infants can potentially only present with increased irritability and decreased appetite.
+Children who have darker skin can have a different presentation in that the redness of the skin involved in the rash and the ring of paleness around the mouth can be less obvious. Suspicion based on accompanying symptoms and diagnostic studies are important in these cases.
+Course => Following exposure to Streptococcus, it takes 12 hours to 7 days for the onset of the symptoms. This may include fever, fatigue, and sore throat. The characteristic scarlatiniform rash then comes 12–48 hours later. During the first few days of the rash development and rapid generalization, the Pastia's Lines and strawberry tongue will also present. The rash starts fading within 3–4 days followed by the desquamation of the rash which will last several weeks to a month. If the case of scarlet fever is uncomplicated, recovery from the fever and clinical symptoms other than the process of desquamation occurs in 5–10 days.
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DISNET disease texts/100 Clean Disease Texts/Scleroderma.txt

+Scleroderma is caused by genetic and environmental factors. Mutations in HLA genes seem to play a crucial role in the pathogenesis of some cases (but not all), likewise silica, aromatic and chlorinated solvents, ketones, trichloroethylene, welding fumes and white spirits exposure seems to contribute to the condition in a small proportion of affected persons.
+Typical scleroderma is classically defined as symmetrical skin thickening, with about 70% of cases also presenting with Raynaud's phenomenon, nail-fold capillary changes and antinuclear antibodies. Affected individuals may or may not experience systemic organ involvement. There is no single test for scleroderma that works all of the time and hence the diagnosis is often a matter of exclusion. Atypical scleroderma may show any variation of these changes without skin changes or with finger swelling only.
+Laboratory testing can show antitopoisomerase antibodies, like anti-scl70 (causing a diffuse systemic form), or anticentromere antibodies (causing a limited systemic form and the CREST syndrome). Other autoantibodies can be seen, such as anti-U3 or anti-RNA polymerase.
+Differential => Diseases that are often in the differential include:
+- Eosinophilia, a condition in which there are too many eosinophils (a type of immune cell that attacks parasites and is involved in certain allergic reactions) in the blood.
+- Eosinophilia-myalgia syndrome, a form of eosinophilia that is caused by L-tryptophan supplements.
+- Eosinophilic fasciitis, a disease that affects the connective tissues surrounding skeletal muscles, bones, blood vessels and nerves in the arms and legs.
+- Graft-versus-host disease, an autoimmune condition that occurs as a result of bone marrow transplants in which the immune cells from the transplanted bone marrow attack the host's body.
+- Mycosis fungoides, a type of cutaneous T cell lymphoma, a rare cancer that causes rashes all over the body.
+- Nephrogenic systemic fibrosis, a condition usually caused by kidney failure that causes fibrosis (thickening) of the tissues.
+- Primary biliary cirrhosis, an autoimmune disease of the liver.
+- Primary pulmonary hypertension
+- Complex regional pain syndrom.
+Classification => Scleroderma is characterised by the appearance of circumscribed or diffuse, hard, smooth, ivory-colored areas that are immobile and which give the appearance of hidebound skin, a disease occurring in both localised and systemic forms:
+- Localised scleroderma Localised morphea Morphea-lichen sclerosus et atrophicus overlap Generalised morphea Atrophoderma of Pasini and Pierini Pansclerotic morphea Morphea profunda Linear scleroderma
+- Localised morphea
+- Morphea-lichen sclerosus et atrophicus overlap
+- Generalised morphea
+- Atrophoderma of Pasini and Pierini
+- Pansclerotic morphea
+- Morphea profunda
+- Linear scleroderma
+- Systemic scleroderma CREST syndrome Progressive systemic sclerosis
+- CREST syndrome
+- Progressive systemic sclerosi.
+Potential signs and symptoms include:
+- Cardiovascular: Raynaud's phenomenon (is the presenting symptom in 30% of affected persons, occurs in 95% of affected individuals at some time during their illness); healed pitting ulcers on the fingertips; skin and mucousal telangiectasis; palpitations, irregular heart rate and fainting due to conduction abnormalities, hypertension and congestive heart failure.
+- Digestive: gastroesophageal reflux disease, bloating, indigestion, loss of appetite, diarrhoea alternating with constipation, sicca syndrome and its complications, loosening of teeth and hoarseness (due to acid reflux).
+- Pulmonary: progressive worsening of shortness of breath, chest pain (due to pulmonary artery hypertension) and dry, persistent cough due to interstitial lung disease.
+- Musculoskeletal: joint, muscle aches, loss of joint range of motion, carpal tunnel syndrome and muscle weakness.
+- Genitourinary: erectile dysfunction, dyspareunia, scleroderma renal crises and kidney failure.
+- Other: facial pain due to trigeminal neuralgia, hand paresthesias, headache, stroke, fatigue, calcinosis and weight loss
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DISNET disease texts/100 Clean Disease Texts/Snakebite.txt

+In the developing world most snakebites occur in those who work outside such as farmers, hunters, and fishermen. They often happen when a person steps on the snake or approaches it too closely. In the United States and Europe snakebites most commonly occur in those who keep them as pets.
+The type of snake that most often delivers serious bites depends on the region of the world. In Africa it is mambas, Egyptian cobras, puff adders, and carpet vipers. In the Middle East it is carpet vipers and elapids. In Central and South America it is snakes of the Bothrops and Crotalus types, the latter including rattlesnakes. In North America, rattlesnakes are the primary concern, and up to 95% of all snakebite-related deaths in the United States are attributed to the western and eastern diamondback rattlesnakes. In South Asia it was previously believed that Indian cobras, common kraits, Russell's viper and carpet vipers were the most dangerous; other snakes, however, may also cause significant problems in this area of the world.
+The most common symptom of all snakebites is overwhelming fear, which contributes to other symptoms, including nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin. Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and people may have unwarranted thoughts of imminent death.
+Dry snakebites and those inflicted by a non-venomous species can still cause severe injury. There are several reasons for this: a snakebite may become infected, with the snake's saliva and fangs sometimes harboring pathogenic microbial organisms, including Clostridium tetani. Infection is often reported with viper bites whose fangs are capable of deep puncture wounds. Bites may cause anaphylaxis in certain people.
+Most snakebites, whether by a venomous snake or not, will have some type of local effect. There is minor pain and redness in over 90 percent of cases, although this varies depending on the site. Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within five minutes. This area may also bleed and blister and can eventually lead to tissue necrosis. Other common initial symptoms of pit viper and viper bites include lethargy, bleeding, weakness, nausea, and vomiting. Symptoms may become more life-threatening over time, developing into hypotension, tachypnea, severe tachycardia, severe internal bleeding, altered sensorium, kidney failure, and respiratory failure.
+Bites caused by some snakes, such as the kraits, coral snake, Mojave rattlesnake, and the speckled rattlesnake, reportedly cause little or no pain despite being serious potentially life-threatening injuries. Those bitten may also describe a "rubbery", "minty", or "metallic" taste if bitten by certain species of rattlesnake. Spitting cobras and rinkhalses can spit venom in a person's eyes. This results in immediate pain, ophthalmoparesis, and sometimes blindness.
+Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly healed wounds. Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the skin.
+Venom emitted from elapids, including sea snakes, kraits, cobras, king cobra, mambas, and many Australian species, contain toxins which attack the nervous system, causing neurotoxicity. The person may present with strange disturbances to their vision, including blurriness. Paresthesia throughout the body, as well as difficulty in speaking and breathing, may be reported. Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. If not treated immediately they may die from respiratory failure.
+Venom emitted from some types of cobras, almost all vipers and some sea snakes causes necrosis of muscle tissue. Muscle tissue will begin to die throughout the body, a condition known as rhabdomyolysis. Rhabdomyolysis can result in damage to the kidneys as a result of myoglobin accumulation in the renal tubules. This, coupled with hypotension, can lead to acute renal failure, and, if left untreated, eventually death.
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DISNET disease texts/100 Clean Disease Texts/Soy allergy.txt

+Diagnosis of soy allergy is based on the person's history of allergic reactions, skin prick test (SPT), patch test and measurement of soy protein specific serum immunoglobulin E (IgE or sIgE). A negative IgE test does not rule out non-IgE mediated allergy, also described as cell-mediated allergy. SPT and sIgE have sensitivities of 55% and 83% respectively, and specificities of 68% and 38%. These numbers mean that either test may miss diagnosing an existing soy allergy, and that both can also be positive for other food allergens. Confirmation is by double-blind, placebo-controlled food challenges, conducted by an allergy specialist.
+Food allergies can have fast onset (from seconds to one hour) or slow onset (from hours to several days) depending on mechanism. Symptoms may include: rash, hives, itching of mouth, lips, tongue, throat, eyes, skin, or other areas, swelling of lips, tongue, eyelids, or the whole face, difficulty swallowing, runny or congested nose, hoarse voice, wheezing, shortness of breath, diarrhea, abdominal pain, lightheadedness, fainting, nausea and vomiting. Symptoms of allergies vary from person to person and may vary from incident to incident. Serious danger regarding allergies can begin when the respiratory tract or blood circulation is affected. The former can be indicated by wheezing, a blocked airway and cyanosis, the latter by weak pulse, pale skin, and fainting. When these symptoms occur the allergic reaction is called anaphylaxis. Anaphylaxis occurs when IgE antibodies are involved, and areas of the body that are not in direct contact with the food become affected and show severe symptoms. Untreated, this can proceed to vasodilation, a low blood pressure situation called anaphylactic shock, and death (very rare).
+Non-IgE mediated reactions are slower to appear, and tend to manifest as gastrointestinal symptoms, without cutaneous or respiratory symptoms. Within non-IgE reactions, clinicians distinguish among food protein-induced enterocolitis syndrome (FPIES), food protein-induced allergic proctocolitis (FPIAP) and food protein-induced enteropathy (FPE). Common trigger foods for all are soy infant formula, and also cow's milk formula. FPIAP is considered to be at the milder end of the spectrum, and is characterized by intermittent bloody stools. FPE is identified by chronic diarrhea which will resolve when the offending food is removed from the infant's diet. FPIES can be severe, characterized by persistent vomiting 1 – 4 hours after an allergen-containing food, to the point of lethargy. Watery and sometimes bloody diarrhea can develop 5 – 10 hours after the triggering meal, to the point of dehydration and low blood pressure. Infants reacting to soy formula may also react to cow's milk formula. International consensus guidelines have been established for the diagnosis and treatment of FPIES.
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DISNET disease texts/100 Clean Disease Texts/Streptococcal pharyngitis.txt

+Strep throat is caused by group A beta-hemolytic streptococcus (GAS or S. Pyogenes). Other bacteria such as non–group A beta-hemolytic streptococci and fusobacterium may also cause pharyngitis. It is spread by direct, close contact with an infected person; thus crowding, as may be found in the military and schools, increases the rate of transmission. Dried bacteria in dust are not infectious, although moist bacteria on toothbrushes or similar items can persist for up to fifteen days. Contaminated food can result in outbreaks, but this is rare. Of children with no signs or symptoms, 12% carry GAS in their pharynx, and, after treatment, approximately 15% of those remain positive, and are true "carriers".
+Points Probability of Strep Management headingBody 1 or fewer <10% No antibiotic or culture needed 2 11–17% Antibiotic based on culture or RADT 3 28–35% 4 or 5 52% Empiric antibiotics.
+A number of scoring systems exist to help with diagnosis; however, their use is controversial due to insufficient accuracy. The modified Centor criteria are a set of five criteria; the total score indicates the probability of a streptococcal infection.
+One point is given for each of the criteria:
+- Absence of a cough
+- Swollen and tender cervical lymph nodes
+- Temperature >38.0 °C (100.4 °F)
+- Tonsillar exudate or swelling
+- Age less than 15 (a point is subtracted if age >44.
+A score of one may indicated no treatment or culture is needed, or it may indicate the need to perform further testing if other high risk factors exist, such as a family member having the disease.
+The Infectious Disease Society of America recommends against empirical treatment and considers antibiotics only appropriate when given after a positive test. Testing is not needed in children under three as both group A strep and rheumatic fever are rare, unless a child has a sibling with the disease.
+Laboratory testing => A throat culture is the gold standard for the diagnosis of streptococcal pharyngitis, with a sensitivity of 90–95%. A rapid strep test (also called rapid antigen detection testing or RADT) may also be used. While the rapid strep test is quicker, it has a lower sensitivity (70%) and statistically equal specificity (98%) as a throat culture. In areas of the world where rheumatic fever is uncommon, a negative rapid strep test is sufficient to rule out the disease.
+A positive throat culture or RADT in association with symptoms establishes a positive diagnosis in those in which the diagnosis is in doubt. In adults, a negative RADT is sufficient to rule out the diagnosis. However, in children a throat culture is recommended to confirm the result. Asymptomatic individuals should not be routinely tested with a throat culture or RADT because a certain percentage of the population persistently "carries" the streptococcal bacteria in their throat without any harmful results.
+As the symptoms of streptococcal pharyngitis overlap with other conditions, it can be difficult to make the diagnosis clinically. Coughing, nasal discharge, diarrhea, and red, irritated eyes in addition to fever and sore throat are more indicative of a viral sore throat than of strep throat. The presence of marked lymph node enlargement along with sore throat, fever, and tonsillar enlargement may also occur in infectious mononucleosis.
+The typical signs and symptoms of streptococcal pharyngitis are a sore throat, fever of greater than 38 °C (100 °F), tonsillar exudates (pus on the tonsils), and large cervical lymph nodes.
+Other symptoms include: headache, nausea and vomiting, abdominal pain, muscle pain, or a scarlatiniform rash or palatal petechiae, the latter being an uncommon but highly specific finding.
+Symptoms typically begin one to three days after exposure and last seven to ten days.
+Strep throat is unlikely when any of the symptoms of red eyes, hoarseness, runny nose, or mouth ulcers are present. It is also unlikely when there is no fever.
+- Mouth wide open showing the throat A throat infection which on culture tested positive for group A streptococcus. Note the large tonsils with white exudate.
+- Mouth wide open showing the throat Note the petechiae, or small red spots, on the soft palate. This is an uncommon but highly specific finding in streptococcal pharyngitis.
+- A set of large tonsils in the back of the throat, covered in white exudate. A culture positive case of streptococcal pharyngitis with typical tonsillar exudate in an 8-year-old
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DISNET disease texts/100 Clean Disease Texts/Subdural hematoma.txt

+Subdural hematomas are most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. Subdural hematomas due to head injury are described as traumatic. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces. Subdural hemorrhage is a classic finding in shaken baby syndrome, in which similar shearing forces classically cause intra-and pre-retinal hemorrhages. Subdural hematoma is also commonly seen in the elderly and in alcoholics, who have evidence of cerebral atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants or antiplatelet drugs, such as warfarin and aspirin. Patients on these medications can have a subdural hematoma after a relatively minor traumatic event. A further cause can be a reduction in cerebral spinal fluid pressure which can create a low pressure in the subarachnoid space, pulling the arachnoid away from the dura mater and leading to a rupture of the blood vessels.
+Risk factors => Factors increasing the risk of a subdural hematoma include very young or very old age. As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears. This and the fact that the elderly have more brittle veins make chronic subdural bleeds more common in older patients. Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults. For this reason, subdural hematoma is a common finding in shaken baby syndrome. In juveniles, an arachnoid cyst is a risk factor for a subdural hematoma.
+Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, dementia, and the presence of a cerebrospinal fluid leak.
+It is important that a person receive medical assessment, including a complete neurological examination, after any head trauma. A CT scan or MRI scan will usually detect significant subdural hematomas.
+Subdural hematomas occur most often around the tops and sides of the frontal and parietal lobes. They also occur in the posterior cranial fossa, and near the falx cerebri and tentorium cerebelli. Unlike epidural hematomas, which cannot expand past the sutures of the skull, subdural hematomas can expand along the inside of the skull, creating a concave shape that follows the curve of the brain, stopping only at the dural reflections like the tentorium cerebelli and falx cerebri.
+On a CT scan, subdural hematomas are classically crescent-shaped, with a concave surface away from the skull. However, they can have a convex appearance, especially in the early stage of bleeding. This may cause difficulty in distinguishing between subdural and epidural hemorrhages. A more reliable indicator of subdural hemorrhage is its involvement of a larger portion of the cerebral hemisphere since it can cross suture lines, unlike an epidural hemorrhage. Subdural blood can also be seen as a layering density along the tentorium cerebelli. This can be a chronic, stable process, since the feeding system is low-pressure. In such cases, subtle signs of bleeding such as effacement of sulci or medial displacement of the junction between gray matter and white matter may be apparent.
+Fresh subdural bleeding is hyperdense, but becomes more hypodense over time due to dissolution of cellular elements. After somewhere between 3–14 days, the bleeding becomes isodense with brain tissue and may therefore be missed. Subsequently, it will become more hypodense than brain tissue.
+Hematoma type Epidural Subdural v t e Location Involved vessel Symptoms (depend on severity) CT appearance headingBody Between the skull and the outer endosteal layer of the dura mater Between dura mater and arachnoid mater. Temperoparietal locus (most likely)-Middle meningeal artery Frontal locus-anterior ethmoidal artery Occipital locus-transverse or sigmoid sinuses Vertex locus-superior sagittal sinus Bridging veins Lucid interval followed by unconsciousness Gradually increasing headache and confusion Biconvex lens Crescent-shaped.
+Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.
+Other signs and symptoms of subdural hematoma can include any combination of the following:
+- A history of recent head injury
+- Loss of consciousness or fluctuating levels of consciousness
+- Irritability
+- Seizures
+- Pain
+- Numbness
+- Headache (either constant or fluctuating)
+- Dizziness
+- Disorientation
+- Amnesia
+- Weakness or lethargy
+- Nausea or vomiting
+- Loss of appetite
+- Personality changes
+- Inability to speak or slurred speech
+- Ataxia, or difficulty walking
+- Loss of muscle control
+- Altered breathing patterns
+- Hearing loss or hearing ringing (tinnitus)
+- Blurred Vision
+- Deviated gaze, or abnormal movement of the eyes.
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DISNET disease texts/100 Clean Disease Texts/Superior mesenteric artery syndrome.txt

+Retroperitoneal fat and lymphatic tissue normally serve as a cushion for the duodenum, protecting it from compression by the SMA. SMA syndrome is thus triggered by any condition involving an insubstantial cushion and narrow mesenteric angle. SMA syndrome can present in two forms: chronic/congenital or acute/induced.
+Patients with the chronic, congenital form of SMA syndrome predominantly have a lengthy or even lifelong history of abdominal complaints with intermittent exacerbations depending on the degree of duodenal compression. Risk factors include anatomic characteristics such as: aesthenic (very thin or "lanky") body build, an unusually high insertion of the duodenum at the ligament of Treitz, a particularly low origin of the SMA, or intestinal malrotation around an axis formed by the SMA. Predisposition is easily aggravated by any of the following: poor motility of the digestive tract, retroperitional tumors, loss of appetite, malabsorption, cachexia, exaggerated lumbar lordosis, visceroptosis, abdominal wall laxity, peritoneal adhesions, abdominal trauma, rapid linear adolescent growth spurt, weight loss, starvation, catabolic states (as with cancer and burns), and history of neurological injury.
+The acute form of SMA syndrome develops rapidly after traumatic incidents that forcibly hyper-extend the SMA across the duodenum, inducing the obstruction, or sudden weight loss for any reason. Causes include prolonged supine bed rest, scoliosis surgery, left nephrectomy, ileo-anal pouch surgery.
+It is important to note, however, that while SMA syndrome can mimic an eating disorder, distinguishing the two conditions is extremely important, as misdiagnosis in this situation can be dangerous.
+Diagnosis is very difficult, and usually one of exclusion. SMA syndrome is thus considered only after patients have undergone an extensive evaluation of their gastrointestinal tract including upper endoscopy, and evaluation for various malabsorptive, ulcerative and inflammatory instestinal conditions with a higher diagnostic frequency. Diagnosis may follow x-ray examination revealing duodenal dilation followed by abrupt constriction proximal to the overlying SMA, as well as a delay in transit of four to six hours through the gastroduodenal region. Standard diagnostic exams include abdominal and pelvic computed tomography (CT) scan with oral and IV contrast, upper gastrointestinal series (UGI), and, for equivocal cases, hypotonic duodenography. In addition, vascular imaging studies such as ultrasound and contrast angiography may be used to indicate increased bloodflow velocity through the SMA or a narrowed SMA angle.
+Despite multiple case reports, there has been controversy surrounding the diagnosis and even the existence of SMA syndrome since symptoms do not always correlate well with radiologic findings, and may not always improve following surgical correction. However, the reason for the persistence of gastrointestinal symptoms even after surgical correction in some cases has been traced to the remaining prominence of reversed peristalsis in contrast to direct peristalsis.
+Since females between the ages of 10 and 30 are most frequently afflicted, it is not uncommon for physicians to initially and incorrectly assume that emaciation is a choice of the patient instead of a consequence of SMA syndrome. Patients in the earlier stages of SMA syndrome often remain unaware that they are ill until substantial damage to their health is done, since they may attempt to adapt to the condition by gradually decreasing their food intake or naturally gravitating toward a lighter and more digestible diet.
+- Upper gastrointestinal series showing extreme duodenal dilation (white arrow) abruptly preceding constriction by the SMA.
+- Play media Ultrasound showing SMA syndrome
+- Ultrasound showing SMA syndrome
+- A diagram of a healthy mesenteric angle.
+- A diagram of a compressed duodenum due to a reduced mesenteric angle.
+Signs and symptoms include early satiety, nausea, vomiting, extreme "stabbing" postprandial abdominal pain (due to both the duodenal compression and the compensatory reversed peristalsis), abdominal distention/distortion, burping (eructation), external hypersensitivity or tenderness of the abdominal area, reflux, and heartburn. In infants, feeding difficulties and poor weight gain are also frequent symptoms.
+In some cases of SMA syndrome, severe malnutrition accompanying spontaneous wasting may occur. This, in turn, increases the duodenal compression, which worsens the underlying cause, creating a cycle of worsening symptoms.
+"Food fear" is a common development among patients with the chronic form of SMA syndrome. For many, symptoms are partially relieved when in the left lateral decubitus or knee-to-chest position, or in the prone (face down) position. A Hayes maneuver (pressure applied below the umbilicus in cephalad and dorsal direction) elevates the root of the SMA, also slightly easing the constriction. Symptoms can be aggravated when leaning to the right or taking a supine (face up) position.
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DISNET disease texts/100 Clean Disease Texts/Taeniasis.txt

+Diagnosis of taeniasis is mainly using stool sample, particularly by identifying the eggs. However, this has limitation at the species level because tapeworms basically have similar eggs. Examination of the scolex or the gravid proglottids can resolve the exact species. But body segments are not often available, therefore, laborious histological observation of the uterine branches and PCR detection of ribosomal 5.8S gene are sometimes necessary. Ziehl–Neelsen stain is also used for T. Saginata and T. Solium, in most cases only the former will stain, but the method is not entirely reliable. Loop-mediated isothermal amplification (LAMP) is highly sensitive (~2.5 times that of multiplex PCR), without false positives, for differentiating the taenid species from faecal samples.
+To date the most relevant test for T. Asiatica is by enzyme-linked immunoelectrotransfer blot (EITB). EITB can effectively identify asiatica from other taenid infections since the serological test indicates an immunoblot band of 21.5 kDa exhibited specifically by T. Asiatica. Even though it gives 100% sensitivity, it has not been tested with human sera for cross-reactivity, and it may show a high false positive result.
+Taeniasis is generally asymptomatic and is diagnosed when a portion of the worm is passed in the stool. It is not fatal, although cysticercosis can cause epilepsy and neurocysticercosis can be fatal.
+Taenia solium => Infection by T. Solium is normally asymptomatic. Heavy infection is indicated by intestinal irritation, anaemia, and indigestion.
+There are accidental consumptions of eggs of T. Solium from contaminated vegetables or water. The eggs enter the intestine where they develop into larvae. The larvae enter the bloodstream and invade host tissues. This clinical condition, called cysticercosis, is the most frequent and severe disease caused by any tapeworm. It can lead to severe headaches, dizziness, occasional seizures, dementia, hypertension, lesions in the brain, blindness, tumor-like growths, and low eosinophil levels. It is the cause of major neurological problems, such as hydrocephalus, paraplegy, meningitis, convulsions, and even death.
+Taenia saginata => Taenia saginata infection is asymptomatic, but heavy infection causes weight loss, dizziness, abdominal pain, diarrhea, headaches, nausea, constipation, chronic indigestion, and loss of appetite. It can cause antigen reaction that induce allergic reaction. It is also a rare cause of ileus, pancreatitis, cholecystitis, and cholangitis.
+Taenia asiatica => Taenia asiatica is also usually asymptomatic. The only severe case was in a 60-year-old woman at the Mackay Memorial Hospital in Taiwan. Her stomach and intestine were severely damaged with active bleeding from ulcers caused by a single tapeworm.
+In pigs, the cysticercus can produce cysticercosis. Cysts develop in liver and lungs. (T. Saginata does not cause cysticercosis.) Due to its biological similarity to T. Solium, which is the major cause of neurocysticercosis, T. Asiatica may also cause cysticercosis.
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DISNET disease texts/100 Clean Disease Texts/Tetanus.txt

+Tetanus is caused by the tetanus bacterium Clostridium tetani. Tetanus is an international health problem, as C. Tetani spores are ubiquitous. Spores can be introduced into the body through a puncture wound (penetrating trauma). Due to C. Tetani being an anaerobic bacterium, it and its endospores thrive in environments that lack oxygen, such as a puncture wound.
+The disease occurs almost exclusively in persons inadequately immunized. It is more common in hot, damp climates with soil rich in organic matter. Manure-treated soils may contain spores, as they are widely distributed in the intestines and feces of many animals such as horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. In agricultural areas, a significant number of human adults may harbor the organism.
+The spores can also be found on skin surfaces and in contaminated heroin. Heroin users, particularly those that inject the drug subcutaneously, appear to be at high risk of contracting tetanus. Rarely, tetanus can be contracted through surgical procedures, intramuscular injections, compound fractures, and dental infections. The bite of a dog can transmit tetanus.
+Tetanus is often associated with rust, especially rusty nails. Although rust itself does not cause tetanus, objects that accumulate rust are often found outdoors or in places that harbour anaerobic bacteria. Additionally, the rough surface of rusty metal provides a habitat for C. Tetani, while a nail affords a means to puncture skin and deliver endospores deep within the body at the site of the wound. An endospore is a non-metabolizing survival structure that begins to metabolize and cause infection once in an adequate environment. Hence, stepping on a nail (rusty or not) may result in a tetanus infection, as the low-oxygen (anaerobic) environment may exist under the skin, and the puncturing object can deliver endospores to a suitable environment for growth.
+There are currently no blood tests for diagnosing tetanus. The diagnosis is based on the presentation of tetanus symptoms and does not depend upon isolation of the bacterium, which is recovered from the wound in only 30% of cases and can be isolated from patients without tetanus. Laboratory identification of C. Tetani can be demonstrated only by production of tetanospasmin in mice. Having recently experienced head trauma may indicate cephalic tetanus if no other diagnosis has been made.
+The "spatula test" is a clinical test for tetanus that involves touching the posterior pharyngeal wall with a soft-tipped instrument and observing the effect. A positive test result is the involuntary contraction of the jaw (biting down on the "spatula") and a negative test result would normally be a gag reflex attempting to expel the foreign object. A short report in The American Journal of Tropical Medicine and Hygiene states that, in a patient research study, the spatula test had a high specificity (zero false-positive test results) and a high sensitivity (94% of infected patients produced a positive test).
+Tetanus often begins with mild spasms in the jaw muscles—also known as lockjaw or trismus. The spasms can also affect the facial muscles resulting in an appearance called risus sardonicus. Chest, neck, back, abdominal muscles, and buttocks may be affected. Back muscle spasms often cause arching, called opisthotonos. Sometimes the spasms affect muscles that help with breathing, which can lead to breathing problems.
+Prolonged muscular action causes sudden, powerful, and painful contractions of muscle groups, which is called "tetany". These episodes can cause fractures and muscle tears. Other symptoms include drooling, excessive sweating, fever, hand or foot spasms, irritability, difficulty swallowing, suffocation, heart attack, breathing problems, irregular heartbeat, and uncontrolled urination or defecation.
+Even with treatment, about 10% of people who contract tetanus die. The mortality rate is higher in unvaccinated people and people over 60 years of age.
+Incubation period => The incubation period of tetanus may be up to several months, but is usually about ten days. In general, the farther the injury site is from the central nervous system, the longer the incubation period. The shorter the incubation period, the more severe the symptoms. In neonatal tetanus, symptoms usually appear from 4 to 14 days after birth, averaging about 7 days. On the basis of clinical findings, four different forms of tetanus have been described.
+Generalized tetanus => Generalized tetanus is the most common type of tetanus, representing about 80% of cases. The generalized form usually presents with a descending pattern. The first sign is trismus, or lockjaw, and the facial spasms called risus sardonicus, followed by stiffness of the neck, difficulty in swallowing, and rigidity of pectoral and calf muscles. Other symptoms include elevated temperature, sweating, elevated blood pressure, and episodic rapid heart rate. Spasms may occur frequently and last for several minutes with the body shaped into a characteristic form called opisthotonos. Spasms continue for up to four weeks, and complete recovery may take months. Sympathetic overactivity (SOA) is common in severe tetanus and manifests as labile hypertension, tachycardia, dysrhythmia, peripheral vasculature constriction, profuse sweating, fever, increased carbon dioxide output, increased catecholamine excretion and late development of hypotension. Death can occur within four days.
+Neonatal tetanus is a form of generalized tetanus that occurs in newborns, usually those born to mothers who themselves have not been vaccinated. If the mother has been vaccinated against tetanus, the infants acquire passive immunity and are thus protected. It usually occurs through infection of the unhealed umbilical stump, particularly when the stump is cut with a non-sterile instrument. As of 1998 neonatal tetanus was common in many developing countries and was responsible for about 14% (215,000) of all neonatal deaths. In 2010 the worldwide death toll was 58,000 newborns. As the result of a public health campaign, the death toll from neonatal tetanus was reduced by 90% between 1990 and 2010, and by 2013 the disease had been largely eliminated from all but 25 countries. Neonatal tetanus is rare in developed countries.
+Local tetanus => Local tetanus is an uncommon form of the disease, in which patients have persistent contraction of muscles in the same anatomic area as the injury. The contractions may persist for many weeks before gradually subsiding. Local tetanus is generally milder; only about 1% of cases are fatal, but it may precede the onset of generalized tetanus.
+Cephalic tetanus => Cephalic tetanus is the rarest form of the disease (0.9–3% of cases) and is limited to muscles and nerves in the head. It usually occurs after trauma to the head area, including skull fracture, laceration, eye injury, dental extraction, and otitis media, but it has been observed from injuries to other parts of the body. Paralysis of the facial nerve is most frequently implicated, which may cause lockjaw, facial palsy, or ptosis, but other cranial nerves can also be affected. Cephalic tetanus may progress to a more generalized form of the disease. Due to its rarity, clinicians may be unfamiliar with the clinical presentation and may not suspect tetanus as the illness. Treatment can be complicated as symptoms may be concurrent with the initial injury that caused the infection. Cephalic tetanus is more likely than other forms of tetanus to be fatal, with the progression to generalized tetanus carrying a 15–30% case fatality rate.
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DISNET disease texts/100 Clean Disease Texts/Tethered spinal cord syndrome.txt

+Tethered spinal cord can be caused by various conditions but the main cause is when tissue attachments limit the movement of the spinal cord in the spinal column which causes abnormal stretching of the cord. The tethered spinal cord syndrome is correlated with having the causes:
+- Spina bifida Occulta Mylomeningocele Meningocele
+- Occulta
+- Mylomeningocele
+- Meningocele
+- History of spinal trauma
+- History of spinal surgery
+- Tumor(s) in the spinal column
+- Thickened and/or tight filum terminale
+- Lipoma(s) in the spinal column
+- Dermal Sinus Tract (congenital deformity)
+- Diastematomyelia (split spinal cord).
+Tethered spinal cord is a disorder and not a mechanism so it does not spread to other people and there are no measures that can be done to prevent it beforehand. The only preventative measure that is successful is to surgically untether the spinal cord though there might already be irreversible damage.
+Tethered spinal cord and spina bifida => In tethered spinal cord cases spina bifida can be accompanied by tethering of the spinal cord but in rare cases with Spina bifida occulta. Tethering of the spinal cord tends to occur in the cases of Spina bifida with mylomeningocele. In a normal person the spine grows faster than the spinal cord during development which causes the end of the spinal cord to appear to rise relative to the bony spine next to it. By the time of birth the spinal cord is located between L1 and L2. In a baby with Spina bifida the spinal cord is still attached to the skin around it preventing it from rising properly. This occurs because the spinal cord in a child with Spina bifida is low lying and tethered at the bottom. At the time of birth the mylomeningocele is separated from the skin but the spinal cord is still stuck in the same place. As the child begins to grow the spinal cord remains in the same place becoming stretched out causing the tight cord and the tethering at the end. With this type of tethering there is an interference with the blood supply to the nerves and body which can then cause the deterioration of the body causing orthopedic, neurological, and urological problems. With milder forms of Spina bifida such as Occulta, may be related to the degree of strain on the cord which can become worse with physical activity, injury, pregnancy, bone spurs, or spinal stenosis. The tethered cord in this case might not be diagnosed until adulthood when it worsens and can still cause neurological, orthopedic, and urological dysfunctions.
+For children younger than eight weeks of age (and possibly in utero), a tethered cord may be observed using ultrasonography. Ultrasonography may still be useful through age 5 in limited circumstances.
+MRI imaging appears to be the gold standard for diagnosing a tethered cord.
+A tethered cord is often diagnosed as a "low conus. " The conus medullaris (or lower termination of the spinal cord) normally terminates at or above the L1 – 2 disk space (where L1 is the first, or topmost lumbar vertebra). After about 3 months of age, a conus below the L1 – 2 disk space may indicate a tethered cord and termination below L3 – 4 is unmistakably tethered. "Cord tethering is often assumed when the conus is below the normal L2 – 3 level.
+TCS, however, is a clinical diagnosis that should be based on "neurological and musculoskeletal signs and symptoms. Imaging features are in general obtained to support rather than make the diagnosis. " Clinical evaluation may include a simple rectal examination and may also include invasive or non-invasive urological examination. "Bladder dysfunction occurs in ~40% of patients affected by tethered cord syndrome.. T may be the earliest sign of the syndrome. ".
+In children, symptoms may include:
+- Lesions, hairy patches, dimples, or fatty tumours on the lower back
+- Foot and spinal deformities
+- Weakness in the legs (loss of muscle strength and tone)
+- Change in or abnormal gait including awkwardness while running or wearing the tips or side of one shoe
+- Low back pain
+- Scoliosis (abnormal curvature of the spine to the left or right)
+- Urinary irregularities (incontinence or retention).
+Tethered spinal cord syndrome may go undiagnosed until adulthood, when sensory, motor, bowel, and bladder control issues emerge. This delayed presentation of symptoms relates to the degree of strain on the spinal cord over time.
+Tethering may also develop after spinal cord injury. Scar tissue can block the flow of fluids around the spinal cord. Fluid pressure may cause cysts to form in the spinal cord, a condition called syringomyelia. This can lead to additional loss of movement or feeling, or the onset of pain or autonomic nervous system symptoms.
+In adults, onset of symptoms typically include:
+- Severe pain (in the lower back and radiating into the legs, groin, and perineum)
+- Bilateral muscle weakness and numbness
+- Loss of feeling and movement in lower extremities
+- Urinary irregularities (incontinence or retention)
+- Bowel control issue.
+Neurological symptoms can include a mixed picture of upper and lower motor neuron findings, such as amyotrophy, hyperreflexia, and pathologic plantar response, occurring in the same limb. Profound sensory changes, such as loss of pain, temperature, and proprioceptive sensations, are common. Last, progressive symptoms of a neuropathic bladder are noted on over 70% of adult patients, versus only 20% to 30% of children. These symptoms include urinary frequency and urgency, feeling of incomplete voiding, poor voluntary control, and urge and stress incontinence. Chronic recurrent infections are common and occasionally lead to nephrolithiasis (kidney stones), renal failure, or renal transplantation. Female patients also give a history of ineffective labor and postpartum rectal prolapse, presumably due to an atonic pelvic floor.
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DISNET disease texts/100 Clean Disease Texts/Thyroid storm.txt

+The transition from hyperthyroidism to thyroid storm is typically triggered by a non-thyroidal insult including, but not limited to fever, sepsis, dehydration, myocardial infarction, and psychiatric diseases. Individuals are at higher risk of thyroid storm if their hyperthyroidism is incompletely treated or if their anti-thyroid drugs are discontinued. Many of these individuals have underlying primary causes of hyperthyroidism (Graves disease, toxic multi-nodular goiter, solitary toxic adenoma). However, thyroid storm can occur in individuals with unrecognized thyrotoxicosis experiencing non-thyroid surgery, labor, infection, or exposure to certain medications and radiocontrast dyes.
+The diagnosis of thyroid storm is based on the presence of symptoms consistent with severe hyperthyroidism, as outlined in the Signs and symptoms section above. Multiple approaches have been proposed to calculate the probability of thyroid storm based on clinical criteria, however, none have been universally adopted by clinicians. For instance, Burch and Wartofsky published the Burch-Wartofsky point scale (BWPS) in 1993, assigning a numerical value based on the presence of specific signs and symptoms organized within the following categories: temperature, cardiovascular dysfunction (including heart rate and presence of atrial fibrillation or congestive heart failure), central nervous system (CNS) dysfunction, gastrointestinal or liver dysfunction and presence of a precipitating event. A Burch-Wartofsky score below 25 is not suggestive of thyroid storm whereas 25 to 45 suggests impending thyroid storm and greater than 45 suggests current thyroid storm. Alternatively, the Japanese Thyroid Association (JTA) criteria, derived from a large cohort of patients with thyroid storm in Japan and published in 2012, provide a qualitative method to determine the probability of thyroid storm. The JTA criteria separate the diagnosis of thyroid storm into definite versus suspected based on the specific combination of signs and symptoms a patient exhibits and require elevated free triiodothyronine (T3) or free thyroxine (T4) for definite thyroid storm.
+Temperature Score Heart Rate Score Symptoms of Heart Failure Score Presence of Atrial Fibrillation Score Symptoms of CNS Dysfunction Score Gastrointestinal or Liver Dysfunction Score Presence of Precipitating Event Score headingBody 99.0 to 99.9 5 90 to109 5 None 0 Absent 0 None 0 None 0 None 0 100.0 to 100.9 10 110 to 119 10 Mild (i.e. Pedal edema) 5 Present 10 Mild (e. G. Showing signs of agitation) 10 Moderate (e. G. Diarrhea, nausea, vomiting or abdominal pain) 10 Present 10 101.0 to 101.9 15 120 to 129 15 Moderate (i.e. Bibasilar rales) 10 Moderate (e. G. Delirium, psychosis, lethargy) 20 Severe (i.e. Unexplained jaundice) 20 102.0 to 102.9 20 130 to 139 20 Severe (i.e. Pulmonary edema) 15 Severe (e. G. Seizure or coma) 30 103 to 103.9 25 Greater than or equal to 140 25 Greater than or equal to 104 30.
+Laboratory findings => As with hyperthyroidism, TSH is suppressed. Both free and serum (or total) T3 and T4 are elevated. An elevation in thyroid hormone levels is suggestive of thyroid storm when accompanied by signs of severe hyperthyroidism but is not diagnostic as it may also correlate with uncomplicated hyperthyroidism. Moreover, serum T3 may be normal in critically ill patients due to decreased conversion of T4 to T3. Other potential abnormalities include the following:
+- Hyperglycemia likely due to catecholamine-mediated effects on insulin release and metabolism as well as increased glycogenolysis, evolving into hypoglycemia when glycogen stores are depleted
+- Elevated aspartate aminotransferase (AST), bilirubin and lactate dehydrogenase (LDH)
+- Hypercalcemia and elevated alkaline phosphatase due to increased bone resorption
+- Elevated white blood cell count.
+Thyroid storm is characterized by an acute onset of symptoms of hyperthyroidism (fast heart rate, restlessness, agitation) accompanied by other features such as fever (temperatures often above 40 °C/104 °F), mental status changes, diarrhea, and vomiting.
+Individuals can exhibit varying signs of organ dysfunction. Patients may experience liver dysfunction, and yellow discoloration of the skin is considered a poor prognostic sign. Heart (cardiac) symptoms include abnormal heart rhythms, decreased blood flow to the heart and heart attacks, and congestive heart failure, which may lead to cardiovascular collapse. Mortality can be as high as 20 – 30%.
+In some situations, individuals may not experience the classic signs of restlessness and agitation, but instead present with apathetic signs of weakness and confusion.
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DISNET disease texts/100 Clean Disease Texts/Thyrotoxic periodic paralysis.txt

+Genetics => Genetic mutations in the L-type calcium channel α1-subunit (Cav1.1) have been described in Southern Chinese with TPP. The mutations are located in a different part of the gene from those described in the related condition familial periodic paralysis. In TPP, the mutations described are single-nucleotide polymorphisms located in the hormone response element responsive to thyroid hormone, implying that transcription of the gene and production of ion channels may be altered by increased thyroid hormone levels. Furthermore, mutations have been reported in the genes coding for potassium voltage-gated channel, Shaw-related subfamily, member 4 (Kv3.4) and sodium channel protein type 4 subunit alpha (Na41.4).
+Of people with TPP, 33% from various populations were demonstrated to have mutations in KCNJ18, the gene coding for Kir2.6, an inward-rectifier potassium ion channel. This gene, too, harbors a thyroid response element.
+Certain forms of human leukocyte antigen (HLA)—especially B46, DR9, DQB1*0303, A2, Bw22, AW19, B17, and DRW8—are more common in TPP. Linkage to particular forms of HLA, which plays a central role in the immune response, might imply an immune system cause, but it is uncertain whether this directly causes TPP or whether it increases the susceptibility to Graves' disease, a known autoimmune disease.
+Thyroid disease => The most common underlying form of thyroid disease associated with TPP is Graves' disease, a syndrome due to an autoimmune reaction that leads to overproduction of thyroid hormone. TPP has also been described in people with other thyroid problems such as thyroiditis, toxic nodular goiter, toxic adenoma, TSH-producing pituitary adenoma, excessive ingestion of thyroxine or iodine, and amiodarone-induced hyperthyroidism.
+Hypokalemia (low blood potassium levels) commonly occurs during attacks; levels below 3.0 mmol/l are typically encountered. Magnesium and phosphate levels are often found to be decreased. Creatine kinase levels are elevated in two thirds of cases, usually due to a degree of muscle injury; severe elevations suggestive of rhabdomyolysis (muscle tissue destruction) are rare. Electrocardiography (ECG/EKG) may show tachycardia (a fast heart rate) due to the thyroid disease, abnormalities due to cardiac arrhythmia (atrial fibrillation, ventricular tachycardia), and conduction changes associated with hypokalemia (U waves, QRS widening, QT prolongation, and T wave flattening). Electromyography shows changes similar to those encountered in myopathies (muscle diseases), with a reduced amplitude of the compound muscle action potentials (CMAPs); they resolve when treatment has commenced.
+TPP is distinguished from other forms of periodic paralysis (especially hypokalemic periodic paralysis) with thyroid function tests on the blood. These are normal in the other forms, and in thyrotoxicosis the levels of thyroxine and triiodothyronine are elevated, with resultant suppression of TSH production by the pituitary gland. Various other investigations are usually performed to separate the different causes of hyperthyroidism.
+An attack often begins with muscle pain, cramping, and stiffness. This is followed by weakness or paralysis that tends to develop rapidly, usually in late evening or the early hours of the morning. The weakness is usually symmetrical; the limb muscles closer to the trunk (proximal) are predominantly affected, and weakness tends to start in the legs and spread to the arms. Muscles of the mouth and throat, eyes, and breathing are usually not affected, but occasionally weakness of the respiratory muscles can cause life-threatening respiratory failure. Attacks typically resolve within several hours to several days, even in the absence of treatment. On neurological examination during an attack, flaccid weakness of the limbs is noted; reflexes are usually diminished, but the sensory system is unaffected. Mental status is not affected.
+Attacks may be brought on by physical exertion, drinking alcohol, or eating food high in carbohydrates or salt. This may explain why attacks are more common in summer, when more people drink sugary drinks and engage in exercise. Exercise-related attacks tend to occur during a period of rest immediately after exercise; exercise may therefore be recommended to abort an attack.
+There may be symptoms of thyroid overactivity, such as weight loss, a fast heart rate, tremor, and perspiration; but such symptoms occur in only half of all cases. The most common type of hyperthyroidism, Graves' disease, may additionally cause eye problems (Graves' ophthalmopathy) and skin changes of the legs (pretibial myxedema). Thyroid disease may also cause muscle weakness in the form of thyrotoxic myopathy, but this is constant rather than episodic.
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DISNET disease texts/100 Clean Disease Texts/Tonsillitis.txt

+The most common cause is viral infection and includes adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. It can also be caused by Epstein-Barr virus, herpes simplex virus, cytomegalovirus, or HIV. The second most common cause is bacterial infection of which the predominant is Group A β-hemolytic streptococcus (GABHS), which causes strep throat. Less common bacterial causes include: Staphylococcus aureus (including methicillin resistant Staphylococcus aureus or MRSA), Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae, Bordetella pertussis, Fusobacterium sp., Corynebacterium diphtheriae, Treponema pallidum, and Neisseria gonorrhoeae.
+Anaerobic bacteria have been implicated in tonsillitis and a possible role in the acute inflammatory process is supported by several clinical and scientific observations.
+Under normal circumstances, as viruses and bacteria enter the body through the nose and mouth, they are filtered in the tonsils. Within the tonsils, white blood cells of the immune system destroy the viruses or bacteria by producing inflammatory cytokines like phospholipase A2, which also lead to fever. The infection may also be present in the throat and surrounding areas, causing inflammation of the pharynx.
+Sometimes, tonsillitis is caused by an infection of spirochaeta and treponema, in this case called Vincent's angina or Plaut-Vincent angina.
+The diagnosis of group A beta-hemolytic streptococcus (GABHS) tonsillitis can be confirmed by culture of samples obtained by swabbing both tonsillar surfaces and the posterior pharyngeal wall and plating them on sheep blood agar medium. The isolation rate can be increased by incubating the cultures under anaerobic conditions and using selective growth media. A single throat culture has a sensitivity of 90–95% for the detection of GABHS (which means that GABHS is actually present 5–10% of the time culture suggests that it is absent). This small percentage of false-negative results are part of the characteristics of the tests used but are also possible if the patient has received antibiotics prior to testing. Identification requires 24 to 48 hours by culture but rapid screening tests (10–60 minutes), which have a sensitivity of 85–90%, are available. Older antigen tests detect the surface Lancefield group A carbohydrate. Newer tests identify GABHS serotypes using nucleic acid (DNA) probes or polymerase chain reaction. Bacterial culture may need to be performed in cases of a negative rapid streptococcal test.
+True infection with GABHS, rather than colonization, is defined arbitrarily as the presence of >10 colonies of GABHS per blood agar plate. However, this method is difficult to implement because of the overlap between carriers and infected patients. An increase in antistreptolysin O (ASO) streptococcal antibody titer 3–6 weeks following the acute infection can provide retrospective evidence of GABHS infection and is considered definitive proof of GABHS infection.
+Increased values of secreted phospholipase A2 and altered fatty acid metabolism in patients with tonsillitis may have diagnostic utility.
+Common signs and symptoms include:
+- sore throat
+- red, swollen tonsils
+- pain when swallowing
+- high temperature (fever)
+- headache
+- tiredness
+- chills
+- a general sense of feeling unwell (malaise)
+- white pus-filled spots on the tonsils
+- swollen lymph nodes (glands) in the neck
+- pain in the ears or neck
+- weight loss
+- difficulty ingesting and swallowing meal/liquid intake
+- difficulty sleepin.
+Less common symptoms include:
+- nausea
+- fatigue
+- stomach ache
+- vomiting
+- furry tongue
+- bad breath (halitosis)
+- voice changes
+- difficulty opening the mouth (trismus)
+- loss of appetite
+- anxiety/fear of chokin.
+In cases of acute tonsillitis, the surface of the tonsil may be bright red and with visible white areas or streaks of pus.
+Tonsilloliths occur in up to 10% of the population frequently due to episodes of tonsillitis.
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DISNET disease texts/100 Clean Disease Texts/Trichinosis.txt

+The classical agent is T. Spiralis (found worldwide in many carnivorous and omnivorous animals, both domestic and sylvatic), but there are also seven primarily sylvatic species of Trichinella now recognized:
+- T. Spiralis is most adapted to swine, most pathogenic in humans and is cosmopolitan in distribution.
+- T. Britovi is the second most common species to infect humans; it is distributed throughout Europe, Asia, and northern and western Africa, usually in wild carnivores, wild boar and domesticated pigs.
+- T. Murrelli also infects humans, especially from black bear meat; it is distributed among wild carnivores in North America.
+- T. Nativa, which has a high resistance to freezing, is found in the Arctic and subarctic regions; reservoir hosts include polar bears, Arctic foxes, walruses and other wild game.
+- T. Nelsoni, found in east African predators and scavengers, has been documented to cause a few human cases.
+- T. Papuae infects both mammals and reptiles, including crocodiles, humans, wild pigs and domestic pigs; this species, found in Papua New Guinea and Thailand, is also nonencapsulated.
+- T. Pseudospiralis infects birds and mammals, and has demonstrated infection in humans; it is a nonencapsulated species.
+- T. Zimbabwensis can infect mammals, and possibly humans; this nonencapsulated species was detected in crocodiles in Africa.
+- Taxonomy => Kingdom: Animalia
+- Phylum: Nematoda
+- Class: Adenophorea
+- Order: Trichurida
+- Family: Trichinellidae
+- Genus: Trichinell.
+The typical life cycle for T. Spiralis involves humans, pigs, and rodents. A pig becomes infected when it eats infectious cysts in raw meat, often porcine carrion or a rat (sylvatic cycle). A human becomes infected by consuming raw or undercooked infected pork (domestic cycle). In the stomach, the cysts from infected undercooked meat are acted on by pepsin and hydrochloric acid, which help release the larvae from the cysts into the stomach. The larvae then migrate to the small intestine, and burrow into the intestinal mucosa, where they molt four times before becoming adults.
+Thirty to 34 hours after the cysts were originally ingested, the adults mate, and within five days produce larvae. Adult worms can only reproduce for a limited time, because the immune system will eventually expel them from the small intestine. The larvae then use their piercing mouthpart, called the "stylet", to pass through the intestinal mucosa and enter the lymphatic vessels, and then enter the bloodstream.
+The larvae travel by capillaries to various organs, such as the retina, myocardium, or lymph nodes; however, only larvae that migrate to skeletal muscle cells survive and encyst. The larval host cell becomes a nurse cell, in which the larva will be encapsulated, potentially for the life of the host. The development of a capillary network around the nurse cell completes encystation of the larva. Trichinosis is not soil-transmitted, as the parasite does not lay eggs, nor can it survive long outside a host.
+Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, and laboratory testing.
+Exposure history => An epidemiological investigation can be done to determine a patient's exposure to raw infected meat. Often, an infection arises from home-preparation of contaminated meat, in which case microscopy of the meat may be used to determine the infection. Exposure determination does not have to be directly from a laboratory-confirmed infected animal. Indirect exposure criteria include the consumption of products from a laboratory-confirmed infected animal, or sharing of a common exposure with a laboratory-confirmed infected human.
+Clinical diagnosis => Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness, splinter hemorrhage, nonspecific gastroenteritis, and muscle pain. The case definition for trichinosis at the European Center for Disease Control states "at least three of the following six: fever, muscle soreness and pain, gastrointestinal symptoms, facial edema, eosinophilia, and subconjuctival, subungual, and retinal hemorrhages. ".
+Laboratory testing => Blood tests and microscopy can be used to aid in the diagnosis of trichinosis. Blood tests include a complete blood count for eosinophilia, creatine phosphokinase activity, and various immunoassays such as ELISA for larval antigens.
+The great majority of trichinosis infections have either minor or no symptoms and no complications. There are two main phases for the infection: enteral (affecting the intestines) and parenteral (outside the intestines). The symptoms vary depending on the phase, species of Trichinella, quantity of encysted larvae ingested, age, sex, and host immunity.
+Enteral phase => A large burden of adult worms in the intestines promotes symptoms such as nausea, heartburn, dyspepsia, and diarrhea from two to seven days after infection, while small worm burdens generally are asymptomatic. Eosinophilia presents early and increases rapidly.
+Parenteral phase => The severity of symptoms caused by larval migration from the intestines depends on the number of larvae produced. As the larvae migrate through tissue and vessels, the body's inflammatory response results in edema, muscle pain, fever, and weakness. A classic sign of trichinosis is periorbital edema, swelling around the eyes, which may be caused by vasculitis. Splinter hemorrhage in the nails is also a common symptom.
+They may very rarely cause enough damage to produce serious neurological deficits (such as ataxia or respiratory paralysis) from worms entering the central nervous system. The CNS is compromised by trichinosis in 10–24% of reported cases of cerebral venous sinus thrombosis, a very rare form of stroke (3 – 4 cases per million annual incidence in adults). Trichinosis can be fatal depending on the severity of the infection; death can occur 4–6 weeks after the infection, and is usually caused by myocarditis, encephalitis, or pneumonia.
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DISNET disease texts/100 Clean Disease Texts/Tropical sprue.txt

+The cause of tropical sprue is not known. It may be caused by persistent bacterial, viral, amoebal, or parasitic infections. Folic acid deficiency, effects of malabsorbed fat on intestinal motility, and persistent small intestinal bacterial overgrowth may combine to cause the disorder. A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved in the aetiology of post-infectious IBS.
+Diagnosis of tropical sprue can be complicated because many diseases have similar symptoms. The following investigation results are suggestive:
+- Abnormal flattening of villi and inflammation of the lining of the small intestine, observed during an endoscopic procedure.
+- Presence of inflammatory cells (most often lymphocytes) in the biopsy of small intestine tissue.
+- Low levels of vitamins A, B12, E, D, and K, as well as serum albumin, calcium, and folate, revealed by a blood test.
+- Excess fat in the feces (steatorrhoea).
+- Thickened small bowel folds seen on imaging.
+Tropical sprue is largely limited to within about 30 degrees north and south of the equator. Recent travel to this region is a key factor in diagnosing this disease in residents of countries outside of that geographical region.
+Other conditions which can resemble tropical sprue need to be differentiated. Coeliac disease (also known as coeliac sprue or gluten sensitive enteropathy), has similar symptoms to tropical sprue, with the flattening of the villi and small intestine inflammation and is caused by an autoimmune disorder in genetically susceptible individuals triggered by ingested gluten. Malabsorption can also be caused by protozoan infections, tuberculosis, HIV/AIDS, immunodeficiency, chronic pancreatitis and inflammatory bowel disease. Environmental enteropathy is a less severe, subclinical condition similar to tropical sprue.
+The illness usually starts with an attack of acute diarrhoea, fever and malaise following which, after a variable period, the patient settles into the chronic phase of diarrhoea, steatorrhoea, weight loss, anorexia, malaise, and nutritional deficiencies. The symptoms of tropical sprue are:
+- Diarrhoea
+- Steatorrhoea or fatty stool (often foul-smelling and whitish in colour)
+- Indigestion
+- Cramps
+- Weight loss and malnutrition
+- Fatigu.
+Left untreated, nutrient and vitamin deficiencies may develop in patients with tropical sprue. These deficiencies may have these symptoms:
+- Vitamin A deficiency: hyperkeratosis or skin scales
+- Vitamin B12 and folic acid deficiencies: anaemia
+- Vitamin D and calcium deficiencies: spasm, bone pain, numbness, and tingling sensation
+- Vitamin K deficiency: bruise
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DISNET disease texts/100 Clean Disease Texts/Typhoid fever.txt

+The bacterium that causes typhoid fever may be spread through poor hygiene habits and public sanitation conditions, and sometimes also by flying insects feeding on feces. Public education campaigns encouraging people to wash their hands after defecating and before handling food are an important component in controlling spread of the disease. According to statistics from the United States Centers for Disease Control and Prevention (CDC), the chlorination of drinking water has led to dramatic decreases in the transmission of typhoid fever in the United States.
+Bacteria => The cause is the bacterium Salmonella Typhi, also known as Salmonella enterica serotype Typhi.
+There are two main types of Typhi namely the ST1 and ST2 based on MLST subtyping scheme, which are currently widespread globally.
+Diagnosis is made by any blood, bone marrow or stool cultures and with the Widal test (demonstration of antibodies against Salmonella antigens O-somatic and H-flagellar). In epidemics and less wealthy countries, after excluding malaria, dysentery, or pneumonia, a therapeutic trial time with chloramphenicol is generally undertaken while awaiting the results of the Widal test and cultures of the blood and stool.
+The Widal test is time-consuming, and prone to significant false positive results. The test may be also falsely negative in the early course of illness. However, unlike Typhidot test Widal test quantifies the specimen with titres.
+Typhidot is a medical test consisting of a dot ELISA kit that detects IgM and IgG antibodies against the outer membrane protein (OMP) of the Salmonella typhi. The typhidot test becomes positive within 2–3 days of infection and separately identifies IgM and IgG antibodies. The test is based on the presence of specific IgM and IgG antibodies to a specific 50Kd OMP antigen, which is impregnated on nitrocellulose strips. IgM shows recent infection whereas IgG signifies remote infection. The most important limitation of this test is that it is not quantitative and result is only positive or negative.
+The term 'enteric fever' is a collective term that refers to severe typhoid and paratyphoid.
+Classically, the course of untreated typhoid fever is divided into four distinct stages, each lasting about a week. Over the course of these stages, the patient becomes exhausted and emaciated.
+- In the first week, the body temperature rises slowly, and fever fluctuations are seen with relative bradycardia (Faget sign), malaise, headache, and cough. A bloody nose (epistaxis) is seen in a quarter of cases, and abdominal pain is also possible. A decrease in the number of circulating white blood cells (leukopenia) occurs with eosinopenia and relative lymphocytosis; blood cultures are positive for Salmonella Typhi or S. Paratyphi. The Widal test is usually negative in the first week.
+- In the second week, the person is often too tired to get up, with high fever in plateau around 40 °C (104 °F) and bradycardia (sphygmothermic dissociation or Faget sign), classically with a dicrotic pulse wave. Delirium is frequent, often calm, but sometimes agitated. This delirium gives to typhoid the nickname of "nervous fever". Rose spots appear on the lower chest and abdomen in around a third of patients. Rhonchi are heard in lung bases.
+- The abdomen is distended and painful in the right lower quadrant, where borborygmi can be heard. Diarrhea can occur in this stage: six to eight stools in a day, green, comparable to pea soup, with a characteristic smell. However, constipation is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender, and liver transaminases are elevated. The Widal test is strongly positive, with antiO and antiH antibodies. Blood cultures are sometimes still positive at this stage.
+- (The major symptom of this fever is that the fever usually rises in the afternoon up to the first and second week.)
+- In the third week of typhoid fever, a number of complications can occur: Intestinal haemorrhage due to bleeding in congested Peyer's patches; this can be very serious, but is usually not fatal. Intestinal perforation in the distal ileum: this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicaemia or diffuse peritonitis sets in. Encephalitis Respiratory diseases such as pneumonia and acute bronchitis Neuropsychiatric symptoms (described as "muttering delirium" or "coma vigil"), with picking at bedclothes or imaginary objects. Metastatic abscesses, cholecystitis, endocarditis, and osteitis The fever is still very high and oscillates very little over 24 hours. Dehydration ensues, and the patient is delirious (typhoid state). One-third of affected individuals develop a macular rash on the trunk. Platelet count goes down slowly and risk of bleeding rises.
+- Intestinal haemorrhage due to bleeding in congested Peyer's patches; this can be very serious, but is usually not fatal.
+- Intestinal perforation in the distal ileum: this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicaemia or diffuse peritonitis sets in.
+- Encephalitis
+- Respiratory diseases such as pneumonia and acute bronchitis
+- Neuropsychiatric symptoms (described as "muttering delirium" or "coma vigil"), with picking at bedclothes or imaginary objects.
+- Metastatic abscesses, cholecystitis, endocarditis, and osteitis
+- The fever is still very high and oscillates very little over 24 hours. Dehydration ensues, and the patient is delirious (typhoid state). One-third of affected individuals develop a macular rash on the trunk.
+- Platelet count goes down slowly and risk of bleeding rises.
+- By the end of third week, the fever starts subsidin
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DISNET disease texts/100 Clean Disease Texts/Upper respiratory tract infection.txt

+In terms of pathophysiology, rhino virus infection resembles the immune response. The viruses do not cause damage to the cells of the upper respiratory tract but rather cause changes in the tight junctions of epithelial cells. This allows the virus to gain access to tissues under the epithelial cells and initiate the innate and adaptive immune responses.
+Up to 15% of acute pharyngitis cases may be caused by bacteria, most commonly Streptococcus pyogenes, a group A streptococcus in streptococcal pharyngitis ("strep throat"). Other bacterial causes are Streptococcus pneumoniae, Haemophilus influenzae, Corynebacterium diphtheriae, Bordetella pertussis, and Bacillus anthracis.
+Sexually transmitted infections have emerged as causes of oral and pharyngeal infections.
+Symptoms Allergy URI Influenza headingBody Itchy, watery eyes Common Rare (conjunctivitis may occur with adenovirus) Soreness behind eyes, sometimes conjunctivitis Nasal discharge Common Common Common Nasal congestion Common Common Sometimes Sneezing Very common Very common Sometimes Sore throat Sometimes (post-nasal drip) Very common Sometimes Cough Sometimes Common (mild to moderate, hacking) Common (dry cough, can be severe) Headache Uncommon Rare Common Fever Never Rare in adults, possible in children Very common 100–102 °F (or higher in young children), lasting 3–4 days; may have chills Malaise Sometimes Sometimes Very common Fatigue, weakness Sometimes Sometimes Very common (can last for weeks, extreme exhaustion early in course) Muscle pain Never Slight Very common (often severe).
+In uncomplicated colds, cough and nasal discharge may persist for 14 days or more even after other symptoms have resolved. Acute upper respiratory tract infections include rhinitis, pharyngitis/tonsillitis and laryngitis often referred to as a common cold, and their complications: sinusitis, ear infection and sometimes bronchitis (though bronchi are generally classified as part of the lower respiratory tract.) Symptoms of URTIs commonly include cough, sore throat, runny nose, nasal congestion, headache, low-grade fever, facial pressure and sneezing.
+Symptoms of rhinovirus in children usually begin 1–3 days after exposure. The illness usually lasts 7–10 more days.
+Color or consistency changes in mucous discharge to yellow, thick, or green are the natural course of viral upper respiratory tract infection and not an indication for antibiotics.
+Group A beta hemolytic streptococcal pharyngitis/tonsillitis (strep throat) typically presents with a sudden onset of sore throat, pain with swallowing and fever. Strep throat does not usually cause runny nose, voice changes, or cough.
+Pain and pressure of the ear caused by a middle ear infection (otitis media) and the reddening of the eye caused by viral conjunctivitis are often associated with upper respiratory infections.
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DISNET disease texts/100 Clean Disease Texts/Vascular dementia.txt

+Vascular dementia can be caused by ischemic or hemorrhagic infarcts affecting multiple brain areas, including the anterior cerebral artery territory, the parietal lobes, or the cingulate gyrus. On rare occasion, infarcts in the hippocampus or thalamus are the cause of dementia. Brain vascular lesions can also be the result of diffuse cerebrovascular disease, such as small vessel disease.
+Risk factors for vascular dementia include age, hypertension, smoking, hypercholesterolemia, diabetes mellitus, cardiovascular disease, and cerebrovascular disease. Other risk factors include geographic origin, genetic predisposition, and prior strokes.
+Vascular dementia can sometimes be triggered by cerebral amyloid angiopathy, which involves accumulation of beta amyloid plaques in the walls of the cerebral arteries, leading to breakdown and rupture of the vessels. Since amyloid plaques are a characteristic feature of Alzheimer's Disease, vascular dementia may occur as a consequence. Cerebral amyloid angiopathy can, however, appear in people with no prior dementia condition. Some beta amyloid plaques are often present in cognitively normal elderly persons.
+Several specific diagnostic criteria can be used to diagnose vascular dementia, including the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, the International Classification of Diseases, Tenth Edition (ICD-10) criteria, the National Institute of Neurological Disorders and Stroke criteria, Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria, the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski Ischemic Score (after Vladimir Hachinski).
+The recommended investigations for cognitive impairment include: blood tests (for anemia, vitamin deficiency, thyrotoxicosis, infection, etc.), chest X-Ray, ECG, and neuroimaging, preferably a scan with a functional or metabolic sensitivity beyond a simple CT or MRI. When available as a diagnostic tool, single photon emission computed tomography (SPECT) and positron emission tomography (PET) neuroimaging may be used to confirm a diagnosis of multi-infarct dementia in conjunction with evaluations involving mental status examination. In a person already having dementia, SPECT appears to be superior in differentiating multi-infarct dementia from Alzheimer's disease, compared to the usual mental testing and medical history analysis. Advances have led to the proposal of new diagnostic criteria.
+The screening blood tests typically include full blood count, liver function tests, thyroid function tests, lipid profile, erythrocyte sedimentation rate, C reactive protein, syphilis serology, calcium serum level, fasting glucose, urea, electrolytes, vitamin B-12, and folate. In selected patients, HIV serology and certain autoantibody testing may be done.
+Mixed dementia is diagnosed when people have evidence of Alzheimer's disease and cerebrovascular disease, either clinically or based on neuro-imaging evidence of ischemic lesions.
+Pathology => Gross examination of the brain may reveal noticeable lesions and damage to blood vessels. Accumulation of various substances such as lipid deposits and clotted blood appear on microscopic views. The white matter is most affected, with noticeable atrophy (tissue loss), in addition to calcification of the arteries. Microinfarcts may also be present in the gray matter (cerebral cortex), sometimes in large numbers. Although atheroma of the major cerebral arteries is typical in vascular dementia, smaller vessels and arterioles are mainly affected.
+Differentiating the different dementia syndromes can be challenging, due to the frequently overlapping clinical features and related underlying pathology. In particular, Alzheimer's dementia often co-occurs with vascular dementia.
+People with vascular dementia present with progressive cognitive impairment, acutely or subacutely as in mild cognitive impairment, frequently step-wise, after multiple cerebrovascular events (strokes). Some people may appear to improve between events and decline after more silent strokes. A rapidly deteriorating condition may lead to death from a stroke, heart disease, or infection.
+Signs and symptoms are cognitive, motor, behavioral, and for a significant proportion of patients also affective. These changes typically occur over a period of 5–10 years. Signs are typically the same as in other dementias, but mainly include cognitive decline and memory impairment of sufficient severity as to interfere with activities of daily living, sometimes with presence of focal neurologic signs, and evidence of features consistent with cerebrovascular disease on brain imaging (CT or MRI). The neurologic signs localizing to certain areas of the brain that can be observed are hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, as well as gait and swallowing difficulties. People have patchy deficits in terms of cognitive testing. They tend to have better free recall and fewer recall intrusions when compared with patients with Alzheimer's disease. In the more severely affected patients, or patients affected by infarcts in Wernicke's or Broca's areas, specific problems with speaking called dysarthrias and aphasias may be present.
+In small vessel disease, the frontal lobes are often affected. Consequently, patients with vascular dementia tend to perform worse than their Alzheimer's disease counterparts in frontal lobe tasks, such as verbal fluency, and may present with frontal lobe problems: apathy, abulia, problems with attention, orientation, and urinary incontinence. They tend to exhibit more perseverative behavior. VaD patients may also present with general slowing of processing ability, difficulty shifting sets, and impairment in abstract thinking. Apathy early in the disease is more suggestive of vascular dementia.
+Rare genetic disorders which result in vascular lesions in the brain have other patterns of presentation. As a rule, they tend to present earlier in life and have a more aggressive course. In addition, infectious disorders, such as syphilis, can lead to arterial damage, strokes, and bacterial inflammation of the brain.
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DISNET disease texts/100 Clean Disease Texts/Waterhouse–Friderichsen syndrome.txt

+Multiple species of bacteria can be associated with the condition:
+- Meningococcus is another term for the bacterial species Neisseria meningitidis; blood infection with said species usually underlies WFS. While many infectious agents can infect the adrenals, an acute, selective infection is usually meningococcus.
+- Pseudomonas aeruginosa can also cause WFS.
+- WFS can also be caused by Streptococcus pneumoniae infections, a common bacterial pathogen typically associated with meningitis in the adult and elderly population.
+- Mycobacterium tuberculosis could also cause WFS. Tubercular invasion of the adrenal glands could cause hemorrhagic destruction of the glands and cause mineralocorticoid deficiency.
+- Staphylococcus aureus has recently also been implicated in pediatric WFS.
+- It can also be associated with Haemophilus influenzae.
+Viruses may also be implicated in adrenal problems:
+- Cytomegalovirus can cause adrenal insufficiency, especially in the immunocompromised.
+- Ebola virus infection may also cause similar acute adrenal failure. Citation needed.
+Leukocytosis Acidosis Hyperkalemia Hyponatremia Abnormal complete blood count Acute kidney injury C reactive protein Acth test TFT.
+Waterhouse-Friderichsen Syndrome can be caused by a number of different organisms (see below). When caused by Neisseria meningitidis, WFS is considered the most severe form of meningococcal sepsis. The onset of the illness is nonspecific with fever, rigors, vomiting, and headache. Soon a rash appears; first macular, not much different from the rose spots of typhoid, and rapidly becoming petechial and purpuric with a dusky gray color. Low blood pressure (hypotension) develops and rapidly leads to septic shock. The cyanosis of extremities can be extreme and the patient is very prostrated or comatose. In this form of meningococcal disease, meningitis generally does not occur. Low levels of blood glucose and sodium, high levels of potassium in the blood, and the ACTH stimulation test demonstrate the acute adrenal failure. Leukocytosis need not be extreme and in fact leukopenia may be seen and it is a very poor prognostic sign. C-reactive protein levels can be elevated or almost normal. Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of disseminated intravascular coagulation (DIC). Acidosis and acute kidney failure can be seen as in any severe sepsis. Meningococci can be readily cultured from blood or cerebrospinal fluid, and can sometimes be seen in smears of cutaneous lesions. Difficulty swallowing, atrophy of the tongue, and cracks at the corners of the mouth are also characteristic features.
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DISNET disease texts/100 Clean Disease Texts/Weight loss.txt

+Disease-related => Disease-related malnutrition can be considered in four categories:
+Problem Cause headingBody Impaired intake Poor appetite can be a direct symptom of an illness, or an illness could make eating painful or induce nausea. Illness can also cause food aversion. Inability to eat can result from: diminished consciousness or confusion, or physical problems affecting the arm or hands, swallowing or chewing. Eating restrictions may also be imposed as part of treatment or investigations. Lack of food can result from: poverty, difficulty in shopping or cooking, and poor quality meals. Impaired digestion and/or absorption This can result from conditions that affect the digestive system. Altered requirements Changes to metabolic demands can be caused by illness, surgery and organ dysfunction. Excess nutrient losses Losses from the gastrointestinal can occur because of symptoms such as vomiting or diarrhea, as well as fistulae and stomas. There can also be losses from drains, including nasogastric tubes. Other losses: Conditions such as burns can be associated with losses such as skin exudates.
+Weight loss issues related to specific diseases include:
+- As chronic obstructive pulmonary disease (COPD) advances, about 35% of patients experience severe weight loss called pulmonary cachexia, including diminished muscle mass. Around 25% experience moderate to severe weight loss, and most others have some weight loss. Greater weight loss is associated with poorer prognosis. Theories about contributing factors include appetite loss related to reduced activity, additional energy required for breathing, and the difficulty of eating with dyspnea (labored breathing).
+- Cancer, a very common and sometimes fatal cause of unexplained (idiopathic) weight loss. About one-third of unintentional weight loss cases are secondary to malignancy. Cancers to suspect in patients with unexplained weight loss include gastrointestinal, prostate, hepatobilary (hepatocellular carcinoma, pancreatic cancer), ovarian, hematologic or lung malignancies.
+- People with HIV often experience weight loss, and it is associated with poorer outcomes. Wasting syndrome is an AIDS-defining condition.
+- Gastrointestinal disorders are another common cause of unexplained weight loss – in fact they are the most common non-cancerous cause of idiopathic weight loss. Possible gastrointestinal etiologies of unexplained weight loss include: celiac disease, peptic ulcer disease, inflammatory bowel disease (crohn's disease and ulcerative colitis), pancreatitis, gastritis, diarrhea and many other GI conditions.
+- Infection. Some infectious diseases can cause weight loss. Fungal illnesses, endocarditis, many parasitic diseases, AIDS, and some other subacute or occult infections may cause weight loss.
+- Renal disease. Patients who have uremia often have poor or absent appetite, vomiting and nausea. This can cause weight loss.
+- Cardiac disease. Cardiovascular disease, especially congestive heart failure, may cause unexplained weight loss.
+- Connective tissue disease
+- Neurologic disease, including dementia
+- Oral, taste or dental problems (including infections) can reduce nutrient intake leading to weight loss.
+Therapy-related => Medical treatment can directly or indirectly cause weight loss, impairing treatment effectiveness and recovery that can lead to further weight loss in a vicious cycle.
+Many patients will be in pain and have a loss of appetite after surgery. Part of the body's response to surgery is to direct energy to wound healing, which increases the body's overall energy requirements. Surgery affects nutritional status indirectly, particularly during the recovery period, as it can interfere with wound healing and other aspects of recovery. Surgery directly affects nutritional status if a procedure permanently alters the digestive system. Enteral nutrition (tube feeding) is often needed. However a policy of 'nil by mouth' for all gastrointestinal surgery has not been shown to benefit, with some suggestion it might hinder recovery.
+Early post-operative nutrition is a part of Enhanced Recovery After Surgery protocols. These protocols also include carbohydrate loading in the 24 hours before surgery, but earlier nutritional interventions have not been shown to have a significant impact.
+Some medications can cause weight loss, while others can cause weight gain.
+Social conditions => Social conditions such as poverty, social isolation and inability to get or prepare preferred foods can cause unintentional weight loss, and this may be particularly common in older people. Nutrient intake can also be affected by culture, family and belief systems. Ill-fitting dentures and other dental or oral health problems can also affect adequacy of nutrition.
+Loss of hope, status or social contact and spiritual distress can cause depression, which may be associated with reduced nutrition, as can fatigue.
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DISNET disease texts/100 Clean Disease Texts/Whipple's disease.txt

+Common clinical signs and symptoms of Whipple's disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of non-destructive seronegative arthritis, often of large joints.
+Diagnosis is made by biopsy, usually by duodenal endoscopy, which reveals PAS-positive macrophages in the lamina propria containing non-acid-fast gram-positive bacilli. Immunohistochemical staining for antibodies against T. Whipplei has been used to detect the organism in a variety of tissues, and a PCR-based assay is also available. PCR can be confirmatory if performed on blood, vitreous fluid, synovial fluid, heart valves, or cerebrospinal fluid. PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipple's disease, but that a negative PCR is most likely indicative of a healthy individual.
+Endoscopy of the duodenum and jejunum can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipple's disease, and small bowel X-rays may show some thickened folds. Other pathological findings may include enlarged mesenteric lymph nodes, hypercellularity of lamina propria with "foamy macrophages", and a concurrent decreased number of lymphocytes and plasma cells, per high power field view of the biopsy.
+A D-Xylose test can be performed, which is where the patient will consume 4.5g of D-xylose, a sugar, by mouth. The urine excretion of D-Xylose is then measured after 5 hours. The majority of D-Xylose is absorbed normally, and should be found in the urine. If the D-Xylose is found to be low in the urine, this suggests an intestinal malabsorption problem such as bacterial overgrowth of the proximal small intestine, Whipple's Disease, or an autoimmune with diseases such as Celiac's Disease (allergy to gluten) or Crohn's Disease (autoimmune disease affecting the small intestine). With empiric antibiotic treatment after an initial positive D-Xylose test, and if a follow-up D-Xylose test is positive (decreased urine excretion) after antibiotic therapy, then this would signify it is not bacterial overgrowth of the proximal small intestine. Since Whipple's disease is so rare, a follow-up positive D-Xylose test more likely indicates a non-infectious etiology and more likely an autoimmune etiology. Clinical correlation is recommended to rule out Whipple's disease.
+The most common symptoms are diarrhea, abdominal pain, weight loss, and joint pains. The joint pains may be due to migratory non-deforming arthritis, which may occur many years before any digestive tract symptoms develop; they tend to involve the large joints but can occur in any pattern and tend not to damage the joint surface to the point that the joint becomes deformed. Fever and chills occur in a small proportion of people.
+In its more advanced form, malabsorption (insufficient absorption of nutrients from the diet) leads to wasting and the enlargement of lymph nodes in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing steatorrhea (fatty, offensive stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of albumin, a blood protein, which may lead to peripheral edema caused by the lowered oncotic pressures.
+Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as uveitis, may occur; this is typically associated with deteriorating vision and pain in the affected eye. Endocarditis (infection of the heart valve) has been reported in a small number of cases, sometimes in people with no other symptoms of Whipple's disease; this is typically noticed as breathlessness and leg swelling due to fluid accumulation as the heart is unable to pump fluid through the body.
+Of those affected by Whipple's disease, 10–40% of people have problems related to the involvement of the brain; the symptoms relate to the part of the brain that is affected. The most common problems are dementia, memory loss, confusion, and decreased level of consciousness. Eye movement disturbances and myorhythmia (rapidly repetitive movements of the muscles) of the face, together referred to as oculomasticatory myorhythmia, are highly characteristic for Whipple's disease. Weakness and poor coordination of part of the body, headaches, seizures, as well as a number of more uncommon neurological features, are present in some cases.
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DISNET disease texts/100 Clean Disease Texts/Xerostomia.txt

+A diagnosis of hyposalivation is based predominantly on the clinical signs and symptoms. There is little correlation between symptoms and objective tests of salivary flow, such as sialometry. This test is simple and noninvasive, and involves measurement of all the saliva a patient can produce during a certain time, achieved by dribbling into a container. Sialometery can yield measures of stimulated salivary flow or unstimulated salivary flow. Stimulated salivary flow rate is calculated using a stimulant such as 10% citric acid dropped onto the tongue, and collection of all the saliva that flows from one of the parotid papillae over five or ten minutes. Unstimulated whole saliva flow rate more closely correlates with symptoms of xerostomia than stimulated salivary flow rate. Sialography involves introduction of radio-opaque dye such as iodine into the duct of a salivary gland. It may show blockage of a duct due to a calculus. Salivary scintiscanning using technetium is rarely used. Other medical imaging that may be involved in the investigation include chest x-ray (to exclude sarcoidosis), ultrasonography and magnetic resonance imaging (to exclude Sjögren's syndrome or neoplasia). A minor salivary gland biopsy, usually taken from the lip, may be carried out if there is a suspicion of organic disease of the salivary glands. Blood tests and urinalysis may be involved to exclude a number of possible causes. To investigate xerophthalmia, the Schirmer test of lacrimal flow may be indicated. Slit-lamp examination may also be carried out.
+True hyposalivation may give the following signs and symptoms:
+- Dental caries (xerostomia related caries) – Without the anticariogenic actions of saliva, tooth decay is a common feature and may progress much more aggressively than it would otherwise ("rampant caries"). It may affect tooth surfaces that are normally spared, e. G., cervical caries and root surface caries. This is often seen in patients who have had radiotherapy involving the major salivary glands, termed radiation-induced caries. Therefore it's important that any products used in managing dry mouth symptoms are sugar-free, as the presence of sugars in the mouth support the growth of oral bacteria, resulting in acid production and development of dental caries.
+- Acid erosion. Saliva acts as a buffer and helps to prevent demineralization of teeth.
+- Oral candidiasis – A loss of the antimicrobial actions of saliva may also lead to opportunistic infection with Candida species.
+- Ascending (suppurative) sialadenitis – an infection of the major salivary glands (usually the parotid gland) that may be recurrent. It is associated with hyposalivation, as bacteria are able to enter the ductal system against the diminished flow of saliva. There may be swollen salivary glands even without acute infection, possibly caused by autoimmune involvement.
+- Dysgeusia – altered taste sensation (e. G., a metallic taste) and dysosmia, altered sense of smell.
+- Intraoral halitosis – possibly due to increased activity of halitogenic biofilm on the posterior dorsal tongue (although dysgeusia may cause a complaint of nongenuine halitosis in the absence of hyposalivation).
+- Oral dysesthesia – a burning or tingling sensation in the mouth.
+- Saliva that appears thick or ropey.
+- Mucosa that appears dry.
+- A lack of saliva pooling in the floor of the mouth during examination.
+- Dysphagia – difficulty swallowing and chewing, especially when eating dry foods. Food may stick to the tissues during eating.
+- The tongue may stick to the palate, causing a clicking noise during speech, or the lips may stick together.
+- Gloves or a dental mirror may stick to the tissues.
+- Fissured tongue with atrophy of the filiform papillae and a lobulated, erythematous appearance of the tongue.
+- Saliva cannot be "milked" (expressed) from the parotid duct.
+- Difficulty wearing dentures, e. G., when swallowing or speaking. There may be generalized mucosal soreness and ulceration of the areas covered by the denture.
+- Mouth soreness and oral mucositis.
+- Lipstick or food may stick to the teeth.
+- A need to sip drinks frequently while talking or eating.
+- Dry, sore, and cracked lips and angles of mouth.
+- Thirst.
+However, sometimes the clinical findings do not correlate with the symptoms experienced. E. G., a person with signs of hyposalivation may not complain of xerostomia. Conversely a person who reports experiencing xerostomia may not show signs of reduced salivary secretions (subjective xerostomia). In the latter scenario, there are often other oral symptoms suggestive of oral dysesthesia ("burning mouth syndrome"). Some symptoms outside the mouth may occur together with xerostomia.
+These include:
+- Xerophthalmia (dry eyes).
+- Inability to cry.
+- Blurred vision.
+- Photophobia (light intolerance).
+- Dryness of other mucosae, e. G., nasal, laryngeal, and/or genital.
+- Burning sensation.
+- Itching or grittiness.
+- Dysphonia (voice changes).
+There may also be other systemic signs and symptoms if there is an underlying cause such as Sjögren's syndrome, for example, joint pain due to associated rheumatoid arthritis.
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DISNET disease texts/100 Original Disease Texts/Acute decompensated heart failure.txt

+Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), abnormal heart rhythms (such as atrial fibrillation), uncontrolled high blood pressure, or the person's failure to maintain a fluid restriction, diet, or medication.[3] Other well recognized precipitating factors include anemia and hyperthyroidism which place additional strain on the heart muscle. Excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones, may also precipitate decompensation.[4]
+Acute myocardial infarction can precipitate acute decompensated heart failure and will necessitate emergent revascularization with thrombolytics, percutaneous coronary intervention, or coronary artery bypass graft.
+A jugular venous distension is the most sensitive clinical sign for acute decompensation.[5]
+Difficulty breathing, a cardinal symptom of left ventricular failure, may manifest with progressively increasing severity as the following:
+Difficulty breathing with physical activity (exertional dyspnea)&Difficulty breathing while lying flat (orthopnea)&Episodes of waking up from sleep gasping for air (paroxysmal nocturnal dyspnea)&Acute pulmonary edem
+Other cardiac symptoms of heart failure include chest pain/pressure and palpitations. Common noncardiac signs and symptoms of heart failure include loss of appetite, nausea, weight loss, bloating, fatigue, weakness, low urine output, waking up at night to urinate, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion.[2]
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DISNET disease texts/100 Original Disease Texts/Acute intermittent porphyria.txt

+Urine and serum show raised levels of porphobilinogen.
+Assay the red blood cells for the level of porphobilinogen deaminase.
+Testing[edit] => Porphobilinogen&Porphobilinogen deaminase&Sodium&Potassium&Anti-nuclear antibody[9]&Creatinine&Creatine kinase[10]&White blood cell&Aspartate transaminase&Alanine transaminase&Epinephrine[11]&Norepinephrine[11
+Signs and symptoms of AIP can be variable. Severe and poorly localized abdominal pain is a very common symptom (found in 95% of those affected by AIP). Urinary signs and symptoms such as painful urination, urinary retention, urinary incontinence, or dark urine have also been known to occur. Psychiatric signs and symptoms of AIP may manifest as anxiety, paranoia, irritability, delusions, hallucinations, confusion, and depression.[4] Signs that suggest increased activity of the sympathetic nervous system may be evident including tachycardia, hypertension, palpitations, orthostatic hypotension, sweating, restlessness, and tremor. Other neurologic signs and symptoms of AIP include seizures, peripheral neuropathy, abnormal sensations, chest pain, leg pain, back pain or headache, and coma. Nausea, vomiting, constipation, and diarrhea can also occur. Proximal muscle weakness typically beginning in the arms is characteristic; there can be muscle pain, tingling, numbness, weakness or paralysis;[5] muscle weakness seen in AIP can progress to include the muscles of breathing causing respiratory failure and can be fatal.[citation needed]
+AIP patients have an increased risk of developing hepatocellular carcinoma, melanoma, lymphoma, chronic hypertension, chronic kidney disease, and chronic pain.[6]
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DISNET disease texts/100 Original Disease Texts/Anthrax.txt

+Bacillus anthracis is a rod-shaped, Gram-positive, aerobic bacterium about 1 by 9 μm in size.[2] It was shown to cause disease by Robert Koch in 1876 when he took a blood sample from an infected cow, isolated the bacteria, and put them into a mouse.[21] The bacterium normally rests in endospore form in the soil, and can survive for decades in this state. Herbivores are often infected whilst grazing, especially when eating rough, irritant, or spiky vegetation; the vegetation has been hypothesized to cause wounds within the gastrointestinal tract permitting entry of the bacterial endospores into the tissues, though this has not been proven. Once ingested or placed in an open wound, the bacteria begin multiplying inside the animal or human and typically kill the host within a few days or weeks. The endospores germinate at the site of entry into the tissues and then spread by the circulation to the lymphatics, where the bacteria multiply.
+The production of two powerful exotoxins and lethal toxin by the bacteria causes death. Veterinarians can often tell a possible anthrax-induced death by its sudden occurrence, and by the dark, nonclotting blood that oozes from the body orifices. Most anthrax bacteria inside the body after death are outcompeted and destroyed by anaerobic bacteria within minutes to hours post mortem. However, anthrax vegetative bacteria that escape the body via oozing blood or through the opening of the carcass may form hardy spores. These vegetative bacteria are not contagious.[22] One spore forms per one vegetative bacterium. The triggers for spore formation are not yet known, though oxygen tension and lack of nutrients may play roles. Once formed, these spores are very hard to eradicate.
+The infection of herbivores (and occasionally humans) by the inhalational route normally proceeds as follows: Once the spores are inhaled, they are transported through the air passages into the tiny air sacs (alveoli) in the lungs. The spores are then picked up by scavenger cells (macrophages) in the lungs and are transported through small vessels (lymphatics) to the lymph nodes in the central chest cavity (mediastinum). Damage caused by the anthrax spores and bacilli to the central chest cavity can cause chest pain and difficulty in breathing. Once in the lymph nodes, the spores germinate into active bacilli that multiply and eventually burst the macrophages, releasing many more bacilli into the bloodstream to be transferred to the entire body. Once in the blood stream, these bacilli release three proteins named lethal factor, edema factor, and protective antigen. The three are not toxic by themselves, but their combination is incredibly lethal to humans.[23] Protective antigen combines with these other two factors to form lethal toxin and edema toxin, respectively. These toxins are the primary agents of tissue destruction, bleeding, and death of the host. If antibiotics are administered too late, even if the antibiotics eradicate the bacteria, some hosts still die of toxemia because the toxins produced by the bacilli remain in their system at lethal dose levels.
+Bacillus anthracis&Color-enhanced scanning electron micrograph shows splenic tissue from a monkey with inhalational anthrax; featured are rod-shaped bacilli (yellow) and an erythrocyte (red)&Gram-positive anthrax bacteria (purple rods) in cerebrospinal fluid: If present, a Gram-negative bacterial species would appear pink. (The other cells are white blood cells.
+Exposure[edit] => The spores are able to survive in harsh conditions for decades or even centuries.[24] Such spores can be found on all continents, including Antarctica.[25] Disturbed grave sites of infected animals have been known to cause infection after 70 years.[26]
+Occupational exposure to infected animals or their products (such as skin, wool, and meat) is the usual pathway of exposure for humans. Workers who are exposed to dead animals and animal products are at the highest risk, especially in countries where anthrax is more common. Anthrax in livestock grazing on open range where they mix with wild animals still occasionally occurs in the United States and elsewhere. Many workers who deal with wool and animal hides are routinely exposed to low levels of anthrax spores, but most exposure levels are not sufficient to develop anthrax infections. A lethal infection is reported to result from inhalation of about 10,000–20,000 spores, though this dose varies among host species.[27] Little documented evidence is available to verify the exact or average number of spores needed for infection.
+Historically, inhalational anthrax was called woolsorters' disease because it was an occupational hazard for people who sorted wool. Today, this form of infection is extremely rare in advanced nations, as almost no infected animals remain.
+Anthrax can enter the human body through the intestines (ingestion), lungs (inhalation), or skin (cutaneous) and causes distinct clinical symptoms based on its site of entry. In general, an infected human will be quarantined. However, anthrax does not usually spread from an infected human to a noninfected human.[28] But, if the disease is fatal to the person's body, its mass of anthrax bacilli becomes a potential source of infection to others and special precautions should be used to prevent further contamination. Inhalational anthrax, if left untreated until obvious symptoms occur, is usually fatal.[28]
+Anthrax can be contracted in laboratory accidents or by handling infected animals or their wool or hides.[29] It has also been used in biological warfare agents and by terrorists to intentionally infect as exemplified by the 2001 anthrax attacks.[30]
+Various techniques may be used for the direct identification of B. anthracis in clinical material. Firstly, specimens may be Gram stained. Bacillus spp. are quite large in size (3 to 4 μm long), they may grow in long chains, and they stain Gram-positive. To confirm the organism is B. anthracis, rapid diagnostic techniques such as polymerase chain reaction-based assays and immunofluorescence microscopy may be used.[33]
+All Bacillus species grow well on 5% sheep blood agar and other routine culture media. Polymyxin-lysozyme-EDTA-thallous acetate can be used to isolate B. anthracis from contaminated specimens, and bicarbonate agar is used as an identification method to induce capsule formation. Bacillus spp. usually grow within 24 hours of incubation at 35°C, in ambient air (room temperature) or in 5% CO2. If bicarbonate agar is used for identification, then the medium must be incubated in 5% CO2. B. anthracis colonies are medium-large, gray, flat, and irregular with swirling projections, often referred to as having a "medusa head" appearance, and are not hemolytic on 5% sheep blood agar. The bacteria are not motile, susceptible to penicillin, and produce a wide zone of lecithinase on egg yolk agar. Confirmatory testing to identify B. anthracis includes gamma bacteriophage testing, indirect hemagglutination, and enzyme-linked immunosorbent assay to detect antibodies.[34] The best confirmatory precipitation test for anthrax is the Ascoli test.
+Cutaneous anthrax, also known as Hide porter's disease, is when anthrax occurs on the skin. It is the most common form (>90% of anthrax cases). Cutaneous anthrax is also the least dangerous form of anthrax (less than 1% mortality rate with treatment).[2] Cutaneous anthrax presents as a boil-like skin lesion that eventually forms an ulcer with a black center (eschar). The black eschar often shows up as a large, painless, necrotic ulcer (beginning as an irritating and itchy skin lesion or blister that is dark and usually concentrated as a black dot, somewhat resembling bread mold) at the site of infection. In general, cutaneous infections form within the site of spore penetration between two and five days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections normally do not cause pain. Nearby lymph nodes may become infected, reddened, swollen, and painful. A scab forms over the lesion soon, and falls off in a few weeks. Complete recovery may take longer.[15] Cutaneous anthrax is typically caused when B. anthracis spores enter through cuts on the skin. This form is found most commonly when humans handle infected animals and/or animal products.
+Cutaneous anthrax is rarely fatal if treated,[16] because the infection area is limited to the skin, preventing the lethal factor, edema factor, and protective antigen from entering and destroying a vital organ. Without treatment, about 20% of cutaneous skin infection cases progress to toxemia and death.
+Lungs[edit] => Respiratory infection in humans is relatively rare and presents as two stages.[17] It infects the lymph nodes in the chest first, rather than the lungs themselves, a condition called hemorrhagic mediastinitis, causing bloody fluid to accumulate in the chest cavity, therefore causing shortness of breath. The first stage causes cold and flu-like symptoms. Symptoms include fever, shortness of breath, cough, fatigue, and chills. This can last hours to days. Often, many fatalities from inhalational anthrax are when the first stage is mistaken for the cold or flu and the victim does not seek treatment until the second stage, which is 90% fatal. The second (pneumonia) stage occurs when the infection spreads from the lymph nodes to the lungs. Symptoms of the second stage develop suddenly after hours or days of the first stage. Symptoms include high fever, extreme shortness of breath, shock, and rapid death within 48 hours in fatal cases. Historical mortality rates were over 85%,[18] but when treated early (seen in the 2001 anthrax attacks), observed case fatality rate dropped to 45%.[16][18] Distinguishing pulmonary anthrax from more common causes of respiratory illness is essential to avoiding delays in diagnosis and thereby improving outcomes. An algorithm for this purpose has been developed.[19]
+Gastrointestinal[edit] => Gastrointestinal (GI) infection is most often caused by consuming anthrax-infected meat and is characterized by diarrhea, potentially with blood, abdominal pains, acute inflammation of the intestinal tract, and loss of appetite.[20] Occasional vomiting of blood can occur. Lesions have been found in the intestines and in the mouth and throat. After the bacterium invades the gastrointestinal system, it spreads to the bloodstream and throughout the body, while continuing to make toxins. GI infections can be treated, but usually result in fatality rates of 25 to 60%, depending upon how soon treatment commences. This form of anthrax is the rarest form.
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DISNET disease texts/100 Original Disease Texts/Arterial embolism.txt

+In addition to evaluating the symptoms above, the health care provider may find decreased or no blood pressure in the arm or leg.[1]
+Tests to determine any underlying cause for thrombosis or embolism and to confirm presence of the obstruction may include:
+Doppler ultrasound, especially duplex ultrasonography.[2] It may also involve transcranial doppler exam of arteries to the brain[2]&Echocardiography,[2] sometimes involving more specialized techniques such as Transesophageal echocardiography (TEE)[2] or myocardial contrast echocardiography (MCE) to diagnose myocardial infarction[2]&Arteriography of the affected extremity or organ[1][2] Digital subtraction angiography is useful in individuals where administration of radiopaque contrast material must be kept to a minimum.[1]&Magnetic resonance imaging (MRI)[2]&Blood tests for measuring elevated enzymes in the blood, including cardiac-specific troponin T and/or troponin I, myoglobins, and creatine kinase isoenzymes.[1] These indicate embolisation to the heart that has caused myocardial infarction. Myoglobins and creatine kinase are also elevated in the blood in embolisation in other locations.&Blood cultures may be done to identify the organism responsible for any causative infection[1]&Electrocardiography (ECG) for detecting myocardial infarction[1]&Angioscopy using a flexible fiberoptic catheter inserted directly into an artery.[1
+Symptoms may begin quickly or slowly depending on the size of the embolus and how much it blocks the blood flow.[2] Symptoms of embolisation in an organ vary with the organ involved but commonly include:
+Pain in the involved body part[2]&Temporarily[2] decreased organ functio
+Later symptoms are closely related to infarction of the affected tissue. This may cause permanently decreased organ function.
+For example, symptoms of myocardial infarction mainly include chest pain, dyspnea, diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations.
+Symptoms of limb infarction include coldness,[1][2] decreased or no pulse beyond the site of blockage,[1][2] pain,[1][2] muscle spasm,[2] numbness and tingling,[1][2] pallor[1][2] and muscle weakness,[1][2] possibly to the grade of paralysis[1] in the affected limb.
+Commonly occluded sites[edit] => Arterial emboli often occur in the legs and feet. Some may occur in the brain, causing a stroke, or in the heart, causing a heart attack. Less common sites include the kidneys, intestines, and eyes.[2]
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DISNET disease texts/100 Original Disease Texts/Arteriovenous malformation.txt

+AVMs are diagnosed primarily by the following methods:
+Computerized tomography (CT) scan is a noninvasive X-ray to view the anatomical structures within the brain to detect blood in or around the brain. A newer technology called CT angiography involves the injection of contrast into the blood stream to view the arteries of the brain. This type of test provides the best pictures of blood vessels through angiography and soft tissues through CT.&Magnetic resonance imaging (MRI) scan is a noninvasive test, which uses a magnetic field and radio-frequency waves to give a detailed view of the soft tissues of the brain.&Magnetic resonance angiography (MRA) – scans created using magnetic resonance imaging to specifically image the blood vessels and structures of the brain. A magnetic resonance angiogram can be an invasive procedure, involving the introduction of contrast dyes (e.g., gadolinium MR contrast agents) into the vasculature of a patient using a catheter inserted into an artery and passed through the blood vessels to the brain. Once the catheter is in place, the contrast dye is injected into the bloodstream and the MR images are taken. Additionally or alternatively, flow-dependent or other contrast-free magnetic resonance imaging techniques can be used to determine the location and other properties of the vasculature
+AVMs can occur in various parts of the body:
+brain (cerebral AV malformation)&spleen[6]&lung[7]&kidney[8]&spinal cord[9]&liver[10]&intercostal space[11]&iris[12]&spermatic cord[13]&extremities – arm, shoulder, etc
+AVMs may occur in isolation or as a part of another disease (for example, Von Hippel-Lindau disease or hereditary hemorrhagic telangiectasia).
+AVMs have been shown to be associated with aortic stenosis.[14]
+Bleeding from an AVM can be relatively mild or devastating. It can cause severe and less often fatal strokes. If a cerebral AVM is detected before a stroke occurs, usually the arteries feeding blood into the nidus can be closed off to avert the danger. However, interventional therapy may also be relatively risky.
+Symptoms of AVM vary according to the location of the malformation. Roughly 88%[1] of people with an AVM are asymptomatic; often the malformation is discovered as part of an autopsy or during treatment of an unrelated disorder (called in medicine an "incidental finding"); in rare cases, its expansion or a micro-bleed from an AVM in the brain can cause epilepsy, neurological deficit, or pain.
+The most general symptoms of a cerebral AVM include headaches and epileptic seizures, with more specific symptoms occurring that normally depend on the location of the malformation and the individual. Such possible symptoms include:[2]
+Difficulties with movement coordination, including muscle weakness and even paralysis;&Vertigo (dizziness);&Difficulties of speech (dysarthria) and communication, such as aphasia;&Difficulties with everyday activities, such as apraxia;&Abnormal sensations (numbness, tingling, or spontaneous pain);&Memory and thought-related problems, such as confusion, dementia or hallucinations
+Cerebral AVMs may present themselves in a number of different ways:
+Bleeding (45% of cases)&Acute onset of severe headache. May be described as the worst headache of the patient's life. Depending on the location of bleeding, may be associated with new fixed neurologic deficit. In unruptured brain AVMs, the risk of spontaneous bleeding may be as low as 1% per year. After a first rupture, the annual bleeding risk may increase to more than 5%.[3]&Seizure or brain seizure (46%) Depending on the place of the AVM, it can cause loss of vision in one place.&Headache (34%)&Progressive neurologic deficit (21%) May be caused by mass effect or venous dilatations. Presence and nature of the deficit depend on location of lesion and the draining veins.[4]&May be caused by mass effect or venous dilatations. Presence and nature of the deficit depend on location of lesion and the draining veins.[4]&Pediatric patients Heart failure Macrocephaly Prominent scalp veins&Heart failure&Macrocephaly&Prominent scalp vein
+Pulmonary arteriovenous malformations[edit] => In the lungs, pulmonary arteriovenous malformations have no symptoms in up to 29% of all cases.[5]
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DISNET disease texts/100 Original Disease Texts/Ascites.txt

+Causes of high serum-ascites albumin gradient (SAAG or transudate) are:[5]
+Cirrhosis – 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)&Heart failure – 3%&Hepatic venous occlusion: Budd–Chiari syndrome or veno-occlusive disease&Constrictive pericarditis&Kwashiorkor (childhood protein-energy malnutrition
+Causes of low SAAG ("exudate") are:
+Cancer (metastasis and primary peritoneal carcinomatosis) – 10%&Infection: Tuberculosis – 2% or spontaneous bacterial peritonitis&Pancreatitis – 1%&Serositis&Nephrotic syndrome[6]&Hereditary angioedema[7
+Other rare causes:
+Meigs syndrome&Vasculitis&Hypothyroidism&Renal dialysis&Peritoneum mesothelioma&Abdominal tuberculosis&Mastocytosi
+Routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend a diagnostic paracentesis be performed if the ascites is new or if the patient with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as microbiological culture, Gram stain and cytopathology.[5]
+The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.[8] A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive as a cause.
+Ultrasound investigation is often performed prior to attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detecting Budd-Chiari syndrome (thrombosis of the hepatic vein) and portal vein thrombosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. An abdominal CT scan is a more accurate alternate to reveal abdominal organ structure and morphology.[citation needed]
+Classification[edit] => Ascites exists in three grades:[9]
+Grade 1: mild, only visible on ultrasound and CT&Grade 2: detectable with flank bulging and shifting dullness&Grade 3: directly visible, confirmed with the fluid wave/thrill tes
+Mild ascites is hard to notice, but severe ascites leads to abdominal distension. Patients with ascites generally will complain of progressive abdominal heaviness and pressure as well as shortness of breath due to mechanical impingement on the diaphragm.
+Ascites is detected on physical examination of the abdomen by visible bulging of the flanks in the reclining patient ("flank bulging"), "shifting dullness" (difference in percussion note in the flanks that shifts when the patient is turned on the side) or in massive ascites with a "fluid thrill" or "fluid wave" (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite side of the abdomen).
+Other signs of ascites may be present due to its underlying cause. For instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the liver) patients may also complain of leg swelling, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance.
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DISNET disease texts/100 Original Disease Texts/Autonomic dysreflexia.txt

+The most common symptoms of autonomic hyperreflexia seen in people with spinal cord injury are loss of bowel and bladder function, resulting in impaction in the case of the bowels and distention in case of the bladder. These are generally found in patients with a spinal cord injury above the T6 (6th thoracic vertebral) level, but can occur in patients with a transection as low as T10 (10th thoracic vertebral) level.
+The risk is greatest with cervical spinal cord lesions and is rare with lesions below T6 thoracic vertebrae. It has rarely been reported in spinal cord lesions as low as T10. The first episode may occur weeks to years after spinal cord injury takes place, but most people at risk (80%) develop their first episode within the first year after injury. Once a person has their first episode of autonomic dysreflexia, the next 7–10 days are critical because there is a high incidence of recurrence within that time.[2] Some people describe this predisposition as an easily excitable autonomic nervous system.[2]
+Another causative factor may be an undetected urinary tract infection. The difficulty in assessing this may be complicated with the usage of indwelling or suprapubic catheters. When a painful stimulus occurs, as when voiding is interrupted or a bowel obstruction occurs, nerve impulses are sent to the brain via the spinal cord.[5] However, in spinal cord transection, these impulses are unable to travel past the injury. This results in a spinal cord reflex to the autonomic nervous system in response to pain. In patients with spinal cord transection, types of stimulation that are tolerated by healthy people create an excessive response from the person's nervous system.
+Other causes include medication side effects and various disease processes. The use of stimulants such as cocaine and amphetamines which can result in urinary retention, and the use of CNS depressants and other psychoactive drugs can also lead to urinary retention and constipation thus leading to autonomic dysreflexia when in use over an extended period of time. Guillain–Barré syndrome is a demyelinating disease that can result in peripheral paralysis and can progress to encompass autonomic functions, leading to a loss of normal respiratory, bladder and bowel function resulting in autonomic dysreflexia. Severe head trauma and other brain injuries[6] can instigate autonomic dysreflexia at the central nervous system by interfering with the reception of the signal that brings the urge to void the bladder and bowels and with the voluntary ability to micturate and defecate. Other causal theories for autonomic dysreflexia include noxious stimuli, or painful stimuli arising from the peripheral sensory neurons. These stimuli are interrupted in their journey to the brain due to a transection of the spine result in a paradoxical stimulation of autonomic pathways of the autonomic nervous system.
+Pain[edit] => Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. (Note: Not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli in normal people, e.g. broken bones, will not result in AD, and may in fact even go unnoticed.) However, different studies have found that activation of pain receptors in muscle and skin below the lesion in spinal cord injured individuals did not trigger AD.[7][8] These studies suggests that not all noxious stimuli are reliable triggers of AD, and because non-noxious stimuli can also trigger AD, attribution of an episode of AD to noxious stimuli may cause clinicians to overlook underlying non-noxious triggers. As a result, non-noxious trigger factors remain undetected, prolonging an episode of AD. They concluded that when deducing the potential causes of AD it is important to consider non-noxious sources of stimulation in addition to noxious triggers. Current assessment of autonomic dysreflexia in patients with known causative factors include palpation of the bladder and bowel and can also include bladder scan.
+The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance. In autonomic dysreflexia, patients will experience hypertension, sweating, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may suffer from headaches and blurred vision. Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe. Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms are usually experiencing essential hypertension, not autonomic dysreflexia. Aggressive treatment of these elderly patients with rapidly acting antihypertensive medications can have disastrous results.
+This condition is distinct and usually episodic, with the people experiencing remarkably high blood pressure (often with systolic readings over 200 mm. Hg), intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision.[2] An elevation of 40 mm Hg over baseline systolic should be suspicious for dysreflexia.
+Complications[edit] => Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue ulcers or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers.
+Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes.[2]
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DISNET disease texts/100 Original Disease Texts/Benzodiazepine withdrawal syndrome.txt

+In severe cases, the withdrawal reaction or protracted withdrawal may exacerbate or resemble serious psychiatric and medical conditions, such as mania, schizophrenia, agitated depression, panic disorder, generalised anxiety disorder, and complex partial seizures and, especially at high doses, seizure disorders.[22] Failure to recognize discontinuation symptoms can lead to false evidence for the need to take benzodiazepines, which in turn leads to withdrawal failure and reinstatement of benzodiazepines, often to higher doses. Pre-existing disorder or other causes typically do not improve, whereas symptoms of protracted withdrawal gradually improve over the ensuing months.[22] For this reason at least six months should have elapsed after benzodiazepines cessation before re-evaluating the symptoms and updating a diagnosis.[citation needed]
+Symptoms may lack a psychological cause and can fluctuate in intensity with periods of good and bad days until eventual recovery.[90][91]
+Withdrawal effects caused by sedative-hypnotics discontinuation, such as benzodiazepines, barbiturates, or alcohol, can cause serious medical complications. They are cited to be more hazardous to withdraw from than opioids.[26] Users typically receive little advice and support for discontinuation.[27] Some withdrawal symptoms are identical to the symptoms for which the medication was originally prescribed,[21] and can be acute or protracted in duration. Onset of symptoms from long half-life benzodiazepines might be delayed for up to three weeks, although withdrawal symptoms from short-acting ones often present early, usually within 24–48 hours.[28] There may be no fundamental differences in symptoms from either high or low dose discontinuation, but symptoms tend to be more severe from higher doses.[29]
+Daytime reemergence and rebound withdrawal symptoms, sometimes confused with interdose withdrawal, may occur once dependence has set in. 'Reemergence' is the return of symptoms for which the drug was initially prescribed, in contrast, 'rebound' symptoms are a return of the symptoms for which the benzodiazepine was initially taken, but at a more intense level than before; whereas 'interdose withdrawal' is when a prior dosage of drug wears off and beginnings of an entirely new cycle of withdrawal sets in, the symptoms of which dissipate upon taking the next dosage but afterwhich yet another entirely new cycle of withdrawal begins when that dosage wears off, a new onset of withdrawal between each dosage thus called 'interdose withdrawal' and if not properly treated can recur indefinitely in a vicious circle (for which consider a benzo with a long half life (e.g. Valium) so the drug does not wear off between doses).[30] Withdrawal symptoms may appear for the first time during dose reduction, and include insomnia, anxiety, distress, weight loss, dizziness, night sweats, shakes, muscle twitches, aphasia, panic attacks, depression, derealization, paranoia, etc., and are more commonly associated with short-acting benzodiazepines discontinuation, like triazolam.[22][31] Daytime symptoms can occur after a few days to a few weeks of administration of nightly benzodiazepine use[32][33] or z-drugs such as zopiclone;[34] withdrawal-related insomnia rebounds worse than baseline[35][36] even when benzodiazepines are used intermittently.[37]
+The following symptoms may emerge during gradual or abrupt dosage reduction:
+Akathisia&Agitation and Anxiety,[25] possible terror and panic attacks[1][38]&Blurred vision[38]&Chest pain[38]&Depersonalization[39]&Depression (can be severe),[40] possible suicidal ideation&Derealisation (feelings of unreality)[41]&Dilated pupils[22]&Dizziness[38]&Dry mouth[38]&Dysphoria[42][43]&Elevation in blood pressure[44]&Fatigue and weakness[38]&Gastrointestinal disturbance (including nausea, diarrhea, vomiting)[45][46][46][47]&Hearing disturbance[38]&Headache[1]&Hot and cold spells[38]&Hyperosmia[48]&Hypertension[49]&Hypnagogic hallucinations[17]&Hypochondriasis[38]&Increased sensitivity to touch[41]&Increased urinary frequency[38]&Insomnia[45]&Impaired memory and concentration[1][38]&Loss of appetite and weight loss[50]&Mild to moderate Aphasia[48]&Mood swings[38]&Muscular spasms, cramps, discomfort or fasciculations[51]&Nightmares[45]&Obsessive compulsive disorder[52][53]&Paraesthesia[38][41][48][5][54]&Paranoia[48]&Perspiration[1]&Photophobia[48]&Postural hypotension[45]&REM sleep rebound[55]&Restless legs syndrome[24]&Stiffness[38]&Taste and smell disturbances[38]&Tachycardia[56]&Tinnitus[57]&Tremor[58][59]&Visual disturbances[41
+Rapid discontinuation may result in a more serious syndrome
+Catatonia, which may result in death[60][61][62]&Confusion[25]&Convulsions,[25] which may result in death[63][64]&Coma[65] (rare)&Delirium tremens[66][67][67]&Hyperthermia[45]&Mania[68][69]&Neuroleptic malignant syndrome-like event[70][71] (rare)&Organic brain syndrome[72]&Post-traumatic stress disorder[24]&Psychosis[73][74]&Suicidal ideation[75] or suicide[2][3]&Violence and aggression[38][76
+As withdrawal progresses, patients often find their physical and mental health improves with improved mood and improved cognition.
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DISNET disease texts/100 Original Disease Texts/Blastomycosis.txt

+Blastomycosis is caused by the dimorphic microfungus Blastomyces dermatitidis, a member of the phylum Ascomycota in the family Ajellomycetaceae. It has been recognised as the asexual state of Ajellomyces dermatitidis. In endemic areas, the fungus lives in soil and rotten wood near lakes and rivers. Although it has never been directly observed growing in nature, it is thought to grow there as a cottony white mold, similar to the growth seen in artificial culture at 25 °C. The moist, acidic soil in the surrounding woodland harbors the fungus.
+Spectrum of disease[edit] => Blastomycosis manifests as a primary lung infection in about 70% of cases.[5] The onset is relatively slow and symptoms are suggestive of pneumonia, often leading to initial treatment with antibacterials. Occasionally, if a lesion is seen on X-ray in a cigarette smoker, the disease may be misdiagnosed as carcinoma, leading to swift excision of the pulmonary lobe involved. Upper lung lobes are involved somewhat more frequently than lower lobes.[5] If untreated, many cases progress over a period of months to years to become disseminated blastomycosis. In these cases, the large Blastomyces yeast cells translocate from the lungs and are trapped in capillary beds elsewhere in the body, where they cause lesions. The skin is the most common organ affected, being the site of lesions in approximately 60% of cases.[5] The signature image of blastomycosis in textbooks is the indolent, verrucous or ulcerated dermal lesion seen in disseminated disease. Osteomyelitis is also common (12–60% of cases). Other recurring sites of dissemination are the genitourinary tract (kidney, prostate, epididymis; collectively ca. 25% of cases) and the brain (3–10% of cases).[5]
+An uncommon but very dangerous type of primary blastomycosis manifests as acute respiratory distress syndrome (ARDS); for example, this was seen in 9 of 72 blastomycosis cases studied in northeast Tennessee.[6] Such cases may follow massive exposure, e.g., during brush clearing operations. The fatality rate in the ARDS cases in the Tennessee study was 89%, while in non-ARDS cases of pulmonary blastomycosis, the fatality rate was 10%.
+Once suspected, the diagnosis of blastomycosis can usually be confirmed by demonstration of the characteristic broad based budding organisms in sputum or tissues by KOH prep, cytology, or histology.[7] Tissue biopsy of skin or other organs may be required in order to diagnose extra-pulmonary disease. Blastomycosis is histologically associated with granulomatous nodules. Commercially available urine antigen testing appears to be quite sensitive in suggesting the diagnosis in cases where the organism is not readily detected. While culture of the organism remains the definitive diagnostic standard, its slow growing nature can lead to delays in treatment of up to several weeks. However, sometimes blood and sputum cultures may not detect blastomycosis.[citation needed]
+Blastomycosis can present in one of the following ways:
+a flu-like illness with fever, chills, arthralgia (joint pain), myalgia (muscle pain), headache, and a nonproductive cough which resolves within days.&an acute illness resembling bacterial pneumonia, with symptoms of high fever, chills, a productive cough, and pleuritic chest pain.&a chronic illness that mimics tuberculosis or lung cancer, with symptoms of low-grade fever, a productive cough, night sweats, and weight loss.&a fast, progressive, and severe disease that manifests as ARDS, with fever, shortness of breath, tachypnea, hypoxemia, and diffuse pulmonary infiltrates.&skin lesions, usually asymptomatic, can be verrucous (wart-like) or ulcerated with small pustules at the margins.&bone lytic lesions can cause bone or joint pain.&prostatitis may be asymptomatic or may cause pain on urinating.&laryngeal involvement causes hoarseness.&40% immunocompromised individuals have CNS involvement and present as brain abscess, epidural abscess or meningitis
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DISNET disease texts/100 Original Disease Texts/Breast cancer.txt

+Most types of breast cancer are easy to diagnose by microscopic analysis of a sample—or biopsy—of the affected area of the breast. Also, there are types of breast cancer that require specialized lab exams.
+The two most commonly used screening methods, physical examination of the breasts by a healthcare provider and mammography, can offer an approximate likelihood that a lump is cancer, and may also detect some other lesions, such as a simple cyst.[82] When these examinations are inconclusive, a healthcare provider can remove a sample of the fluid in the lump for microscopic analysis (a procedure known as fine needle aspiration, or fine needle aspiration and cytology—FNAC) to help establish the diagnosis. The needle aspiration may be performed in a healthcare provider's office or clinic using local anaesthetic if required.[clarification needed] A finding of clear fluid makes the lump highly unlikely to be cancerous, but bloody fluid may be sent off for inspection under a microscope for cancerous cells. Together, physical examination of the breasts, mammography, and FNAC can be used to diagnose breast cancer with a good degree of accuracy.
+Other options for biopsy include a core biopsy or vacuum-assisted breast biopsy,[83] which are procedures in which a section of the breast lump is removed; or an excisional biopsy, in which the entire lump is removed. Very often the results of physical examination by a healthcare provider, mammography, and additional tests that may be performed in special circumstances (such as imaging by ultrasound or MRI) are sufficient to warrant excisional biopsy as the definitive diagnostic and primary treatment method.
+MRI showing breast cancer&Excised human breast tissue, showing an irregular, dense, white stellate area of cancer 2 cm in diameter, within yellow fatty tissue.&High-grade invasive ductal carcinoma, with minimal tubule formation, marked pleomorphism, and prominent mitoses, 40x field.&Micrograph showing a lymph node invaded by ductal breast carcinoma, with an extension of the tumor beyond the lymph node.&Neuropilin-2 expression in normal breast and breast carcinoma tissue.&F-18 FDG PET/CT: A breast cancer metastasis to the right scapula&Needle breast biopsy.&Elastography shows stiff cancer tissue on ultrasound imaging.&Ultrasound image shows irregularly shaped mass of breast cancer.&Infiltrating (Invasive) breast carcinoma
+Breast cancers are classified by several grading systems. Each of these influences the prognosis and can affect treatment response. Description of a breast cancer optimally includes all of these factors.
+Histopathology. Breast cancer is usually classified primarily by its histological appearance. Most breast cancers are derived from the epithelium lining the ducts or lobules, and these cancers are classified as ductal or lobular carcinoma. Carcinoma in situ is growth of low-grade cancerous or precancerous cells within a particular tissue compartment such as the mammary duct without invasion of the surrounding tissue. In contrast, invasive carcinoma does not confine itself to the initial tissue compartment.[84]&Grade. Grading compares the appearance of the breast cancer cells to the appearance of normal breast tissue. Normal cells in an organ like the breast become differentiated, meaning that they take on specific shapes and forms that reflect their function as part of that organ. Cancerous cells lose that differentiation. In cancer, the cells that would normally line up in an orderly way to make up the milk ducts become disorganized. Cell division becomes uncontrolled. Cell nuclei become less uniform. Pathologists describe cells as well differentiated (low grade), moderately differentiated (intermediate grade), and poorly differentiated (high grade) as the cells progressively lose the features seen in normal breast cells. Poorly differentiated cancers (the ones whose tissue is least like normal breast tissue) have a worse prognosis.&Stage. Breast cancer staging using the TNM system is based on the size of the tumor (T), whether or not the tumor has spread to the lymph nodes (N) in the armpits, and whether the tumor has metastasized (M) (i.e. spread to a more distant part of the body). Larger size, nodal spread, and metastasis have a larger stage number and a worse prognosis. The main stages are: Stage 0 is a pre-cancerous or marker condition, either ductal carcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS). Stages 1–3 are within the breast or regional lymph nodes. Stage 4 is 'metastatic' cancer that has a less favorable prognosis since it has spread beyond the breast and regional lymph nodes.&Stage 0 is a pre-cancerous or marker condition, either ductal carcinoma in situ (DCIS) or lobular carcinoma in situ (LCIS).&Stages 1–3 are within the breast or regional lymph nodes.&Stage 4 is 'metastatic' cancer that has a less favorable prognosis since it has spread beyond the breast and regional lymph nodes
+Stage T1 breast cancer&Stage T2 breast cancer&Stage T3 breast cance
+Receptor status. Breast cancer cells have receptors on their surface and in their cytoplasm and nucleus. Chemical messengers such as hormones bind to receptors, and this causes changes in the cell. Breast cancer cells may or may not have three important receptors: estrogen receptor (ER), progesterone receptor (PR), and HER2. ER+ cancer cells (that is, cancer cells that have estrogen receptors) depend on estrogen for their growth, so they can be treated with drugs to block estrogen effects (e.g. tamoxifen), and generally have a better prognosis. Untreated, HER2+ breast cancers are generally more aggressive than HER2- breast cancers,[87][88] but HER2+ cancer cells respond to drugs such as the monoclonal antibody trastuzumab (in combination with conventional chemotherapy), and this has improved the prognosis significantly.[89] Cells that do not have any of these three receptor types (estrogen receptors, progesterone receptors, or HER2) are called triple-negative, although they frequently do express receptors for other hormones, such as androgen receptor and prolactin receptor.&DNA assays. DNA testing of various types including DNA microarrays have compared normal cells to breast cancer cells. The specific changes in a particular breast cancer can be used to classify the cancer in several ways, and may assist in choosing the most effective treatment for that DNA type
+Stage 1A breast cancer&Stage 1B breast cancer&Stage 2A breast cancer&Stage 2A breast cancer&Stage 2B breast cancer&Stage 2B breast cancer&Stage 2B breast cancer&Stage 3A breast cancer&Stage 3A breast cancer&Stage 3A breast cancer&Stage 3B breast cancer&Stage 3B breast cancer&Stage 4 breast cance
+The first noticeable symptom of breast cancer is typically a lump that feels different from the rest of the breast tissue. More than 80% of breast cancer cases are discovered when the woman feels a lump.[18] The earliest breast cancers are detected by a mammogram.[19] Lumps found in lymph nodes located in the armpits[18] can also indicate breast cancer.
+Indications of breast cancer other than a lump may include thickening different from the other breast tissue, one breast becoming larger or lower, a nipple changing position or shape or becoming inverted, skin puckering or dimpling, a rash on or around a nipple, discharge from nipple/s, constant pain in part of the breast or armpit, and swelling beneath the armpit or around the collarbone.[20] Pain ("mastodynia") is an unreliable tool in determining the presence or absence of breast cancer, but may be indicative of other breast health issues.[18][19][21]
+Inflammatory breast cancer is a particular type of breast cancer which can pose a substantial diagnostic challenge. Symptoms may resemble a breast inflammation and may include itching, pain, swelling, nipple inversion, warmth and redness throughout the breast, as well as an orange-peel texture to the skin referred to as peau d'orange.[18] As inflammatory breast cancer does not present as a lump there can sometimes be a delay in diagnosis.
+Another reported symptom complex of breast cancer is Paget's disease of the breast. This syndrome presents as skin changes resembling eczema, such as redness, discoloration, or mild flaking of the nipple skin. As Paget's disease of the breast advances, symptoms may include tingling, itching, increased sensitivity, burning, and pain. There may also be discharge from the nipple. Approximately half of women diagnosed with Paget's disease of the breast also have a lump in the breast.[22]
+In rare cases, what initially appears as a fibroadenoma (hard, movable non-cancerous lump) could in fact be a phyllodes tumor. Phyllodes tumors are formed within the stroma (connective tissue) of the breast and contain glandular as well as stromal tissue. Phyllodes tumors are not staged in the usual sense; they are classified on the basis of their appearance under the microscope as benign, borderline, or malignant.[23]
+Occasionally, breast cancer presents as metastatic disease—that is, cancer that has spread beyond the original organ. The symptoms caused by metastatic breast cancer will depend on the location of metastasis. Common sites of metastasis include bone, liver, lung and brain.[24] Unexplained weight loss can occasionally signal breast cancer, as can symptoms of fevers or chills. Bone or joint pains can sometimes be manifestations of metastatic breast cancer, as can jaundice or neurological symptoms. These symptoms are called non-specific, meaning they could be manifestations of many other illnesses.[25]
+Most symptoms of breast disorders, including most lumps, do not turn out to represent underlying breast cancer. Fewer than 20% of lumps, for example, are cancerous,[26] and benign breast diseases such as mastitis and fibroadenoma of the breast are more common causes of breast disorder symptoms. Nevertheless, the appearance of a new symptom should be taken seriously by both patients and their doctors, because of the possibility of an underlying breast cancer at almost any age.[27]
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DISNET disease texts/100 Original Disease Texts/Campylobacteriosis.txt

+Campylobacteriosis is caused by Campylobacter bacteria (curved or spiral, motile, non–spore-forming, Gram-negative rods). The disease is usually caused by C. jejuni, a spiral and comma shaped bacterium normally found in cattle, swine, and birds, where it is nonpathogenic, but the illness can also be caused by C. coli (also found in cattle, swine, and birds), C. upsaliensis (found in cats and dogs) and C. lari (present in seabirds in particular).
+One effect of campylobacteriosis is tissue injury in the gut. The sites of tissue injury include the jejunum, the ileum, and the colon. C jejuni appears to achieve this by invading and destroying epithelial cells.
+C. jejuni can also cause a latent autoimmune effect on the nerves of the legs, which is usually seen several weeks after a surgical procedure of the abdomen. The effect is known as an acute idiopathic demyelinating polyneuropathy (AIDP), i.e. Guillain–Barré syndrome, in which one sees symptoms of ascending paralysis, dysaesthesias usually below the waist, and, in the later stages, respiratory failure.
+Some strains of C jejuni produce a cholera-like enterotoxin, which is important in the watery diarrhea observed in infections. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism.
+Campylobacter organisms can be detected by performing a Gram stain of a stool sample with high specificity and a sensitivity of ~60%, but are most often diagnosed by stool culture. Fecal leukocytes should be present and indicate the diarrhea to be inflammatory in nature. Methods currently being developed to detect the presence of campylobacter organisms include antigen testing via an EIA or PCR.
+The prodromal symptoms are fever, headache, and myalgia, which can be severe, lasting as long as 24 hours. After 1–5 days, typically, these are followed by diarrhea (as many as 10 watery, frequently bloody, bowel movements per day) or dysentery, cramps, abdominal pain, and fever as high as 40 °C (104 °F). In most people, the illness lasts for 2–10 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery.
+There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking acute appendicitis. Furthermore, Helicobacter pylori is closely related to Campylobacter and causes peptic ulcer disease.
+Complications[edit] => Complications include toxic megacolon, dehydration and sepsis. Such complications generally occur in young children (< 1 year of age) and immunocompromised people. A chronic course of the disease is possible; this disease process is likely to develop without a distinct acute phase. Chronic campylobacteriosis features a long period of sub-febrile temperature and asthenia; eye damage, arthritis, endocarditis may develop if infection is untreated.
+Occasional deaths occur in young, previously healthy individuals because of blood volume depletion (due to dehydration), and in persons who are elderly or immunocompromised.
+Some individuals (1–2 in 100,000 cases) develop Guillain–Barré syndrome, in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently. This occurs only with infection of C. jejuni and C. upsaliensis.[2]
+Other factors[edit] => In patients with HIV, infections may be more frequent, may cause prolonged bouts of dirty brown diarrhea, and may be more commonly associated with bacteremia and antibiotic resistance. In participants of unprotected anal intercourse, campylobacteriosis is more localized to the distal end of the colon and may be termed a proctocolitis. The severity and persistence of infection in patients with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection.
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DISNET disease texts/100 Original Disease Texts/Carciac myxoma.txt

+Myxomas are the most common type of primary heart tumor.[2]
+The tumor is derived from multipotential mesenchymal cells and may cause a ball valve-type obstruction.
+About 75% of myxomas occur in the left atrium of the heart, usually beginning in the wall that divides the two upper chambers of the heart. The rest are in the right atrium, rarely in the left ventricle. Right atrial myxomas are sometimes associated with tricuspid stenosis and atrial fibrillation.
+Myxomas are more common in women. About 10% of myxomas are passed down through families (inherited), as in Carney syndrome, where several other abnormalities are observed, such as skin myxomas, pigmentation, endocrine hyperactivity, schwannomas and epithelioid blue nevi. Such tumors are called familial myxomas. They tend to occur in more than one part of the heart at a time, and often cause symptoms at a younger age than other myxomas.
+A doctor will listen to the heart with stethoscope. A "tumor plop" (a sound related to movement of the tumor), abnormal heart sounds, or a murmur similar to the mid-diastolic rumble of mitral stenosis may be heard. These sounds may change when the patient changes position.
+Right atrial myxomas rarely produce symptoms until they have grown to be at least 13 cm (about 5 inches) wide.
+Tests may include:
+Echocardiogram and Doppler study&Chest x-ray&CT scan of chest&Heart MRI&Left heart angiography&Right heart angiography&ECG—may show atrial fibrillatio
+Blood tests: A FBC may show anemia and increased WBCs (white blood cells). The erythrocyte sedimentation rate (ESR) is usually increased.
+Echocardiogram of atrial myxoma&Play media Echocardiogram showing atrial myxoma[3]&Echocardiogram showing atrial myxoma[3
+Atrial myxoma and myocardium. H&E stain.&Atrial myxoma. H&E stain.&Atrial myxoma. H&E stain.&Atrial myxoma covered by endothelium. H&E stain
+Symptoms may occur at any time, but most often they accompany a change of body position. Pedunculated myxomas can have a "wrecking ball effect", as they lead to stasis and may eventually embolize themselves. Symptoms may include:
+Shortness of breath with activity&Platypnea – Difficulty breathing in the upright position with relief in the supine position&Paroxysmal nocturnal dyspnea – Breathing difficulty when asleep&Dizziness&Fainting&Palpitations – Sensation of feeling your heart beat&Chest pain or tightness&Sudden Death (In which case the disease is an autopsy finding
+The symptoms and signs of left atrial myxomas often mimic mitral stenosis. General symptoms may also be present, such as:
+Cough&Pulmonary edema, as blood backs up into the pulmonary artery, after increased pressures in the left atrium and atrial dilation&Hemoptysis&Fever&Cachexia – Involuntary weight loss&General discomfort (malaise)&Joint pain&Blue discoloration of the skin, especially the fingers (Raynaud's phenomenon)&Fingers that change color upon pressure or with cold or stress&Clubbing – Curvature of nails accompanied with soft tissue enlargement of the fingers&Swelling – any part of the body&Presystolic heart murmur[1
+These general symptoms may also mimic those of infective endocarditis.
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DISNET disease texts/100 Original Disease Texts/Carrion's disease.txt

+Carrion's disease is caused by Bartonella bacilliformis.[4][7] Recent investigations show that Candidatus Bartonella ancashi may cause verruga peruana, although it may not meet all of Koch's postulates. There has been no experimental reproduction of the Peruvian wart in animals and there is little research on the disease's natural spread or impact in native animals.
+Diagnosis during the acute phase can be made by obtaining a peripheral blood smear with Giemsa stain, Columbia blood agar cultures, immunoblot, indirect immunofluorescence, and PCR. Diagnosis during the chronic phase can be made using a Warthin-Starry stain of wart biopsy, PCR, and immunoblot.
+The clinical symptoms of bartonellosis are pleomorphic and some patients from endemic areas may be asymptomatic. The two classical clinical presentations are the acute phase and the chronic phase, corresponding to the two different host cell types invaded by the bacterium (red blood cells and endothelial cells). An individual can be affected by either or both phases.[2][3]
+Acute phase[edit] => It is also called the hematic phase.[2] The most common findings are fever (usually sustained, but with temperature no greater than 102 °F (39 °C)), pale appearance, malaise, painless liver enlargement, jaundice, enlarged lymph nodes, and enlarged spleen. This phase is characterized by severe hemolytic anemia and transient immunosuppression. The case fatality ratios of untreated patients exceeded 40% but reach around 90% when opportunistic infection with Salmonella spp occurs. In a recent study, the attack rate was 13.8% (123 cases) and the case-fatality rate was 0.7%.
+Other symptoms include a headache, muscle aches, and general abdominal pain.[4] Some studies have suggested a link between Carrion's disease and heart murmurs due to the disease's impact on the circulatory system. In children, symptoms of anorexia, nausea, and vomiting have been investigated as possible symptoms of the disease.[2]
+Most of the mortality of Carrion's disease occurs during the acute phase. Studies vary in their estimates of mortality. In one study, mortality has been estimated as low as just 1% in studies of hospitalized patients, to as high as 88% in untreated, unhospitalized patients.[2] In developed countries, where the disease rarely occurs, it is recommended to seek the advice of a specialist in infectious disease when diagnosed.[5] Mortality is often thought to be due to subsequent infections due to the weakened immune symptoms and opportunistic pathogen invasion, or consequences of malnutrition due to weight loss in children.[2][6] In a study focusing on pediatric and gestational effects of the disease, mortality rates for pregnant women with the acute phase were been estimated at 40% and rates of spontaneous abortion in another 40%.[2]
+Chronic phase[edit] => It is also called the eruptive phase or tissue phase, in which the patients develop a cutaneous rash produced by a proliferation of endothelial cells and is known as "Peruvian warts" or "verruga peruana". Depending on the size and characteristics of the lesions, there are three types: miliary (1–4 mm), nodular or subdermic, and mular (>5mm). Miliary lesions are the most common. The lesions often ulcerate and bleed.[4]
+The most common findings are bleeding of verrugas, fever, malaise, arthralgias (joint pain), anorexia, myalgias, pallor, lymphadenopathy, and liver and spleen enlargement.
+On microscopic examination, the chronic phase and its rash are produced by angioblastic hyperplasia, or the increased rates and volume of cell growth in the tissues that form blood vessels. This results in a loss of contact between cells and a loss of normal functioning.[2][7]
+The chronic phase is the more common phase. Mortality during the chronic phase is very low.[2][4]
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DISNET disease texts/100 Original Disease Texts/Cerebral salt-wasting syndrome.txt

+Signs and symptoms of CSWS include large amounts of urination (at least 3 liters of urine output over a 24-hour period for adults) due to inadequate sodium retention in the body, high amounts of sodium in the urine,[1] low blood sodium concentration,[1] excessive thirst, extreme salt cravings, dysfunction of the autonomic nervous system, and dehydration. Patients often self-medicate by naturally gravitating toward a high-sodium diet and by dramatically increasing their water intake. Advanced symptoms include muscle cramps, lightheadedness, dizziness or vertigo, feelings of anxiety or panic (not mentally induced), increased heart rate or slowed heart rate, low blood pressure and orthostatic hypotension sometimes resulting in fainting.[5] Other symptoms frequently associated with dysautonomia include: headaches, pallor, malaise, facial flushing, constipation or diarrhea, nausea, acid reflux, visual disturbances, numbness, nerve pain, trouble breathing, chest pains, loss of consciousness and seizures.[5]
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DISNET disease texts/100 Original Disease Texts/Cerebrovascular disease.txt

+Congenital[edit] => Congenital diseases are medical conditions that are present at birth that may be associated with inherited through genes.[15] Examples of congenital cerebrovascular diseases include arteriovenous malformations, germinal matrix hemorrhage, and CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy).[8] Arteriovenous malformations are abnormal tangles of blood vessels. Usually, a capillary bed separates arteries from veins, which protects the veins from the higher blood pressures that occur in arteries. In arteriovenous malformations, arteries are directly connected to veins, which increases the risk of venous rupture and hemorrhage. Arteriovenous malformations in the brain have a 2–4% chance of rupture each year. However, many arteriovenous malformations go unnoticed and are asymptomatic throughout a person's lifetime.[16]
+A germinal matrix hemorrhage is bleeding into the brain of premature infants caused by the rupture of fragile blood vessels within the germinal matrix of premature babies.[17] The germinal matrix is a highly vascularized area within an unborn infant's brain from which brain cells, including neurons and glial cells, originate. Infants are at most risk to germinal matrix hemorrhages when they are born prematurely, before 32 weeks.[17] The stresses exposed after birth, along with the fragile blood vessels, increase the risk for hemorrhage. Signs and symptoms include flaccid weakness, seizures, abnormal posturing, or irregular respiration.[17]
+CADASIL is an inherited disorder caused by mutations in the Notch 3 gene located on chromosome 19.[18] The Notch 3 gene codes for a transmembrane protein whose function is not well-known. However, the mutation causes accumulation of this protein within small to medium-sized blood vessels.[18] This disease often presents in early adulthood with migraines, stroke, mood disturbances, and cognitive deterioration. MRI shows white matter changes in the brain and also signs of repeated strokes. The diagnosis can be confirmed by gene testing.[19]
+Acquired[edit] => Acquired cerebrovascular diseases are those that are obtained throughout a person's life that may be preventable by controlling risk factors. The incidence of cerebrovascular disease increases as an individual ages.[20] Causes of acquired cerebrovascular disease include atherosclerosis, embolism, aneurysms, and arterial dissections.[8] Atherosclerosis leads to narrowing of blood vessels and less perfusion to the brain, and it also increases the risk of thrombosis, or a blockage of an artery, within the brain. Major modifiable risk factors for atherosclerosis include:[21]
+Hypertension&Smoking&Obesity&Diabetes
+Controlling these risk factors can reduce the incidence of atherosclerosis and stroke.[22] Atrial fibrillation is also a major risk factor for strokes. Atrial fibrillation causes blood clots to form within the heart, which may travel to the arteries within the brain and cause an embolism. The embolism prevents blood flow to the brain, which leads to a stroke.
+An aneurysm is an abnormal bulging of small sections of arteries, which increases the risk of artery rupture. Intracranial aneurysms are a leading cause of subarachnoid hemorrhage, or bleeding around the brain within the subarachnoid space. There are various hereditary disorders associated with intracranial aneurysms, such as Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, and familial hyperaldosteronism type I.[23][24][25] However, individuals without these disorders may also obtain aneurysms. The American Heart Association and American Stroke Association recommend controlling modifiable risk factors including smoking and hypertension.[26]
+Arterial dissections are tears of the internal lining of arteries, often associated with trauma.[27] Dissections within the carotid arteries or vertebral arteries may compromise blood flow to the brain due to thrombosis, and dissections increase the risk of vessel rupture.[28]
+Idiopathic[edit] => Idiopathic diseases are those that occur spontaneously without a known cause.[29] Moyamoya is an example of an idiopathic cerebrovascular disorder that results in narrowing and occlusion of intracranial blood vessels.[8] The most common presentation is stroke or transient ischemic attack, but cognitive decline within children may also be a presenting symptom.[8][11] The disease may begin to show symptoms beginning in adolescence, but some may not have symptoms until adulthood.[11]
+The most common presentation of cerebrovascular diseases is an acute stroke, which occurs when blood supply to the brain is compromised.[11] Symptoms of stroke are usually rapid in onset, and may include weakness of one side of the face or body, numbness on one side of the face or body, inability to produce or understand speech, vision changes, and balance difficulties.[12] Hemorrhagic strokes can present with a very severe, sudden headache associated with vomiting, neck stiffness, and decreased consciousness.[11] Symptoms vary depending on the location and the size of the area of involvement of the stroke. Edema, or swelling, of the brain may occur which increases intracranial pressure and may result in brain herniation. A stroke may result in coma or death if it involves key areas of the brain.[13]
+Other symptoms of cerebrovascular disease include migraines, seizures, epilepsy, or cognitive decline. However, cerebrovascular disease may go undetected for years until an acute stroke occurs. In addition, patients with some rare congenital cerebrovascular diseases may begin to have these symptoms in childhood.[14]
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DISNET disease texts/100 Original Disease Texts/Chlamydia infection.txt

+The diagnosis of genital chlamydial infections evolved rapidly from the 1990s through 2006. Nucleic acid amplification tests (NAAT), such as polymerase chain reaction (PCR), transcription mediated amplification (TMA), and the DNA strand displacement amplification (SDA) now are the mainstays. NAAT for chlamydia may be performed on swab specimens sampled from the cervix (women) or urethra (men), on self-collected vaginal swabs, or on voided urine.[26] NAAT has been estimated to have a sensitivity of approximately 90% and a specificity of approximately 99%, regardless of sampling from a cervical swab or by urine specimen.[27] In women seeking an STI clinic and a urine test is negative, a subsequent cervical swab has been estimated to be positive in approximately 2% of the time.[27]
+At present, the NAATs have regulatory approval only for testing urogenital specimens, although rapidly evolving research indicates that they may give reliable results on rectal specimens.
+Because of improved test accuracy, ease of specimen management, convenience in specimen management, and ease of screening sexually active men and women, the NAATs have largely replaced culture, the historic gold standard for chlamydia diagnosis, and the non-amplified probe tests. The latter test is relatively insensitive, successfully detecting only 60–80% of infections in asymptomatic women, and often giving falsely positive results. Culture remains useful in selected circumstances and is currently the only assay approved for testing non-genital specimens. Other method also exist including: ligase chain reaction (LCR), direct fluorescent antibody resting, enzyme immunoassay, and cell culture.[28]
+Women => Chlamydial infection of the cervix (neck of the womb) is a sexually transmitted infection which has no symptoms for 50–70% of women infected. The infection can be passed through vaginal, anal, or oral sex. Of those who have an asymptomatic infection that is not detected by their doctor, approximately half will develop pelvic inflammatory disease (PID), a generic term for infection of the uterus, fallopian tubes, and/or ovaries. PID can cause scarring inside the reproductive organs, which can later cause serious complications, including chronic pelvic pain, difficulty becoming pregnant, ectopic (tubal) pregnancy, and other dangerous complications of pregnancy.
+Chlamydia is known as the "silent epidemic" as in women, it may not cause any symptoms in 70–80% of cases,[11] and can linger for months or years before being discovered. Signs and symptoms may include abnormal vaginal bleeding or discharge, abdominal pain, painful sexual intercourse, fever, painful urination or the urge to urinate more often than usual (urinary urgency).
+For sexually active women who are not pregnant, screening is recommended in those under 25 and others at risk of infection.[12] Risk factors include a history of chlamydial or other sexually transmitted infection, new or multiple sexual partners, and inconsistent condom use.[13] Guidelines recommend all women attending for emergency contraceptive are offered Chlamydia testing, with studies showing up to 9% of women aged <25 years had Chlamydia.[14]
+Men => In men, those with a chlamydial infection show symptoms of infectious inflammation of the urethra in about 50% of cases.[11] Symptoms that may occur include: a painful or burning sensation when urinating, an unusual discharge from the penis, testicular pain or swelling, or fever. If left untreated, chlamydia in men can spread to the testicles causing epididymitis, which in rare cases can lead to sterility if not treated.[11] Chlamydia is also a potential cause of prostatic inflammation in men, although the exact relevance in prostatitis is difficult to ascertain due to possible contamination from urethritis.[15]
+Chlamydia conjunctivitis or trachoma was once the most important cause of blindness worldwide, but its role diminished from 15% of blindness cases by trachoma in 1995 to 3.6% in 2002.[16][17] The infection can be spread from eye to eye by fingers, shared towels or cloths, coughing and sneezing and eye-seeking flies.[18] Newborns can also develop chlamydia eye infection through childbirth (see below). Using the SAFE strategy (acronym for surgery for in-growing or in-turned lashes, antibiotics, facial cleanliness, and environmental improvements), the World Health Organization aims for the global elimination of trachoma by 2020 (GET 2020 initiative).[19][20]
+Joints => Chlamydia may also cause reactive arthritis—the triad of arthritis, conjunctivitis and urethral inflammation—especially in young men. About 15,000 men develop reactive arthritis due to chlamydia infection each year in the U.S., and about 5,000 are permanently affected by it. It can occur in both sexes, though is more common in men.
+Infants => As many as half of all infants born to mothers with chlamydia will be born with the disease. Chlamydia can affect infants by causing spontaneous abortion; premature birth; conjunctivitis, which may lead to blindness; and pneumonia.[21] Conjunctivitis due to chlamydia typically occurs one week after birth (compared with chemical causes (within hours) or gonorrhea (2–5 days)).
+Other conditions => A different serovar of Chlamydia trachomatis is also the cause of lymphogranuloma venereum, an infection of the lymph nodes and lymphatics. It usually presents with genital ulceration and swollen lymph nodes in the groin, but it may also manifest as rectal inflammation, fever or swollen lymph nodes in other regions of the body.[22]
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DISNET disease texts/100 Original Disease Texts/Cholesterol embolism.txt

+It is relatively unusual (25% of the total number of cases) for cholesterol emboli to occur spontaneously; this usually happens in people with severe atherosclerosis of the large arteries such as the aorta. In the other 75% it is a complication of medical procedures involving the blood vessels, such as vascular surgery or angiography. In coronary catheterization, for instance, the incidence is 1.4%.[5] Furthermore, cholesterol embolism may develop after the commencement of anticoagulants or thrombolytic medication that decrease blood clotting or dissolve blood clots, respectively. They probably lead to cholesterol emboli by removing blood clots that cover up a damaged atherosclerotic plaque; cholesterol-rich debris can then enter the bloodsteam.[3]
+Differential diagnosis[edit] => Findings on general investigations (such as blood tests) are not specific for cholesterol embolism, which makes diagnosis difficult. The main problem is the distinction between cholesterol embolism and vasculitis (inflammation of the small blood vessels), which may cause very similar symptoms - especially the skin findings and the kidney dysfunction.[3] Worsening kidney function after an angiogram may also be attributed to kidney damage by substances used during the procedure (contrast nephropathy). Other causes that may lead to similar symptoms include ischemic renal failure (kidney dysfunction due to an interrupted blood supply), a group of diseases known as thrombotic microangiopathies and endocarditis (infection of the heart valves with small clumps of infected tissue embolizing through the body).[3]
+Blood and urine[edit] => Tests for inflammation (C-reactive protein and the erythrocyte sedimentation rate) are typically elevated, and abnormal liver enzymes may be seen.[3] If the kidneys are involved, tests of renal function (such as urea and creatinine) are elevated.[3] The complete blood count may show particularly high numbers of a type of white blood cell known as eosinophils (more than 0.5 billion per liter); this occurs in only 60-80% of cases, so normal eosinophil counts do not rule out the diagnosis.[3][5] Examination of the urine may show red blood cells (occasionally in casts as seen under the microscope) and increased levels of protein; in a third of the cases with kidney involvement, eosinophils can also be detected in the urine.[3] If vasculitis is suspected, complement levels may be determined as reduced levels are often encountered in vasculitis; complement is a group of proteins that forms part of the innate immune system. Complement levels are frequently reduced in cholesterol embolism, limiting the use of this test in the distinction between vasculitis and cholesterol embolism.[6]
+Tissue diagnosis[edit] => The microscopic examination of tissue (histology) gives the definitive diagnosis. The diagnostic histopathologic finding is intravascular cholesterol crystals, which are seen as cholesterol clefts in routinely processed tissue (embedded in paraffin wax).[7] The cholesterol crystals may be associated with macrophages, including giant cells, and eosinophils.
+The sensitivity of small core biopsies is modest, due to sampling error, as the process is often patchy. Affected organs show the characteristic histologic changes in 50-75% of the clinically diagnosed cases.[3][5] Non-specific tissue findings suggestive of a cholesterol embolization include ischemic changes, necrosis and unstable-appearing complex atherosclerotic plaques (that are cholesterol-laden and have a thin fibrous cap). While biopsy findings may not be diagnostic, they have significant value, as they help exclude alternate diagnoses, e.g. vasculitis, that often cannot be made confidently based on clinical criteria.
+The symptoms experienced in cholesterol embolism depend largely on the organ involved. Non-specific symptoms often described are fever, muscle ache and weight loss. Embolism to the legs causes a mottled appearance and purple discoloration of the toes, small infarcts and areas of gangrene due to tissue death that usually appear black, and areas of the skin that assume a marbled pattern known as livedo reticularis.[3] The pain is usually severe and requires opiates. If the ulcerated plaque is below the renal arteries the manifestations appear in both lower extremities. Very rarely the ulcerated plaque is below the aortic bifurcation and those cases the changes occur only in one lower extremity.
+Kidney involvement leads to the symptoms of renal failure, which are non-specific but usually cause nausea, reduced appetite (anorexia), raised blood pressure (hypertension), and occasionally the various symptoms of electrolyte disturbance such as an irregular heartbeat. Some patients report hematuria (bloody urine) but this may only be detectable on microscopic examination of the urine. Increased amounts of protein in the urine may cause edema (swelling) of the skin (a combination of symptoms known as nephrotic syndrome).[3]
+If emboli have spread to the digestive tract, reduced appetite, nausea and vomiting may occur, as well as nonspecific abdominal pain, gastrointestinal hemorrhage (vomiting blood, or admixture of blood in the stool), and occasionally acute pancreatitis (inflammation of the pancreas).[3]
+Both the central nervous system (brain and spinal cord) and the peripheral nervous system may be involved. Emboli to the brain may cause stroke-like episodes, headache and episodes of loss of vision in one eye (known as amaurosis fugax).[3] Emboli to the eye can be seen by ophthalmoscopy and are known as plaques of Hollenhorst.[4] Emboli to the spinal cord may cause paraparesis (decreased power in the legs) or cauda equina syndrome, a group of symptoms due to loss of function of the distal part of the spinal cord - loss of control over the bladder, rectum and skin sensation around the anus.[3] If the blood supply to a single nerve is interrupted by an embolus, the result is loss of function in the muscles supplied by that nerve; this phenomenon is called a mononeuropathy.[3]
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DISNET disease texts/100 Original Disease Texts/Coccidioidomycosis.txt

+It must rain first to start the cycle of initial growth of the fungus underneath the soil.[11] In soil (and in agar media), Coccidioides exist in filament form. It forms hyphae in both horizontal and vertical directions. Over a prolonged dry period, cells within hyphae degenerate to form alternating barrel-shaped cells (arthroconidia). Arthroconidia are light-weight and carried by air currents. This happens when the soil is disturbed often by clearing trees, construction and farming. As the population grows, so have all these industries, causing a potential cascade effect. The more land that is cleared, the more arid the soil, the riper the environment for Coccidioides.[12] These spores can be easily inhaled without the person knowing. On arriving in alveoli, they enlarge in size to become spherules, and internal septations develop. This division of cells is made possible by the optimal temperature inside the body.[13] Septations develop and form endospores within the spherule. Rupture of spherules release these endospores, which in turn repeat the cycle and spread the infection to adjacent tissues within the body of the infected individual. Nodules can form in lungs surrounding these spherules. When they rupture, they release their contents into bronchi, forming thin-walled cavities. These cavities can result in symptoms like characteristic chest pain, coughing up blood, and persistent cough. In individuals with a weakened immune system, the infection can spread through the blood. On rare occasion it can enter the body through a break in the skin, causing infection.[13]
+Coccidioidomycosis diagnosis relies on a combination of an infected person's signs and symptoms, findings on radiographic imaging, and laboratory results.[1] The disease is commonly misdiagnosed as bacterial community-acquired pneumonia.[1] The fungal infection can be demonstrated by microscopic detection of diagnostic cells in body fluids, exudates, sputum and biopsy tissue by methods of Papanicolaou or Grocott's methenamine silver staining. These stains can demonstrate spherules and surrounding inflammation.
+With specific nucleotide primers, C.immitis DNA can be amplified by polymerase chain reaction (PCR). It can also be detected in culture by morphological identification or by using molecular probes that hybridize with C.immitis RNA. C. immitis and C. posadasii cannot be distinguished on cytology or by symptoms, but only by DNA PCR.
+An indirect demonstration of fungal infection can be achieved also by serologic analysis detecting fungal antigen or host IgM or IgG antibody produced against the fungus. The available tests include the tube-precipitin (TP) assays, complement fixation assays, and enzyme immunoassays. TP antibody is not found in cerebrospinal fluid (CSF). TP antibody is specific and is used as a confirmatory test, whereas ELISA is sensitive and thus used for initial testing.
+If the meninges are affected, CSF will show abnormally low glucose levels in CSF, an increased level of protein in the CSF, and lymphocytic pleocytosis. Rarely, CSF eosinophilia is present.
+Imaging[edit] => Chest x-rays rarely demonstrate nodules or cavities in the lungs, but these images commonly demonstrate lung opacification, pleural effusions, or enlargement of lymph nodes associated with the lungs.[1] Computed tomography scans of the chest are better able to detect these changes than chest x-rays.[1]
+An estimated 60% of people infected with the fungi responsible for coccidioidomycosis have minimal to no symptoms, while 40% will have a range of possible clinical symptoms.[1][7] Of those who do develop symptoms, the primary infection is most often respiratory, with symptoms resembling bronchitis or pneumonia that resolve over a matter of a few weeks. In endemic regions, coccidioidomycosis is responsible for 20% of cases of community-acquired pneumonia.[7] Notable coccidioidomycosis signs and symptoms include a profound feeling of tiredness, fever, cough, headaches, rash, muscle pain, and joint pain.[1] Fatigue can persist for many months after initial infection.[7] The classic triad of coccidioidomycosis known as "desert rheumatism" includes the combination of fever, joint pains, and erythema nodosum.[1]
+Nearly 3% to 5% of infected individuals do not recover from the initial acute infection and develop a chronic infection. This can take the form of chronic lung infection or widespread disseminated infection (affecting the tissues lining the brain, soft tissues, joints, and bone). Chronic infection is responsible for most of the morbidity and mortality. Chronic fibrocavitary disease is manifested by cough, sputum, fevers, night sweats and weight loss.[7] Osteomyelitis, including involvement of the spine, and meningitis which may occur months to years after initial infection. Severe lung disease may develop in HIV-infected persons.[8]
+Types[edit] => After Coccidioides infection, coccidioidomycosis begins with Valley fever, which is its initial acute form. Valley fever may progress to the chronic form and then to disseminated coccidioidomycosis. Therefore, Coccidioidomycosis may be divided into the following types:[9]
+Complications[edit] => Serious complications may occur in patients who have weakened immune systems, including severe pneumonia with respiratory failure and bronchopleural fistulas requiring resection, lung nodules, and possible disseminated form, where the infection spreads throughout the body.[7] The disseminated form of coccidioidomycosis can devastate the body, causing skin ulcers, abscesses, bone lesions, swollen joints with severe pain, heart inflammation, urinary tract problems, and inflammation of the brain's lining, which can lead to death.[10]
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DISNET disease texts/100 Original Disease Texts/Conversion disorder.txt

+Exclusion of neurological disease[edit] => Conversion disorder presents with symptoms that typically resemble a neurological disorder such as stroke, multiple sclerosis, epilepsy or hypokalemic periodic paralysis. The neurologist must carefully exclude neurological disease, through examination and appropriate investigations.[9] However, it is not uncommon for patients with neurological disease to also have conversion disorder.[10]
+In excluding neurological disease, the neurologist has traditionally relied partly on the presence of positive signs of conversion disorder, i.e. certain aspects of the presentation that were thought to be rare in neurological disease but common in conversion. The validity of many of these signs has been questioned, however, by a study showing that they also occur in neurological disease.[11] One such symptom, for example, is la belle indifférence, described in DSM-IV as "a relative lack of concern about the nature or implications of the symptoms". In a later study, no evidence was found that patients with functional symptoms are any more likely to exhibit this than patients with a confirmed organic disease.[12] In DSM-V, la belle indifférence was removed as a diagnostic criteria.
+Another feature thought to be important was that symptoms tended to be more severe on the non-dominant (usually left) side of the body. There have been a number of theories about this, such as the relative involvement of cerebral hemispheres in emotional processing, or more simply, that it was "easier" to live with a functional deficit on the non-dominant side. However, a literature review of 121 studies established that this was not true, with publication bias the most likely explanation for this commonly held view.[13] Although agitation is often assumed to be a positive sign of conversion disorder, release of epinephrine is a well-demonstrated cause of paralysis from hypokalemic periodic paralysis.[14]
+Misdiagnosis does sometimes occur. In a highly influential[15] study from the 1960s, Eliot Slater demonstrated that misdiagnoses had occurred in one third of his 112 patients with conversion disorder.[16] Later authors have argued that the paper was flawed, however,[17][18] and a meta-analysis has shown that misdiagnosis rates since that paper was published are around 4%, the same as for other neurological diseases.[9]
+Exclusion of feigning[edit] => Conversion disorder is unique in ICD-10 in explicitly requiring the exclusion of deliberate feigning. Unfortunately, this is likely to be demonstrable only where the patient confesses, or is "caught out" in a broader deception, such as a false identity.[19] One neuroimaging study suggested that feigning may be distinguished from conversion by the pattern of frontal lobe activation;[20] however, this was a piece of research, rather than a clinical technique.[citation needed] True rates of feigning in medicine remain unknown.[citation needed] However, it is believed that feigning of conversion disorder is no more likely than of other medical conditions.[citation needed]
+Psychological mechanism[edit] => The psychological mechanism of conversion can be the most difficult aspect of a conversion diagnosis. Even if there is a clear antecedent trauma or other possible psychological trigger, it is still not clear exactly how this gives rise to the symptoms observed. Patients with medically unexplained neurological symptoms may not have any psychological stressor, hence the use of the term "functional neurological symptom disorder" in DSM-V as opposed to "conversion disorder", and DSM-V's removal of the need for a psychological trigger.
+Conversion disorder begins with some stressor, trauma, or psychological distress. Usually the physical symptoms of the syndrome affect the senses or movement. Common symptoms include blindness, partial or total paralysis, inability to speak, deafness, numbness, difficulty swallowing, incontinence, balance problems, seizures, tremors, and difficulty walking. These symptoms are attributed to conversion disorder when a medical explanation for the afflictions cannot be found.[6] Symptoms of conversion disorder usually occur suddenly. Conversion disorder is typically seen in individuals aged 10 to 35,[7] and affects between 0.011% and 0.5% of the general population.[8]
+Conversion disorder can present with motor or sensory symptoms including any of the following:
+Motor symptoms or deficits:
+Impaired coordination or balance&Weakness/paralysis of a limb or the entire body (hysterical paralysis or motor conversion disorders)&Impairment or loss of speech (hysterical aphonia)&Difficulty swallowing (dysphagia) or a sensation of a lump in the throat&Urinary retention&Psychogenic non-epileptic seizures or convulsions&Persistent dystonia&Tremor, myoclonus or other movement disorders&Gait problems (astasia-abasia)&Loss of consciousness (fainting
+Sensory symptoms or deficits:
+Impaired vision (hysterical blindness), double vision&Impaired hearing (deafness)&Loss or disturbance of touch or pain sensatio
+Conversion symptoms typically do not conform to known anatomical pathways and physiological mechanisms. It has sometimes been stated that the presenting symptoms tend to reflect the patient's own understanding of anatomy and that the less medical knowledge a person has, the more implausible are the presenting symptoms.[7] However, no systematic studies have yet been performed to substantiate this statement.[citation needed]
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DISNET disease texts/100 Original Disease Texts/Cryoglobulinemia.txt

+Cryoglobulinemia and cryoglobulinemic disease must be distinguished from cryofibrinogenemia or cryofibrinogenemic disease, conditions which involve the cold-induced intravascular deposition of circulating native fibrinogens.[13][14] The cryoglobulins in plasma or serum precipitate at lower temperatures (e.g. 4°C). Since cryofibrinogens are present in plasma but greatly depleted in serum, precipitation tests for them are positive in plasma but negative in serum.[14] Cryofibrinogenemia is occasionally found in cases of cryoglobulinemic disease.[15] Cryoglobulinemic disease must also be distinguished from frostbite as well as numerous other conditions that have a clinical (particularly cutaneous) presentation similar to cryoglobulinemic disease but are not exacerbated by cold temperature, e.g. dysfibrinogenemia and dysfibrinogenemic disease (conditions involving the intravascular deposition of genetically abnormal circulating fibrinogens), purpura fulminans, cholesterol emboli, warfarin necrosis, ecthyma gangrenosum, and various hypercoagulable states.[15]
+Rheumatoid factor is a sensitive test for cryoglobulinemia. The precipitated cryoglobulins are examined by immunoelectrophoresis and immunofixation to detect and quantify the presence of monoclonal IgG, IgM, IgA, κ light chain, or λ light chain immunoglobins. Other routine tests include measuring blood levels of rheumatoid factor activity, complement C4, other complement components, and hepatitic C antigen. Biopsies of skin lesions and, where indicated, kidney or other tissues can help in determining the nature of the vascular disease (immunoglobulin deposition, cryoglobulinemic vasculitis, or, in cases showing the presence of cryfibrinogenemia, fibrinogen deposition. In all events, further studies to determine the presence of hematological, infections, and autoimmune disorders are conducted on the basis of these findings as well as each cases clinical findings.[2][12][15]
+The clinical features of cryoglobulinemic disease can reflect those due not only to the circulation of cryoglobulins but also to any underlying hematological premalignant or malignant disorder, infectious disease, or autoimmune syndrome. The following sections of clinical features focuses on those attributed to the cryoglobulins. Cryoglobulins cause tissue damage by three mechanisms; they can: a) increase blood viscosity thereby reducing blood flow to tissues to cause the hyperviscosity syndrome (i.e. headache, confusion, blurry or loss of vision, hearing loss, and epistaxis; b) deposit in small arteries and capillaries thereby plugging these blood vessels and causing infarction and necrosis of tissues including in particular skin, distal extremities, and kidneys; and c) in type II and type III disease, deposit on the epithelium of blood vessels and activate the blood complement system to form pro-inflammatory elements such as C5a thereby initiating the systemic vascular inflammatory reaction termed cryoglobulinemic vasculitis.[2][9]
+Essential cryoglobulinemic disease[edit] => The signs and symptoms in the increasingly rare cases of cryoglobulinemic disease that cannot be attributed to an underlying disease generally resemble those of patients suffering Type II and III (i.e. mixed) cryoglobulinemic disease.[9][11]
+Type I cryoglobulinemic disease[edit] => Signs and symptoms due to the cryoglobulins of type I disease reflect the hyperviscosity and deposition of cryoglobulins within the blood vessels which reduce or stop blood perfusion to tissues. These events occur particularly in cases where blood cryoglobulin levels of monoclonal IgM are high in patients with IgM MGUS, smoldering Waldenström's macroglobulinemia, or Waldenström's macroglobulinemia and in uncommon cases where the levels of monoclonal IgA, IgG, free κ light chains, or free λ light chains are extremely high in patients with non-IgM MGUS, non-IgM smoldering multiple myeloma, or multiple myeloma. The interruption of blood flow to neurological tissues can cause symptoms of confusion, headache, hearing loss, and peripheral neuropathy. Interruption of blood flow to other tissues in type I disease can cause cutaneous manifestations of purpura, acrocyanosis, necrosis, ulcers, and livedo reticularis; spontaneous nose bleeds, joint pain, membranoproliferative glomerulonephritis; and cardiovascular disturbances such as shortness of breath, hypoxemia, and congestive heart failure.[2][9]
+Types II and III cryoglobulinemic disease[edit] => Types II and III (or mixed or variant) cryoglobulinemic disease may also present with symptoms and signs of blood hyperviscosity and intravascular cryoglobulin deposition but also include those attributable to cryoglobulinemic vasculitis. "Meltzer's triad" of palpable purpura, joint pain, and generalized weakness occurs in ~33% of patients presenting with type II or type III disease. One or more skin lesions including palpable purpura, ulcers, digital gangrene, and areas of necrosis occur in 69-89% of these mixed disease cases (see attached photograph); less common findings include painful peripheral neuropathy (19-44% of cases), kidney disease (primarily membranoproliferative glomerulonephritis (30%), joint pain (28%), and, less commonly, dry eye syndrome, Raynaud phenomenon (i.e. episodic painful reductions in blood flow to the fingers and toes).[9][12] While the glomerulonephritis occurring in mixed disease appears to be due to inflammatory vasculitis, the glomerulonephritis occurring in type I disease appears due to the interruption of blood flow.[12] The hematological, infectious, and autoimmune diseases underlying type II cryoglobulinemic disease and the infectious and autoimmune diseases underlying type III cryoglobulinemic disease are also critical parts of the disease's clinical findings.
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DISNET disease texts/100 Original Disease Texts/Diphtheria.txt

+The current clinical case definition of diphtheria used by the United States' Centers for Disease Control and Prevention is based on both laboratory and clinical criteria.
+Laboratory criteria[edit] => Isolation of C. diphtheriae from a Gram stain or throat culture from a clinical specimen,[9]&Histopathologic diagnosis of diphtheria by Albert's stai
+Clinical criteria[edit] => Upper respiratory tract illness with sore throat&Low-grade fever (above 39 °C (102 °F) is rare)&An adherent, dense, grey pseudomembrane covering the posterior aspect of the pharynx: in severe cases, it can extend to cover the entire tracheobronchial tree
+Case classification[edit] => Probable: a clinically compatible case that is not laboratory-confirmed and is not epidemiologically linked to a laboratory-confirmed case&Confirmed: a clinically compatible case that is either laboratory-confirmed or epidemiologically linked to a laboratory-confirmed cas
+Empirical treatment should generally be started in a patient in whom suspicion of diphtheria is high.
+The symptoms of diphtheria usually begin two to seven days after infection. Symptoms of diphtheria include fever of 38 °C (100.4 °F) or above, chills, fatigue, bluish skin coloration (cyanosis), sore throat, hoarseness, cough, headache, difficulty swallowing, painful swallowing, difficulty breathing, rapid breathing, foul-smelling and bloodstained nasal discharge, and lymphadenopathy.[8][9] Within two to three days, diphtheria may destroy healthy tissues in the respiratory system. The dead tissue forms a thick, gray coating that can build up in the throat or nose. This thick gray coating is called a “pseudomembrane.” It can cover tissues in the nose, tonsils, voice box, and throat, making it very hard to breathe and swallow.[10] Symptoms can also include cardiac arrhythmias, myocarditis, and cranial and peripheral nerve palsies.
+Diphtheritic croup[edit] => Laryngeal diphtheria can lead to a characteristic swollen neck and throat, or "bull neck". The swollen throat is often accompanied by a serious respiratory condition, characterized by a brassy or "barking" cough, stridor, hoarseness, and difficulty breathing, and historically referred to variously as "diphtheritic croup",[11] "true croup",[12][13] or sometimes simply as "croup".[14] Diphtheritic croup is extremely rare in countries where diphtheria vaccination is customary. As a result, the term "croup" nowadays most often refers to an unrelated viral illness that produces similar but milder respiratory symptoms.[15]
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DISNET disease texts/100 Original Disease Texts/Erysipelas.txt

+Most cases of erysipelas are due to Streptococcus pyogenes (also known as beta-hemolytic group A streptococci), although non-group A streptococci can also be the causative agent. Beta-hemolytic, non-group A streptococci include Streptococcus agalactiae, also known as group B strep or GBS. Historically, the face was most affected; today, the legs are affected most often.[3] The rash is due to an exotoxin, not the Streptococcus bacteria, and is found in areas where no symptoms are present; e.g., the infection may be in the nasopharynx, but the rash is found usually on the upper dermis and superficial lymphatics.
+Erysipelas infections can enter the skin through minor trauma, insect bites, dog bites, eczema, athlete's foot, surgical incisions and ulcers and often originate from streptococci bacteria in the subject's own nasal passages. Infection sets in after a small scratch or abrasion spreads, resulting in toxaemia.
+Erysipelas does not affect subcutaneous tissue. It does not release pus, only serum or serous fluid. Subcutaneous edema may lead the physician to misdiagnose it as cellulitis, but the style of the rash is much more well circumscribed and sharply marginated than the rash of cellulitis.
+Risk factors[edit] => This disease is most common among the elderly, infants, and children. People with immune deficiency, diabetes, alcoholism, skin ulceration, fungal infections, and impaired lymphatic drainage (e.g., after mastectomy, pelvic surgery, bypass grafting) are also at increased risk.
+This disease is diagnosed mainly by the appearance of well-demarcated rash and inflammation. Blood cultures are unreliable for diagnosis of the disease, but may be used to test for sepsis. Erysipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, and diffuse inflammatory carcinoma of the breast.
+Erysipelas can be distinguished from cellulitis by its raised advancing edges and sharp borders. Elevation of the antistreptolysin O titer occurs after around 10 days of illness.
+Affected individuals typically develop symptoms including high fevers, shaking, chills, fatigue, headaches, vomiting, and general illness within 48 hours of the initial infection. The erythematous skin lesion enlarges rapidly and has a sharply demarcated, raised edge. It appears as a red, swollen, warm, and painful rash, similar in consistency to an orange peel. More severe infections can result in vesicles (pox or insect bite-like marks), blisters, and petechiae (small purple or red spots), with possible skin necrosis (death). Lymph nodes may be swollen, and lymphedema may occur. Occasionally, a red streak extending to the lymph node can be seen.
+The infection may occur on any part of the skin, including the face, arms, fingers, legs, and toes; it tends to favour the extremities. Fat tissue and facial areas, typically around the eyes, ears, and cheeks, are most susceptible to infection. Repeated infection of the extremities can lead to chronic swelling (lymphangitis).
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DISNET disease texts/100 Original Disease Texts/Erythema nodosum.txt

+EN is associated with a wide variety of conditions, including:
+In about 30–50% of cases, the cause of EN is unknown.[8]
+Streptococcal infection which, in children, is by far the most common precipitant,[7]&Primary infection of Tuberculosis&Mycoplasma pneumoniae&Histoplasma capsulatum&Yersinia&Epstein-Barr virus&Coccidioides immitis (Valley fever)&Cat scratch diseas
+Inflammatory bowel disease (IBD)&Behçet's disease&Sarcoidosi
+Sulfonamides&Penicillins&Oral contraceptives&Bromides&Hepatitis B vaccination[10
+Non-Hodgkins lymphoma (NHL)&Carcinoid tumours&Pancreatic cance
+EN may also be due to excessive antibody production in lepromatous leprosy leading to deposition of immune complexes.[11]
+There is an association with the HLA-B27 histocompatibility antigen, which is present in 65% of patients with erythema nodosum.[12]
+A useful mnemonic for causes is SORE SHINS (Streptococci, OCP, Rickettsia, Eponymous (Behçet), Sulfonamides, Hansen's Disease (Leprosy), IBD, NHL, Sarcoidosis.[13]
+Erythema nodosum is diagnosed clinically. A biopsy can be taken and examined microscopically to confirm an uncertain diagnosis.[3] Microscopic examination usually reveals a neutrophilic infiltrate surrounding capillaries that results in septal thickening, with fibrotic changes in the fat around blood vessels. A characteristic microscopic finding is radial granulomas, well-defined nodular aggregates of histiocytes surrounding a stellate cleft.[4]
+Additional evaluation should be performed to determine the underlying cause of erythema nodosum. This may include a full blood count, erythrocyte sedimentation rate (ESR), antistreptolysin-O (ASO) titer and throat culture, urinalysis, intradermal tuberculin test, and a chest x-ray.[15] The ESR is typically high, the C-reactive protein elevated, and the blood showing an increase in white blood cells.[3]
+The ESR is initially very high, and falls as the nodules of erythema nodosum. The ASO titer is high in cases associated with a streptococcal throat infection. A chest X-ray should be performed to rule out pulmonary diseases, in particular sarcoidosis and Löfgren syndrome.[3]
+Pre-eruptive phase[edit] => The first signs of erythema nodosum are often flu-like symptoms such as a fever, cough, malaise, and aching joints. Some people also experience stiffness or swelling in the joints and weight loss.[2]
+Eruptive stage[edit] => Erythema nodosum is characterised by 1–2-inch (25–51 mm) nodules (rounded lumps) below the skin surface, usually on the shins. These subcutaneous nodules can appear anywhere on the body, but the most common sites are the shins, arms, thighs, and torso. Each nodule typically disappears after around two weeks, though new one may continue to form for up to six or eight weeks.[2] A new nodule usually appears red and is hot and firm to touch. The redness starts to fade and it gradually becomes softer and smaller until it disappears. Each nodule usually heals completely without scarring over the course of about two weeks.[2][3] Joint pain and inflammation sometimes continues for several weeks or months after the nodules appear.[4]
+Less common variants of erythema nodosum include:
+Ulcerating forms, seen in Crohn's disease&Erythema contusiforme, when a subcutaneous hemorrhage (bleeding under the skin) occurs with a erythema nodosum lesion, causing the lesion to look like a contusion (bruise)&Erythema nodosum migrans (also known as subacute nodular migratory panniculitis), a rare form of chronic erythema nodosum characterized by asymmetrical nodules that are mildly tender and migrate over time.[5][6][7
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DISNET disease texts/100 Original Disease Texts/Ethylene glycol poisoning.txt

+As many of the clinical signs and symptoms of ethylene glycol poisoning are nonspecific and occur in many poisonings the diagnosis is often difficult.[24] It is most reliably diagnosed by the measurement of the blood ethylene glycol concentration. Ethylene glycol in biological fluids can be determined by gas chromatography.[25] Many hospital laboratories do not have the ability to perform this blood test and in the absence of this test the diagnosis must be made based on the clinical presentation of the patient.[7] In this situation a helpful test to diagnose poisoning is the measurement of the osmolal gap. The patients' serum osmolality is measured by freezing point depression and then compared with the predicted osmolality based on the patients' measured sodium, glucose, blood urea nitrogen, and any ethanol that may have been ingested. The presence of a large osmolal gap supports a diagnosis of ethylene glycol poisoning. However, a normal osmolar gap does not rule out ethylene glycol exposure because of wide individual variability.[26][27]
+The increased osmolal gap is caused by the ethylene glycol itself. As the metabolism of ethylene glycol progresses there will be less ethylene glycol and this will decrease the blood ethylene glycol concentration and the osmolal gap making this test less useful.[28] Additionally, the presence of other alcohols such as ethanol, isopropanol, or methanol or conditions such as alcoholic or diabetic ketoacidosis, lactic acidosis, or kidney failure may also produce an elevated osmolal gap leading to a false diagnosis.[7]
+Other laboratory abnormalities may suggest poisoning, especially the presence of a metabolic acidosis, particularly if it is characterized by a large anion gap. Large anion gap acidosis is usually present during the initial stage of poisoning. However, acidosis has a large number of differential diagnosis, including poisoning from methanol, salicylates, iron, isoniazid, paracetamol, theophylline, or from conditions such as uremia or diabetic and alcoholic ketoacidosis. The diagnosis of ethylene glycol poisoning should be considered in any patient with a severe acidosis.[7] Urine microscopy can reveal needle or envelope-shaped calcium oxalate crystals in the urine which can suggest poisoning; although these crystals may not be present until the late stages of poisoning.[29] Finally, many commercial radiator antifreeze products have fluorescein added to enable radiator leaks to be detected using a Wood's lamp. Following ingestion of antifreeze products containing ethylene glycol and fluorescein, a Wood's lamp may reveal fluorescence of a patient’s mouth area, clothing, vomitus, or urine which can help to diagnose poisoning.[30][31]
+Signs of ethylene glycol poisoning depend upon the time after ingestion.[6] Symptoms usually follow a three-step progression, although poisoned individuals will not always develop each stage.[7][8]
+Stage 1 (30 minutes to 12 hours) consists of neurological and gastrointestinal symptoms and looks similar to alcohol poisoning.[9] Poisoned individuals may appear to be intoxicated, dizzy, lacking coordination of muscle movements, drooling, depressed,[6] and have slurred speech, seizuring, abnormal eye movements, headaches, and confusion.[9] Irritation to the stomach may cause nausea and vomiting.[7] Also seen are excessive thirst and urination.[9] Over time, the body metabolizes ethylene glycol into other toxins.&Stage 2 (12 to 36 hours) where signs of "alcohol" poisoning appear to resolve, underlying severe internal damage is still occurring.[9] An elevated heart rate, hyperventilation or increased breathing effort, and dehydration may start to develop, along with high blood pressure and metabolic acidosis.[9] These symptoms are a result of accumulation of organic acids formed by the metabolism of ethylene glycol. Additionally low calcium concentrations in the blood, overactive muscle reflexes, muscle spasms, QT interval prolongation, and congestive heart failure may occur. If untreated, death most commonly occurs during this period.[7]&Stage 3 (24 to 72 hours) kidney failure is the result of ethylene glycol poisoning. In cats, this stage occurs 12–24 hours after getting into antifreeze; in dogs, at 36–72 hours after getting into antifreeze.[9] During this stage, severe kidney failure is developing secondary to calcium oxalate crystals forming in the kidneys.[9] Severe lethargy, coma, depression, vomiting, seizures, drooling, and inappetance may be seen.[9] Other symptoms include acute tubular necrosis, red blood cells in the urine, excess proteins in the urine, lower back pain, decreased or absent production of urine, elevated blood concentration of potassium, and acute kidney failure.[10][11] If kidney failure occurs it is typically reversible, although weeks or months of supportive care including hemodialysis may be required before kidney function returns.[7
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DISNET disease texts/100 Original Disease Texts/Felty's syndrome.txt

+The cause of Felty's syndrome is unknown, but it has been found to be more common in those with chronic rheumatoid arthritis. Some patients have Human Leukocytic Antigen (HLA-DR4) in their serum. This syndrome is mostly present in people having extra articular manifestations of rheumatoid arthritis. People with this syndrome are at risk of infection because they have a low white blood cell count.[13]
+This condition affects less than 1% of patients with rheumatoid arthritis.[9] The presence of three conditions: rheumatoid arthritis, an enlarged spleen (splenomegaly), and an abnormally low white blood cell count are indications that Felty's syndrome is possibly occurring. This condition as a whole is difficult to diagnose due to its complexity given a combination of disorders. It is commonly overlooked or misdiagnosed as other conditions (e.g., leukemia, systemic lupus erythrematosus)[3] because of the rarity and lack of good understanding about it. An acronym can be used to make recognizing this disease somewhat easier:
+S: Splenomegaly
+A: Anemia
+N: Neutropenia
+T: Thrombocytopenia
+A: Arthritis (rheumatoid)
+Conditions of the Blood[edit] => A complete blood count (CBC) can be done to diagnose anemia (normochromic, normocytic), thrombocytopenia, and neutropenia.[10] Abnormal liver function tests are commonly used to help in diagnosis as the spleen and liver are strongly affected by one another.
+Splenomegaly[edit] => If rheumatoid arthritis is present and other symptoms occur that are not commonly found within RA itself, such as a palpable spleen, further testing should be done. A palpable spleen is not always a clinical significance, therefore CT scan, MRI, or ultrasound can be administered in order to help diagnose the condition. According to Poulin et al, dimensional guidelines for diagnosing splenomegaly are as follows:[11]
+Moderate if the largest dimension is 11-20 cm&Severe if the largest dimension is greater than 20 c
+Rheumatoid Arthritis[edit] => RA in patients with Felty's syndrome is chronic (after 10-15 years), and presents with increased severity along with extra articular manifestations.[6] RA can be mistaken for other conditions such as gout if not clinically diagnosed. Diagnosis can be confirmed by use of X-rays or synovial fluid analysis. [12]
+The symptoms of Felty's syndrome are similar to those of rheumatoid arthritis. Patients suffer from painful, stiff, and swollen joints, most commonly in the joints of the hands, feet, and arms. In some affected individuals, Felty's syndrome may develop during a period when the symptoms and physical findings associated with rheumatoid arthritis have subsided or are not present; in this case, Felty's syndrome may remain undiagnosed. In more rare instances, the development of Felty's syndrome may precede the development of the symptoms and physical findings associated with rheumatoid arthritis.
+Felty's syndrome is also characterized by an abnormally enlarged spleen (splenomegaly) and abnormally low levels of certain white blood cells (neutropenia). As a result of neutropenia, affected individuals are increasingly susceptible to certain infections. Keratoconjunctivitis sicca may occur due to secondary Sjorgen's syndrome. Individuals with Felty's syndrome may also experience fever, weight loss, and/or fatigue. In some cases, affected individuals may have discoloration (abnormal brown pigmentation) of the skin, particularly of the leg, sores (ulcers) on the lower leg, and/or an abnormally large liver (hepatomegaly). In addition, affected individuals may have abnormally low levels of circulating red blood cells (anemia), a decrease in circulating blood platelets that assist in blood clotting functions (thrombocytopenia), abnormal liver function tests and/or inflammation of the blood vessels (vasculitis).[8]
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DISNET disease texts/100 Original Disease Texts/Food intolerance.txt

+Reactions to chemical components of the diet are more common than true food allergies.[citation needed] Although, there is no evidence to support this. They are caused by various organic chemicals occurring naturally in a wide variety of foods, both of animal and vegetable origin more often than to food additives, preservatives, colourings and flavourings, such as sulfites or dyes.[13] Both natural and artificial ingredients may cause adverse reactions in sensitive people if consumed in sufficient amount, the degree of sensitivity varying between individuals.
+Pharmacological responses to naturally occurring compounds in food, or chemical intolerance, can occur in individuals from both allergic and non-allergic family backgrounds. Symptoms may begin at any age, and may develop quickly or slowly. Triggers may range from a viral infection or illness to environmental chemical exposure. It occurs more commonly in women, which may be because of hormone differences, as many food chemicals mimic hormones.[citation needed]
+A deficiency in digestive enzymes can also cause some types of food intolerances. Lactose intolerance is a result of the body not producing sufficient lactase to digest the lactose in milk;[25][26] dairy foods which are lower in lactose, such as cheese, are less likely to trigger a reaction in this case. Another carbohydrate intolerance caused by enzyme deficiency is hereditary fructose intolerance.
+Celiac disease, an autoimmune disorder caused by an immune response to the protein gluten, results in gluten intolerance and can lead to temporary lactose intolerance.[27][28]
+The most widely distributed naturally occurring food chemical capable of provoking reactions is salicylate,[18] although tartrazine and benzoic acid are well recognised in susceptible individuals.[29][30][31] Benzoates and salicylates occur naturally in many foods, including fruits, juices, vegetables, spices, herbs, nuts, tea, wines, and coffee. Salicylate sensitivity causes reactions to not only aspirin and NSAIDs but also foods in which salicylates naturally occur, such as cherries.
+Other natural chemicals which commonly cause reactions and cross reactivity include amines, nitrates, sulphites and some antioxidants. Chemicals involved in aroma and flavour are often suspect.[20][32][33][34]
+The classification or avoidance of foods based on botanical families bears no relationship to their chemical content and is not relevant in the management of food intolerance.[citation needed]
+Salicylate-containing foods include apples, citrus fruits, strawberries, tomatoes, and wine, while reactions to chocolate, cheese, bananas, avocado, tomato or wine point to amines as the likely food chemical. Thus, exclusion of single foods does not necessarily identify the chemical responsible as several chemicals can be present in a food, the patient may be sensitive to multiple food chemicals and reaction more likely to occur when foods containing the triggering substance are eaten in a combined quantity that exceeds the patient's sensitivity thresholds. People with food sensitivities have different sensitivity thresholds, and so more sensitive people will react to much smaller amounts of the substance.[5][9][20][33][34] [35][36][37][38][39]
+Diagnosis of food intolerance can include hydrogen breath testing for lactose intolerance and fructose malabsorption, professionally supervised elimination diets, and ELISA testing for IgG-mediated immune responses to specific foods. It is important to be able to distinguish between food allergy, food intolerance, and autoimmune disease in the management of these disorders.[41] Non-IgE-mediated intolerance is more chronic, less acute, less obvious in its clinical presentation, and often more difficult to diagnose than allergy, as skin tests and standard immunological studies are not helpful.[8] Elimination diets must remove all poorly tolerated foods, or all foods containing offending compounds. Clinical investigation is generally undertaken only for more serious cases, as for minor complaints which do not significantly limit the person's lifestyle the cure may be more inconvenient than the problem.[5]
+IgG4 tests are invalid; IgG4 presence indicates that the person has been repeatedly exposed to food proteins recognized as foreign by the immune system which is a normal physiological response of the immune system after exposure to food components.[42][1] Although elimination of foods based on IgG-4 testing in IBS patients resulted in an improvement in symptoms,[43] the positive effects of food elimination were more likely due to wheat and milk elimination than IgG-4 test-determined factors.[44] The IgG-4 test specificity is questionable as healthy individuals with no symptoms of food intolerance also test positive for IgG-4 to several foods.[45]
+Diagnosis is made using medical history and cutaneous and serological tests to exclude other causes, but to obtain final confirmation a Double Blind Controlled Food Challenge must be performed.[6] Treatment can involve long-term avoidance,[46] or if possible re-establishing a level of tolerance.
+Today there are many methods available such as Cytotoxic testing, MRT testing, Elisa Testing and Microarray Elisa Testing. Allergy US reviewed these methods and Microarray technology appears to be the most reliable among them. http://allergyus.com/food-intolerance-tests-in-usa/.[47][48][49]
+Food intolerance is more chronic, less acute, less obvious in its presentation, and often more difficult to diagnose than a food allergy.[8] Symptoms of food intolerance vary greatly, and can be mistaken for the symptoms of a food allergy. While true allergies are associated with fast-acting immunoglobulin IgE responses, it can be difficult to determine the offending food causing a food intolerance because the response generally takes place over a prolonged period of time. Thus, the causative agent and the response are separated in time, and may not be obviously related. Food intolerance symptoms usually begin about half an hour after eating or drinking the food in question, but sometimes symptoms may be delayed by up to 48 hours.[9]
+Food intolerance can present with symptoms affecting the skin, respiratory tract, gastrointestinal tract (GIT) either individually or in combination. On the skin may include skin rashes, urticaria (hives),[10] angioedema,[11] dermatitis,[12] and eczema.[13] Respiratory tract symptoms can include nasal congestion, sinusitis, pharyngeal irritations, asthma and an unproductive cough. GIT symptoms include mouth ulcers, abdominal cramp, nausea, gas, intermittent diarrhea, constipation, irritable bowel syndrome (IBS),[6][7][9] and may include anaphylaxis.[13]
+Food intolerance has been found associated with irritable bowel syndrome and inflammatory bowel disease,[14] chronic constipation,[15] chronic hepatitis C infection,[16] eczema,[17] NSAID intolerance,[18] respiratory complaints,[19] including asthma,[20] rhinitis and headache,[21][22] functional dyspepsia,[23] eosinophilic esophagitis[9] and ENT illnesses.[21][24]
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DISNET disease texts/100 Original Disease Texts/GM1 gangliosidoses.txt

+Types[edit] => GM1 has three forms: early infantile, late infantile, and adult.
+Early infantile GM1[edit] => Symptoms of early infantile GM1 (the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver enlargement (hepatomegaly), spleen enlargement (splenomegaly), coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response to sound, and problems with gait.
+About half of affected patients develop cherry-red spots in the eye.
+Children may be deaf and blind by age 1 and often die by age 3 from cardiac complications or pneumonia.[1]
+Autosomal recessive disorder; beta-galactosidase deficiency; neuronal storage of GM1 ganglioside and visceral storage of galactosyl oligosaccharides and keratan sulfate.&Early psychomotor deterioration: decreased activity and lethargy in the first weeks; never sit; feeding problems - failure to thrive; visual failure (nystagmus noted) by 6 months; initial hypotonia; later spasticity with pyramidal signs; secondary microcephaly develops; decerebrate rigidity by 1 year and death by age 1–2 years (due to pneumonia and respiratory failure); some have hyperacusis.&Macular cherry-red spots in 50% by 6–10 months; corneal opacities in some&Facial dysmorphology: frontal bossing, wide nasal bridge, facial edema (puffy eyelids); peripheral edema, epicanthus, long upper lip, microretrognathia, gingival hypertrophy (thick alveolar ridges), macroglossia&Hepatomegaly by 6 months and splenomegaly later; some have cardiac failure&Skeletal deformities: flexion contractures noted by 3 months; early subperiosteal bone formation (may be present at birth); diaphyseal widening later; demineralization; thoracolumbar vertebral hypoplasia and beaking at age 3–6 months; kyphoscoliosis. *Dysostosis multiplex (as in the mucopolysaccharidoses)&10–80% of peripheral lymphocytes are vacuolated; foamy histiocytes in bone marrow; visceral mucopolysaccharide storage similar to that in Hurler disease; GM1 storage in cerebral gray matter is 10-fold elevated (20–50-fold increased in viscera)&Galactose-containing oligosacchariduria and moderate keratan sulfaturia&Morquio disease Type B: Mutations with higher residual beta-galactosidase activity for the GM1 substrate than for keratan sulfate and other galactose-containing oligosaccharides have minimal neurologic involvement but severe dysostosis resembling Morquio disease type A (Mucopolysaccharidosis type 4)
+[2]
+Late infantile GM1[edit] => Onset of late infantile GM1 is typically between ages 1 and 3 years.
+Neurological symptoms include ataxia, seizures, dementia, and difficulties with speech.
+Adult GM1[edit] => Onset of adult GM1 is between ages 3 and 30.
+Symptoms include muscle atrophy, neurological complications that are less severe and progress at a slower rate than in other forms of the disorder, corneal clouding in some patients, and dystonia (sustained muscle contractions that cause twisting and repetitive movements or abnormal postures). Angiokeratomas may develop on the lower part of the trunk of the body. Most patients have a normal size liver and spleen.
+Prenatal diagnosis is possible by measurement of Acid Beta Galactosidase in cultured amniotic cells.
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DISNET disease texts/100 Original Disease Texts/Gastroparesis.txt

+Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.
+It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves.[6] The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis.[7] Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease.[8] It may also occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis.
+Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery.[9] Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.
+Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection.[citation needed] Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.
+Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.[10] A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest.[4] Neither theory has been proven definitively.
+Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency,[citation needed] as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCl) in order to properly empty itself of a meal.
+Gastroparesis can be diagnosed with tests such as x-rays, manometry, and gastric emptying scans.[11] The clinical definition for gastroparesis is based solely on the emptying time of the stomach (and not on other symptoms), and severity of symptoms does not necessarily correlate with the severity of gastroparesis. Therefore, some patients may have marked gastroparesis with few, if any, serious complications.[citation needed]
+The most common symptoms of gastroparesis are the following:[2]
+Chronic nausea (93%)&Vomiting (especially of undigested food) (68–84%)&Abdominal pain (46–90%)&A feeling of fullness after eating just a few bites (60–86%
+Other symptoms include the following:
+Abdominal bloating&Body aches (myalgia)&Erratic blood glucose levels&Gastroesophageal reflux (GERD)&Heartburn&Lack of appetite&Morning nausea&Muscle weakness&Night sweats&Palpitations&Spasms of the stomach wall&Constipation or infrequent bowel movements&Weight loss, malnutrition&Weight gain[3
+Morning nausea may also indicate gastroparesis. Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.[4]
+Primary complications of gastroparesis include:
+Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)[5]&General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it&Severe fatigue and weight loss due to calorie deficit&Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)[5]&Bacterial infection due to overgrowth in undigested food[5
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DISNET disease texts/100 Original Disease Texts/Generalized anxiety disorder.txt

+Genetics[edit] => Genes are attributed about a third of general anxiety disorder's variance.[13] Individuals with a genetic predisposition for GAD are more likely to develop GAD, especially in response to a life stressor.[14]
+Substance-induced[edit] => Long-term use of benzodiazepines can worsen underlying anxiety,[15][16] with evidence that reduction of benzodiazepines can lead to a lessening of anxiety symptoms.[17] Similarly, long-term alcohol use is associated with anxiety disorders,[18] with evidence that prolonged abstinence can result in a disappearance of anxiety symptoms.[19] However, it can take up to two years for anxiety symptoms to return to baseline in about a quarter of people recovering from alcoholism.[20]
+In one study in 1988–90, illness in approximately half of patients attending mental health services at British hospital psychiatric clinic, for conditions including anxiety disorders such as panic disorder or social phobia, was determined to be the result of alcohol or benzodiazepine dependence. In these patients, anxiety symptoms, while worsening initially during the withdrawal phase, disappeared with abstinence from benzodiazepines or alcohol. Sometimes anxiety pre-existed alcohol or benzodiazepine dependence, but the dependence was acting to keep the anxiety disorders going and often progressively making them worse. Recovery from benzodiazepines tends to take a lot longer than recovery from alcohol, but people can regain their previous good health.[20]
+Tobacco smoking has been established as a risk factor for developing anxiety disorders.[21] Excessive caffeine usage has been linked to anxiety.[22]
+DSM-5 criteria[edit] => The diagnostic criteria for GAD as defined by the Diagnostic and Statistical Manual of Mental Disorders DSM-5 (2013),[2] published by the American Psychiatric Association, are paraphrased as follows:[2]
+Too much anxiety or worry over more than six months. This is present most of the time in regards to many activities.&Inability to manage these symptoms&At least three of the following occur: Note: Only one item is required in children. Restlessness Tires easily Problems concentrating Irritability Muscle tension. Problems with sleep&Restlessness&Tires easily&Problems concentrating&Irritability&Muscle tension.&Problems with sleep&Symptoms result in problems with functioning.&Symptoms are not due to medications, drugs, other physical health problems&Symptoms do not fit better with another psychiatric problem such as panic disorde
+No major changes to GAD have occurred since publication of the Diagnostic and Statistical Manual of Mental Disorders (2004); minor changes include wording of diagnostic criteria.[24]
+ICD-10 criteria[edit] => ICD-10 Generalized anxiety disorder "F41.1"[25] Note: For children different criteria may be applied (see F93.80).
+A period of at least six months with prominent tension, worry, and feelings of apprehension, about everyday events and problems.&At least four symptoms out of the following list of items must be present, of which at least one from items (1) to (4). Autonomic arousal symptoms (1) Palpitations or pounding heart, or accelerated heart rate. (2) Sweating. (3) Trembling or shaking. (4) Dry mouth (not due to medication or dehydration). Symptoms concerning chest and abdomen (5) Difficulty breathing. (6) Feeling of choking. (7) Chest pain or discomfort. (8) Nausea or abdominal distress (e.g. churning in the stomach). Symptoms concerning brain and mind (9) Feeling dizzy, unsteady, faint or light-headed. (10) Feelings that objects are unreal (derealization), or that one's self is distant or "not really here" (depersonalization). (11) Fear of losing control, going crazy, or passing out. (12) Fear of dying. General symptoms (13) Hot flashes or cold chills. (14) Numbness or tingling sensations. Symptoms of tension (15) Muscle tension or aches and pains. (16) Restlessness and inability to relax. (17) Feeling keyed up, or on edge, or of mental tension. (18) A sensation of a lump in the throat or difficulty with swallowing. Other non-specific symptoms (19) Exaggerated response to minor surprises or being startled. (20) Difficulty in concentrating or mind going blank, because of worrying or anxiety. (21) Persistent irritability. (22) Difficulty getting to sleep because of worrying.&The disorder does not meet the criteria for panic disorder (F41.0), phobic anxiety disorders (F40.-), obsessive-compulsive disorder (F42.-) or hypochondriacal disorder (F45.2).&Most commonly used exclusion criteria: not sustained by a physical disorder, such as hyperthyroidism, an organic mental disorder (F0) or psychoactive substance-related disorder (F1), such as excess consumption of amphetamine-like substances, or withdrawal from benzodiazepines.[5
+History of diagnosis[edit] => The American Psychiatric Association introduced GAD as a diagnosis in the DSM-III in 1980, when anxiety neurosis was split into GAD and panic disorder. [26] The definition in the DSM-III required uncontrollable and diffuse anxiety or worry that is excessive and unrealistic and persists for 1 month or longer. High rates in comorbidity of GAD and major depression led many commentators to suggest that GAD would be better conceptualized as an aspect of major depression instead of an independent disorder.[27] Many critics stated that the diagnostic features of this disorder were not well established until the DSM-III-R.[28] Since comorbidity of GAD and other disorders decreased with time, the DSM-III-R changed the time requirement for a GAD diagnosis to 6 months or longer.[29] The DSM-IV changed the definition of excessive worry and the number of associated psychophysiological symptoms required for a diagnosis.[27] Another aspect of the diagnosis the DSM-IV clarified was what constitutes a symptom as occurring "often".[30] The DSM-IV also required difficulty controlling the worry to be diagnosed with GAD. The DSM-5 emphasized that excessive worrying had to occur more days than not and on a number of different topics.[28] It has been stated that the constant changes in the diagnostic features of the disorder have made assessing epidemiological statistics such as prevalence and incidence difficult, as well as increasing the difficulty for researchers in identifying the biological and psychological underpinnings of the disorder. Consequently, making specialized medications for the disorder is more difficult as well. This has led to the continuation of GAD being medicated heavily with SSRIs.[28]
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DISNET disease texts/100 Original Disease Texts/Helicobacter pylori.txt

+Colonization with H. pylori is not a disease in and of itself, but a condition associated with a number of disorders of the upper gastrointestinal tract.[13] Testing for H. pylori is recommended if peptic ulcer disease or low-grade gastric MALT lymphoma is present, after endoscopic resection of early gastric cancer, first-degree relatives with gastric cancer, and in certain cases of dyspepsia,[64] not routinely.[13] Several ways of testing exist. One can test noninvasively for H. pylori infection with a blood antibody test, stool antigen test, or with the carbon urea breath test (in which the patient drinks 14C—or 13C-labelled urea, which the bacterium metabolizes, producing labelled carbon dioxide that can be detected in the breath).[64] Also, a urine ELISA test with a 96% sensitivity and 79% specificity is available. None of the test methods is completely failsafe. Even biopsy is dependent on the location of the biopsy. Blood antibody tests, for example, range from 76% to 84% sensitivity. Some drugs can affect H. pylori urease activity and give false negatives with the urea-based tests. The most accurate method for detecting H. pylori infection is with a histological examination from two sites after endoscopic biopsy, combined with either a rapid urease test or microbial culture.[65]
+Up to 85% of people infected with H. pylori never experience symptoms or complications.[10] Acute infection may appear as an acute gastritis with abdominal pain (stomach ache) or nausea.[3] Where this develops into chronic gastritis, the symptoms, if present, are often those of non-ulcer dyspepsia: stomach pains, nausea, bloating, belching, and sometimes vomiting or black stool.[11][12]
+Individuals infected with H. pylori have a 10 to 20% lifetime risk of developing peptic ulcers and a 1 to 2% risk of acquiring stomach cancer.[5][13] Inflammation of the pyloric antrum is more likely to lead to duodenal ulcers, while inflammation of the corpus (body of the stomach) is more likely to lead to gastric ulcers and gastric carcinoma.[14][15] However, H. pylori possibly plays a role only in the first stage that leads to common chronic inflammation, but not in further stages leading to carcinogenesis.[9] A meta-analysis conducted in 2009 concluded the eradication of H. pylori reduces gastric cancer risk in previously infected individuals, suggesting the continued presence of H. pylori constitutes a relative risk factor of 65% for gastric cancers; in terms of absolute risk, the increase was from 1.1% to 1.7%.[16]
+H. pylori has been associated with colorectal polyps and colorectal cancer.[17] It may also be associated with eye disease.[18]
+Pain typically occurs when the stomach is empty, between meals and in the early morning hours, but it can also occur at other times. Less common ulcer symptoms include nausea, vomiting, and loss of appetite. Bleeding can also occur; prolonged bleeding may cause anemia leading to weakness and fatigue. If bleeding is heavy, hematemesis, hematochezia, or melena may occur.[19]
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DISNET disease texts/100 Original Disease Texts/Hemolytic-uremic syndrome.txt

+The similarities between HUS, aHUS, and TTP make differential diagnosis essential.[7][8] All three of these systemic TMA-causing diseases are characterized by thrombocytopenia[14] and microangiopathic hemolysis,[6][14] plus one or more of the following: neurological symptoms (e.g., confusion,[6][22] cerebral convulsions,[22] seizures[19]); renal impairment[14] (e.g., elevated creatinine,[15] decreased estimated glomerular filtration rate [eGFR],[15] abnormal urinalysis[44]); and gastrointestinal (GI) symptoms (e.g., diarrhea,[17][20] nausea/vomiting,[19] abdominal pain,[19] gastroenteritis[14][17]).The presence of diarrhea does not exclude aHUS as the cause of TMA, as 28% of patients with aHUS present with diarrhea and/or gastroenteritis.[16][17] First diagnosis of aHUS is often made in the context of an initial, complement-triggering infection, and Shiga-toxin has also been implicated as a trigger that identifies patients with aHUS.[39] Additionally, in one study, mutations of genes encoding several complement regulatory proteins were detected in 8 of 36 (22%) patients diagnosed with STEC-HUS.[45] However, the absence of an identified complement regulatory gene mutation does not preclude aHUS as the cause of the TMA, as approximately 50% of patients with aHUS lack an identifiable mutation in complement regulatory genes.[17]
+Diagnostic work-up supports the differential diagnosis of TMA-causing diseases. A positive Shiga-toxin/EHEC test confirms a cause for STEC-HUS,[23][31] and severe ADAMTS13 deficiency (i.e., ≤5% of normal ADAMTS13 levels) confirms a diagnosis of TTP.[46]
+STEC-HUS occurs after ingestion of a strain of bacteria expressing Shiga toxin(s), usually types of E. coli, that expresses verotoxin (also called Shiga-like toxin). E. coli can produce stx1 and/or stx2 Shiga toxins, the latter being more dangerous. A combination of both toxins in certain ratios is usually associated with HUS. These Shiga toxins bind GB3 receptors, globotriaosylceramide, which are present in renal tissue more than any other tissue and are also found in central nervous system neurons and other tissue. Children have more GB3 receptors than adults which may be why children are more susceptible to HUS. Cattle, swine, deer, and other mammals do not have GB3 receptors, but can be asymptomatic carriers of Shiga toxin-producing bacteria. Some humans can also be asymptomatic carriers. Once the bacteria colonizes, diarrhea followed by bloody diarrhea, hemorrhagic colitis, typically follows. HUS develops about 5–10 days after onset of diarrhea, with decreased urine output (oliguria), blood in the urine (hematuria), kidney failure, thrombocytopenia (low levels of platelets) and destruction of red blood cells (microangiopathic hemolytic anemia). Hypertension is common. In some cases, there are prominent neurologic changes.[9][10][11]
+Patients with HUS commonly exhibit the signs and symptoms of thrombotic microangiopathy (TMA), which can include abdominal pain,[12] low platelet count,[13] elevated lactate dehydrogenase LDH, a chemical released from damaged cells, and which is therefore a marker of cellular damage)[14] decreased haptoglobin (indicative of the breakdown of red blood cells)[14] anemia (low red blood cell count)/schistocytes (damaged red blood cells),[13][14] elevated creatinine (a protein waste product generated by muscle metabolism and eliminated renally,[15] proteinuria (indicative of kidney injury),[16] confusion,[12] fatigue,[17] edema (swelling),[18] nausea/vomiting,[19] and diarrhea.[20] Additionally, patients with aHUS typically present with an abrupt onset of systemic signs and symptoms such as acute kidney failure,[13] hypertension (high blood pressure),[17] myocardial infarction (heart attack),[21] stroke,[12] lung complications,[21] pancreatitis (inflammation of the pancreas),[19] liver necrosis (death of liver cells or tissue),[13][17] encephalopathy (brain dysfunction),[17] seizure,[22] and coma.[23] Failure of neurologic, cardiac, renal, and gastrointestinal (GI) organs, as well as death, can occur unpredictably at any time, either very quickly or following prolonged symptomatic or asymptomatic disease progression.[6][7][13][16][24]
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DISNET disease texts/100 Original Disease Texts/Herpes labialis.txt

+Herpes labialis infection occurs when the herpes simplex virus comes into contact with oral mucosal tissue or abraded skin of the mouth. Infection by the type 1 strain of herpes simplex virus (HSV-1) is most common; however, cases of oral infection by the type 2 strain are increasing.[11] Specifically, type 2 has been implicated as causing 10–15% of oral infections.
+Cold sores are the result of the virus reactivating in the body. Once HSV-1 has entered the body, it never leaves. The virus moves from the mouth to remain latent in the central nervous system. In approximately one-third of people, the virus can "wake up" or reactivate to cause disease. When reactivation occurs, the virus travels down the nerves to the skin where it may cause blisters (cold sores) around the lips, in the mouth or, in about 10% of cases, on the nose, chin, or cheeks.
+Cold sore outbreaks may be influenced by stress, menstruation, sunlight, sunburn, fever, dehydration, or local skin trauma. Surgical procedures such as dental or neural surgery, lip tattooing, or dermabrasion are also common triggers. HSV-1 can in rare cases be transmitted to newborn babies by family members or hospital staff who have cold sores; this can cause a severe disease called neonatal herpes simplex.
+The colloquial term for this condition, "cold sore" comes from the fact that herpes labialis is often triggered by fever, for example, as may occur during an upper respiratory tract infection (i.e. a cold).[15]
+People can transfer the virus from their cold sores to other areas of the body, such as the eye, skin, or fingers; this is called autoinoculation. Eye infection, in the form of conjunctivitis or keratitis, can happen when the eyes are rubbed after touching the lesion. Finger infection (herpetic whitlow) can occur when a child with cold sores or primary HSV-1 infection sucks his fingers.
+Blood tests for herpes may differentiate between type 1 and type 2. When a person is not experiencing any symptoms, a blood test alone does not reveal the site of infection. Genital herpes infections occurred with almost equal frequency as type 1 or 2 in younger adults when samples were taken from genital lesions. Herpes in the mouth is more likely to be caused by type 1, but (see above) also can be type 2. The only way to know for certain if a positive blood test for herpes is due to infection of the mouth, genitals, or elsewhere, is to sample from lesions. This is not possible if the afflicted individual is asymptomatic.
+Herpes infections usually show no symptoms;[1] when symptoms do appear they typically resolve within two weeks.[11] The main symptom of oral infection is inflammation of the mucosa of the cheek and gums—known as acute herpetic gingivostomatitis—which occurs within 5–10 days of infection. Other symptoms may also develop, including headache, nausea, dizziness and painful ulcers—sometimes confused with canker sores—fever, and sore throat.[11]
+Primary HSV infection in adolescents frequently manifests as severe pharyngitis with lesions developing on the cheek and gums. Some individuals develop difficulty in swallowing (dysphagia) and swollen lymph nodes (lymphadenopathy).[11] Primary HSV infections in adults often results in pharyngitis similar to that observed in glandular fever (infectious mononucleosis), but gingivostomatitis is less likely.
+Recurrent oral infection is more common with HSV-1 infections than with HSV-2. Symptoms typically progress in a series of eight stages:
+Latent (weeks to months incident-free): The remission period; After initial infection, the viruses move to sensory nerve ganglia (trigeminal ganglion),[12] where they reside as lifelong, latent viruses. Asymptomatic shedding of contagious virus particles can occur during this stage.&Prodromal (day 0–1): Symptoms often precede a recurrence. Symptoms typically begin with tingling (itching) and reddening of the skin around the infected site. This stage can last from a few days to a few hours preceding the physical manifestation of an infection and is the best time to start treatment.&Inflammation (day 1): Virus begins reproducing and infecting cells at the end of the nerve. The healthy cells react to the invasion with swelling and redness displayed as symptoms of infection.&Pre-sore (day 2–3): This stage is defined by the appearance of tiny, hard, inflamed papules and vesicles that may itch and are painfully sensitive to touch. In time, these fluid-filled blisters form a cluster on the lip (labial) tissue, the area between the lip and skin (vermilion border), and can occur on the nose, chin, and cheeks.&Open lesion (day 4): This is the most painful and contagious of the stages. All the tiny vesicles break open and merge to create one big, open, weeping ulcer. Fluids are slowly discharged from blood vessels and inflamed tissue. This watery discharge is teeming with active viral particles and is highly contagious. Depending on the severity, one may develop a fever and swollen lymph glands under the jaw.[13]&Crusting (day 5–8): A honey/golden crust starts to form from the syrupy exudate. This yellowish or brown crust or scab is not made of active virus but from blood serum containing useful proteins such as immunoglobulins. This appears as the healing process begins. The sore is still painful at this stage, but, more painful, however, is the constant cracking of the scab as one moves or stretches their lips, as in smiling or eating. Virus-filled fluid will still ooze out of the sore through any cracks.&Healing (day 9–14): New skin begins to form underneath the scab as the virus retreats into latency. A series of scabs will form over the sore (called Meier Complex), each one smaller than the last. During this phase irritation, itching, and some pain are common.&Post-scab (12–14 days): A reddish area may linger at the site of viral infection as the destroyed cells are regenerated. Virus shedding can still occur during this stage
+The recurrent infection is thus often called herpes simplex labialis. Rare reinfections occur inside the mouth (intraoral HSV stomatitis) affecting the gums, alveolar ridge, hard palate, and the back of the tongue, possibly accompanied by herpes labialis.[11]
+A lesion caused by herpes simplex can occur in the corner of the mouth and be mistaken for angular cheilitis of another cause. Sometimes termed "angular herpes simplex".[14] A cold sore at the corner of the mouth behaves similarly to elsewhere on the lips. Rather than utilizing antifungal creams, angular herpes simplex is treated in the same way as a cold sore, with topical antiviral drugs.
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DISNET disease texts/100 Original Disease Texts/Hypercalcaemia.txt

+Primary hyperparathyroidism and malignancy account for about 90% of cases of hypercalcaemia.[8][9]
+Parathyroid function[edit] => Primary hyperparathyroidism Solitary parathyroid adenoma Primary parathyroid hyperplasia Parathyroid carcinoma Multiple endocrine neoplasia (MEN1 & MEN2A) Familial isolated hyperparathyroidism[10]&Solitary parathyroid adenoma&Primary parathyroid hyperplasia&Parathyroid carcinoma&Multiple endocrine neoplasia (MEN1 & MEN2A)&Familial isolated hyperparathyroidism[10]&Lithium use&Familial hypocalciuric hypercalcemia/familial benign hypercalcemia[11][12][13
+Solid tumour with metastasis (e.g. breast cancer or classically squamous cell carcinoma, which can be PTHrP-mediated)&Solid tumour with humoral mediation of hypercalcaemia (e.g. lung cancer, most commonly non-small cell lung cancer[14] or kidney cancer, phaeochromocytoma)&Haematologic cancers (multiple myeloma, lymphoma, leukaemia)&Ovarian small cell carcinoma of the hypercalcemic typ
+Vitamin-D disorders[edit] => Hypervitaminosis D (vitamin D intoxication)&Elevated 1,25(OH)2D (see calcitriol under Vitamin D) levels (e.g. sarcoidosis and other granulomatous diseases such as tuberculosis)&Idiopathic hypercalcaemia of infancy[15]&rebound hypercalcaemia after rhabdomyolysi
+High bone-turnover rates[edit] => Hyperthyroidism&Multiple myeloma&Prolonged immobilization&Paget's disease&Thiazide use&Vitamin A intoxicatio
+Kidney failure[edit] => Severe secondary hyperparathyroidism&Tertiary hyperparathyroidism&Aluminium intoxication&Milk-alkali syndrom
+Other[edit] => Adrenal insufficiency&Zollinger Ellison syndrom
+Abnormal heart rhythms can also result, and ECG findings of a short QT interval[16] suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction.[17] Hypercalcaemia has also been known to cause an ECG finding mimicking hypothermia, known as an Osborn wave.[18]
+The neuromuscular symptoms of hypercalcemia are caused by a negative bathmotropic effect due to the increased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, increased calcium raises the threshold for depolarization.[5] This results in diminished deep tendon reflexes (hyporeflexia), and skeletal muscle weakness.[6] There is a general mnemonic for remembering the effects of hypercalcaemia: "Stones, Bones, Groans, Thrones and Psychiatric Overtones"
+Stones (renal or biliary) (see calculus)&Bones (bone pain)&Groans (abdominal pain, nausea and vomiting)&Thrones (polyuria) resulting in dehydration&Psychiatric overtones (Depression 30–40%, anxiety, cognitive dysfunction, insomnia, coma
+Other symptoms include cardiac arrhythmias (especially in those taking digoxin), fatigue, nausea, vomiting (emesis), anorexia, abdominal pain, constipation, & paralytic ileus. If renal impairment occurs as a result, manifestations can include polyuria, nocturia, and polydipsia.[6] Psychiatric manifestation can include emotional instability, confusion, delirium, psychosis, & stupor.[6] Limbus sign seen in eye due to hypercalcemia.[citation needed]
+Hypercalcemia can result in an increase in heart rate[7] and a positive inotropic effect (increase in contractility).
+Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/l).[6] Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result. The high levels of calcium ions decrease the neuron membrane permeability to sodium ions, thus decreasing excitability, which leads to hypotonicity of smooth and striated muscle. This explains the fatigue, muscle weakness, low tone and sluggish reflexes in muscle groups. The sluggish nerves also explain drowsiness, confusion, hallucinations, stupor and / or coma. In the gut this causes constipation. Hypocalcaemia causes the opposite by the same mechanism.[citation needed]
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DISNET disease texts/100 Original Disease Texts/Hyperosmolar hyperglycemic state.txt

+The main risk factor is a history of diabetes mellitus type 2.[4] Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1.[3][4] Triggers include infections, stroke, trauma, certain medications, and heart attacks.[4]
+Other risk factors:
+Lack of sufficient insulin (but enough to prevent ketosis)[5]&Poor kidney function[5]&Poor fluid intake (dehydration)[5]&Older age (50–70 years)[5]&Certain medical conditions (cerebral vascular injury, myocardial infarction, sepsis)[5]&Some medications (glucocorticoids, beta-blockers, thiazide diuretics, calcium channel blockers, phenytoin)[5
+Criteria[edit] => According to the American Diabetes Association, diagnostic features include:[7][8]
+Plasma glucose level >30 mmol/L (>600 mg/dL)&Serum osmolality >320 mOsm/kg&Profound dehydration, up to an average of 9L (and therefore substantial thirst (polydipsia))&Serum pH >7.40 [5]&Bicarbonate >15 mEq/L&Small ketonuria (~+ on dipstick) and absent-to-low ketonemia (<3 mmol/L)&Some alteration in consciousness&BUN > 30 md/dL (increased)[5]&Creatinine > 1.5 mg/dL (increased)[5
+Imaging[edit] => Cranial imaging is not used for diagnosis of this condition. However, if MRI is performed, it may show cortical restricted diffusion with unusual characteristics of reversible T2 hypointensity in the subcortical white matter.[9]
+Differential diagnosis[edit] => The major differential diagnosis is diabetic ketoacidosis (DKA). In contrast to DKA, serum glucose levels in HHS are extremely high, usually greater than 40-50 mmol/L (600 mg/dL).[5] Metabolic acidosis is absent or mild.[5] A temporary state of confusion (delirium) is also more common in HHS than DKA. HHS also tends to affect older people more. DKA may have fruity breath, and rapid and deep breathing.[5]
+DKA often has serum glucose level greater than 300 mg/dL (HHS is >600 mg/dL).[5] DKA usually occurs in type 1 diabetics whereas HHS is more common in type 2 diabetics.[5] DKA is characterized by a rapid onset, and HHS occurs gradually over a few days.[5] DKA also is characterized by ketosis due to the breakdown of fat for energy.[5]
+Both DKA and HHS may show symptoms of dehydration, increased thirst, increased urination, increased hunger, weight loss, nausea, vomiting, abdominal pain, blurred vision, headaches, weakness, and low blood pressure with standing.[5]
+Symptoms of high blood sugar including increased thirst (polydipsia), increased volume of urination (polyurea), and increase hunger (polyphagia).[5]
+Symptoms of HHS include:
+Altered level of consciousness&Neurologic signs including: blurred vision, headaches, focal seizures, myoclonic jerking, reversible paralysis[5]&Motor abnormalities including flaccidity, depressed reflexes, tremors or fasiciculations&Hyperviscosity and increased risk of blood clot formation&Dehydration [5]&Weight loss[5]&Nausea, vomiting, and abdominal pain[5]&Weakness[5]&Low blood pressure with standing[5
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DISNET disease texts/100 Original Disease Texts/Hypervitaminosis A.txt

+Hypervitaminosis A results from excessive intake of preformed vitamin A. A genetic variance in tolerance to vitamin A intake may occur.[22] Children are particularly sensitive to vitamin A, with daily intakes of 1500 IU/kg body weight reportedly leading to toxicity.[20]
+Types of vitamin A[edit] => Provitamin carotenoids - such as beta carotene - are “largely impossible” to cause toxicity, as their conversion to retinol is highly regulated.[20] No vitamin A toxicity has ever been reported from ingestion of excessive amounts.[23] Overconsumption of beta carotene can only cause carotenosis, a harmless and reversible cosmetic condition in which the skin turns orange.&Preformed vitamin A absorption and storage in the liver occur very efficiently until a pathologic condition develops.[20] When ingested, 70-90% of preformed vitamin A is absorbed and used.[20
+Sources of toxicity[edit] => Diet - liver is high in vitamin A. The liver of certain animals — including the polar bear, bearded seal,[24][25] walrus,[26] moose,[27] — are particularly toxic.&Supplements - usually when taken above recommended dosages - can be toxic. Cod liver oil is particularly high in vitamin A.&Medications - at high doses of vitamin A - are often used on long-term basis in numerous preventive and therapeutic medical applications, which may lead to hypervitaminosis A.[28
+Types of toxicity[edit] => Acute toxicity occurs over a period of hours or a few days, and is less of a problem than chronic toxicity.&Chronic toxicity - ingestion of high amounts of preformed vitamin A for months or years - results from daily intakes greater than 25,000 IU for 6 years or longer and more than 100,000 IU for 6 months or longer - are considered toxic
+Tests[edit] => Tests may include:[1]
+bone X-rays&blood calcium test&cholesterol test&liver function test&blood test for vitamin
+Retinol concentrations are nonsensitive indicators[edit] => Assessing vitamin A status in persons with subtoxicity or toxicity is complicated because serum retinol concentrations are not sensitive indicators in this range of liver vitamin A reserves.[20] The range of serum retinol concentrations under normal conditions is 1–3 μmol/l and, because of homeostatic regulation, that range varies little with widely disparate vitamin A intakes[20]
+Retinol esters have been used as markers[edit] => Retinyl esters can be distinguished from retinol in serum and other tissues and quantified with the use of methods such as high-performance liquid chromatography.[20]
+Elevated amounts of retinyl ester (i.e., > 10% of total circulating vitamin A) in the fasting state have been used as markers for chronic hypervitaminosis A in humans and monkeys.[20] This increased retinyl ester may be due to decreased hepatic uptake of vitamin A and the leaking of esters into the bloodstream from saturated hepatic stellate cells.[20]
+Symptoms may include:[1]
+Abnormal softening of the skull bone (craniotabes—infants and children)&Blurred vision&Bone pain or swelling&Bulging fontanelle (infants)&Changes in consciousness&Decreased appetite&Dizziness&Double vision (young children)&Drowsiness&Headache&Gastric mucosal calcinosis[2]&Heart valve calcification[3]&Hypercalcemia&Increased intracranial pressure manifesting as cerebral edema, papilledema, and headache[4] (may be referred to as Idiopathic intracranial hypertension)&Irritability&Liver damage[5][6][7][8][9][10][11][12][13]&Nausea&Poor weight gain (infants and children)&Skin and hair changes&Cracking at corners of the mouth&Hair loss&Higher sensitivity to sunlight&Oily skin and hair (seborrhea)&Premature epiphyseal closure[14][15][16][17][18]&Skin peeling, itching&Spontaneous fracture[19][20]&Yellow discoloration of the skin (aurantiasis cutis)&Uremic pruritus[21]&Vision changes&Vomitin
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DISNET disease texts/100 Original Disease Texts/Hypocalcaemia.txt

+Hypoparathyroidism is a common cause of hypocalcemia. Calcium is tightly regulated by the parathyroid hormone (PTH). In response to low calcium levels, PTH induces the kidneys to reabsorb calcium, the kidneys to increase production of calcitriol (the active form of vitamin D) thereby increasing intestinal absorption of calcium, and the bones to release calcium. These actions lead to a re-balance in the blood calcium levels. However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the parathyroid glands via parathyroidectomy or neck dissection for head and neck cancers. Hypoparathyroidism may also be due to autoimmune destruction of the glands.[citation needed]
+Eating disorders&Prolonged vomiting (e.g. with a viral illness)&Exposure to mercury, including infantile acrodynia&Excessive dietary magnesium, as with supplementation.[citation needed]&Excessive dietary zinc, as with supplementation (causes rapid hypocalcemia).&Prolonged use of medications/laxatives containing magnesium&Chelation therapy for metal exposure, particularly EDTA&Osteoporosis treatment or preventive agents, such as bisphosphonates and denosumab.&Agents for the treatment of hypercalcemia, such as Calcitonin.&Chronic kidney failure&Absent active vitamin D Decreased dietary intake Decreased sun exposure Defective Vitamin D metabolism Anticonvulsant therapy Vitamin-D dependent rickets, type I&Decreased dietary intake&Decreased sun exposure&Defective Vitamin D metabolism Anticonvulsant therapy Vitamin-D dependent rickets, type I&Anticonvulsant therapy&Vitamin-D dependent rickets, type I&Ineffective active vitamin D Intestinal malabsorption Vitamin-D dependent rickets, type II&Intestinal malabsorption&Vitamin-D dependent rickets, type II&Pseudohypoparathyroidism&Severe acute hyperphosphataemia&Tumour lysis syndrome&Acute kidney failure Rhabdomyolysis (initial stage)&Rhabdomyolysis (initial stage)&Exposure to hydrofluoric acid which can be fatal if 2.5% of skin is exposed[9]&As a complication of pancreatitis&Alkalosis, often caused by hyperventilation As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation. Tetany may also be seen with this condition.&As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation.&Tetany may also be seen with this condition.&Neonatal hypocalcemia Very low birth weight (less than 1500 grams) Gestational age less than 32 weeks&Very low birth weight (less than 1500 grams)&Gestational age less than 32 week
+Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the measured level of calcium. A corrected calcium level based on the albumin level is: Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0 - serum albumin [g/dL]).[11]
+The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers,reduced calcium lowers the threshold for depolarization.[7] The symptoms can be recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth.[citation needed]
+Petechiae which appear as on-off spots, then later become confluent, and appear as purpura (larger bruised areas, usually in dependent regions of the body).&Oral, perioral and acral paresthesias, tingling or 'pins and needles' sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.&Carpopedal and generalized tetany (unrelieved and strong contractions of the hands, and in the large muscles of the rest of the body) are seen.&Latent tetany Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic) Chvostek's sign (tapping of the inferior portion of the cheekbone will produce facial spasms)[8]&Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic)&Chvostek's sign (tapping of the inferior portion of the cheekbone will produce facial spasms)[8]&Tendon reflexes are hyperactive&Life-threatening complications Laryngospasm Cardiac arrhythmias&Laryngospasm&Cardiac arrhythmias&Effects on cardiac output Negative chronotropic effect, or a decrease in heart rate. Negative inotropic effect, or a decrease in contractility&Negative chronotropic effect, or a decrease in heart rate.&Negative inotropic effect, or a decrease in contractility&&ECG changes include the following: Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the patient at high risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death, unless the patient can be medically or electrically cardioverted and returned to a normal cardiac rhythm.)&Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the patient at high risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death, unless the patient can be medically or electrically cardioverted and returned to a normal cardiac rhythm.
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DISNET disease texts/100 Original Disease Texts/Hypomagnesemia.txt

+Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium (hypermagnesemia), however, are nearly always caused by a medical treatment. Up to 12 percent of all people admitted to hospital and as high as 60–65% of people in the intensive care unit (ICU) have hypomagnesemia.[5][6] Hypomagnesemia is probably underdiagnosed, as testing for serum magnesium levels is not routine.
+Low levels of magnesium in blood may mean that there is not enough magnesium in the diet, the intestines are not absorbing enough magnesium, or the kidneys are excreting too much magnesium. Deficiencies may be due to the following conditions:
+Drugs[edit] => Alcoholism. Hypomagnesemia occurs in 30% of alcohol abusers and in 85% of delirium tremens inpatients, due to malnutrition and chronic diarrhea.[citation needed] Alcohol stimulates the kidneys' excretion of magnesium, which is also increased because of alcoholic and diabetic ketoacidosis, low blood phosphate levels, and hyperaldosteronism resulting from liver disease. Also, hypomagnesemia is related to thiamine deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate
+Medications[edit] => Loop and thiazide diuretic use (the most common cause of hypomagnesemia)[7]&Antibiotics (i.e. aminoglycoside, amphotericin, pentamidine, gentamicin, tobramycin, viomycin) block resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia.[citation needed]&Long term use of proton-pump inhibitors such as omeprazole.[8][9]&Other drugs. Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect.[7] Adrenergics, displace magnesium into the cell Cisplatin, stimulates kidney excretion Ciclosporin, stimulates kidney excretion Mycophenolate mofetil&Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect.[7]&Adrenergics, displace magnesium into the cell&Cisplatin, stimulates kidney excretion&Ciclosporin, stimulates kidney excretion&Mycophenolate mofeti
+Genetic causes[edit] => Gitelman-like diseases, which include the syndromes caused by genetic mutations in SLC12A3, CLNCKB,[10] BSND, KCNJ10, FXYD2, HNF1B or PCBD1. In these diseases, the hypomagnesemia is accompanied by other defects in electrolyte handling such as hypocalciuria and hypokalemia. The genes involved in this group of diseases all encode proteins that are involved in reabsorbing electrolytes (including magnesium) in the distal convoluted tubule of the kidney.[3]&Hypercalciuric hypomagnesemic syndromes, which encompass the syndromes caused by mutations in CLDN16, CLDN19, CASR or CLCNKB. In these diseases, reabsorption of divalent cations (such as magnesium and calcium) in the thick ascending limb of Henle's loop of the kidney is impaired. This results in loss of magnesium and calcium in the urine.[3]&Mitochondriopathies, such as caused by mutations in SARS2, MT-TI or as seen with Kearns-Sayre syndrome.[3]&Other genetic causes of hypomagnesemia, such as mutations in TRPM6, CNNM2, EGF, EGFR, KCNA1 or FAM111A. Many of the proteins encoded by these genes play a role in the transcellular absorption of magnesium in the distal convoluted tubule.[3
+Metabolic abnormalities[edit] => Insufficient selenium,[11] vitamin D, sunlight exposure or vitamin B6.[citation needed]&Gastrointestinal causes: the distal tractus digestivus secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohn's disease, ulcerative colitis, Whipple's disease and celiac sprue can all cause hypomagnesemia.&Postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant.[citation needed
+Other[edit] => Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines.&Malabsorption&Acute pancreatitis&Fluoride poisoning&Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications.[12
+The diagnosis can be made by finding a plasma magnesium concentration of less than 0.6 mmol/L (1.46 mg/dl).[2] Since most magnesium is intracellular, a body deficit can be present with a normal plasma concentration.
+The ECG may show a tachycardia with a prolonged QT interval, which has been noted in proton pump inhibitor-associated hypomagnesemia.[16]
+Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, hypokalemia, hypoparathyroidism which might result in hypocalcemia, chondrocalcinosis, spasticity and tetany, epileptic seizures, basal ganglia calcifications and in extreme and prolonged cases coma, intellectual disability or death.[3] Other symptoms that have been suggested to be associated with hypomagnesemia are athetosis, jerking, nystagmus, and an extensor plantar reflex, confusion, disorientation, hallucinations, depression, hypertension and fast heart rate.[citation needed]
+People being treated on an intensive care unit who have a low magnesium level may have a higher risk of requiring mechanical ventilation, and death.[4]
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DISNET disease texts/100 Original Disease Texts/Hypovolemia.txt

+Common causes of hypovolemia are[4]
+Loss of blood (external or internal bleeding or blood donation[5])&Loss of plasma (severe burns[6][7] and lesions discharging fluid)&Loss of body sodium and consequent intravascular water; e.g. diarrhea or vomitin
+Excessive sweating is not a cause of hypovolemia, because the body eliminates significantly more water than sodium.[8]
+Clinical symptoms may not be present until 10–20% of total whole-blood volume is lost.
+Hypovolemia can be recognized by tachycardia, diminished blood pressure,[9] and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.
+Note that in children compensation can result in an artificially high blood pressure despite hypovolemia. Children will typically compensate (maintain blood pressure despite loss of blood volume) for a longer period than adults, but will deteriorate rapidly and severely once they do begin to decompensate. This is another reason (aside from initial lower blood volume) that even the possibility of internal bleeding in children should almost always be treated aggressively.
+Obvious signs of external bleeding should be noted while remembering that people can bleed to death internally without any external blood loss. ("Blood on the floor, plus 4 more" = intrathoracic, intraperitoneal, retroperitoneal, pelvis/thigh)
+There should be considered possible mechanisms of injury that may have caused internal bleeding, such as ruptured or bruised internal organs. If trained to do so and if the situation permits, there should be conducted a secondary survey and checked the chest and abdomen for pain, deformity, guarding, discoloration or swelling. Bleeding into the abdominal cavity can cause the classical bruising patterns of Grey Turner's sign or Cullen's sign.
+Usually referred to as a "class" of shock. Most sources state that there are 4 stages of hypovolemic shock;[10] however, a number of other systems exist with as many as 6 stages.[11]
+The 4 stages are sometimes known as the "Tennis" staging of hypovolemic shock, as the stages of blood loss (under 15% of volume, 15–30% of volume, 30–40% of volume and above 40% of volume) mimic the scores in a game of tennis: 15, 15–30, 30–40 and 40.[12] It is basically the same as used in classifying bleeding by blood loss.
+The signs and symptoms of the major stages of hypovolemic shock include:[13]
+Stage 1 Stage 2 Stage 3 Stage 4  headingBody  Blood loss Up to 15% (750 mL) 15–30% (750–1500 mL) 30–40% (1500–2000 mL) Over 40% (over 2000 mL) Blood pressure Normal (Maintained by vasoconstriction) Increased diastolic BP Systolic BP < 100 Systolic BP < 70 Heart rate Normal Slight tachycardia (> 100 bpm) Tachycardia (> 120 bpm) Extreme tachycardia (> 140 bpm) with weak pulse Respiratory rate Normal Increased (> 20) Tachypneic (> 30) Extreme tachypnea Mental status Normal Slight anxiety, restless Altered, confused Decreased LOC, lethargy, coma Skin Pallor Pale, cool, clammy Increased diaphoresis Extreme diaphoresis; mottling possible Capillary refill Normal Delayed Delayed Absent Urine output Normal 20–30 mL/h 20 mL/h Negligible
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DISNET disease texts/100 Original Disease Texts/Inborn error of metabolism.txt

+Dozens of congenital metabolic diseases are now detectable by newborn screening tests, especially the expanded testing using mass spectrometry. This is an increasingly common way for the diagnosis to be made and sometimes results in earlier treatment and a better outcome. There is a revolutionary Gas chromatography–mass spectrometry-based technology with an integrated analytics system, which has now made it possible to test a newborn for over 100 mm genetic metabolic disorders.
+Because of the multiplicity of conditions, many different diagnostic tests are used for screening. An abnormal result is often followed by a subsequent "definitive test" to confirm the suspected diagnosis.
+Common screening tests used in the last sixty years:
+Ferric chloride test (turned colors in reaction to various abnormal metabolites in urine)&Ninhydrin paper chromatography (detected abnormal amino acid patterns)&Guthrie bacterial inhibition assay (detected a few amino acids in excessive amounts in blood) The dried blood spot can be used for multianalyte testing using Tandem Mass Spectrometry (MS/MS). This given an indication for a disorder. The same has to be further confirmed by enzyme assays, IEX-Ninhydrin, GC/MS or DNA Testing.&Quantitative measurement of amino acids in plasma and urine&IEX-Ninhydrin post column derivitization liquid ion-exchange chromatography (detected abnormal amino acid patterns and quantitative analysis)&Urine organic acid analysis by gas chromatography–mass spectrometry&Plasma acylcarnitines analysis by mass spectrometry&Urine purines and pyrimidines analysis by gas chromatography-mass spectrometr
+Specific diagnostic tests (or focused screening for a small set of disorders):
+Tissue biopsy or necropsy: liver, muscle, brain, bone marrow&Skin biopsy and fibroblast cultivation for specific enzyme testing&Specific DNA testin
+A 2015 review reported that even with all these diagnostic tests, there are cases when "biochemical testing, gene sequencing, and enzymatic testing can neither confirm nor rule out an IEM, resulting in the need to rely on the patient's clinical course."[3]
+Because of the enormous number of these diseases and wide range of systems affected, nearly every "presenting complaint" to a doctor may have a congenital metabolic disease as a possible cause, especially in childhood. The following are examples of potential manifestations affecting each of the major organ systems.
+Growth failure, failure to thrive, weight loss&Ambiguous genitalia, delayed puberty, precocious puberty&Developmental delay, seizures, dementia, encephalopathy, stroke&Deafness, blindness, pain agnosia&Skin rash, abnormal pigmentation, lack of pigmentation, excessive hair growth, lumps and bumps&Dental abnormalities&Immunodeficiency, low platelet count, low red blood cell count, enlarged spleen, enlarged lymph nodes&Many forms of cancer&Recurrent vomiting, diarrhea, abdominal pain&Excessive urination, kidney failure, dehydration, edema&Low blood pressure, heart failure, enlarged heart, hypertension, myocardial infarction&Liver enlargement, jaundice, liver failure&Unusual facial features, congenital malformations&Excessive breathing (hyperventilation), respiratory failure&Abnormal behavior, depression, psychosis&Joint pain, muscle weakness, cramps&Hypothyroidism, adrenal insufficiency, hypogonadism, diabetes mellitu
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DISNET disease texts/100 Original Disease Texts/Influenza.txt

+Symptom: sensitivity specificity Fever Cough Nasal congestion  headingBody  68–86% 25–73% 84–98% 7–29% 68–91% 19–41% All three findings, especially fever, were less sensitive in people over 60 years of age.
+Approximately 33% of people with influenza are asymptomatic.[14]
+Symptoms of influenza can start quite suddenly one to two days after infection. Usually the first symptoms are chills or a chilly sensation, but fever is also common early in the infection, with body temperatures ranging from 38 to 39 °C (approximately 100 to 103 °F).[15] Many people are so ill that they are confined to bed for several days, with aches and pains throughout their bodies, which are worse in their backs and legs.[16] Symptoms of influenza may include:
+Fever and chills&Cough&Nasal congestion&Runny nose&Sneezing&Sore throat&Hoarseness&Ear pressure&Earache&Muscle aches&Fatigue&Headache&Irritated, watering eyes&Reddened eyes, skin (especially face), mouth, throat and nose&Petechial rash[17]&In children, gastrointestinal symptoms such as diarrhea, vomiting, and abdominal pain,[18][19] (may be severe in children with influenza B)[20
+It can be difficult to distinguish between the common cold and influenza in the early stages of these infections.[21] Influenza is a mixture of symptoms of common cold and pneumonia, body ache, headache, and fatigue. Diarrhea is not normally a symptom of influenza in adults,[12] although it has been seen in some human cases of the H5N1 "bird flu"[22] and can be a symptom in children.[18] The symptoms most reliably seen in influenza are shown in the adjacent table.[12]
+Since antiviral drugs are effective in treating influenza if given early (see treatment section, below), it can be important to identify cases early. Of the symptoms listed above, the combinations of fever with cough, sore throat and/or nasal congestion can improve diagnostic accuracy.[23] Two decision analysis studies[24][25] suggest that during local outbreaks of influenza, the prevalence will be over 70%,[25] and thus patients with any of these combinations of symptoms may be treated with neuraminidase inhibitors without testing. Even in the absence of a local outbreak, treatment may be justified in the elderly during the influenza season as long as the prevalence is over 15%.[25]
+The available laboratory tests for influenza continue to improve. The United States Centers for Disease Control and Prevention (CDC) maintains an up-to-date summary of available laboratory tests.[26] According to the CDC, rapid diagnostic tests have a sensitivity of 50–75% and specificity of 90–95% when compared with viral culture.[27] These tests may be especially useful during the influenza season (prevalence=25%) but in the absence of a local outbreak, or peri-influenza season (prevalence=10%[25]).
+Occasionally, influenza can cause severe illness including primary viral pneumonia or secondary bacterial pneumonia.[28][29] The obvious symptom is trouble breathing. In addition, if a child (or presumably an adult) seems to be getting better and then relapses with a high fever, that is a danger sign since this relapse can be bacterial pneumonia.[30]
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DISNET disease texts/100 Original Disease Texts/Intention tremor.txt

+Intention tremors are common among individuals with multiple sclerosis (MS). One common symptom of multiple sclerosis is ataxia, a lack of coordinated muscle movement caused by cerebellar lesions characteristic of multiple sclerosis. The disease often destroys physical and cognitive function of individuals.
+Intention tremors can be a first sign of multiple sclerosis, since loss or deterioration of motor function and sensitivity are often one of the first symptoms of cerebellar lesions.[1][4]
+Intention tremors have a variety of other recorded causes as well. These include a variety of neurological disorders, such as stroke, alcoholism, alcohol withdrawal, peripheral neuropathy, Wilson's disease, Creutzfeldt–Jakob disease, Guillain–Barré syndrome and fragile X syndrome, as well as brain tumors, low blood sugar, hyperthyroidism, hypoparathyroidism, insulinoma, normal aging, and traumatic brain injury.[1][5][6][7] Holmes tremor, a rubral or midbrain tremor, is another form of tremor that includes intention tremors, among other symptoms. This disease affects the proximal muscles of the head, shoulders, and neck. Tremors of this disease occur at frequencies of 2–4 Hz or more.[8]
+Intention tremor is also known to be associated with infections, West Nile virus, rubella, H. influenza, rabies, and varicella.[1][9] A variety of poisons have been shown to cause intention tremor, including mercury, methyl bromide, and phosphine.[1][10][11] In addition, vitamin deficiencies have been linked to intention tremor, especially deficiency in vitamin E.[12] Pharmacological agents such as anti-arrhythmic drugs, anti-epileptic agents, benzodiazepine, cyclosporine, lithium, neuroleptics, and stimulants have been known to cause intention tremor.[3] Some ordinary activities including ingesting too much caffeine, cigarettes, and alcohol, along with stress, anxiety, fear, anger and fatigue have also been shown to cause intention tremor by negatively affecting the cerebellum, brainstem, or thalamus, as discussed in mechanisms.[5]
+A working diagnosis is made from a neurological examination and evaluation. Parts of a complete examination include a physical examination, MRI, patient history, and electrophysiological and accelerometric studies. A diagnosis of solely intention tremor can only be made if the tremor is of low frequency (below 5 Hz) and without the presence of any resting tremors.[1] Electrophysiological studies can be useful in determining frequency of the tremor, and accelerometric studies quantify tremor amplitude. MRI is used to locate damage to and degradation of the cerebellum that may be causing the intention tremor. Focal lesions such as neoplasms, tumors, hemorrhages, demyelination, or other damage may be causing dysfunction of the cerebellum and correspondingly the intention tremor.[14]
+Physical tests are an easy way to determine the severity of the intention tremor and impairment of physical activity. Common tests that are used to assess intention tremor are the finger-to-nose and heel-to-shin tests. In a finger-to-nose test, a physician has the individual touch their nose with their finger while monitoring for irregularity in timing and control of the movement. An individual with intention tremors will have coarse side-to-side movements that increase in severity as the finger approaches the nose. Similarly, the heel-to-shin test evaluates intention tremors of the lower extremities. In such a test, the individual, in a supine position, places one heel on top of the opposite knee and is then instructed to slide the heel down the shin to the ankle while being monitored for coarse and irregular side-to-side movement as the heel approaches the ankle. Important historical elements to the diagnosis of intention tremor are:
+age at onset&mode of onset (sudden or gradual)&anatomical affected sites&rate of progression&exacerbating and remitting factors&alcohol abuse&family history of tremor[15]&current medications[12
+Secondary symptoms commonly observed are dysarthria (a speech disorder characterized by poor articulation and slurred speech), nystagmus (rapid involuntary eye movement, especially rolling of the eyes), gait problems (abnormality in walking), and postural tremor or titubation (to-and-fro movements of the neck and trunk). A postural tremor may also accompany intention tremors.[1][12]
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DISNET disease texts/100 Original Disease Texts/Intraparenchymal hemorrhage.txt

+Hypertension&Arteriovenous malformation&Aneurysm rupture&Cerebral amyloid angiopathy&Intracranial neoplasm&Coagulopathy&Hemorrhagic transformation of an ischemic infarct&Cerebral venous thrombosis&Sympathomimetic drug abuse&Moyamoya&Sickle cell disease&Eclampsia or postpartum vasculopathy&Infection&Vasculitis&Neonatal intraventricular hemorrhage&Traum
+In younger patients, vascular malformations, specifically AVMs and cavernous angiomas are more common causes for hemorrhage. In addition, venous malformations are associated with hemorrhage.
+In the elderly population, amyloid angiopathy is associated with cerebral infarcts as well as hemorrhage in superficial locations, rather than deep white matter or basal ganglia. These are usually described as "lobar". These bleedings are not associated with systemic amyloidosis.
+Hemorrhagic neoplasms are more complex, heterogeneous bleeds often with associated edema. These hemorrhages are related to tumor necrosis, vascular invasion and neovascularity. Glioblastomas are the most common primary malignancies to hemorrhage while thyroid, renal cell carcinoma, melanoma, and lung cancer are the most common causes of hemorrhage from metastatic disease.
+Other causes of intraparenchymal hemorrhage include hemorrhagic transformation of infarction which is usually in a classic vascular distribution and is seen in approximately 24 to 48 hours following the ischemic event. This hemorrhage rarely extends into the ventricular system.
+Computed tomography (CT scan): A CT scan may be normal if it is done soon after the onset of symptoms. A CT scan is the best test to look for bleeding in or around your brain. In some hospitals, a perfusion CT scan may be done to see where the blood is flowing and not flowing in your brain.
+Magnetic resonance imaging (MRI scan): A special MRI technique (diffusion MRI) may show evidence of an ischemic stroke within minutes of symptom onset. In some hospitals, a perfusion MRI scan may be done to see where the blood is flowing and not flowing in your brain.
+Angiogram: a test that looks at the blood vessels that feed the brain. An angiogram will show whether the blood vessel is blocked by a clot, the blood vessel is narrowed, or if there is an abnormality of a blood vessel known as an aneurysm.
+Carotid duplex: A carotid duplex is an ultrasound study that assesses whether or not you have atherosclerosis (narrowing) of the carotid arteries. These arteries are the large blood vessels in your neck that feed your brain.
+Transcranial Doppler (TCD): Transcranial Doppler is an ultrasound study that assesses whether or not you have atherosclerosis (narrowing) of the blood vessels inside of your brain. It can also be used to see if you have emboli (blood clots) in your blood vessels.
+Clinical manifestations of intraparenchymal hemorrhage are determined by the size and location of hemorrhage, but may include the following:
+Hypertension, fever, or cardiac arrhythmias&Nuchal rigidity&Subhyaloid retinal hemorrhages&Altered level of consciousness&Anisocoria, Nystagmus&Focal neurological deficits&Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia, neglect, or apraxia&Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion&Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia&Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion&Brain stem - Tetraparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability&Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousnes
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DISNET disease texts/100 Original Disease Texts/Itch.txt

+Infections[edit] => Allergic reaction to contact with specific chemicals, such as urushiol, derived from poison ivy or poison oak, or Balsam of Peru, found in many foods and fragrances.[7][8] Certain allergens may be diagnosed in a patch test.[9][10]&Body louse, found in substandard living conditions&Cutaneous larva migrans, a skin disease&Head lice, if limited to the neck and scalp&Herpes, a viral disease&Insect bites, such as those from mosquitos or chiggers&Photodermatitis – sunlight reacts with chemicals in the skin, leading to the formation of irritant metabolites&Pubic lice, if limited to the genital area&Scabies, especially when several other persons in close contact also itch&Shaving, which may irritate the skin&Swimmer's itch, a short-term immune reaction&Varicella – i.e. chickenpox, prevalent among young children and highly contagiou
+Environmental and allergic[edit] => Foreign objects on the skin are the most common cause of non-pathological itching.&Urticaria (also called hives) usually causes itchin
+Skin disorders[edit] => Dandruff – an unusually large amount of flaking is associated with this sensation&Punctate palmoplantar keratoderma, a group of disorders characterized by abnormal thickening of the palms and soles&Skin conditions (such as psoriasis, eczema, sunburn, athlete's foot, and hidradenitis suppurativa). Most are of an inflammatory nature.&Scab healing, scar growth, and the development or emergence of moles, pimples, and ingrown hairs from below the epidermis&Xerosis – dry skin, the most common cause,[citation needed] frequently seen in the winter and also associated with older age, frequent bathing in hot showers or baths, and high-temperature and low-humidity environment
+Medical disorders[edit] => Diabetes mellitus, a group of metabolic diseases in which a person has high blood sugar&Hyperparathyroidism, overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH)[11]&Iron deficiency anemia, a common anemia (low red blood cell or hemoglobin levels)&Jaundice and cholestasis – bilirubin is a skin irritant at high concentrations&Malignancy or internal cancer, such as lymphoma or Hodgkin's disease[12]&Polycythemia, which can cause generalized itching due to increased histamines&Psychiatric disease ("psychogenic itch", as may be seen in delusional parasitosis)&Thyroid illness&Uraemia – the itching sensation this causes is known as uremic pruritu
+Medication[edit] => Drugs (such as opioids) that activate histamine (H1) receptors or trigger histamine release&Chloroquine, a dru
+Related to pregnancy[edit] => Gestational pemphigoid, a dermatosis of pregnancy&Intrahepatic cholestasis of pregnancy, a medical condition in which cholestasis occurs&Pruritic urticarial papules and plaques of pregnancy (PUPPP), a chronic hives-like ras
+Other[edit] => Menopause, or changes in hormonal balances associated with agin
+Pain and itch have very different behavioral response patterns. Pain evokes a withdrawal reflex, which leads to retraction and therefore a reaction trying to protect an endangered part of the body. Itch in contrast creates a scratch reflex, which draws one to the affected skin site. Itch generates stimulus of a foreign object underneath or upon the skin and also the urge to remove it. For example, responding to a local itch sensation is an effective way to remove insects from one's skin.
+Scratching has traditionally been regarded as a way to relieve oneself by reducing the annoying itch sensation. However, there are hedonic aspects of scratching, as one would find noxious scratching highly pleasurable.[2] This can be problematic with chronic itch patients, such as ones with atopic dermatitis, who may scratch affected spots until they no longer produce a pleasant or painful sensation, instead of when the itch sensation disappears.[4] It has been hypothesized that motivational aspects of scratching include the frontal brain areas of reward and decision making. These aspects might therefore contribute to the compulsive nature of itch and scratching.[2]
+Contagious itch[edit] => Events of "contagious itch" are very common occurrences. Even a discussion on the topic of itch can give one the desire to scratch. Itch is likely to be more than a localized phenomenon in the place we scratch. Results from a study showed that itching and scratching were induced purely by visual stimuli in a public lecture on itching. The sensation of pain can also be induced in a similar fashion, often by listening to a description of an injury, or viewing an injury itself.
+There is little detailed data on central activation for contagious itching, but it is hypothesized that a human mirror neuron system exists in which we imitate certain motor actions when we view others performing the same action. A similar phenomenon in which mirror neurons are used to explain the cause is contagious yawning.[2]
+Pain inhibition by itching[edit] => The sensation of itch can be reduced by many painful sensations. Studies done in the last decade have shown that itch can be inhibited by many other forms of painful stimuli, such as noxious heat,[5] physical rubbing/scratching, noxious chemicals, and electric shock.[6]
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DISNET disease texts/100 Original Disease Texts/Juvenile dermatomyositis.txt

+The underlying cause of JDM is unknown. It most likely has a genetic component, as other autoimmune disease tend to run in the families of patients. The disease is usually triggered by a condition that causes immune system activity that does not stop as it should, but the trigger is almost certainly not the cause in most cases. Common triggers include immunizations, infections, injuries, and sunburn.
+Proximal muscle weakness, characteristic skin rash and elevated muscle enzymes are routinely used to identify JDM. Typical magnetic resonance imaging and muscle biopsy changes are considered the next most useful diagnostic criteria, followed by myopathic changes on electromyogram, calcinosis, dysphonia and nailfold capillaroscopy. Other useful criteria include myositis-specific or -related antibodies, nailfold capillaroscopy, factor VIII-related antigen, muscle ultrasound, calcinosis and neopterin.[4]
+The vasculitis caused by JDMS manifests itself predominantly in two ways:
+One is a distinctive rash. The rash often affects the face, eyelids, and hands, and sometimes the skin above joints, including the knuckles, knees, elbows, etc. The color of the rash is a pinkish purple, and is called heliotrope (after a flower of the same name with approximately this color). On the hands and face, the rash very closely resembles allergies, eczema, fifth disease, or other more common skin condition, but the heliotrope color is unique to the inflammatory process of JDMS. Some children develop calcinosis, which are calcium deposits under the skin. The rash is the source of the "dermato-" part of the name of the disease.
+The second symptom caused by vasculitis is muscle inflammation. This symptom is the source of the "-myositis" part of the name of the disease ("myo" = muscle, "-itis" = inflammation of). Muscle Inflammation causes muscle weakness, which can cause fatigue, clumsiness, not keeping up physically with peers, and eventually inability to perform tasks like climbing stairs, lifting objects, and performing other manual tasks. Other signs may include falling, dysphonia, or dysphagia. The muscle weakness often causes a medical misdiagnosis of muscular dystrophy or other muscle disease. Some patients develop contractures, when the muscle shortens and causes joints to stay bent; exercise, occupational therapy, and physical therapy can prevent this. The muscles first affected tend to be proximal (i.e., neck, shoulders, back, and abdominal). About half of children with JDMS also have pain in their muscles.[1]
+Other symptoms may include irritability, weight loss, and mouth ulcers.[2] When a child becomes irritable, fatigued, reluctant to socialize, and the face becomes flushed easily, physicians refer to this constellation of symptoms as "misery."[3]
+Progression[edit] => The speed of the progression of JDMS is highly variable. Nearly all JDM patients have some skin involvement. The JDMS rash usually occurs as the initial symptom. Sometimes it is so slight as not to be recognized for what it is until muscle symptoms appear. Sometimes muscle symptoms never appear at all or occur very gradually over the course of months, and sometimes going from normal strength to being unable to walk within days. Usually, muscle symptoms appear weeks to months after the onset of the rash.
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DISNET disease texts/100 Original Disease Texts/Kaposi's sarcoma.txt

+Kaposi's sarcoma-associated herpesvirus (KSHV), also called HHV-8 is present in almost 100% of Kaposi sarcoma lesions, whether HIV-related, classic, endemic, or iatrogenic.[14]
+Transmission[edit] => In Europe and North America, KSHV is transmitted through saliva. Thus, kissing is a theoretical risk factor for transmission. Higher rates of transmission among gay and bisexual men have been attributed to "deep kissing" sexual partners with KSHV.[15] Another alternative theory suggests that use of saliva as a sexual lubricant might be a major mode for transmission. Prudent advice is to use commercial lubricants when needed and avoid deep kissing with partners with KSHV infection or whose status is unknown.
+KSHV is also transmissible via organ transplantation[16] and blood transfusion.[17] Testing for the virus before these procedures is likely to effectively limit iatrogenic transmission.
+Classification[edit] => HHV-8, is responsible for all varieties of KS. Since Moritz Kaposi first described this cancer, the disease has been reported in five separate clinical settings, with different presentations, epidemiology, and prognoses.[18]:599 All of these forms are infected with KSHV and are different manifestations of the same disease but have differences in clinical aggressiveness, prognosis and treatment.
+Classic Kaposi sarcoma most commonly appears early on the toes and soles as reddish, violaceous, or bluish-black macules and patches that spread and coalesce to form nodules or plaques.[18]:599 A small percentage of these patients may have visceral lesions. In most cases the treatment involves surgical removal of the lesion. The condition tends to be indolent and chronic, affecting elderly men from the Mediterranean region, Arabian countries[19] or of Eastern European descent. Countries bordering the Mediterranean basin have higher rates of KSHV/HHV-8 infection than the remainder of Europe.[20][21]&Endemic KS, which has two types. Although this may be present worldwide, it has been originally described later in young African people, mainly from sub-Saharan Africa. This variant is not related to HIV infection[22][23] and is a more aggressive disease that infiltrates the skin extensively.[24][25] African lymphadenopathic Kaposi sarcoma is aggressive, occurring in children under 10 years of age, presenting with lymph node involvement, with or without skin lesions.[18]:599 African cutaneous Kaposi sarcoma presents with nodular, infiltrative, vascular masses on the extremities, mostly in men between the ages of 20 and 50, and is endemic in tropical Africa.[18]:599&African lymphadenopathic Kaposi sarcoma is aggressive, occurring in children under 10 years of age, presenting with lymph node involvement, with or without skin lesions.[18]:599&African cutaneous Kaposi sarcoma presents with nodular, infiltrative, vascular masses on the extremities, mostly in men between the ages of 20 and 50, and is endemic in tropical Africa.[18]:599&Immunosuppression-associated Kaposi sarcoma had been described, but only rarely until the advent of calcineurin inhibitors (such as ciclosporines, which are inhibitors of T-cell function) for transplant patients in the 1980s, when its incidence grew rapidly. The tumor arises either when an HHV 8-infected organ is transplanted into someone who has not been exposed to the virus or when the transplant recipient already harbors pre-existing HHV 8 infection.[26][27] Unlike classic Kaposi sarcoma, the site of presentation is more variable.[18]:60
+AIDS-associated Kaposi sarcoma typically presents with cutaneous lesions that begin as one or several red to purple-red macules, rapidly progressing to papules, nodules, and plaques, with a predilection for the head, back, neck, trunk, and mucous membranes. In more advanced cases, they can be found in the stomach and intestines, the lymph nodes, and the lungs.[18]:599 KS-AIDS stimulated the greatest interest as one of the first illnesses associated with AIDS, and was first described in 1981.[28][29][30] It is over 300 times more common in AIDS patients than in renal transplant recipients. In this case, HHV 8 is sexually transmitted among people also at risk for sexually transmitted HIV infection.[31
+Although KS may be suspected from the appearance of lesions and the patient's risk factors, definite diagnosis can be made only by biopsy and microscopic examination. Detection of the KSHV protein LANA in tumor cells confirms the diagnosis.
+In differential diagnosis, arteriovenous malformations, pyogenic granuloma and other vascular proliferations can be microscopically confused with KS.[38]
+KS lesions are nodules or blotches that may be red, purple, brown, or black, and are usually papular.
+They are typically found on the skin, but spread elsewhere is common, especially the mouth, gastrointestinal tract and respiratory tract. Growth can range from very slow to explosively fast, and is associated with significant mortality and morbidity.[10]
+Commonly affected areas include the lower limbs, back, face, mouth, and genitalia. The lesions are usually as described above, but may occasionally be plaque-like (often on the soles of the feet) or even involved in skin breakdown with resulting fungating lesions. Associated swelling may be from either local inflammation or lymphoedema (obstruction of local lymphatic vessels by the lesion). Skin lesions may be quite disfiguring for the sufferer, and a cause of much psychosocial pathology.
+The mouth is involved in about 30% of cases, and is the initial site in 15% of AIDS-related KS. In the mouth, the hard palate is most frequently affected, followed by the gums.[11] Lesions in the mouth may be easily damaged by chewing and bleed or suffer secondary infection, and even interfere with eating or speaking.
+Gastrointestinal tract[edit] => Involvement can be common in those with transplant-related or AIDS-related KS, and it may occur in the absence of skin involvement. The gastrointestinal lesions may be silent or cause weight loss, pain, nausea/vomiting, diarrhea, bleeding (either vomiting blood or passing it with bowel motions), malabsorption, or intestinal obstruction.[12]
+Respiratory tract[edit] => Involvement of the airway can present with shortness of breath, fever, cough, hemoptysis (coughing up blood), or chest pain, or as an incidental finding on chest x-ray.[13] The diagnosis is usually confirmed by bronchoscopy when the lesions are directly seen, and often biopsied.
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DISNET disease texts/100 Original Disease Texts/Lambert–Eaton myasthenic syndrome.txt

+LEMS is often associated with lung cancer (50–70%), specifically small-cell carcinoma,[1] making LEMS a paraneoplastic syndrome.[4] Of the people with small-cell lung cancer, 1–3% have LEMS.[3] In most of these cases, LEMS is the first symptom of the lung cancer, and it is otherwise asymptomatic.[3]
+LEMS may also be associated with autoimmune diseases, such as hypothyroidism (an underactive thyroid gland) or diabetes mellitus type 1.[1][5] Myasthenia gravis, too, may happen in the presence of tumors (thymoma, a tumor of the thymus in the chest); people with MG without a tumor and people with LEMS without a tumor have similar genetic variations that seem to predispose them to these diseases.[3] HLA-DR3-B8 (an HLA subtype), in particular, seems to predispose to LEMS.[5]
+The diagnosis is usually made on electromyography (EMG), which is one of the standard tests in the investigation of otherwise unexplained muscle weakness. This involves the insertion of small needles into the nerves supplying several muscles, administering small electrical impulses through these needles, and measuring the electrical response of the muscle in question. Two EMG investigations can be characteristic in LEMS: compound motor action potentials (CMAPs) and single-fiber examination.[1]
+CMAPs show small amplitudes but normal latency and conduction velocities. If repeated impulses are administered (2 per second or 2 Hz), it is normal for CMAP amplitudes to become smaller as the acetylcholine in the motor end plate is depleted. In LEMS, this decrease is larger than observed normally. Eventually, stored acetylcholine is made available, and the amplitudes increase again. In LEMS, this remains insufficient to reach a level sufficient for transmission of an impulse from nerve to muscle; all can be attributed to insufficient calcium in the nerve terminal. A similar pattern is witnessed in myasthenia gravis. In LEMS, in response to exercising the muscle, the CMAP amplitude increases greatly (over 200%, often much more). This also occurs on the administration of a rapid burst of electrical stimuli (20 impulses per second for 10 seconds). This is attributed to the influx of calcium in response to these stimuli.[1][3] On single-fiber examination, features may include increased jitter (seen in other diseases of neuromuscular transmission) and blocking.[1]
+Blood tests may be performed to exclude other causes of muscle disease (elevated creatine kinase may indicate a myositis, and abnormal thyroid function tests may indicate thyrotoxic myopathy). Antibodies against voltage-gated calcium channels can be identified in 85% of people with EMG-confirmed LEMS.[1] Once LEMS is diagnosed, investigations such as a CT scan of the chest are usually performed to identify any possible underlying lung tumors. Around 50–60% of these are discovered immediately after the diagnosis of LEMS. The remainder is diagnosed later, but usually within two years and typically within four years.[3] As a result, scans are typically repeated every six months for the first two years after diagnosis.[1] While CT of the lungs is usually adequate, a positron emission tomography scan of the body may also be performed to search for an occult tumour, particularly of the lung.[6]
+The weakness from LEMS typically involves the muscles of the proximal arms and legs (the muscles closer to the trunk). In contrast to myasthenia gravis, the weakness affects the legs more than the arms. This leads to difficulties climbing stairs and rising from a sitting position. Weakness is often relieved temporarily after exertion or physical exercise. High temperatures can worsen the symptoms. Weakness of the bulbar muscles (muscles of the mouth and throat) is occasionally encountered.[1] Weakness of the eye muscles is uncommon. Some may have double vision, drooping of the eyelids and difficulty swallowing,[1] but generally only together with leg weakness; this too distinguishes LEMS from myasthenia gravis, in which eye signs are much more common.[3] In the advanced stages of the disease, weakness of the respiratory muscles may occur.[1] Some may also experience problems with coordination (ataxia).[4]
+Three-quarters of people with LEMS also have disruption of the autonomic nervous system. This may be experienced as a dry mouth, constipation, blurred vision, impaired sweating, and orthostatic hypotension (falls in blood pressure on standing, potentially leading to blackouts). Some report a metallic taste in the mouth.[1]
+On neurological examination, the weakness demonstrated with normal testing of power is often less severe than would be expected on the basis of the symptoms. Strength improves further with repeated testing, e.g. improvement of power on repeated hand grip (a phenomenon known as "Lambert's sign"). At rest, reflexes are typically reduced; with muscle use, reflex strength increases. This is a characteristic feature of LEMS. The pupillary light reflex may be sluggish.[1]
+In LEMS associated with lung cancer, most have no suggestive symptoms of cancer at the time, such as cough, coughing blood, and unintentional weight loss.[3] LEMS associated with lung cancer may be more severe.[4]
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DISNET disease texts/100 Original Disease Texts/Laryngitis.txt

+Laryngitis can be infectious as well as noninfectious in origin. The resulting inflammation of the vocal folds results in a distortion of the sound produced there.[1] It normally develops in response to either an infection, trauma to the vocal folds, or allergies.[3] Chronic laryngitis may also be caused by more severe problems, such as nerve damage, sores, polyps, or hard and thick lumps (nodules) on the vocal cords.[4]
+Viral[edit] => Most acute cases of laryngitis are caused by viral infections,[1] the most common of which tend to be rhinovirus, influenza virus, parainfluenza virus, adenovirus, coronavirus, and RSV. In patients who have a compromised immune system, other viruses such as herpes, HIV and coxsackievirus may also be potential causes
+Bacterial[edit] => This is another major cause of acute laryngitis, and may develop in conjunction with or due to a viral infection.[1] Common bacterial strains are; group A streptococcus, Streptococcus pneumoniae, C. diphtheriae, M. catarrhalis, Haemophilus influenzae, Bordetella pertussis, Bacillus anthracis, and M. tuberculosis. In developing countries, more unusual bacterial causes may occur such as mycobacterial and syphilitic, though these may occur in developed nations as well.[1
+Fungal[edit] => Laryngitis caused by fungal infection is common but not frequently diagnosed according to a review by BMJ and can account for up to 10% of acute laryngitis cases.[1] Patients with both functioning and impaired immune systems can develop fungal laryngitis, which may develop as a result of recent antibiotic or inhaled corticosteroids use.[1] Certain strains of fungi that may cause laryngitis include; Histoplasma, Blastomyces, Candida (especially in immunocompromised persons), and Cryptococcus and Coccidioides
+Trauma[edit] => Often due to excessive use of the vocal folds such as excessive yelling, screaming, singing. Though this often results in damage to the outer layers of the vocal folds, the subsequent healing may lead to changes in the physiology of the folds.[1] Another potential cause of inflammation may be overuse of the vocal cords.[5] [6] [7] [8] [9] Laryngeal trauma, including iatrogenic (caused by endotracheal intubation), can also result in inflammation of the vocal cords.[11
+Allergies[edit] => Findings are unclear as to whether asthma may cause symptoms commonly associated with laryngitis.[1] Some researchers have posited that allergic causes of laryngitis are often misdiagnosed as being the result of acid reflux.[12
+Reflux[edit] => One possible explanation of chronic laryngitis is that inflammation is caused by gastro-oesophageal reflux which causes subsequent irritation of the vocal folds.[13
+Autoimmune disorders[edit] => Approximately between 30-75% of persons with rheumatoid arthritis report symptoms of laryngitis.[1]&Symptoms of laryngitis are present in only 0.5-5% of people that have sarcoidosis.[1] According to a meta-analysis by Silva et al. (2007), this disease is often an uncommon cause of laryngeal symptoms and is frequently misdiagnosed as another voice disorder.[14
+Acute laryngitis&Chronic laryngitis Granulomatous laryngitis Pseudomyxomatous laryngitis&Granulomatous laryngitis&Pseudomyxomatous laryngiti
+Visual diagnosis[edit] => The larynx itself will often show erythema (reddening) and edema (swelling). This can be seen with laryngoscopy or stroboscopy (method depends on the type of laryngitis).[7]:108 Other features of the laryngeal tissues may include
+Redness of the laryngeal tissues (acute)&Dilated blood vessels (acute)&Thick, yet dry laryngal tissue (chronic)&Stiff vocal folds&Sticky secretions between the vocal folds and nearby structures (the interarytenoid region
+Referral[edit] => Some signs and symptoms indicate the need for early referral.[1] These include
+Difficulty swallowing&Vocal stridor&Ear pain&Recent weight loss&History of smoking&Current or recent radiotherapy treatment (in the neck region)&Recent neck surgery or surgery involving endotracheal tubing&Person is a professional voice user (teacher, singer, actor, call center worker, and so on
+The primary symptom of laryngitis is a hoarse voice.[7]:108 Because laryngitis can have various causes, other signs and symptoms may vary.[8] They can include
+Dry or sore throat&Coughing (both a causal factor and a symptom of laryngitis)&Frequent throat clearing&Increased saliva production&Dysphagia (difficulty swallowing)&Sensation of swelling in the area of the larynx (discomfort in the front of the neck)&Globus pharyngeus (feeling like there is a lump in the throat)&Cold or flu-like symptoms (which, like a cough, may also be a causal factor for laryngitis)&Swollen lymph nodes in the throat, chest, or face&Fever&General muscle pain (myalgia)&Shortness of breath, predominantly in childre
+Voice quality[edit] => Aside from a hoarse-sounding voice, changes to pitch and volume may occur with laryngitis. Speakers may experience a lower or higher pitch than normal, depending on whether their vocal folds are swollen or stiff.[1][9] They may also have breathier voices, as more air flows through the space between the vocal folds (the glottis), quieter volume[10] and a reduced range.[1][1]
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DISNET disease texts/100 Original Disease Texts/Lateral medullary syndrome.txt

+It is the clinical manifestation resulting from occlusion of the posterior inferior cerebellar artery (PICA) or one of its branches or of the vertebral artery, in which the lateral part of the medulla oblongata infarcts, resulting in a typical pattern. The most commonly affected artery is the vertebral artery, followed by the PICA, superior middle and inferior medullary arteries.
+Since lateral medullary syndrome is often caused by a stroke, diagnosis is time dependent. Diagnosis is usually done by assessing vestibular-related symptoms in order to determine where in the medulla that the infarction has occurred. Head Impulsive Nystagmus Test of Skew (HINTS) examination of oculomotor function is often performed, along with computed tomography (CT) or magnetic resonance imaging (MRI) to assist in stroke detection. Standard stroke assessment must be done to rule out a concussion or other head trauma.[2]
+This syndrome is characterized by sensory deficits that affect the trunk and extremities contralaterally (opposite to the lesion), and sensory deficits of the face and cranial nerves ipsilaterally (same side as the lesion). Specifically a loss of pain and temperature sensation if the lateral spinothalamic tract is involved. The cross body finding is the chief symptom from which a diagnosis can be made.
+Patients often have difficulty walking or maintaining balance (ataxia), or difference in temperature of an object based on which side of the body the object of varying temperature is touching. Some patients may walk with a slant or suffer from skew deviation and illusions of room tilt. The nystagmus is commonly associated with vertigo spells. These vertigo spells can result in falling, caused from the involvement of the region of Deiters’ nucleus.
+Common symptoms with lateral medullary syndrome may include difficulty swallowing, or dysphagia. This can be caused by the involvement of the nucleus ambiguous, as it supplies the vagus and glossopharyngeal nerves. Slurred speech (dysarthria), and disordered vocal quality (dysphonia) are also common. The damage to the cerebellum or the inferior cerebellar peduncle can cause ataxia. Damage to the hypothalamospinal fibers disrupts sympathetic nervous system relay and gives symptoms that are similar to the symptoms caused by Horner syndrome – such as miosis, anhidrosis and partial ptosis.
+Palatal myoclonus, the twitching of the muscles of the mouth, may be observed due to disruption of the central tegmental tract. Other symptoms include: hoarseness, nausea, vomiting, a decrease in sweating, problems with body temperature sensation, dizziness, difficulty walking, and difficulty maintaining balance. Lateral medullary syndrome can also cause bradycardia, a slow heart rate, and increases or decreases in the patients average blood pressure. [1]
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DISNET disease texts/100 Original Disease Texts/MERRF syndrome.txt

+The cause of MERRF disorder is due to the mitochondrial genomes mutation. This means that its a pathogenic variants in mtDNA and is transmitted by maternal inheritance. A four points mutations in the genome can be identified which are associated with MERRF: A8344G, T8356C, G8361A, and G8363A. The point mutation A8344G is mostly associated with MERRF,[6] in a study published by Paul Jose Lorenzoni from the Department of neurology at University of Panama[7] stated that 80% of the patients with MERRF disease exhibited this point mutation.This point mutation disrupts the mitochondrial gene for tRNA-Lys and so disrupts synthesis of proteins essential for oxidative phosphorylation.The remaining mutations only account for 10% of cases, and the remaining 10% of he patients with MERRF did not have an identifiable mutation in the mitochondrial DNA.
+Many genes are involved.[8] These genes include:
+MT-TK[9]&MT-TL1&MT-TH[5]&MT-TS1[10]&MT-TS2&MT-TF[11
+It involves the following characteristics:
+progressive myoclonic epilepsy&"Ragged Red Fibers" - clumps of diseased mitochondria accumulate in the subsarcolemmal region of the muscle fiber and appear as "Ragged Red Fibers" when muscle is stained with modified Gömöri trichrome stain
+There is currently no cure for MERRF.
+The diagnosis varies from individual to individual, each is evaluated and diagnosed according to their age, clinical phenotype and pressed inheritance pattern.[14] If the Individual has been experiencing myoclonus the doctor will run a series of genetic studies to determine if its a mitochondrial disorder.
+The molecular genetic studies are run to identify the reason of for the mutations underlying the mitochondrial dysfunction. This approach will avoid the need for a muscle biopsy or an exhaustive metabolic evaluation. After the sequencing the mitochondrial genomes, four points mutations in the genome can be identified which are associated with MERRF: A8344G, T8356C, G8361A, and G8363A. The point mutation[9] A8344G is mostly associated with MERRF,[6] in a study published by Paul Jose Lorenzoni from the Department of neurology at University of Panama[7] stated that 80% of the patients with MERRF disease exhibited this point mutation. The remaining mutations only account for 10% of cases, and the remaining 10% of the patients with MERRF did not have an identifiable mutation in the mitochondrial DNA.[12]
+If a patient does not exhibit mitochondrial DNA mutations, there are other ways that they can be diagnosed with MERRF. They can go through computed tomography (CT) or magnetic resonance imaging (MRI).The classification for the severity of MERRF syndrome is difficult to distinguish since most individuals will exhibit multi-symptoms.[12] For children with complex neurologic or multi-system involvement, as the one described below, is often necessary.[4]
+History and Physical Examination of the patient[edit] => A detailed family history should be obtained from at least three generations. In particularly a history to determine if there has been any neonatal and childhood deaths: Also a way to determine if any one of the family members exhibit any of the features of the multi-system disease. Specifically if there has been a maternal inheritance, when the disease is transmitted to females only, or if there is a family member who experienced a multi system involvement such as:[14] Brain condition that a family member has been record to have such as seizures, dystonia, ataxia, or stroke like episodes.The eyes with optic atrophy, the skeletal muscle where there has been a history of myalgia, weakness or ptosis. Also in the family history look for neuropathy and dysautonomia, or observe heart conditions such ascardiomyopathy. The patients history might also exhibit a problem in their kidney, such as proximal nephron dysfunction. An endocrine condition, for example diabetes and hypoparathyroidism. The patient might have also had gastrointestinal condition which could have been due to liver disease, episodes of nausea or vomiting. Multiple lipomas in the skin, sideroblastic anemia and pancytopenia in the metabolic system or short stature might all be examples of patients with possible symptoms of MERRF disease.
+An individual displaying MERRFs syndrome will manifest not only a single symptom, but regularly patients display more than one affected body part at a time. It has been observed that patients with MERRF syndrome will primarily display Myoclonus as a first symptom, along with it they can also manifest seizures, cerebellar ataxia and myopathy.[3] Secondary features include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity or multiple lipomata. Additional symptoms include dementia, optic atrophy, bilateral deafness and peripheral neuropathy, spasticity, lipomatosis, and/or cardiomyopathy with wolff parkinson-white syndrome. Most patients will not exhibit all of these symptoms, however more than one of these symptoms will be present in a patient who has been diagnosed with MERRFS disease. Due to the multi-symptoms presented by the individual, the severity of the syndrome is very difficult to evaluate.[5] Mitochondrial disorders may present at any age, and this holds truth for MERRS, since it forms part of them. Therefore, if a patient is presenting some of these symptoms, the doctor is able to narrow it down to MEERF mitochondrial disorder.[4]
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DISNET disease texts/100 Original Disease Texts/Metal fume fever.txt

+Metal fume fever is due to the inhalation of certain metals, either as fine dust or most commonly as fumes. Simple metal compounds such as oxides are equally capable of causing it. The effects of particularly toxic compounds, such as nickel carbonyl, are not considered merely metal fume fever.[citation needed]
+Exposure usually arises through hot metalworking processes, such as smelting and casting of zinc alloys, welding of galvanized metals, brazing, or soldering. If the metal concerned is particularly high-risk, the residue from cold sanding processes may also cause fume fever, even if the dose is lower. It may also be caused by electroplated surfaces or metal-rich anti-corrosion paint, such as cadmium passivated steel or zinc chromate primer on aluminium aircraft parts. Exposure has also been reported in use of lead-free ammunition, by the harder steel core stripping excess metal from the jacket of the bullet and barrel of the rifle.[9]
+The most plausible metabolic source of the symptoms is a dose-dependent release of certain cytokines, an event which occurs by inhaling metal oxide fumes that injure the lung cells. This is not an allergic reaction, though allergic reactions to metal fumes can occur.[10]
+Diagnosis is primarily anecdotal, that is, it depends upon a good occupational history. Diagnosis of metal fume fever can be easily missed because the complaints are non-specific, resemble a number of other common illnesses, and presentation occurs typically 2–4 hours after the exposure.[11] When respiratory symptoms are prominent, metal fume fever may be confused with acute bronchitis or pneumonia. The diagnosis is based primarily upon a history of exposure to metal oxide fumes. Cain and Fletcher (2010) report a case of metal fume fever that was diagnosed only by taking a full occupational history and by close collaboration between primary and secondary health care personnel.[12]
+Physical symptoms vary among persons exposed, depending largely upon the stage in the course of the syndrome during which examination occurs. Patients may present with wheezing or crackles in the lungs. They typically have an increased white blood cell count, and urine, blood plasma and skin zinc levels may (unsurprisingly) be elevated. Chest X-ray abnormalities may also be present.[10]
+An interesting feature of metal fume fever involves rapid adaptation to the development of the syndrome following repeated metal oxide exposure. Workers with a history of recurrent metal fume fever often develop a tolerance to the fumes. This tolerance, however, is transient, and only persists through the work week. After a weekend hiatus, the tolerance has usually disappeared. This phenomenon of tolerance is what led to the name "Monday Fever".[citation needed]
+In 2006, approximately 700 metal fume exposures were reported to the United States Poison control center. The American Welding Society estimated that 2500 employees in the steel industry develop metal fume fever in the US each year and that the majority of the cases are not reported.[citation needed]
+The signs and symptoms are generally flu-like. They include fever, chills, nausea, headache, fatigue, muscle aches, joint pains, lack of appetite, shortness of breath, pneumonia, chest pain, change in blood pressure, and coughing. A sweet or metallic taste in the mouth may also be reported, along with a dry or irritated throat which may lead to hoarseness.[7] Symptoms of a more severe metal toxicity may also include a burning sensation in the body, shock, no urine output, collapse, convulsions, shortness of breath, yellow eyes or yellow skin, rash, vomiting, watery or bloody diarrhea or low or high blood pressure, which require prompt medical attention.[8] Flu-like symptoms normally disappear within 24 to 48 hours. Full recovery often requires one to three weeks.[citation needed]
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DISNET disease texts/100 Original Disease Texts/Morvan's syndrome.txt

+General symptoms[edit] => In one of the few reported cases, the subject presented with muscle weakness and fatigue, muscle twitching, excessive sweating and salivation, small joint pain, itching and weight loss. The subject also developed confusional episodes with spatial and temporal disorientation, visual and auditory hallucinations, complex behavior during sleep and progressive nocturnal insomnia associated with diurnal drowsiness. There was also severe constipation, urinary incontinence, and excessive lacrimation. When left alone, the subject would slowly lapse into a stuporous state with dreamlike episodes characterized by complex and quasi-purposeful gestures and movements (enacted dreams). Marked hyperhidrosis and excessive salivation were evident. Neurological examination disclosed diffuse muscle twitching and spontaneous and reflex myoclonus, slight muscle atrophy in the limbs, absence of tendon reflexes in the lower limbs and diffuse erythema especially on the trunk with scratching lesions of the skin.[4] Compulsive behaviours, stereotypies and reduplicative paramnesias can be part of the CNS spectrum.[7]
+Insomnia[edit] => In all of the reported cases, the need for sleep was severely reduced and in some cases not necessary. The duration of sleep in one case decreased to about 2–4 hours per 24-hour period.[8] Clinical features pertaining to insomnia include daytime drowsiness associated with a loss of ability to sleep, intermingled with confusional oneiric status, and the emergence of atypical REM sleep from wakefulness. The Polysomnogram (PSG) picture of this disease is characterized by an inability to generate physiological sleep (key features are the suppression of the hallmarks of stage 2 non-REM sleep: spindles and K complexes) and by the emergence of REM sleep without atonia. The involvement of the thalamus and connected limbic structures in the pathology indicate the prominent role that the limbic thalamus plays in the pathophysiology of sleep.[3] In a case documented in 1974, PSG findings documented the sustained absence of all sleep rhythms for up to a period of 4 months.[5]
+Electroencephalography (EEG) in one case was dominated by "wakefulness" and “subwakefulness” states alternating or intermingled with short (< 1 min) atypical REM sleep phases, characterized by a loss of muscle atonia. The “subwakefulness” state was characterized by 4–6 Hz theta activity intermingled with fast activity and desynchronized lower voltage theta activity, behaviourally associated with sleep-like somatic and autonomic behavior. The subject was said to suffer from “agrypnia excitata”, which consists of severe total insomnia of long duration associated with decreased vigilance, mental confusion, hallucinations, motor agitation, and complex motor behavior mimicking dreams, and autonomic activation. CNS and autonomic symptoms were caused by impaired corticolimbic control of the subcortical structures regulating the sleep-wake and autonomic functions.[4]
+Neuromyotonia[edit] => Neuromyotonia refers to muscle twitching and cramping at rest that is exacerbated with exercise. It is caused by sustained or repetitive spontaneous muscle activity of peripheral nerve origin. Myokymia, or spontaneous rippling and twitching movements of muscles, is a visible component of neuromyotonia. Electromyography (EMG) discloses spontaneous, repetitive motor unit or single fiber discharges firing in irregular rhythmic bursts at high intraburst frequencies.[1] Some of the muscles exhibiting twitching include the bilateral gastrocnemii, quadriceps femoris, biceps brachii, and right masseter.[8] In vivo electrophysiological studies suggest at least some dysfunction of the muscle cell membrane.[6] In the examined muscles, no abnormal insertional activity or fibrillation potentials were noted. Nerve conduction studies were normal.[4]
+Other symptoms[edit] => Breathing difficulties can occur, resulting from neuromyotonic activity of the laryngeal muscles. Laryngeal spasm possibly resulting from neuromyotonia has been described previously, and this highlights that, in patients with unexplained laryngospasm, neuromytonia should be added to the list of differential diagnoses.[6]
+Studies have shown subtly decreased metabolism on positron emission tomography (PET) and single photon emission computed tomography (SPECT) in the left inferior frontal and left temporal lobes.[8] and or basal ganglia hypermetabolism.[7] Ancillary laboratory tests including MRI and brain biopsy have confirmed temporal lobe involvement. Cranial MRI shows increased signal in the hippocampus.[9]
+Cerebral spinal fluid (CSF) shows normal protein, glucose, white blood cell, and IgG index but there are weak oligoclonal bands, absent in the blood. Marked changes in circadian serum levels of neurohormones and increased levels of peripheral neurotransmitters were also observed. The absence of morphological alterations of the brain pathology, the suggestion of diffusion of IgG into the thalamus and striatum, more marked than in the cortex (consistent with effects on the thalamolimbic system) the oligoclonal bands in the CSF and the amelioration after PE all strongly support an antibody-mediated basis for the condition.[4] Raised CSF IgG concentrations and oligoclonal bands have been reported in patients with psychosis. Anti-acetylcholine receptors (anti-AChR) antibodies have also been detected in patients with thymoma, but without clinical manifestations of myasthenia gravis.[1] There have also been reports of non-paraneoplastic limbic encephalitis associated with raised serum VGKC suggesting that these antibodies may give rise to a spectrum of neurological disease presenting with symptoms arising peripherally, centrally, or both. Yet, in two cases, oligoclonal bands were absent in the CSF and serum, and CSF immunoglobulin profiles were unremarkable.[2]
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DISNET disease texts/100 Original Disease Texts/Myocarditis.txt

+A large number of causes of myocarditis have been identified, but often a cause cannot be found. In Europe and North America, viruses are common culprits. Worldwide, however, the most common cause is Chagas' disease, an illness endemic to Central and South America that is due to infection by the protozoan Trypanosoma cruzi.[10] Many of the causes listed below, particularly those involving protozoa, fungi, parasites, allergy, autoimmune disorders, and drugs are also causes of eosinophilic myocarditis.
+Infections[edit] => Viral (adenovirus, parvovirus B19, coxsackie virus, HIV, enterovirus, rubella virus, polio virus, cytomegalovirus, human herpesvirus 6 and possibly hepatitis C)&Protozoan (Trypanosoma cruzi causing Chagas disease and Toxoplasma gondii)&Bacterial (Brucella, Corynebacterium diphtheriae, gonococcus, Haemophilus influenzae, Actinomyces, Tropheryma whipplei, Vibrio cholerae, Borrelia burgdorferi, leptospirosis, and Rickettsia, Mycoplasma pneumoniae)&Fungal (Aspergillus)&Parasitic (ascaris, Echinococcus granulosus, Paragonimus westermani, schistosoma, Taenia solium, Trichinella spiralis, visceral larva migrans, and Wuchereria bancrofti
+Bacterial myocarditis is rare in patients without immunodeficiency.
+Toxins[edit] => Drugs, including alcohol, anthracyclines and some other forms of chemotherapy, and antipsychotics, e.g. clozapine, also some designer drugs such as mephedrone[12
+Immunologic[edit] => Allergic (acetazolamide, amitriptyline)&Rejection after a heart transplant&Autoantigens (scleroderma, systemic lupus erythematosus, sarcoidosis, systemic vasculitis such as eosinophilic granulomatosis with polyangiitis, and granulomatosis with polyangiitis, Kawasaki disease)&Toxins (arsenic, toxic shock syndrome toxin, carbon monoxide, or snake venom)&Heavy metals (copper or iron
+Physical agents[edit] => Electric shock, hyperpyrexia, and radiatio
+Myocarditis refers to an underlying process that causes inflammation and injury of the heart. It does not refer to inflammation of the heart as a consequence of some other insult. Many secondary causes, such as a heart attack, can lead to inflammation of the myocardium and therefore the diagnosis of myocarditis cannot be made by evidence of inflammation of the myocardium alone.[15][16]
+Myocardial inflammation can be suspected on the basis of electrocardiographic (ECG) results, elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.[10]
+The ECG findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis).[10]
+The gold standard is still biopsy of the myocardium, in general done in the setting of angiography. A small tissue sample of the endocardium and myocardium is taken, and investigated by a pathologist by light microscopy and—if necessary—immunochemistry and special staining methods. Histopathological features are myocardial interstitium with abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure.[10]
+Cardiac magnetic resonance imaging (cMRI or CMR) has been shown to be very useful in diagnosing myocarditis by visualizing markers for inflammation of the myocardium.[17] Recently, consensus criteria for the diagnosis of myocarditis by CMR have been published.[18]
+Play media Ultrasound showing cardiogenic shock due to myocarditis[19]&Play media Ultrasound showing cardiogenic shock due to myocarditis[19]&Play media Ultrasound showing cardiogenic shock due to myocarditis[19
+The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium or to the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include the following:[10]
+Chest pain (often described as "stabbing" in character)&Congestive heart failure (leading to swelling, shortness of breath and liver congestion)&Palpitations (due to abnormal heart rhythms)&Sudden death (in young adults, myocarditis causes up to 20% of all cases of sudden death)[11]&Fever (especially when infectious, e.g. in rheumatic fever)&Symptoms in young children tend to be more nonspecific, with generalized malaise, poor appetite, abdominal pain, and chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing, and is often mistaken for asthma
+Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, rash, diarrhea, joint pains, and easily becoming tired.
+Myocarditis is often associated with pericarditis, and many people with myocarditis present with signs and symptoms that suggest myocarditis and pericarditis at the same time.
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DISNET disease texts/100 Original Disease Texts/Necatoriasis.txt

+Necatoriasis is caused by N. americanus. N. americanus can be divided into two areas – larvae and adult stage. The third stage larvae are guided to human skin by following thermal gradients.[3] Typically, the larvae enter through the hands and feet following contact with contaminated soil. A papular, pruritic, itchy rash will develop around the site of entry into the human host.[4] This is also known as "ground itch". Generally, migration through the lungs is asymptomatic but a mild cough and pharyngeal irritation may occur during larval migration in the airways. Once larvae break through the alveoli and are swallowed, they enter the gastrointestinal tract and attach to the intestinal mucosa where they mature into adult worms. The hookworms attach to the mucosal lining using their cutting plates which allows them to penetrate blood vessels and feed on the host's blood supply. Each worm consumes 30μl of blood per day. The major issue results from this intestinal blood loss which can lead to iron-deficiency anemia in moderate to heavy infections. Other common symptoms include epigastric pain and tenderness, nausea, exertional dyspnea, pain in lower extremities and in joints, sternal pain, headache, fatigue, and impotence.[5] Death is rare in humans.
+The standard method for diagnosing necatoriasis is through identification of N. americanus eggs in a fecal sample using a microscope. Eggs can be difficult to visualize in a lightly infected sample so a concentration method is generally used such as flotation or sedimentation.[6] However, the eggs of A. duodenale and N. americanus cannot be distinguished; thus, the larvae must be examined to identify these hookworms. Larvae cannot be found in stool specimens unless the specimen was left at ambient temperature for a day or more.
+The most common technique used to diagnose a hookworm infection is to take a stool sample, fix it in 10% formalin, concentrate it using the formalin-ethyl acetate sedimentation technique, and then create a wet mount of the sediment for viewing under a microscope.
+When adult worms attach to the villi of the small intestine, they suck on the host's blood, which may cause abdominal pain, diarrhea, cramps, and weight loss that can lead to anorexia. Heavy infections can lead to the development of iron deficiency and hypochromic microcytic anemia. This form of anemia in children can give rise to physical and mental retardation. Infection caused by cutaneous larvae migrans, a skin disease in humans, is characterized by skin ruptures and severe itching.[2]
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DISNET disease texts/100 Original Disease Texts/Nicotine poisoning.txt

+Increased nicotine or cotinine (the nicotine metabolite) is detected in urine or blood, or serum nicotine concentrations increase.
+Nicotine poisoning tends to produce symptoms that follow a biphasic pattern. The initial symptoms are mainly due to stimulatory effects and include nausea and vomiting, excessive salivation, abdominal pain, pallor, sweating, hypertension, tachycardia, ataxia, tremor, headache, dizziness, muscle fasciculations, and seizures.[4] After the initial stimulatory phase, a later period of depressor effects can occur and may include symptoms of hypotension and bradycardia, central nervous system depression, coma, muscular weakness and/or paralysis, with difficulty breathing or respiratory failure.[1][4][26][27]
+From September 1, 2010 to December 31, 2014, there were at least 21,106 traditional cigarette calls to US poison control centers.[28] During the same period, the ten most frequent adverse effects to traditional cigarettes reported to US poison control centers were vomiting (80.0%), nausea (9.2%), drowsiness (7.8%), cough (7.2%), agitation (6.6%), pallor (3.0%), tachycardia (2.5%), diaphoresis (1.5%), dizziness (1.5%), and diarrhea (1.4%).[28] 95% of traditional cigarette calls were related to children 5 years old or less.[28] Most of the traditional cigarette calls were a minor effect.[28]
+Calls to US poison control centers related to e-cigarette exposures involved inhalations, eye exposures, skin exposures, and ingestion, in both adults and young children.[29] Minor, moderate, and serious adverse effects involved adults and young children.[28] Minor effects correlated with e-cigarette liquid poisoning were tachycardia, tremor, chest pain and hypertension.[30] More serious effects were bradycardia, hypotension, nausea, respiratory paralysis, atrial fibrillation and dyspnea.[30] The exact correlation is not fully known between these effects and e-cigarettes.[30] 58% of e-cigarette calls to US poison control centers were related to children 5 years old or less.[28] E-cigarette calls had a greater chance to report an adverse effect and a greater chance to report a moderate or major adverse effect than traditional cigarette calls.[28] Most of the e-cigarette calls were a minor effect.[28]
+From September 1, 2010 to December 31, 2014, there were at least 5,970 e-cigarette calls to US poison control centers.[28] During the same period, the ten most frequent adverse effects to e-cigarettes and e-liquid reported to US poison control centers were vomiting (40.4%), eye irritation or pain (20.3%), nausea (16.8%), red eye or conjunctivitis (10.5%), dizziness (7.5%), tachycardia (7.1%), drowsiness (7.1%), agitation (6.3%), headache (4.8%), and cough (4.5%).[28]
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DISNET disease texts/100 Original Disease Texts/Non-alcoholic fatty liver disease.txt

+Diet[edit] => Soft drinks have been linked to NAFLD due to high concentrations of fructose, which may be present either in high-fructose corn syrup or, in similar quantities, as a metabolite of sucrose. The quantity of fructose delivered by soft drinks may cause increased deposition of fat in the abdomen.[11][12]
+Genetics[edit] => Native American men have a high prevalence of non-alcoholic fatty liver disease.[citation needed] Two genetic mutations for this susceptibility have been identified, and these mutations provided clues to the mechanism of NASH and related diseases.[citation needed]
+Polymorphisms (genetic variations) in the single-nucleotide polymorphisms (SNPs) T455C and C482T in APOC3 are associated with fatty liver disease, insulin resistance, and possibly hypertriglyceridemia. 95 healthy Asian Indian men and 163 healthy non-Asian Indian men around New Haven, Connecticut were genotyped for polymorphisms in those SNPs. 20% homogeneous wild both loci. Carriers of T-455C, C-482T, or both (not additive) had a 30% increase in fasting plasma apolipoprotein C3, 60% increase in fasting plasma triglyceride and retinal fatty acid ester, and 46% reduction in plasma triglyceride clearance. Prevalence of non-alcoholic fatty liver disease was 38% in carriers, 0% wild (normal). Subjects with fatty liver disease had marked insulin resistance.[13]
+Drugs[edit] => NAFLD can also be caused by some medications (drug-induced illness):[4]
+Amiodarone&Antiviral drugs (nucleoside analogues)&Aspirin rarely as part of Reye's syndrome in children&Corticosteroids&Methotrexate&Tamoxifen&Tetracyclin
+Common findings are elevated liver enzymes and a liver ultrasound showing steatosis. An ultrasound may also be used to exclude gallstone problems (cholelithiasis). A liver biopsy (tissue examination) is the only test widely accepted as definitively distinguishing NASH from other forms of liver disease and can be used to assess the severity of the inflammation and resultant fibrosis.[4]
+Non-invasive diagnostic tests have been developed, such as FibroTest, that estimates liver fibrosis,[15] and SteatoTest, that estimates steatosis,[16] however their use has not been widely adopted.[17] Apoptosis has been indicated as a potential mechanism of hepatocyte injury as caspase-cleaved cytokeratin 18 (M30-Apoptosense ELISA) in serum/plasma is often elevated in patients with NASH and tests based on these parameters have been developed;[18] however, as the role of oncotic necrosis has yet to be examined it is unknown to what degree apoptosis acts as the predominant form of injury.[19][20]
+Other diagnostic tests are available. Relevant blood tests include erythrocyte sedimentation rate, glucose, albumin, and kidney function. Because the liver is important for making proteins used in coagulation some coagulation related studies are often carried out especially the INR (international normalized ratio). In people with fatty liver with associated inflammatory injury (steatohepatitis) blood tests are usually used to rule out viral hepatitis (hepatitis A, B, C and herpes viruses like EBV or CMV), rubella, and autoimmune related diseases. Hypothyroidism is more prevalent in NASH patients which would be detected by determining the TSH.[21]
+It has been suggested that in cases involving overweight patients whose blood tests do not improve on losing weight and exercising that a further search of other underlying causes is undertaken. This would also apply to those with fatty liver who are very young or not overweight or insulin-resistant. In addition those whose physical appearance indicates the possibility of a congenital syndrome, have a family history of liver disease, have abnormalities in other organs, and those that present with moderate to advanced fibrosis or cirrhosis.[22]
+Most people with NAFLD have few or no symptoms. Patients may complain of fatigue, malaise, and dull right-upper-quadrant abdominal discomfort. Mild jaundice may be noticed, although this is rare. More commonly NAFLD is diagnosed following abnormal liver function tests during routine blood tests. By definition, alcohol consumption of over 20 g/day (about 25 ml/day of net ethanol) excludes the condition.[4]
+NAFLD is associated with insulin resistance and metabolic syndrome (obesity, combined hyperlipidemia, diabetes mellitus (type II), and high blood pressure).[4][1] Recent research has shown that NAFLD increases the risk of cardiovascular diseases,[8] such as cardiac arrhythmias.[9][10]
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DISNET disease texts/100 Original Disease Texts/Non-small-cell lung carcinoma.txt

+Smoking is by far the leading risk factor for lung cancer.[36] Cigarette smoke contains more than 6,000 components, many of which lead to DNA damage[37] (see table of tobacco-related DNA damages in Tobacco smoking).
+Other causes include radon, exposure to secondhand smoke, exposure to substances such as asbestos, chromium, nickel, beryllium, soot, or tar, family history of lung cancer, and air pollution.[4] [36]
+In general, DNA damage appears to be the primary underlying cause of cancer.[38] Though most DNA damages are repairable,[37] leftover un-repaired DNA damages from cigarette smoke are the likely cause of NSCLC.
+DNA replication past an un-repaired damage can give rise to a mutation because of inaccurate translesion synthesis. In addition, during repair of DNA double-strand breaks, or repair of other DNA damages, incompletely cleared sites of repair can lead to epigenetic gene silencing.[39][40]
+Many of the symptoms of NSCLC can be signs of other diseases, but having chronic or overlapping symptoms may be a signal of the presence of the disease. Some symptoms are indicators of less advanced cases while some may signal that the cancer has spread. Some of the symptoms of less advanced cancer include chronic cough, coughing up blood, chest pain, hoarseness, shortness of breath, wheezing, chest pain, weight loss, and loss of appetite.[14] A few more symptoms associated with the early progression of the disease are feeling weak, being very tired, having trouble swallowing, swelling in the face or neck, and continuous or recurring infections like bronchitis or pneumonia.[4][14][15] Signs of more advanced cases include bone pain, nervous system changes (headache, weakness, dizziness, balance problems, seizures), jaundice, lumps near the surface of the body, numbness of extremities due to Pancoast Syndrome, and nausea, vomiting and constipation brought on by hypercalcemia.[14][15] Some more of the symptoms that indicate further progression of the cancer include shortness of breath, superior vena cava syndrome, trouble swallowing, large amounts of mucus, weakness, fatigue, and hoarseness.[15]
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DISNET disease texts/100 Original Disease Texts/Normal pressure hydrocephalus.txt

+Diagnosis of NPH is usually first led by brain imaging, either CT or MRI, to rule out any mass lesions in the brain. This is then followed by lumbar puncture and evaluation of clinical response to removal of CSF. This can be followed by continuous external lumbar CSF drainage during 3 or 4 days.
+CT scan may show enlarged ventricles without convolutional atrophy.&MRI may show some degree of transependymal migration of CSF surrounding the ventricles on T2/FLAIR sequence. Imaging however cannot differentiate between pathologies with similar clinical picture like Alzheimer's dementia, vascular dementia or Parkinson's disease.[6]&Following imaging, lumbar puncture is usually the first step in diagnosis and the CSF opening pressure is measured carefully. In most cases, CSF pressure is usually above 155 mmH2O. Clinical improvement after removal of CSF (30 mL or more) has a high predictive value for subsequent success with shunting. This is called the "lumbar tap test" or Miller Fisher test. On the contrary, a "negative" test has a very low predictive accuracy, as many patients may improve after a shunt in spite of lack of improvement after CSF removal.&Infusion test is a test that may have higher sensitivity and specificity than a lumbar puncture, but is not performed in most centers. The outflow conductance (Cout) of the cerebrospinal fluid (CSF) system is a parameter considered by some centers to be predictive in selection for hydrocephalus surgery. Cout can be determined through an infusion test. This is not a test that is normally performed prior to shunting, but may become more accepted.&In some centers, External lumbar drainage has been shown to have the highest sensitivity and specificity with regards to predicting a successful outcome following surgery.[7
+Types[edit] => There are two types of normal pressure hydrocephalus: idiopathic and secondary. The secondary type of NPH can be due to a subarachnoid hemorrhage, head trauma, tumor, infection in the central nervous system, or a complication of cranial surgery.[8]
+NPH may exhibit a classic triad of clinical findings (known as the Adams triad or Hakim's triad) of urinary incontinence, gait disturbance, and dementia (commonly referred to as "wet, wacky and wobbly" or "weird walking water").
+Gait disturbance is typically the initial and most prominent symptom of the triad and may be progressive, due to expansion of the ventricular system, particularly at the level of the lateral ventricles, leading to traction on the corticospinal tract motor fibers descending to the lumbosacral spinal cord. The gait disturbance can be classified as mild (cautious gait or difficulty with tandem gait), marked (evident difficulty walking or considerable unstable gait) or severe (unaided gait not possible)[2] In the early stages, most often this gait disturbance occurs in the form of unsteadiness and impaired balance, especially when encountering stairs and curbs. Weakness and tiredness of the legs may also be part of the complaint, although examination discloses no paresis or ataxia.[3] Often a mobility aid is used for added stability, once the patient has reached the mild to marked stage. Such aids may include a quad cane or wheeled walker. The patient's gait at the marked stage will often show a decrease in step height and foot-floor clearance, as well as a decrease in walking speed. This style is often referred to as a magnetic gait, in which the feet appear to be stuck to the walking surface, and is considered the characteristic gait disturbance of NPH. The gait may begin to mimic a Parkinsonian gait, with short shuffling steps and stooped, forward-leaning posture, but there is no rigidity or tremor. An increased tendency to fall backwards is also seen, and a broad-based gait may be employed by the patient in order to increase their base of support and thereby their stability. In the very late stages, the patient can progress from an inability to walk, to an inability to stand, sit, rise from a chair or turn over in bed; this advanced stage is referred to as "hydrocephalic astasia-abasia".[3]&Dementia is predominantly frontal lobe in nature and of the subcortical type of dementia. It presents in the form of abulia, forgetfulness, inertia, inattention, decreased speed of complex information procession (also described as a dullness in thinking and actions), and disturbed manipulation of acquired knowledge, which is reflective of the loss of integrity of the frontal lobes.[4] Memory problems are usually a component of the overall problem and have been predominant in some cases, which can lead to the misdiagnosis of Alzheimer's disease. However, in NPH there may be an obvious discrepancy between (often severely) impaired recall and intact or much less impaired recognition. The dementia is thought to result from traction on frontal and limbic fibers that also run in the periventricular region.&Urinary incontinence appears late in the illness, and is found to be of the spastic hyperreflexic, increased-urgency type associated with decreased inhibition of bladder contractions and detrusor instability.[4] In the most severe cases, bladder hyperreflexia is associated with a lack of concern for micturition due to the severe frontal lobe cognitive impairment.[4] This is also known as "frontal lobe incontinence", where the patient becomes indifferent to their recurrent urinary symptoms
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DISNET disease texts/100 Original Disease Texts/Obesity hypoventilation syndrome.txt

+Formal criteria for diagnosis of OHS are:[1][2][3]
+Body mass index over 30 kg/m2 (a measure of obesity, obtained by taking one's weight in kilograms and dividing it by one's height in meters squared)&Arterial carbon dioxide level over 45 mmHg or 6.0 kPa as determined by arterial blood gas measurement&No alternative explanation for hypoventilation, such as use of narcotics, severe obstructive or interstitial lung disease, severe chest wall disorders such as kyphoscoliosis, severe hypothyroidism (underactive thyroid), neuromuscular disease or congenital central hypoventilation syndrom
+If OHS is suspected, various tests are required for its confirmation. The most important initial test is the demonstration of elevated carbon dioxide in the blood. This requires an arterial blood gas determination, which involves taking a blood sample from an artery, usually the radial artery. Given that it would be complicated to perform this test on every patient with sleep-related breathing problems, some suggest that measuring bicarbonate levels in normal (venous) blood would be a reasonable screening test. If this is elevated (27 mmol/l or higher), blood gasses should be measured.[2]
+To distinguish various subtypes, polysomnography is required. This usually requires brief admission to a hospital with a specialized sleep medicine department where a number of different measurements are conducted while the subject is asleep; this includes electroencephalography (electronic registration of electrical activity in the brain), electrocardiography (same for electrical activity in the heart), pulse oximetry (measurement of oxygen levels) and often other modalities.[1] Blood tests are also recommended for the identification of hypothyroidism and polycythemia.[1][2]
+To distinguish between OHS and various other lung diseases that can cause similar symptoms, medical imaging of the lungs (such as a chest X-ray or CT/CAT scan), spirometry, electrocardiography and echocardiography may be performed. Echo- and electrocardiography may also show strain on the right side of the heart caused by OHS, and spirometry may show a restrictive pattern related to obesity.[2]
+Most people with obesity hypoventilation syndrome have concurrent obstructive sleep apnea, a condition characterized by snoring, brief episodes of apnea (cessation of breathing) during the night, interrupted sleep and excessive daytime sleepiness. In OHS, sleepiness may be worsened by elevated blood levels of carbon dioxide, which causes drowsiness ("CO2 narcosis"). Other symptoms present in both conditions are depression, and hypertension (high blood pressure) that is difficult to control with medication.[1] The high carbon dioxide can also cause headaches, which tend to be worsening in the morning.[4]
+The low oxygen level leads to physiologic constriction of the pulmonary arteries to correct ventilation-perfusion mismatching, which puts excessive strain on the right side of the heart. When this leads to right sided heart failure, it is known as cor pulmonale.[1] Symptoms of this disorder occur because the heart has difficulty pumping blood from the body through the lungs. Fluid may, therefore, accumulate in the skin of the legs in the form of edema (swelling), and in the abdominal cavity in the form of ascites; decreased exercise tolerance and exertional chest pain may occur. On physical examination, characteristic findings are the presence of a raised jugular venous pressure, a palpable parasternal heave, a heart murmur due to blood leaking through the tricuspid valve, hepatomegaly (an enlarged liver), ascites and leg edema.[5] Cor pulmonale occurs in about a third of all people with OHS.[2]
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DISNET disease texts/100 Original Disease Texts/Opioid use disorder.txt

+Opioid use disorder can develop as a result of self-medication, though this is controversial.[20] Scoring systems have been derived to assess the likelihood of opiate addiction in chronic pain patients.[21]
+According to position papers on the treatment of opioid dependence published by the United Nations Office on Drugs and Crime and the World Health Organization, care providers should not treat opioid use disorder as the result of a weak character or will.[22][23] Additionally, detoxification alone does not constitute adequate treatment.
+The DSM-5 guidelines for diagnosis of opioid use disorder require that the individual has significant impairment or distress related to opioid uses.[4] In order to make the diagnosed two or more of eleven criteria must be present in a given year:[4]
+More opioids are taken than intended&The individual is unable to decrease the amount of opioids used&Large amounts of time are spent trying to obtain opioids, use opioids, or recover from taking them&The individual has cravings for opioids&Difficulty fulfilling professional duties at work or school&Continued use of opioids leading to social and interpersonal consequences&Decreased social or recreational activities&Using opioids despite it being physically dangerous settings&Continued use despite opioids worsening physical or psychological health (i.e. depression, constipation)&Tolerance&Withdrawa
+Signs and symptoms include:[4][8]
+Drug seeking behavior&Multiple prescriptions from different providers&Increased use over time&Opioid cravings&Multiple medical complications from drug use (HIV/AIDS, hospitalizations, abscesses)&Legal or social ramifications secondary to drug use&Withdrawal symptom
+Withdrawal[edit] => Symptoms of withdrawal from opioids include:[18]
+Early symptoms[edit] => Altered perception of temperature (hot/cold flashes)&Agitation&Anxiety&Change in libido (abnormally high or low)&Dehydration&Fatigue&Muscle aches&Mental fog or confusion&Lack of motivation&Increased tearing&Insomnia&Restless legs&Runny nose&Sweating&Yawning&Skin-crawlin
+Late symptoms[edit] => Abdominal cramping&Sneezing&Diarrhea&Dilated pupils&Goose bumps&Nausea&Vomitin
+Opioid intoxication[edit] => Signs and symptoms of opioid intoxication include:[8]
+Decreased perception of pain&Euphoria&Confusion&Desire to sleep&Nausea&Constipation&Miosi
+Signs and symptoms of opioid overdose include, but are not limited to:[19]
+Pin-point pupils may occur. Patient presenting with dilated pupils may still be suffering an opioid overdose.&Decreased heart rate&Decreased body temperature&Decreased breathing&Altered level of consciousness. People may be unresponsive or unconscious.&Pulmonary edema (fluid accumulation in the lungs)&Shock&Deat
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DISNET disease texts/100 Original Disease Texts/Optic neuritis.txt

+The optic nerve comprises axons that emerge from the retina of the eye and carry visual information to the primary visual nuclei, most of which is relayed to the occipital cortex of the brain to be processed into vision. Inflammation of the optic nerve causes loss of vision, usually because of the swelling and destruction of the myelin sheath covering the optic nerve.
+The most common cause is multiple sclerosis or ischemic optic neuropathy (Blood Clot). Blood Clot[3] that supplies the optic nerve.[4] Up to 50% of patients with MS will develop an episode of optic neuritis, and 20-30% of the time optic neuritis is the presenting sign of MS. The presence of demyelinating white matter lesions on brain MRI at the time of presentation of optic neuritis is the strongest predictor for developing clinically definite MS. Almost half of the patients with optic neuritis have white matter lesions consistent with multiple sclerosis.
+Some other common causes of optic neuritis include infection (e.g. Tooth Abscess in upper jaw, syphilis, Lyme disease, herpes zoster), autoimmune disorders (e.g. lupus, neurosarcoidosis, neuromyelitis optica), Pinch in Optic Nerve, Methanol poisoning, B12 deficiency and diabetes . Injury to the eye, which usually does not heal by itself.[5]
+Less common causes are: papilledema, brain tumor or abscess in occipitalregion, Cerebral trauma or hemorrhage, Meningitis Arachnoidal adhesions, sinus thrombosis, Liver Dysfunction or, Late Stage Kidney.
+Cause and Rank based on Deaths Annual Num Cases TOTAL (US) (2011) Annual Cases leading to Optic Neuritis Percent Prognosis and Treatment  headingBody  Multiple Sclerosis (Rank 33) 400, 042 146,232 45% Most Common cause, Almost all patients will experience some form of vision dysfunction. Partial vision loss can occur through the duration of the disease, Total vision loss occurs in severe cases and late stages Blood Clot (Rank 29) (Optic ONLY) 17,000 16,777 5% Reversible if early and before reduced Blood flow causes permanent damage. Nerve Pinch, (0) NOT REPORTED  4% Usually heals itself, Treatment Not needed Injury to Optic Nerve (Including Poisoning, i.e. Methanol) (0) 23,827 20,121 <1% Depends on Severity, Usually Treatable Liver Dysfunction (Rank 19) If untreated can lead to Failure (Rank 8) 141,211 11,982 7% Poor Outcomes and Progresses and can lead to total vision loss Reduced Kidney Function (Treatable with diet change) (Rank 67 - If untreated, can progress to Late Stage with much greater mortality rates. 509,898 16,281 9% Good Outcomes if Early, and can usually be treated with diet changes, Progresses and can lead to total vision loss Late Stage Kidney Failure (Rank 7) 33,212 1,112 2% Poor Outcomes - Usually permanent nerve damage at this stage Papilledema, (Brain tumor or abscess ) (Rank 10) 45,888 9,231 3% Depends on Severity Meningitis (Rank 61) 2,521 189 <1% Depends on Severity Other Infections (Not from Abscess) 5,561  <1% Good Outcomes, Treatable with Antibiotics or other Microbial drugs Diabetes (early Stage Treatable) Late Stage has worse prognosis (Rank 6) 49,562 21,112 15% Type 1 carries poor prognosis, Type 2 can be treated and vision returned Unknown n/a  2%
+Demyelinating recurrent optic neuritis and non-demyelinating (CRION)[edit] => The repetition of an idiopathic optic neuritis is considered a distinct clinical condition, and when it shows demyelination, it has been found to be associated to anti-MOG and AQP4-negative neuromyelitis optica[7]
+When an inflammatory recurrent optic neuritis is not demyelinating, it is called "Chronic relapsing inflammatory optic neuropathy" (CRION)[8]
+When it is anti-MOG related, it is demyelinating and it is considered inside the anti-MOG associated inflammatory demyelinating diseases.
+Major symptoms are sudden loss of vision (partial or complete), sudden blurred or "foggy" vision, and pain on movement of the affected eye. Early symptoms that require investigation include symptoms from multiple sclerosis (twitching, lack of coordination, slurred speech, frequent episodes of partial vision loss or blurred vision), episodes of "disturbed/blackened" rather than blurry indicate moderate stage and require immediate medical attention to prevent further loss of vision. Other early symptoms are reduced night vision, photophobia and red eyes. Many patients with optic neuritis may lose some of their color vision in the affected eye (especially red), with colors appearing subtly washed out compared to the other eye. Patients may also experience difficulties judging movement in depth which can be particular troublesome during driving or sport (Pulfrich effect). Likewise transient worsening of vision with increase of body temperature (Uhthoff's phenomenon) and glare disability are a frequent complaint. However, several case studies in children have demonstrated the absence of pain in more than half of cases (approximately 60%) in their pediatric study population, with the most common symptom reported simply as "blurriness." [1][2] Other remarkable differences between the presentation of adult optic neuritis as compared to pediatric cases include more often unilateral optic neuritis in adults, while children much predominantly present with bilateral involvement.
+On medical examination the head of the optic nerve can easily be visualized by a slit lamp with high plus or by using direct ophthalmoscopy; however, frequently there is no abnormal appearance of the nerve head in optic neuritis (in cases of retrobulbar optic neuritis), though it may be swollen in some patients (anterior papillitis or more extensive optic neuritis). In many cases, only one eye is affected and patients may not be aware of the loss of color vision until they are asked to close or cover the healthy eye.
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DISNET disease texts/100 Original Disease Texts/Orofacial granulomatosis.txt

+The cause of the condition is unknown.[6][4] The disease is characterized by non-caseating granulomatous inflammation.[3] That is, the granulomas do not undergo the caseating ("cheese-like") necrosis typical of the granulomas of tuberculosis.
+There is disagreement as to whether OFG represents an early form of Crohn's disease or sarcoidosis, or whether it is a distinct, but similar clinical entity.[3][7] Crohn's disease can affect any part of gastrointestinal tract, from mouth to anus. When it involves the mouth alone, some authors refer to this as "oral Crohn's disease", distinguishing it from OFG, and others suggest that OFG is the same condition as Crohn's disease when it presents in the oral cavity.
+OFG may represent a delayed hypersensitivity reaction, but the causative antigen(s) is not identified or varies form one individual to the next. Suspected sources of antigens include metals, e.g. cobalt, or additives and preservatives in foods, including benzoates, benzoic acid, cinnamaldehyde, metabisulfates, butylated hydroxyanisole, dodecyl gallate, tartrazine, or menthol,[4][6][8] Examples of foods which may contain these substances include margarine, cinnamon, eggs, chocolate or peppermint oil.[4][6][9]
+Some suggest that infection with atypical mycobacteria could be involved, (paratuberculosis),[4] and that OFG is a reaction to mycobacterial stress protein mSP65 acting as an antigen.[6]
+In response to an antigen, a chronic, submucosal, T cell mediated inflammatory response occurs, which involves cytokines (e.g. tumor necrosis factor alpha), protease-activated receptors, matrix metalloproteinases and cyclooxygenases.[6] The granulomas in OFG form in the lamina propria, and may form adjacent to or within lymphatic vessels.[8] This is thought to cause obstruction of lymphatic drainage and lymphedema which is manifest as swelling clinically.[6]
+There may be a genetic predisposition to the condition.[6] People who develop OFG often have a history of atopy, such as childhood asthma or eczema.[4]
+The diagnosis is usually made by tissue biopsy, however this cannot reliably distinguish between the granulomas of OFG and those of Crohn's disease or sarcoidosis.[8] Other causes of granulomatous inflammation are ruled out, such as sarcoidosis, Crohn's disease, allergic or foreign body reactions and mycobacterial infections.[1]
+Signs and symptoms may include:
+Persistent or recurrent enlargement of the lips, causing them to protrude. If recurrent, the interval during which the lips are enlarged may be weeks or months. The enlargement can cause midline fissuring of the lip ("median cheilitis") or angular cheilitis (sores at the corner of the mouth). The swelling is non-pitting (c.f. pitting edema) and feels soft or rubbery on palpation. The mucous membrane of the lip may be erythemaous (red) and granular.[2] One or both lips may be affected.[4]&Oral ulceration (mouth ulcers) which may be aphthous like, or be more chronic and deep with raised margins. Alternatively, lesions similar to pyostomatitis vegetans may occur in OFG, but this is uncommon.[2]&"Full width" gingivitis[5] (compare with marginal gingivitis).&Gingival enlargement (swelling of the gums).[2]&Fissured tongue (grooves in the tongue).[2]&Enlargement of the mucous membrane of the mouth, which may be associated with cobblestoning and mucosal tags (similar lesions often occur on the intestinal mucosa in Crohn's disease).[2]&Enlargement of the perioral and periorbital soft tissues (the tissues of the face around the mouth and the eyes). The facial skin may be dry, exfoliative (flaking) or erythematous.[2]&Cervical lymphadenopathy (enlarged lymph nodes in the neck).[2]&Facial palsy (weakness and altered sensation of the face).[2
+The enlargement of the tissues of the mouth, lips and face seen in OFG is painless.[1] Melkersson-Rosenthal syndrome is where OFG occurs with fissured tongue and paralysis of the facial nerve.[1] The cause of the facial paralysis is thought to be caused by the formation of granulomas in the facial nerve, which supplies the muscles of facial expression.[2]
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DISNET disease texts/100 Original Disease Texts/Orthostatic hypotension.txt

+Orthostatic hypotension is caused primarily by gravity-induced blood pooling in the lower extremities, which in turn compromises venous return, resulting in decreased cardiac output and subsequent lowering of arterial pressure. For example, changing from a lying position to standing loses about 700 ml of blood from the thorax, with a decrease in systolic and diastolic blood pressures.[4] The overall effect is an insufficient blood perfusion in the upper part of the body.[citation needed]
+Still, the blood pressure does not normally fall very much, because it immediately triggers a vasoconstriction (baroreceptor reflex), pressing the blood up into the body again. (Often, this mechanism is exaggerated and is why diastolic blood pressure is a bit higher when a person is standing up, compared to a person in the horizontal position.) Therefore, a secondary factor that causes a greater than normal fall in blood pressure is often required. Such factors include low blood volume, diseases, and medications.[citation needed]
+Hypovolemia[edit] => Orthostatic hypotension may be caused by low blood volume, bleeding, the excessive use of diuretics, vasodilators, or other types of drugs, dehydration, or prolonged bed rest(immobility); as well as occurring in people with anemia.[5]
+Diseases[edit] => The disorder may be associated with Addison's disease, atherosclerosis (build-up of fatty deposits in the arteries), diabetes, pheochromocytoma, porphyria,[6] and certain neurological disorders, including multiple system atrophy and other forms of dysautonomia. It is also associated with Ehlers–Danlos syndrome and anorexia nervosa. It is also present in many patients with Parkinson's disease resulting from sympathetic denervation of the heart or as a side-effect of dopaminomimetic therapy. This rarely leads to fainting unless the person has developed true autonomic failure or has an unrelated heart problem.[citation needed]
+Another disease, dopamine beta hydroxylase deficiency, also thought to be underdiagnosed, causes loss of sympathetic noradrenergic function and is characterized by a low or extremely low levels of norepinephrine, but an excess of dopamine.[7]
+Quadriplegics and paraplegics also might experience these symptoms due to multiple systems' inability to maintain a normal blood pressure and blood flow to the upper part of the body.[citation needed]
+Orthostatic hypotension can be a side-effect of certain antidepressants, such as tricyclics[8] or monoamine oxidase inhibitors (MAOIs).[9] Marijuana and tetrahydrocannabinol can on occasion produce marked orthostatic hypotension.[10] Alcohol can also potentiate orthostatic hypotension to the point of syncope.[11] Orthostatic hypotension can also be a side effect of alpha-1 blockers (alpha1 adrenergic blocking agents). Alpha1 blockers inhibit vasoconstriction normally initiated by the baroreceptor reflex upon postural change and the subsequent drop in pressure.[12]
+Other factors[edit] => Patients prone to orthostatic hypotension are the elderly, post partum mothers, and those having been on bedrest. People suffering from anorexia nervosa and bulimia nervosa often suffer from orthostatic hypotension as a common side-effect. Consuming alcohol may also lead to orthostatic hypotension due to its dehydrating effects.[citation needed]
+Orthostatic hypotension can be confirmed by measuring a person's blood pressure after lying flat for 5 minutes, then 1 minute after standing, and 3 minutes after standing.[13] Orthostatic hypotension is defined as a fall in systolic blood pressure of at least 20 mmHg and/or in the diastolic blood pressure of at least 10 mmHg between the supine reading and the upright reading. In addition, the heart rate should also be measured for both positions. A significant increase in heart rate from supine to standing may indicate a compensatory effort by the heart to maintain cardiac output or postural orthostatic tachycardia syndrome (POTS). A tilt table test may also be performed.[citation needed]
+Orthostatic hypotension is characterised by symptoms that occur after standing (from lying or sitting), particularly when this is done rapidly. Many report lightheadedness (a feeling that one might be about to faint), sometimes severe. Generalized weakness or tiredness may also occur. Some also report difficulty concentrating, blurred vision, tremulousness, vertigo, anxiety, palpitations (awareness of the heartbeat), feeling sweaty or clammy, and sometimes nausea. A person may look pale.[3]
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DISNET disease texts/100 Original Disease Texts/Pancreatic cancer.txt

+The symptoms of pancreatic adenocarcinoma do not usually appear in the disease's early stages, and are individually not distinctive to the disease.[3][11][30] The symptoms at diagnosis vary according to the location of the cancer in the pancreas, which anatomists divide (from left to right on most diagrams) into the thick head, the neck, and the tapering body, ending in the tail.
+Regardless of a tumor's location, the most common symptom is unexplained weight loss, which may be considerable. A large minority (between 35% and 47%) of people diagnosed with the disease will have had nausea, vomiting or a feeling of weakness. Tumors in the head of the pancreas typically also cause jaundice, pain, loss of appetite, dark urine, and light-colored stools. Tumors in the body and tail typically also cause pain.[30]
+People sometimes have recent onset of atypical type 2 diabetes that is difficult to control, a history of recent but unexplained blood vessel inflammation caused by blood clots (thrombophlebitis) known as Trousseau sign, or a previous attack of pancreatitis.[30] A doctor may suspect pancreatic cancer when the onset of diabetes in someone over 50 years old is accompanied by typical symptoms such as unexplained weight loss, persistent abdominal or back pain, indigestion, vomiting, or fatty feces.[11] Jaundice accompanied by a painlessly swollen gallbladder (known as Courvoisier's sign) may also raise suspicion, and can help differentiate pancreatic cancer from gallstones.[49]
+Medical imaging techniques, such as computed tomography (CT scan) and endoscopic ultrasound (EUS) are used both to confirm the diagnosis and to help decide whether the tumor can be surgically removed (its "resectability").[11] On contrast CT scan, pancreatic cancer typically shows a gradually increasing radiocontrast uptake, rather than a fast washout as seen in a normal pancreas or a delayed washout as seen in chronic pancreatitis.[50] Magnetic resonance imaging and positron emission tomography may also be used,[2] and magnetic resonance cholangiopancreatography may be useful in some cases.[30] Abdominal ultrasound is less sensitive and will miss small tumors, but can identify cancers that have spread to the liver and build-up of fluid in the peritoneal cavity (ascites).[11] It may be used for a quick and cheap first examination before other techniques.[51]
+A biopsy by fine needle aspiration, often guided by endoscopic ultrasound, may be used where there is uncertainty over the diagnosis, but a histologic diagnosis is not usually required for removal of the tumor by surgery to go ahead.[11]
+Liver function tests can show a combination of results indicative of bile duct obstruction (raised conjugated bilirubin, γ-glutamyl transpeptidase and alkaline phosphatase levels). CA19-9 (carbohydrate antigen 19.9) is a tumor marker that is frequently elevated in pancreatic cancer. However, it lacks sensitivity and specificity, not least because 5% of people lack the Lewis (a) antigen and cannot produce CA19-9. It has a sensitivity of 80% and specificity of 73% in detecting pancreatic adenocarcinoma, and is used for following known cases rather than diagnosis.[2][11]
+The most common form of pancreatic cancer (adenocarcinoma) is typically characterized by moderately to poorly differentiated glandular structures on microscopic examination. There is typically considerable desmoplasia or formation of a dense fibrous stroma or structural tissue consisting of a range of cell types (including myofibroblasts, macrophages, lymphocytes and mast cells) and deposited material (such as type I collagen and hyaluronic acid). This creates a tumor microenvironment that is short of blood vessels (hypovascular) and so of oxygen (tumor hypoxia).[2] It is thought that this prevents many chemotherapy drugs from reaching the tumor, as one factor making the cancer especially hard to treat.[2][3]
+Since pancreatic cancer usually does not cause recognizable symptoms in its early stages, the disease is typically not diagnosed until it has spread beyond the pancreas itself.[4] This is one of the main reasons for the generally poor survival rates. Exceptions to this are the functioning PanNETs, where over-production of various active hormones can give rise to symptoms (which depend on the type of hormone).[29]
+Bearing in mind that the disease is rarely diagnosed before the age of 40, common symptoms of pancreatic adenocarcinoma occurring before diagnosis include:
+Pain in the upper abdomen or back, often spreading from around the stomach to the back. The location of the pain can indicate the part of the pancreas where a tumor is located. The pain may be worse at night and may increase over time to become severe and unremitting.[23] It may be slightly relieved by bending forward. In the UK, about half of new cases of pancreatic cancer are diagnosed following a visit to a hospital emergency department for pain or jaundice. In up to two-thirds of people abdominal pain is the main symptom, for 46% of the total accompanied by jaundice, with 13% having jaundice without pain.[11]&Jaundice, a yellow tint to the whites of the eyes or skin, with or without pain, and possibly in combination with darkened urine. This results when a cancer in the head of the pancreas obstructs the common bile duct as it runs through the pancreas.[30]&Unexplained weight loss, either from loss of appetite, or loss of exocrine function resulting in poor digestion.[11]&The tumor may compress neighboring organs, disrupting digestive processes and making it difficult for the stomach to empty, which may cause nausea and a feeling of fullness. The undigested fat leads to foul-smelling, fatty feces that are difficult to flush away.[11] Constipation is common.[31]&At least 50% of people with pancreatic adenocarcinoma have diabetes at the time of diagnosis.[2] While long-standing diabetes is a known risk factor for pancreatic cancer (see Risk factors), the cancer can itself cause diabetes, in which case recent onset of diabetes could be considered an early sign of the disease.[32] People over 50 who develop diabetes have eight times the usual risk of developing pancreatic adenocarcinoma within three years, after which the relative risk declines.[11
+Other findings[edit] => Trousseau's syndrome, in which blood clots form spontaneously in the portal blood vessels, the deep veins of the extremities, or the superficial veins anywhere on the body, may be associated with pancreatic cancer, and is found in about 10% of cases.[3]&Clinical depression has been reported in association with pancreatic cancer in some 10–20% of cases, and can be a hindrance to optimal management. The depression sometimes appears before the diagnosis of cancer, suggesting that it may be brought on by the biology of the disease.[3
+Other common manifestations of the disease include: weakness and tiring easily; dry mouth; sleep problems; and a palpable abdominal mass."[31]
+The spread of pancreatic cancer to other organs (metastasis) may also cause symptoms. Typically, pancreatic adenocarcinoma first spreads to nearby lymph nodes, and later to the liver or to the peritoneal cavity, large intestine or lungs.[3] It is uncommon for it to spread to the bones or brain.[33]
+Cancers in the pancreas may also be secondary cancers that have spread from other parts of the body. This is uncommon, found in only about 2% of cases of pancreatic cancer. Kidney cancer is by far the most common cancer to spread to the pancreas, followed by colorectal cancer, and then cancers of the skin, breast, and lung. Surgery may be performed on the pancreas in such cases, whether in hope of a cure or to alleviate symptoms.[34]
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DISNET disease texts/100 Original Disease Texts/Panic attack.txt

+Long-term, predisposing causes – The onset of panic disorder usually occurs in early adulthood, although it may appear at any age. It occurs more frequently in women and more often in people with above-average intelligence. Various twin studies where one identical twin has an anxiety disorder have reported a 31–88% incidence of the other twin also having an anxiety disorder diagnosis. Environmental factors such as an overcautious view of the world expressed by parents and cumulative stress over time have been found to be correlated with panic attacks.[8]&Biological causes – obsessive compulsive disorder, Postural Orthostatic Tachycardia Syndrome, post traumatic stress disorder, hypoglycemia, hyperthyroidism, Wilson's disease, mitral valve prolapse, pheochromocytoma, and inner ear disturbances (labyrinthitis). Dysregulation of the norepinephrine system in the locus ceruleus, an area of the brain stem, has been linked to panic attacks.[10]&Marijuana – According to the Harvard Mental Health Letter, "the most commonly reported side effects of smoking marijuana are anxiety and panic attacks. Studies report that about 20% to 30% of recreational users experience such problems after smoking marijuana."[11]&Phobias – People will often experience panic attacks as a direct result of exposure to a phobic object or situation.&Short-term triggering causes – Significant personal loss, including an emotional attachment to a romantic partner, life transitions, significant life change.&Maintaining causes – Avoidance of panic-provoking situations or environments, anxious/negative self-talk ("what-if" thinking), mistaken beliefs ("these symptoms are harmful and/or dangerous"), withheld feelings.&Hyperventilation syndrome – Breathing from the chest may cause overbreathing, exhaling excessive carbon dioxide in relation to the amount of oxygen in one's bloodstream. Hyperventilation syndrome can cause respiratory alkalosis and hypocapnia. This syndrome often involves prominent mouth breathing as well. This causes a cluster of symptoms, including rapid heart beat, dizziness, and lightheadedness, which can trigger panic attacks.&Situationally bound panic attacks – Associating certain situations with panic attacks, due to experiencing one in that particular situation, can create a cognitive or behavioral predisposition to having panic attacks in certain situations (situationally bound panic attacks).&Discontinuation or marked reduction in the dose of a substance such as a drug (drug withdrawal), for example an antidepressant (antidepressant discontinuation syndrome), can cause a panic attack
+In adolescents it may in part be due to the social transitions.[12]
+People who have repeated, persistent attacks or feel severe anxiety about having another attack are said to have panic disorder. Panic disorder is strikingly different from other types of anxiety disorders in that panic attacks are often sudden and unprovoked.[13] However, panic attacks experienced by those with panic disorder may also be linked to or heightened by certain places or situations, making daily life difficult.[14]
+Agoraphobia is an anxiety disorder which primarily consists of the fear of experiencing a difficult or embarrassing situation from which the sufferer cannot escape. Panic attacks are commonly linked to agoraphobia and the fear of not being able to escape a bad situation.[15] As the result, severe sufferers of agoraphobia may become confined to their homes, experiencing difficulty traveling from this "safe place".[16] The word "agoraphobia" is an English adoption of the Greek words agora (αγορά) and phobos (φόβος). The term "agora" refers to the place where ancient Greeks used to gather and talk about issues of the city, so it basically applies to any or all public places; however the essence of agoraphobia is a fear of panic attacks especially if they occur in public as the victim may feel like he or she has no escape. In the case of agoraphobia caused by social phobia or social anxiety, sufferers may be very embarrassed by having a panic attack publicly in the first place. This translation is the reason for the common misconception that agoraphobia is a fear of open spaces, and is not clinically accurate. Agoraphobia, as described in this manner, is actually a symptom professionals check for when making a diagnosis of panic disorder. Other syndromes like obsessive compulsive disorder or post traumatic stress disorder and social anxiety disorder can also cause agoraphobia; basically any irrational fear that keeps one from going outside can cause the syndrome.[17][unreliable medical source?]
+People who have had a panic attack in certain situations may develop irrational fears, called phobias, of these situations and begin to avoid them. Eventually, the pattern of avoidance and level of anxiety about another attack may reach the point where individuals with panic disorder are unable to drive or even step out of the house. At this stage, the person is said to have panic disorder with agoraphobia. This can be one of the most harmful side-effects of panic disorder as it can prevent sufferers from seeking treatment in the first place.[citation needed]
+Experimentally induced[edit] => Panic attack symptoms can be experimentally induced in the laboratory by various means. Among them, for research purposes, by administering a bolus injection of the neuropeptide cholecystokinin-tetrapeptide (CCK-4).[18] Various animal models of panic attacks have been experimentally studied.[19]
+DSM-5 diagnostic criteria for a panic attack include a discrete period of intense fear or discomfort, in which four (or more) of the following symptoms developed abruptly and reached a peak within minutes:
+In DSM-5, culture-specific symptoms (e.g., tinnitus, neck soreness, headache, and uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms.
+Some or all of these symptoms can be found in the presence of a pheochromocytoma.
+Screening tools such as the Panic Disorder Severity Scale can be used to detect possible cases of disorder and suggest the need for a formal diagnostic assessment.[28][29]
+People with panic attacks often report a fear of dying or heart attack, flashing vision, faintness or nausea, numbness throughout the body, heavy breathing and hyperventilation, or loss of body control. Some people also suffer from tunnel vision, mostly due to blood flow leaving the head to more critical parts of the body in defense. These feelings may provoke a strong urge to escape or flee the place where the attack began (a consequence of the "fight-or-flight response", in which the hormone causing this response is released in significant amounts). This response floods the body with hormones, particularly epinephrine (adrenaline), which aid it in defending against harm.[8]
+A panic attack is a response of the sympathetic nervous system (SNS). The most common symptoms include trembling, dyspnea (shortness of breath), heart palpitations, chest pain (or chest tightness), hot flashes, cold flashes, burning sensations (particularly in the facial or neck area), sweating, nausea, dizziness (or slight vertigo), light-headedness, hyperventilation, paresthesias (tingling sensations), sensations of choking or smothering, difficulty moving, and derealization. These physical symptoms are interpreted with alarm in people prone to panic attacks. This results in increased anxiety and forms a positive feedback loop.[9]
+Often, the onset of shortness of breath and chest pain are the predominant symptoms. People with a panic attack may incorrectly attribute them to a heart attack and thus trigger seeking treatment in an emergency room. However, since chest pain and shortness of breath are indeed hallmark symptoms of cardiovascular illnesses, including unstable angina and myocardial infarction (heart attack), especially in a person whose mental health status and heart health status are not known, attributing these pains to simple anxiety and not (also) a physical condition is a diagnosis of exclusion (other conditions must be ruled out first) until an electrocardiogram and a mental health assessment have been carried out.
+Panic attacks are distinguished from other forms of anxiety by their intensity and their sudden, episodic nature.[8] They are often experienced in conjunction with anxiety disorders and other psychological conditions, although panic attacks are not generally indicative of a mental disorder.
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DISNET disease texts/100 Original Disease Texts/Paratyphoid fever.txt

+Paratyphoid fever is caused by any of three strains of Salmonella paratyphoid: S. Paratyphi A; S. schottmuelleri (also called S. Paratyphi B); or S. hirschfeldii (also called S. Paratyphi C).
+Transmission[edit] => They are usually spread by eating or drinking food or water contaminated with the feces of an infected person.[1] They may occur when a person who prepares food is infected.[2] Risk factors include poor sanitation as is found among poor crowded populations.[4] Occasionally they may be transmitted by sex. Humans are the only animal infected.[1]
+Paratyphoid B[edit] => Paratyphoid B is more frequent in Europe. It can present as a typhoid-like illness, as a severe gastroenteritis or with features of both. Herpes labialis, rare in true typhoid fever, is frequently seen in paratyphoid B. Diagnosis is with isolation of the agent in blood or stool and demonstration of antibodies antiBH in the Widal test. The disease responds well to chloramphenicol or co-trimoxazole.
+Paratyphoid C[edit] => Paratyphoid C is a rare infection, generally seen in the Far East. It presents as a septicaemia with metastatic abscesses. Cholecystitis is possible in the course of the disease. Antibodies to paratyphoid C are not usually tested and the diagnosis is made with blood cultures. Chloramphenicol therapy is generally effective.
+Carriers[edit] => Humans and, occasionally, domestic animals are the carriers of paratyphoid fever. Members of the same family can be transient or permanent carriers. In most parts of the world, short-term fecal carriers are more common than urinary carriers. The chronic urinary carrier state occurs in those who have schistosomiasis (parasitic blood fluke).
+It is possible to continue to shed Salmonella Paratyphi for up to one year and, during this phase, a person is considered to be a carrier. The chronic carrier state may follow acute illness, mild or even subclinical infections. Chronic carriers are most often women who were infected in their middle age.
+Paratyphoid fever resembles typhoid fever. Infection is characterized by a sustained fever, headache, abdominal pain, malaise, anorexia, a nonproductive cough (in early stage of illness), a relative bradycardia (slow heart rate), and hepatosplenomegaly (an enlargement of the liver and spleen). About 30% of Caucasians develop rosy spots on the central body. In adults, constipation is more common than diarrhea.
+Only 20% to 40% of people initially have abdominal pain. Nonspecific symptoms such as chills, sweating, headache, loss of appetite, cough, weakness, sore throat, dizziness, and muscle pains are frequently present before the onset of fever. Some very rare symptoms are psychosis (mental disorder), confusion, and seizures.
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DISNET disease texts/100 Original Disease Texts/Parry–Romberg syndrome.txt

+The fact that some people affected with this disease have circulating antinuclear antibodies in their serum supports the theory that Parry–Romberg syndrome may be an autoimmune disease, specifically a variant of localized scleroderma.[11] Several instances have been reported where more than one member of a family has been affected, prompting speculation of an autosomal dominant inheritance pattern. However, there has also been at least one report of monozygotic twins in which only one of the twins was affected, casting doubt on this theory. Various other theories about the cause and pathogenesis have been suggested, including alterations in the peripheral sympathetic nervous system (perhaps as a result of trauma or infection involving the cervical plexus or the sympathetic trunk), as the literature reported it following sympathectomy, disorders in migration of cranial neural crest cells, or chronic cell-mediated inflammatory process of the blood vessels. It is likely that the disease results from different mechanisms in different people, with all of these factors potentially being involved.[2]
+Diagnosis can be made solely on the basis of history and physical examination in people who present with only facial asymmetry. For those who report neurological symptoms such as migraine or seizures, MRI scan of the brain is the imaging modality of choice. A diagnostic lumbar puncture and serum test for autoantibodies may also be indicated in people who present with a seizure disorder of recent onset.[6]
+A 3D, soft tissue reconstruction of a CT scan of a 17-year-old girl with Parry Romberg syndrome.&CT scan3D bone reconstruction of a 17-year-old girl with Parry Romberg syndrome
+Initial facial changes usually involve the area of the face covered by the temporal or buccinator muscles. The disease progressively spreads from the initial location, resulting in atrophy of the skin and its adnexa, as well as underlying subcutaneous structures such as connective tissue, (fat, fascia, cartilage, bones) and/or muscles of one side of the face.[2] The mouth and nose are typically deviated towards the affected side of the face.[3]
+The process may eventually extend to involve tissues between the nose and the upper corner of the lip, the upper jaw, the angle of the mouth, the area around the eye and brow, the ear, and/or the neck.[2][3] The syndrome often begins with a circumscribed patch of scleroderma in the frontal region of the scalp which is associated with a loss of hair and the appearance of a depressed linear scar extending down through the midface on the affected side. This scar is referred to as a "coup de sabre" lesion because it resembles the scar of a wound made by a sabre, and is indistinguishable from the scar observed in frontal linear scleroderma.[4][5]
+In 20% of cases, the hair and skin overlying affected areas may become hyperpigmented or hypopigmented with patches of unpigmented skin. In up to 20% of cases the disease may involve the ipsilateral (on the same side) or contralateral (on the opposite side) neck, trunk, arm, or leg.[6] The cartilage of the nose, ear and larynx can be involved. The disease has been reported to affect both sides of the face in 5-10% of the cases.[4]
+Symptoms and physical findings usually become apparent during the first or early during the second decade of life. The average age of onset is nine years of age,[2] and the majority of individuals experience symptoms before 20 years of age. The disease may progress for several years before eventually going into remission (abruptly ceasing).[2]
+Neurological[edit] => Neurological abnormalities are common. Roughly 45% of people with Parry–Romberg syndrome are also afflicted with trigeminal neuralgia (severe pain in the tissues supplied by the ipsilateral trigeminal nerve, including the forehead, eye, cheek, nose, mouth and jaw) and/or migraine (severe headaches that may be accompanied by visual abnormalities, nausea and vomiting).[6][7]
+10% of affected individuals develop a seizure disorder as part of the disease.[6] The seizures are typically Jacksonian in nature (characterized by rapid spasms of a muscle group that subsequently spread to adjacent muscles) and occur on the side contralateral to the affected side of the face.[2] Half of these cases are associated with abnormalities in both the gray and white matter of the brain—usually ipsilateral but sometimes contralateral—that are detectable on magnetic resonance imaging (MRI) scan.[6][8]
+Ocular[edit] => Enophthalmos (recession of the eyeball within the orbit) is the most common eye abnormality observed in Parry–Romberg syndrome. It is caused by a loss of subcutaneous tissue around the orbit. Other common findings include drooping of the eyelid (ptosis), constriction of the pupil (miosis), redness of the conjunctiva, and decreased sweating (anhidrosis) of the affected side of the face. Collectively, these signs are referred to as Horner's syndrome. Other ocular abnormalities include ophthalmoplegia (paralysis of one or more of the extraocular muscles) and other types of strabismus, uveitis, and heterochromia of the iris.[9][10]
+Oral[edit] => The tissues of the mouth, including the tongue, gingiva, teeth and soft palate are commonly involved in Parry–Romberg syndrome.[3] 50% of affected individuals develop dental abnormalities such as delayed eruption, dental root exposure, or resorption of the dental roots on the affected side. 35% have difficulty or inability to normally open the mouth or other jaw symptoms, including temporomandibular joint disorder and spasm of the muscles of mastication on the affected side. 25% experience atrophy of one side of the upper lip and tongue.[6]
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DISNET disease texts/100 Original Disease Texts/Pituitary apoplexy.txt

+Almost all cases of pituitary apoplexy arise from a pituitary adenoma, a benign tumor of the pituitary gland. In 80%, the patient has been previously unaware of this (although some will retrospectively report associated symptoms).[1] It was previously thought that particular types of pituitary tumors were more prone to apoplexy than others, but this has not been confirmed.[2] In absolute terms, only a very small proportion of pituitary tumors eventually undergoes apoplexy. In an analysis of incidentally found pituitary tumors, apoplexy occurred in 0.2% annually, but the risk was higher in tumors larger than 10 mm ("macroadenomas") and tumors that were growing more rapidly; in a meta-analysis, not all these associations achieved statistical significance.[7]
+The majority of cases (60–80%) are not precipitated by a particular cause.[2] A quarter has a history of high blood pressure,[1] but this is a common problem in the general population, and it is not clear whether it significantly increase the risk of apoplexy.[8] A number of cases has been reported in association with particular conditions and situations; it is uncertain whether these were in fact causative.[8] Amongst reported associations are surgery (especially coronary artery bypass graft, where there are significant fluctuations in the blood pressure), disturbances in blood coagulation or medication that inhibits coagulation, radiation therapy to the pituitary, traumatic brain injury, pregnancy (during which the pituitary enlarges) and treatment with estrogens. Hormonal stimulation tests of the pituitary have been reported to provoke episodes. Treatment of prolactinomas (pituitary adenomas that secrete prolactin) with dopamine agonist drugs, as well as withdrawal of such treatment, has been reported to precipitate apoplexy.[1][2][4]
+Hemorrhage from a Rathke's cleft cyst, a remnant of Rathke's pouch that normally regresses after embryological development, may cause symptoms that are indistinguishable from pituitary apoplexy.[4] Pituitary apoplexy is regarded by some as distinct from Sheehan's syndrome, where the pituitary undergoes infarction as a result of prolonged very low blood pressure, particularly when caused by bleeding after childbirth. This condition usually occurs in the absence of a tumor.[4] Others regard Sheehan's syndrome as a form of pituitary apoplexy.[3][9]
+It is recommended that magnetic resonance imaging (MRI) scan of the pituitary gland is performed if the diagnosis is suspected; this has a sensitivity of over 90% for detecting pituitary apoplexy; it may demonstrate infarction (tissue damage due to a decreased blood supply) or hemorrhage.[1] Different MRI sequences can be used to establish when the apoplexy occurred, and the predominant form of damage (hemorrhage or infarction).[2] If MRI is not suitable (e.g. due to claustrophobia or the presence of metal-containing implants), a computed tomography (CT) scan may demonstrate abnormalities in the pituitary gland, although it is less reliable.[1] Many pituitary tumors (25%) are found to have areas of hemorrhagic infarction on MRI scans, but apoplexy is not said to exist unless it is accompanied by symptoms.[1][4]
+In some instances, lumbar puncture may be required if there is a suspicion that the symptoms might be caused by other problems (meningitis or subarachnoid hemorrhage). This is the examination of the cerebrospinal fluid that envelops the brain and the spinal cord; the sample is obtained with a needle that is passed under local anesthetic into the spine. In pituitary apoplexy the results are typically normal, although abnormalities may be detected if blood from the pituitary has entered the subarachnoid space.[2][4] If there is remaining doubt about the possibility of subarachnoid hemorrhage (SAH), a magnetic resonance angiogram (MRI with a contrast agent) may be required to identify aneurysms of the brain blood vessels, the most common cause of SAH.[10]
+Professional guidelines recommend that if pituitary apoplexy is suspected or confirmed, the minimal blood tests performed should include a complete blood count, urea (a measure of renal function, usually performed together with creatinine), electrolytes (sodium and potassium), liver function tests, routine coagulation testing, and a hormonal panel including IGF-1, growth hormone, prolactin, luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, thyroid hormone, and either testosterone in men or estradiol in women.[1]
+Visual field testing is recommended as soon as possible after diagnosis,[1][4] as it quantifies the severity of any optic nerve involvement, and may be required to decide on surgical treatment.[1]
+Acute symptoms[edit] => The initial symptoms of pituitary apoplexy are related to the increased pressure in and around the pituitary gland. The most common symptom, in over 95% of cases, is a sudden-onset headache located behind the eyes or around the temples. It is often associated with nausea and vomiting.[1][2][3] Occasionally, the presence of blood leads to irritation of the lining of the brain, which may cause neck rigidity and intolerance to bright light, as well as a decreased level of consciousness.[1][2][3] This occurs in 24% of cases.[4]
+Pressure on the part of the optic nerve known as the chiasm, which is located above the gland, leads to loss of vision on the outer side of the visual field on both sides, as this corresponds to areas on the retinas supplied by these parts of the optic nerve; it is encountered in 75% of cases.[1] Visual acuity is reduced in half, and over 60% have a visual field defect.[2][4] The visual loss depends on which part of the nerve is affected. If the part of the nerve between the eye and the chiasm is compressed, the result is vision loss in one eye. If the part after the chiasm is affected, visual loss on one side of the visual field occurs.[2]
+Adjacent to the pituitary lies a part of the skull base known as the cavernous sinus. This contains a number of nerves that control the eye muscles. 70% of people with pituitary apoplexy experience double vision due to compression of one of the nerves. In half of these cases, the oculomotor nerve (the third cranial nerve), which controls a number of eye muscles, is affected. This leads to diagonal double vision and a dilated pupil. The fourth (trochlear) and sixth (abducens) cranial nerves are located in the same compartment and can cause diagonal or horizontal double vision, respectively.[1] The oculomotor nerve is predominantly affected as it lies closest to the pituitary.[2][5] The cavernous sinus also contains the carotid artery, which supplies blood to the brain; occasionally, compression of the artery can lead to one-sided weakness and other symptoms of stroke.[1][2][4]
+The pituitary gland consists of two parts, the anterior (front) and posterior (back) pituitary. Both parts release hormones that control numerous other organs. In pituitary apoplexy, the main initial problem is a lack of secretion of adrenocorticotropic hormone (ACTH, corticotropin), which stimulates the secretion of cortisol by the adrenal gland. This occurs in 70% of those with pituitary apoplexy. A sudden lack of cortisol in the body leads to a constellation of symptoms called "adrenal crisis" or "Addisonian crisis" (after a complication of Addison's disease, the main cause of adrenal dysfunction and low cortisol levels).[1] The main problems are low blood pressure (particularly on standing), low blood sugars (which can lead to coma) and abdominal pain; the low blood pressure can be life-threatening and requires immediate medical attention.[6]
+Hyponatremia, an unusually low level of sodium in the blood that may cause confusion and seizures, is found in 40% of cases. This may be caused by low cortisol levels or by inappropriate release of antidiuretic hormone (ADH) from the posterior pituitary.[1] Several other hormonal deficiencies may develop in the subacute phase. 50% have a deficiency in thyroid-stimulating hormone (TSH), leading to undersecretion of thyroid hormone by the thyroid gland and characteristic symptoms such as fatigue, weight gain, and cold intolerance. 75% develop a deficiency to gonadotropins (LH and FSH), which control the reproductive hormone glands. This leads to a disrupted menstrual cycle, infertility and decreased libido.[1]
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DISNET disease texts/100 Original Disease Texts/Polyarteritis nodosa.txt

+There is no association with ANCA, but about 30% of people with PAN have chronic hepatitis B and deposits containing HBsAg-HBsAb complexes in affected vessels, indicating an immune complex–mediated cause in that subset. The cause remains unknown in the remaining cases; there may be causal and clinical distinctions between classic idiopathic PAN, the cutaneous forms of PAN, and the PAN associated with chronic hepatitis.[3] In the pediatric population, cutaneous PAN is frequently associated to streptococcal infections, and positive streptococcal serology is included in the diagnostic criteria.[8]
+No specific lab tests exist for diagnosing polyarteritis nodosa. Diagnosis is generally based on the physical examination and a few laboratory studies that help confirm the diagnosis:
+A patient is said to have polyarteritis nodosa if he or she has three of the 10 signs known as the 1990 American College of Rheumatology (ACR)[9] criteria, when a radiographic or pathological diagnosis of vasculitis is made:
+In polyarteritis nodosa, small aneurysms are strung like the beads of a rosary,[5] therefore making "rosary sign" an important diagnostic feature of the vasculitis.[6] The 1990 ACR criteria were designed for classification purposes only. Nevertheless, their good discriminatory performances, indicated by the initial ACR analysis, suggested their potential usefulness for diagnostic purposes as well. Subsequent studies did not confirm their diagnostic utility, demonstrating a significant dependence of their discriminative abilities on the prevalence of the various vasculitides in the analyzed populations. Recently, an original study, combining the analysis of more than 100 items used to describe patients' characteristics in a large sample of vasculitides with a computer simulation technique designed to test the potential diagnostic utility of the various criteria, proposed a set of eight positively or negatively discriminating items to be used as a screening tool for diagnosis in patients suspected of systemic vasculitis.[11]
+In this disease, symptoms result from ischemic damage to affected organs, often the skin, heart, kidneys, and nervous system. Generalised symptoms include fever, fatigue, weakness, loss of appetite, and weight loss. Muscle and joint aches are common. The skin may show rashes, swelling, ulcers, and lumps.[citation needed] Palpable purpura and livedo reticularis can occur in some patients.
+Nerve involvement may cause sensory changes with numbness, pain, burning, and weakness (peripheral neuropathy). Central nervous system involvement may cause strokes or seizures. Kidney involvement can produce varying degrees of kidney failure, such as hypertension, edema, oliguria, and uremia.[citation needed] Involvement of the arteries of the heart may cause a heart attack, heart failure, and inflammation of the sac around the heart (pericarditis).
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DISNET disease texts/100 Original Disease Texts/Porencephaly.txt

+Porencephaly is a rare disorder. The exact prevalence of porencephaly is not known; however, it has been reported that 6.8% of patients with cerebral palsy or 68% of patients with epilepsy and congenital vascular hemiparesis have porencephaly.[6] Porencephaly has a number of different, often unknown, causes including absence of brain development and destruction of brain tissue. With limited research, the most commonly regarded cause of porencephaly is disturbances in blood circulation, ultimately leading to brain damage.[7] However, a number of different and multiple factors such as abnormal brain development or damage to the brain tissue can also affect the development of porencephaly.[2]
+The following text lists out potential risk factors of developing porencephaly and porencephalic cysts and cavities along with brief description of certain terminologies.[3][7][8][10]
+Lack of oxygen and blood supply to the brain leading to internal bleeding&Cerebral degeneration – loss of neuron structure and function&Maternal cardiac arrest&Trauma during pregnancy&Abdominal trauma&Pathogenic infection&Accidents&Abnormal brain development during birth&Vascular thrombosis – blood clot formation within blood vessels&Hemorrhage – loss of blood outside of the circulatory system&Brain contusion or injury&Multifocal cerebrovascular insufficiency&Placental bleeding – prevention of oxygen and blood supply to infant brain&Maternal toxemia – toxin within circulatory system of mother that is transferred to fetus, causing brain damage&Cerebral hypoxia – reduced oxygen concentration within blood system&Vascular occlusion – blood clotting of vessels&Cystic periventricular leukomalacia&Cerebral atrophy – decrease in neuron number and size and loss of brain mass&Chronic lung disease&Male gender&Endotoxins&Prenatal and postnatal encephalitis and meningitis&Drug abuse of mothe
+Cysts or cavities can occur anywhere within the brain and the locations of these cysts depend highly on the patient. Cysts can develop in the frontal lobe, parietal lobe, forebrain, hindbrain, temporal lobe, or virtually anywhere in the cerebral hemisphere.[8]
+Genetics[edit] => From recent studies, de novo and inherited mutations in the gene COL4A1, suggesting genetic predisposition within the family, that encodes type IV collagen α1 chain has shown to be associated with and present in patients with porencephaly. COL4A1 mutation causes a variety of phenotypes, including porencephaly, infantile hemiplegia, and cerebral small vessel diseases involving both stroke and infarction.[7] Abnormal gene expression of COL4A1 can contribute to the development of porencephaly. COL4A1 gene expresses a type IV collagen (basement protein) that is present in all tissue and blood vessels and is extremely important for the structural stability of vascular basement membranes. The COL4A1 protein provides a strong layer around blood vessels.[11] The mutation can weaken the blood vessels within the brain, elevating the probability of a hemorrhage, and eventually promoting internal bleeding then leading to porencephaly during neurodevelopment of infantile stage.[7] Therefore, the formation of cavities can be a result of hemorrhages which promote cerebral degeneration.[11] In a mouse model, mouse with COL4A1 mutations displayed cerebral hemorrhage, porencephaly, and abnormal development of vascular basement membranes, such as uneven edges, inconsistent shapes, and highly variable thickness.[7] Purposely causing a mutation in the COL4A1 gene caused several mouse to develop cerebral hemorrhage and porencephaly-like diseases. Though, there is no direct correlation between mutations of the COL4A1 gene, it appears that it has an influential effect on the development of porencephaly.[12][13][14]
+Another genetic mutation, factor V G1691A mutation, has been reported to show possible association to the development of porencephaly. A mutation in factor V G1691A increases the risk of thrombosis, blood clots, in neonates, infants, and children.[6] Therefore, 76 porencephalic and 76 healthy infants were investigated for factor V G1691A mutation along with other different prothrombotic risk factors. The results indicated that there was higher prevalence of the factor V G1691A mutation in the porencephalic patient group. The prediction that childhood porencephaly is caused by hypercoagulable state, a condition where one has a higher chance of developing blood clots, was supported by the significance of the factor V G1691A mutation. Also, pregnant women in hypercoagulable state can cause the fetus to have the same risks, therefore possibly causing fetal loss, brain damage, lesions, and infections that lead to porencephaly. However, other different prothrombotic risk factors individually did not reach statistical significance to link it to the development of porencephaly, but a combination of multiple prothrombotic risk factors in the porencephaly group was significant. Overall, factor V G1691A mutation has been linked to the development of porencephaly. However, this one mutation is not the cause of porencephaly, and whether further prothrombiotic risk factors are associated with porencephaly still remains unknown.[6]
+Cocaine and other street drugs[edit] => In utero exposure to cocaine and other street drugs can lead to porencephaly.[15]
+Patients diagnosed with porencephaly display a variety of symptoms, from mild to severe effects on the patient. Patients with severe cases of porencephaly suffer epileptic seizures and developmental delays, whereas patients with a mild case of porencephaly display little to no seizures and healthy neurodevelopment. Infants with extensive defects show symptoms of the disorder shortly after birth, and the diagnosis is usually made before the age of 1.[2][8]
+The following text lists out common signs and symptoms of porencephaly in affected individuals along with a short description of certain terminologies.[2][7][8][9]
+Degenerative or non-degenerative cavities or cysts&Delayed growth and development&Spastic paresis – weakness or loss in voluntary movement&Contractures – painful shortening of muscles affecting motion&Hypotonia – reduced muscle strength&Epileptic seizures and epilepsy – multiple symptoms that involve sudden muscle spasms and loss of consciousness&Macrocephaly – condition where head circumference is larger compared to other children of a certain age&Microcephaly – condition where head circumference is smaller compared to other children of a certain age&Hemiplegia – paralysis of appendages&Tetraplegia – paralysis of limb leading to loss of function&Intellectual and cognitive disability&Poor or absent speech development&Hydrocephalus – accumulation of cerebrospinal fluid in the brain&Mental retardation&Poor motor control, abnormal movements of appendages&Cerebral palsy – a motor condition causing movement disabilities&Blood vascular diseases such as intracerebral hemorrhage and cerebral infarction.&Cerebral white-matter lesion
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DISNET disease texts/100 Original Disease Texts/Prediabetes.txt

+Family history of diabetes&Cardiovascular disease&Increased triglycerides levels&Low levels of good cholesterol (HDL)&Overweight or obesity&Elevated blood pressure[10]&Elevated fasting plasma glucose[10][11]&Women who have had gestational diabetes, had high birth weight babies (greater than 9 lbs.), and/or have polycystic ovarian syndrome (PCOS)[12
+These are associated with insulin resistance and are risk factors for the development of type 2 diabetes mellitus. Those in this stratum (IGT or IFG) are at increased risk of cardiovascular disease. Of the two, impaired glucose tolerance better predicts cardiovascular disease and mortality.[13][14][15]
+In a way, prediabetes is a misnomer since it is an early stage of diabetes. It now is known that the health complications associated with type 2 diabetes often occur before the medical diagnosis of diabetes is made.[16]
+Genetics[edit] => Type 2 DM, which is the condition for which prediabetes is a precursor, has 90–100% concordance in twins; there is no HLA association.[17] Genetics play a relatively small role, however, in the widespread occurrence of type 2 diabetes.[medical citation needed] This may be deduced logically from the huge increase in the occurrence of type 2 diabetes that has correlated with the significant change in western lifestyle and diet.[17] As the human genome is further explored, it is possible that multiple genetic anomalies at different loci will be found that confer varying degrees of predisposition to type 2 diabetes.[18]
+Usually, prediabetes is diagnosed with a blood test:[19]
+Fasting blood sugar (glucose) level of: 110 to 125 mg/dL (6.1 mM/L to 6.9 mM/L) – WHO criteria 100 to 125 mg/dL (5.6 mM/L to 6.9 mM/L) – ADA criteria&110 to 125 mg/dL (6.1 mM/L to 6.9 mM/L) – WHO criteria&100 to 125 mg/dL (5.6 mM/L to 6.9 mM/L) – ADA criteria&Two hour glucose tolerance test after ingesting the standardized 75 Gm glucose solution the blood sugar level of 140 to 199 mg/dL (7.8 to 11.0 mM) [20]&Glycated haemoglobin between 5.7 and 6.4 percent [21
+Glycated hemoglobin is; however, of questionable accuracy and while fasting glucose can indicate the diagnosis when positive if it is negative it is not very accurate.[22] A 2016 review found worse outcomes when blood sugar levels were over 100 mg/dL and glycated haemoglobin over 5.7%.[23]
+Levels above these limits would justify a diagnosis for diabetes.
+Screening[edit] => Fasting plasma glucose screening should begin at age 30–45 and be repeated at least every three years. Earlier and more frequent screening should be conducted in at-risk individuals. The risk factors for which are listed below:
+Family history (parent or sibling)&Dyslipidemia (triglycerides > 200 or HDL < 35)&Overweight or obesity (body mass index > 25)&History of gestational diabetes or infant born with birth weight greater than 9 lb (4 kg)&High risk ethnic group[vague]&Hypertension (systolic blood pressure >140 mmHg or diastolic blood pressure > 90 mmHg)&Prior fasting blood glucose > 99&Known vascular disease&Markers of insulin resistance (PCOS, acanthosis nigricans)[24][25
+Prediabetes typically has no distinct signs or symptoms except the sole sign of high blood sugar. Patients should monitor for signs and symptoms of type 2 diabetes mellitus. These include the following:[8]
+Constant hunger&Unexplained weight loss&Weight gain&Flu-like symptoms, including weakness and fatigue&Blurred vision&Slow healing of cuts or bruises&Tingling or loss of feeling in hands or feet&Recurring gum or skin infections&Recurring vaginal or bladder infections&A high BMI (Body Mass Index) result[9
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DISNET disease texts/100 Original Disease Texts/Pregnancy.txt

+The beginning of pregnancy may be detected either based on symptoms by the woman herself, or by using pregnancy tests. However, an important condition with serious health implications that is quite common is the denial of pregnancy by the pregnant woman. About one in 475 denials will last until around the 20th week of pregnancy. The proportion of cases of denial, persisting until delivery is about 1 in 2500.[53] Conversely, some non-pregnant women have a very strong belief that they are pregnant along with some of the physical changes. This condition is known as a false pregnancy.[54]
+Most pregnant women experience a number of symptoms,[55] which can signify pregnancy. A number of early medical signs are associated with pregnancy.[56][57] These signs include:
+the presence of human chorionic gonadotropin (hCG) in the blood and urine&missed menstrual period&implantation bleeding that occurs at implantation of the embryo in the uterus during the third or fourth week after last menstrual period&increased basal body temperature sustained for over 2 weeks after ovulation&Chadwick's sign (darkening of the cervix, vagina, and vulva)&Goodell's sign (softening of the vaginal portion of the cervix)&Hegar's sign (softening of the uterus isthmus)&Pigmentation of the linea alba – linea nigra, (darkening of the skin in a midline of the abdomen, caused by hyperpigmentation resulting from hormonal changes, usually appearing around the middle of pregnancy).[56][57]&Darkening of the nipples and areolas due to an increase in hormones.[58
+Pregnancy detection can be accomplished using one or more various pregnancy tests,[59] which detect hormones generated by the newly formed placenta, serving as biomarkers of pregnancy.[60] Blood and urine tests can detect pregnancy 12 days after implantation.[61] Blood pregnancy tests are more sensitive than urine tests (giving fewer false negatives).[62] Home pregnancy tests are urine tests, and normally detect a pregnancy 12 to 15 days after fertilization.[63] A quantitative blood test can determine approximately the date the embryo was conceived because HCG doubles every 36 to 48 hours.[42] A single test of progesterone levels can also help determine how likely a fetus will survive in those with a threatened miscarriage (bleeding in early pregnancy).[64]
+Obstetric ultrasonography can detect fetal abnormalities, detect multiple pregnancies, and improve gestational dating at 24 weeks.[65] The resultant estimated gestational age and due date of the fetus are slightly more accurate than methods based on last menstrual period.[66] Ultrasound is used to measure the nuchal fold in order to screen for Downs syndrome.[67]
+The symptoms and discomforts of pregnancy are those presentations and conditions that result from pregnancy but do not significantly interfere with activities of daily living or pose a threat to the health of the mother or baby. This is in contrast to pregnancy complications. Sometimes a symptom that is considered a discomfort can be considered a complication when it is more severe. For example, nausea (morning sickness) can be a discomfort, but if, in combination with significant vomiting it causes a water-electrolyte imbalance, it is a complication known as hyperemesis gravidarum.
+Common symptoms and discomforts of pregnancy include:
+Tiredness.&Constipation&Pelvic girdle pain&Back pain&Braxton Hicks contractions. Occasional, irregular, and often painless contractions that occur several times per day.&Edema (swelling). Common complaint in advancing pregnancy. Caused by compression of the inferior vena cava and pelvic veins by the uterus leads to increased hydrostatic pressure in lower extremities.&Increased urinary frequency. A common complaint, caused by increased intravascular volume, elevated glomerular filtration rate, and compression of the bladder by the expanding uterus.&Urinary tract infection[22]&Varicose veins. Common complaint caused by relaxation of the venous smooth muscle and increased intravascular pressure.&Haemorrhoids (piles). Swollen veins at or inside the anal area. Caused by impaired venous return, straining associated with constipation, or increased intra-abdominal pressure in later pregnancy.[23]&Regurgitation, heartburn, and nausea.&Stretch marks&Breast tenderness is common during the first trimester, and is more common in women who are pregnant at a young age.[24
+In addition, pregnancy may result in pregnancy complication such as deep vein thrombosis or worsening of an intercurrent disease in pregnancy.
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DISNET disease texts/100 Original Disease Texts/Premenstrual syndrome.txt

+While PMS is linked to the luteal phase, the causes of PMS are not clear, but several factors may be involved. Changes in hormones during the menstrual cycle seem to be an important factor; changing hormone levels affect some women more than others. Chemical changes in the brain, stress, and emotional problems, such as depression, do not seem to cause PMS but they may make it worse. Low levels of vitamins and minerals, high sodium, alcohol, and/or caffeine can exacerbate symptoms such as water retention and bloating. PMS occurs more often in women who are between their late 20s and early 40s; have at least 1 child; have a family history of depression; and have a past medical history of either postpartum depression or a mood disorder.
+There are no laboratory tests or unique physical findings to verify the diagnosis of PMS. The three key features[3] are:
+The woman's chief complaint is one or more of the emotional symptoms associated with PMS (most typically irritability, tension, or unhappiness). The woman does not have PMS if she only has physical symptoms, such as cramps or bloating.&Symptoms appear predictably during the luteal (premenstrual) phase, reduce or disappear predictably shortly before or during menstruation, and remain absent during the follicular (preovulatory) phase.&The symptoms must be severe enough to interfere with the woman's everyday life
+Mild PMS is common, and more severe symptoms would qualify as PMDD. PMS is not listed in the DSM-IV, unlike PMDD. To establish a pattern and determine if it is PMDD, a woman's physician may ask her to keep a prospective record of her symptoms on a calendar for at least two menstrual cycles.[6] This will help to establish if the symptoms are, indeed, limited to the premenstrual time, predictably recurring, and disruptive to normal functioning. A number of standardized instruments have been developed to describe PMS, including the Calendar of Premenstrual syndrome Experiences (COPE), the Prospective Record of the Impact and Severity of Menstruation (PRISM), and the Visual Analogue Scales (VAS).[3]
+Other conditions that may better explain symptoms must be excluded.[3] A number of medical conditions are subject to exacerbation at menstruation, a process called menstrual magnification. These conditions may lead the woman to believe that she has PMS, when the underlying disorder may be some other problem, such as anemia, hypothyroidism, eating disorders and substance abuse.[3] A key feature is that these conditions may also be present outside of the luteal phase. Conditions that can be magnified perimenstrually include depression or other affective disorders, migraine, seizure disorders, fatigue, irritable bowel syndrome, asthma, and allergies.[3] Problems with other aspects of the female reproductive system must be excluded, including dysmenorrhea (pain during the menstrual period, rather than before it), endometriosis, perimenopause, and adverse effects produced by oral contraceptive pills.[3]
+The National Institute of Mental Health research definition compares the intensity of symptoms from cycle days 5 to 10 to the six-day interval before the onset of the menstrual period.[3] To qualify as PMS, symptom intensity must increase at least 30% in the six days before menstruation. Additionally, this pattern must be documented for at least two consecutive cycles.
+More than 200 different symptoms have been associated with PMS. Common emotional and non-specific symptoms include stress, anxiety, difficulty with sleep, headache, feeling tired, mood swings, increased emotional sensitivity, and changes in interest in sex.[4]
+Physical symptoms associated with the menstrual cycle include bloating, lower back pain, abdominal cramps, constipation/diarrhea, swelling or tenderness in the breasts, cyclic acne, and joint or muscle pain, and food cravings.[5] The exact symptoms and their intensity vary significantly from woman to woman, and even somewhat from cycle to cycle and over time.[2] Most women with premenstrual syndrome experience only a few of the possible symptoms, in a relatively predictable pattern.[6]
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DISNET disease texts/100 Original Disease Texts/Primary hyperparathyroidism.txt

+The most common cause of primary hyperparathyroidism is a sporadic, single parathyroid adenoma[6] resulting from a clonal mutation (~97%). Less common are parathyroid hyperplasia[7] (~2.5%), parathyroid carcinoma (malignant tumor), and adenomas in more than one gland (together ~0.5%).
+Primary hyperparathyroidism is also a feature of several familial endocrine disorders: Multiple endocrine neoplasia type 1 and type 2A (MEN type 1 and MEN type 2A), and familial hyperparathyroidism.
+Genetic associations include:
+OMIM Name Gene  headingBody  145000 HRPT1 MEN1, HRPT2 145001 HRPT2 HRPT2 610071 HRPT3 unknown at 2p13.3-14[8]
+In all cases, the disease is idiopathic, but is thought to involve inactivation of tumor suppressor genes (Menin gene in MEN1), or involve gain of function mutations (RET proto-oncogene MEN 2a).
+Recently, it was demonstrated that liquidators of the Chernobyl power plant are faced with a substantial risk of primary hyperparathyroidism, possibly caused by radioactive strontium isotopes.[9]
+Primary hyperparathyroidism can also result from pregnancy. It is apparently very rare, with only about 110 cases have so far been reported in world literature, but this is probably a considerable underestimate of its actual prevalence in pregnant women.[10]
+The diagnosis of primary hyperparathyroidism is made by blood tests.
+Serum calcium levels are elevated, and the parathyroid hormone level is abnormally high compared with an expected low level in response to the high calcium. A relatively elevated parathyroid hormone has been estimated to have a sensitivity of 60%-80% and a specificity of approximately 90% for primary hyperparathyroidism.[11]
+A more powerful variant of comparing the balance between calcium and parathyroid hormone is to perform a 3-hour calcium infusion. After infusion, a parathyroid hormone level above a cutoff of 14 ng/l has a sensitivity of 100% and a specificity of 93% in detecting primary hyperparathyroidism, with a confidence interval of 80% to 100%.[12]
+Urinary cAMP is occasionally measured; this is generally elevated.[citation needed]
+Biochemical confirmation of primary hyperparathyroidism is following by investigations to localize the culprit lesion. Primary hyperparathyroidism is most commonly due to solitary parathyroid adenoma. Less commonly it may be due to double parathyroid adenomas or parathyroid hyperplasia. Tc99 sestamibi scan of head, neck and upper thorax is the most commonly used test for localizing parathyroid adenomas having a sensitivity and specificity of 70-80%. Sensitivity falls down to 30% in case of double/multiple parathyroid adenomas or in case of parathyroid hyperplasia. Ultrasonography is also a useful test in localizing suspicious parathyroid lesions.
+The signs and symptoms of primary hyperparathyroidism are those of hypercalcemia. They are classically summarized by "stones, bones, abdominal groans, thrones and psychiatric overtones".
+"Stones" refers to kidney stones, nephrocalcinosis, and diabetes insipidus (polyuria and polydipsia). These can ultimately lead to renal failure.&"Bones" refers to bone-related complications. The classic bone disease in hyperparathyroidism is osteitis fibrosa cystica, which results in pain and sometimes pathological fractures. Other bone diseases associated with hyperparathyroidism are osteoporosis, osteomalacia, and arthritis.&"Abdominal groans" refers to gastrointestinal symptoms of constipation, indigestion, nausea and vomiting. Hypercalcemia can lead to peptic ulcers and acute pancreatitis. The peptic ulcers can be an effect of increased gastric acid secretion by hypercalcemia.[1]&"Thrones" refers to polyuria and constipation&"Psychiatric overtones" refers to effects on the central nervous system. Symptoms include lethargy, fatigue, depression, memory loss, psychosis, ataxia, delirium, and coma
+Left ventricular hypertrophy may also be seen.[2]
+Other signs include proximal muscle weakness, itching, and band keratopathy of the eyes.
+When subjected to formal research, symptoms of depression, pain, and gastric dysfunction seem to correlate with mild cases of hypercalcemia.[3]
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DISNET disease texts/100 Original Disease Texts/Primary sclerosing cholangitis.txt

+The exact cause of primary sclerosing cholangitis is unknown and its pathogenesis is poorly understood.[1] Although PSC is thought to be an autoimmune disease, it does not demonstrate a clear response to immunosuppressants. Thus, many experts believe it to be a complex, multifactorial (including immune-mediated) disorder and perhaps one that encompasses several different hepatobiliary diseases.[10][11]
+Data have provided novel insights suggesting:
+an important association between the intestinal microbiota and PSC[12][13][14] and&a process referred to as cellular senescence and the senescence-associated secretory phenotype (SASP) in the pathogenesis of PSC.[15][16
+In addition, there are longstanding, well-recognized associations between PSC and human leukocyte antigen (HLA) alleles (A1, B8, and DR3).[4]
+PSC is generally diagnosed on the basis of having at least two of three clinical criteria after secondary causes of sclerosing cholangitis have been ruled out:
+serum alkaline phosphatase (ALP) > 1.5x the upper limit of normal for longer than 6 months;&cholangiography demonstrating biliary strictures or irregularity consistent with PSC; and,&liver biopsy consistent with PSC (if available)
+Historically, a cholangiogram would be obtained via endoscopic retrograde cholangiopancreatography (ERCP), which typically reveals "beading" (alternating strictures and dilation) of the bile ducts inside and/or outside the liver. Currently, the preferred option for diagnostic cholangiography, given its non-invasive yet highly accurate nature, is magnetic resonance cholangiopancreatography (MRCP), a magnetic resonance imaging technique. MRCP has unique strengths, including high spatial resolution, and can even be used to visualize the biliary tract of small animal models of PSC.[19]
+Most people with PSC have evidence of autoantibodies and abnormal immunoglobulin levels.[20] For example, approximately 80% of people with PSC have perinuclear anti-neutrophil cytoplasmic antibodies; however, this and other immunoglobulin findings are not specific to those with PSC and are of unclear clinical significance/consequence. Antinuclear antibodies and anti-smooth muscle antibody are found in 20%-50% of PSC patients and, likewise, are not specific for the disease but may identify a subgroup of PSC patients who also have autoimmune hepatitis (i.e. PSC-AIH overlap syndrome).[4]
+Other markers which may be measured and monitored are a complete blood count, serum liver enzymes, bilirubin levels (usually grossly elevated), kidney function, and electrolytes. Fecal fat measurement is occasionally ordered when symptoms of malabsorption (e.g., gross steatorrhea) are prominent.
+The differential diagnosis can include primary biliary cholangitis (formerly referred to as primary biliary cirrhosis), drug-induced cholestasis, cholangiocarcinoma, IgG4-related disease, post-liver transplantation non-anastomotic biliary strictures,[21] and HIV-associated cholangiopathy.[22] Primary sclerosing cholangitis and primary biliary cholangitis are distinct entities and exhibit important differences, including the site of tissue damage within the liver, associations with inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease, response to treatment, and risks of disease progression.[23]
+Nearly half of people with PSC do not have symptoms and are often incidentally discovered to have PSC due to abnormal liver function tests,[1] but a substantial proportion will have debilitating signs and symptoms of the disease.[7] Signs and symptoms of PSC may include severe itching and non-specific fatigue. Yellowing of the skin and white portion of the eyes may also be seen. Enlargement of the liver and spleen are seen in approximately 40% of affected individuals. Abdominal pain affects about 20% of people with PSC.
+Multiple episodes of life-threatening acute cholangitis (infection within the bile ducts) can be seen due to impaired drainage of the bile ducts, which increases the risk of infection.[8]
+Dark urine due to excess conjugated bilirubin, which is water-soluble and excreted by the kidneys (i.e. choluria)&Malabsorption, especially of fat, and steatorrhea (fatty stool), due to an inadequate amount of bile reaching the small intestine, leading to decreased levels of the fat-soluble vitamins, A, D, E, and K
+Portal hypertension, a complication of cirrhosis, which can manifest with esophageal and parastomal varices[9] as well as hepatic encephalopathy (mental status alteration/disturbance caused by liver dysfunction and shunting of blood away from the scarred liver; such that ammonia detoxification is reduced with concomitant encephalopathy)
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DISNET disease texts/100 Original Disease Texts/Reactive hypoglycemia.txt

+The NIH states: "The causes of most cases of reactive hypoglycemia are still open to debate. Some researchers suggest that certain people may be more sensitive to the body’s normal release of the hormone epinephrine, which causes many of the symptoms of hypoglycemia. Others believe deficiencies in glucagon secretion might lead to reactive hypoglycemia.[1]
+Stomach surgery or hereditary fructose intolerance are believed to be causes, albeit uncommon, of reactive hypoglycemia. myo-Inositol or D-chiro-inositol withdrawal can cause temporary reactive hypoglycemia.
+There are different kinds of reactive hypoglycemia:[10]
+Alimentary hypoglycemia (consequence of dumping syndrome; it occurs in about 15% of people who have had stomach surgery)&Hormonal hypoglycemia (e.g., hypothyroidism)&Helicobacter pylori-induced gastritis (some reports suggest this bacteria may contribute to the occurrence of reactive hypoglycemia)[11]&Congenital enzyme deficiencies (hereditary fructose intolerance, galactosemia, and leucine sensitivity of childhood)[12]&Late hypoglycemia (occult diabetes; characterized by a delay in early insulin release from pancreatic β-cells, resulting in initial exaggeration of hyperglycemia during a glucose tolerance test)[13
+"Idiopathic reactive hypoglycemia" is a term no longer used because researchers now know the underlying causes of reactive hypoglycemia and have the tools to perform the diagnosis and the pathophysiological data explaining the mechanisms.[10]
+To check if there is real hypoglycemia when symptoms occur, neither an oral glucose tolerance test nor a breakfast test is effective; instead, a hyperglucidic breakfast test or ambulatory glucose testing is the current standard.[10][14]
+The body requires a relatively constant input of glucose, a sugar produced upon digestion of carbohydrates, for normal functioning. Glucagon and insulin are among the hormones that ensure a normal range of glucose in the human body.[15] Upon consumption of a meal, blood sugar normally rises, which triggers pancreatic cells to produce insulin. This hormone initiates the absorption of the just-digested blood glucose as glycogen into the liver for metabolism or storage, thereby lowering glucose levels in the blood. In contrast, the hormone glucagon is released by the pancreas as a response to lower than normal blood sugar levels. Glucagon initiates uptake of the stored glycogen in the liver into the bloodstream so as to increase glucose levels in the blood.[16] Sporadic, high-carbohydrate snacks and meals are deemed the specific causes of sugar crashes. The “crash” one feels is due to the rapid increase and subsequent decline of blood sugar in the body system as one begins and ceases consumption of high-sugar foods. More insulin than is actually needed is produced in response to the large, rapid ingestion of sugary foods.
+Symptoms vary according to individuals' hydration level and sensitivity to the rate and/or magnitude of decline of their blood glucose concentration. A crash is usually felt within four hours or less of heavy carbohydrate consumption. Symptoms of reactive hypoglycemia include: [6] [7] [8]
+double vision or blurry vision&unclear thinking&insomnia&heart palpitation or fibrillation&fatigue&dizziness&light-headedness&sweating&headaches&depression&nervousness&muscle twitches&irritability&tremors&flushing&craving sweets&increased appetite&rhinitis&nausea, vomiting&panic attack&numbness/coldness in the extremities&confusion&irrationality&bad temper&paleness&cold hands&disorientation&the need to sleep or 'crash'&coma can be a result in severe untreated episode
+The majority of these symptoms, often correlated with feelings of hunger, mimic the effect of inadequate sugar intake as the biology of a crash is similar in itself to the body’s response to low blood sugar levels following periods of glucose deficiency.[9]
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DISNET disease texts/100 Original Disease Texts/Reflex syncope.txt

+Reflex syncope occurs in response to a trigger due to dysfunction of the heart rate and blood pressure regulating mechanism. When heart rate slows, blood pressure drops, and the resulting lack of blood to the brain causes fainting.[7]
+Vasovagal syncope[edit] => Typical triggers include:
+Prolonged standing[5]&Emotional stress[5]&Pain[5]&The sight of blood[5]&Time varying magnetic field[8] (i.e. transcranial magnetic stimulation
+Situational syncope[edit] => After or during urination (micturition syncope)[2]&Straining, such as to have a bowel movement[2]&Coughing[2]&Swallowing[2]&Lifting a heavy weight[2
+Carotid sinus syncope[edit] => Pressing upon a certain spot in the neck.[5] This may happen when wearing a tight collar, shaving, or turning the head.[5]
+In addition to the mechanism described above, a number of other medical conditions may cause syncope. Making the correct diagnosis for loss of consciousness is difficult. The core of the diagnosis of vasovagal syncope rests upon a clear description of a typical pattern of triggers, symptoms, and time course.
+It is pertinent to differentiate lightheadedness, seizures, vertigo, and low blood sugar as other causes.
+In people with recurrent vasovagal syncope, diagnostic accuracy can often be improved with one of the following diagnostic tests:
+A tilt table test (results should be interpreted in the context of patients' clinical presentations and with an understanding of the sensitivity and specificity of the test)[11]&Implantation of an insertable loop recorder&A Holter monitor or event monitor&An echocardiogram&An electrophysiology stud
+Episodes of vasovagal syncope are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger. Before losing consciousness, the individual frequently experiences early signs or symptoms such as lightheadedness, nausea, the feeling of being extremely hot or cold (accompanied by sweating), ringing in the ears, an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak or form words (sometimes combined with mild stuttering), weakness and visual disturbances such as lights seeming too bright, fuzzy or tunnel vision, black cloud-like spots in vision, and a feeling of nervousness can occur as well. The symptoms may become more intense over several seconds to several minutes before the loss of consciousness (if it is lost). Onset usually occurs when a person is sitting up or standing.
+When people lose consciousness, they fall down (unless prevented from doing so) and, when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness. If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a seizure may result from the blood's inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense. Fainting occurs with a loss of oxygen to the brain.[6]
+The autonomic nervous system's physiological state (see below) leading to loss of consciousness may persist for several minutes, so
+If sufferers try to sit or stand when they wake up, they may pass out again&The person may be nauseated, pale, and sweaty for several minutes or hour
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DISNET disease texts/100 Original Disease Texts/Ross River fever.txt

+A blood test is the only way to confirm a case of Ross River Fever. Several types of blood tests may be used to examine antibody levels in the blood. Tests may either look for simply elevated antibodies (which indicate some sort of infection), or specific antibodies to the virus.[3]
+Symptoms of the disease may vary widely in severity, but major indicators are arthralgia, arthritis, fever, and rash.[3] The incubation period is 7–9 days. About a third of infections are asymptomatic, particularly in children.[2][3]
+Acute illness[edit] => About 95% of symptomatic cases report joint pain.[2] This is typically symmetrical and with acute onset, affecting the fingers, toes, ankles, wrists, back, knees and elbows.[3] Fatigue occurs in 90% and fever, myalgia and headache occur in 50–60%.[2]
+A rash occurs in 50% of patients and is widespread and maculopapular. Lymphadenopathy occurs commonly; sore throat and coryza less frequently. Diarrhea is rare. About 50% of people report needing time off work with the acute illness.[2] If the rash is unnoticed, these symptoms are quite easily mistaken for more common illnesses like influenza or the common cold. Recovery from the flu symptoms is expected within a month, but, because the virus currently cannot be removed once infection has occurred secondary symptoms of joint and muscle inflammation, pain and stiffness can last for many years.
+Less common manifestations include splenomegaly, hematuria and glomerulonephritis. Headache, neck stiffness, and photophobia may occur. There have been three case reports suggesting meningitis or encephalitis.
+Chronic illness[edit] => Reports from the 1980s and 1990s suggested RRV infection was associated with arthralgia, fatigue and depression lasting for years.[3] More recent prospective studies have reported a steady improvement in symptoms over the first few months, with 15–66% of patients having ongoing arthralgia at 3 months. Arthralgias have resolved in the majority by 5–7 months. The incidence of chronic fatigue is 12% at 6 months and 9% at 12 months, similar to Epstein-Barr virus and Q fever.[2] The only significant predictor of the likelihood of developing chronic symptoms is the severity of the acute illness itself. No other aspects of the patient's medical or psychiatric history have been found to be predictive. However, in those with the most persisting symptoms (12 months or more), comorbid rheumatologic conditions and/or depression are frequently observed .[2]
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DISNET disease texts/100 Original Disease Texts/Rubella.txt

+The disease is caused by rubella virus, a togavirus that is enveloped and has a single-stranded RNA genome.[19] The virus is transmitted by the respiratory route and replicates in the nasopharynx and lymph nodes. The virus is found in the blood 5 to 7 days after infection and spreads throughout the body. The virus has teratogenic properties and is capable of crossing the placenta and infecting the fetus where it stops cells from developing or destroys them.[10] During this incubation period, the patient is contagious typically for about one week before he/she develops a rash and for about one week thereafter.
+Increased susceptibility to infection might be inherited as there is some indication that HLA-A1 or factors surrounding A1 on extended haplotypes are involved in virus infection or non-resolution of the disease.[20] [21]
+Rubella virus specific IgM antibodies are present in people recently infected by rubella virus, but these antibodies can persist for over a year, and a positive test result needs to be interpreted with caution.[22] The presence of these antibodies along with, or a short time after, the characteristic rash confirms the diagnosis.[23]
+Rubella has symptoms that are similar to those of flu. However, the primary symptom of rubella virus infection is the appearance of a rash (exanthem) on the face which spreads to the trunk and limbs and usually fades after three days (that is why it is often referred to as three-day measles). The facial rash usually clears as it spreads to other parts of the body. Other symptoms include low grade fever, swollen glands (sub-occipital and posterior cervical lymphadenopathy), joint pains, headache, and conjunctivitis.[10]
+The swollen glands or lymph nodes can persist for up to a week and the fever rarely rises above 38 °C (100.4 °F). The rash of German measles is typically pink or light red. The rash causes itching and often lasts for about three days. The rash disappears after a few days with no staining or peeling of the skin. When the rash clears up, the skin might shed in very small flakes where the rash covered it. Forchheimer's sign occurs in 20% of cases, and is characterized by small, red papules on the area of the soft palate.[11]
+Rubella can affect anyone of any age and is generally a mild disease, rare in infants or those over the age of 40. The older the person is the more severe the symptoms are likely to be. Up to 60% of older girls or women experience joint pain or arthritic type symptoms with rubella.[12]
+In children rubella normally causes symptoms which last two days and include:[13]
+Rash beginning on the face which spreads to the rest of the body.&Low fever of less than 38.3 °C (101 °F).&Posterior cervical lymphadenopathy.[14
+In older children and adults additional symptoms may be present including:[13]
+Swollen glands&Coryza (cold-like symptoms)&Aching joints (especially in young women
+Rare problems can occur including the following:
+Brain inflammation&Ear infection [15
+Coryza in rubella may convert to pneumonia, either direct viral pneumonia or secondary bacterial pneumonia, and bronchitis (either viral bronchitis or secondary bacterial bronchitis).[16]
+Rubella can cause congenital rubella syndrome in the newborn. The syndrome (CRS) follows intrauterine infection by the rubella virus and comprises cardiac, cerebral, ophthalmic and auditory defects.[17] It may also cause prematurity, low birth weight, and neonatal thrombocytopenia, anemia and hepatitis. The risk of major defects or organogenesis is highest for infection in the first trimester. CRS is the main reason a vaccine for rubella was developed.[18]
+Many mothers who contract rubella within the first critical trimester either have a miscarriage or a stillborn baby. If the fetus survives the infection, it can be born with severe heart disorders (patent ductus arteriosus being the most common), blindness, deafness, or other life-threatening organ disorders. The skin manifestations are called "blueberry muffin lesions".[18] For these reasons, rubella is included on the TORCH complex of perinatal infections.
+About 100,000 cases of this condition occur each year.[3]
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DISNET disease texts/100 Original Disease Texts/Scarlet fever.txt

+Spread of strep throat occurs by close contact, via respiratory droplets (for example, saliva or nasal discharge).[13] A person in close contact with another person infected with Group A streptococcal pharyngitis has a 35% chance of becoming infected.[18] One in ten children who are infected with Group A streptococcal pharyngitis will develop scarlet fever.[12]
+Although the presentation of scarlet fever can be clinically diagnosed, further testing may be required to distinguish it from other illnesses.[7] Also, history of a recent exposure to someone with strep throat can be useful.[13] There are two methods used to confirm suspicion of scarlet fever rapid antigen detection test and throat culture.[18]
+The rapid antigen detection test is a very specific test but not very sensitive. This means that if the result is positive (indicating that the Group A Strep Antigen was detected and therefore confirming that the patient has a Group A Strep Pharyngitis) then it is appropriate to treat them with antibiotics. However, if the Rapid Antigen Detection Test is negative (indicating that they do not have Group A Strep Pharyngitis), then a throat culture is required to confirm since it could be a false negative result.[26] The throat culture is the current gold standard for diagnosis.[18]
+Serologic testing looks for the antibodies that the body produces against the streptococcal infection including antistreptolysin-O and antideoxyribonuclease B. It takes the body 2–3 weeks to make these antibodies so this type of testing is not useful for diagnosing a current infection. However, it is useful when assessing a patient who may have one of the complications from a previous streptococcal infection.[12][18]
+Throat cultures done after antibiotic therapy can tell you if the infection has been removed. These throat swabs however are not indicated because up to 25% of properly treated individuals can continue to carry the streptococcal infection while asymptomatic.[19]
+Differential diagnosis[edit] => Viral exanthem: Viral infections are often accompanied by a rash which can be described as morbilliform or maculopapular. This type of rash is accompanied by a prodromal period of cough and runny nose in addition to a fever, indicative of a viral process.[14]&Allergic or contact dermatitis: The erythematous appearance of the skin will be in a more localized distribution rather than the diffuse and generalized rash seen in Scarlet Fever.[12]&Drug eruption: These are potential side effects of taking certain drugs such as Penicillin. The reddened maculopapular rash which results can be itchy and be accompanied by a fever.[27]&Kawasaki disease Children with this disease also present with a strawberry tongue and undergo a desquamative process on their palms and soles. However these children tend to be younger than 5 years old, their fever lasts longer (at least five days) and they have additional clinical criteria (including signs such as conjunctival redness and cracked lips) which can help distinguish this from Scarlet Fever.[28]&Toxic shock syndrome: Both Streptococcal and Staphylococcal bacteria can cause this syndrome. Clinical manifestations include diffuse rash and desquamation of the palms and soles. Can be distinguished from Scarlet Fever by low blood pressure, the rash will lack sandpaper texture, and multi-organ system involvement.[29]&Staphylococcal scalded skin syndrome: This is a disease which occurs primarily in young children due to a toxin producing strain of the bacteria Staphylococcus Aureus. The abrupt start of the fever and diffused sunburned appearance of the rash can resemble Scarlet Fever. However, this rash is associated with tenderness and large blister formation. These blisters easily pop and then cause the skin to peel.[30]&Staphylococcal Scarlet Fever: The rash is identical to the streptococcal scarlet fever in distribution and texture however the skin affected by the rash will be tender.[7
+Rash which has a characteristic appearance, spreading pattern, and desquamating process "Strawberry tongue"
+The tongue starts out by having a white coating on it while the papillae of the tongue are swollen and reddened. The protrusion of the red papillae through the white coating gives the tongue a "white strawberry" appearance.&Then a few days later (following the desquamating process, or the shedding of the tissue which created the white coating) the whiteness disappears while the red and enlarged papillae give it the "red strawberry" appearance.[7]&Note that this involvement of the tongue is a part of the rash which is characteristic of scarlet fever.[8
+Pastia's lines[9]
+Lines of petechiae which appear as pink/red areas located in arm pits and elbow pit
+Vomiting and abdominal pain[10]
+Strep throat[edit] => Typical symptoms of streptococcal pharyngitis (also known as strep throat):[10]
+Sore throat, painful swallowing&Fever - typically over 39 °C (102.2 °F)&Fatigue&Enlarged and reddened tonsils with yellow or white exudates present (this is typically an exudative pharyngitis)[11]&Enlarged and tender lymph nodes usually located on the front of the neck[12
+The following symptoms will usually be absent: cough, hoarseness, runny nose, diarrhea, and conjunctivitis.[10] Their presence indicates it is more likely a viral infection.
+Rash[edit] => The rash begins 1–2 days following the onset of symptoms caused by the strep pharyngitis (sore throat, fever, fatigue).[13] This characteristic rash has been denoted as "scarlatiniform" and it appears as a diffuse redness of the skin with small papules, or bumps, which resemble goose pimples.[7][14] These bumps are what give the characteristic sand paper texture to the rash. The reddened skin will blanch when you apply pressure to it. It is possible for the skin to be itchy however it will not be painful.[7] It usually first appears on the trunk and then gradually spreads out to the arms and legs.[14] The palms, soles and face are usually left uninvolved by the rash. The face is however is usually flushed, most prominent in cheeks, with a ring of paleness around the mouth.[15] After the rash spreads, it becomes more pronounced in creases in the skin, such as the skin folds in the inguinal and axillary regions of the body.[9] Also in those areas it is possible for there to be Pastia’s Lines which are petechiae arranged in a linear pattern.[9] Within 1 week of onset the rash begins to fade followed by a longer process of desquamation, or shedding of the outer layer of skin, which lasts several weeks.[12] The desquamation process usually begins on the face and progresses downward on the body.[7] After the desquamation the skin will be left with a sunburned appearance.[13]
+The streptococcal pharyngitis which is the usual presentation of scarlet fever in combination with the characteristic rash commonly involves the tonsils. The tonsils will appear swollen and reddened. The palate and uvula are also commonly affected by the infection. The involvement of the soft palate can be seen as tiny red and round spots known as Forscheimer spots.[11]
+Variable presentations[edit] => The features of scarlet fever can differ depending on the age and race of the person. Children less than 5 years old can have atypical presentations. Children less than 3 years old can present with nasal congestion and a lower grade fever.[16] Infants can potentially only present with increased irritability and decreased appetite.[16]
+Children who have darker skin can have a different presentation in that the redness of the skin involved in the rash and the ring of paleness around the mouth can be less obvious.[7] Suspicion based on accompanying symptoms and diagnostic studies are important in these cases.
+Course[edit] => Following exposure to Streptococcus, it takes 12 hours to 7 days for the onset of the symptoms. This may include fever, fatigue, and sore throat. The characteristic scarlatiniform rash then comes 12–48 hours later. During the first few days of the rash development and rapid generalization, the Pastia's Lines and strawberry tongue will also present.[7] The rash starts fading within 3–4 days followed by the desquamation of the rash which will last several weeks to a month.[13][11] If the case of scarlet fever is uncomplicated, recovery from the fever and clinical symptoms other than the process of desquamation occurs in 5–10 days.[17]
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DISNET disease texts/100 Original Disease Texts/Scleroderma.txt

+Scleroderma is caused by genetic and environmental factors.[13][5][4][14] Mutations in HLA genes seem to play a crucial role in the pathogenesis of some cases (but not all), likewise silica, aromatic and chlorinated solvents, ketones, trichloroethylene, welding fumes and white spirits exposure seems to contribute to the condition in a small proportion of affected persons.[13][5][4][14][15]
+Typical scleroderma is classically defined as symmetrical skin thickening, with about 70% of cases also presenting with Raynaud's phenomenon, nail-fold capillary changes and antinuclear antibodies. Affected individuals may or may not experience systemic organ involvement. There is no single test for scleroderma that works all of the time and hence the diagnosis is often a matter of exclusion. Atypical scleroderma may show any variation of these changes without skin changes or with finger swelling only.[24]
+Laboratory testing can show antitopoisomerase antibodies, like anti-scl70 (causing a diffuse systemic form), or anticentromere antibodies (causing a limited systemic form and the CREST syndrome). Other autoantibodies can be seen, such as anti-U3 or anti-RNA polymerase.[25]
+Differential[edit] => Diseases that are often in the differential include:[26]
+Eosinophilia, a condition in which there are too many eosinophils (a type of immune cell that attacks parasites and is involved in certain allergic reactions) in the blood.&Eosinophilia-myalgia syndrome, a form of eosinophilia that is caused by L-tryptophan supplements.&Eosinophilic fasciitis, a disease that affects the connective tissues surrounding skeletal muscles, bones, blood vessels and nerves in the arms and legs.&Graft-versus-host disease, an autoimmune condition that occurs as a result of bone marrow transplants in which the immune cells from the transplanted bone marrow attack the host's body.&Mycosis fungoides, a type of cutaneous T cell lymphoma, a rare cancer that causes rashes all over the body.&Nephrogenic systemic fibrosis, a condition usually caused by kidney failure that causes fibrosis (thickening) of the tissues.&Primary biliary cirrhosis, an autoimmune disease of the liver.&Primary pulmonary hypertension&Complex regional pain syndrom
+Classification[edit] => Scleroderma is characterised by the appearance of circumscribed or diffuse, hard, smooth, ivory-colored areas that are immobile and which give the appearance of hidebound skin, a disease occurring in both localised and systemic forms:[27]
+Localised scleroderma Localised morphea Morphea-lichen sclerosus et atrophicus overlap Generalised morphea Atrophoderma of Pasini and Pierini Pansclerotic morphea Morphea profunda Linear scleroderma&Localised morphea&Morphea-lichen sclerosus et atrophicus overlap&Generalised morphea&Atrophoderma of Pasini and Pierini&Pansclerotic morphea&Morphea profunda&Linear scleroderma&Systemic scleroderma CREST syndrome Progressive systemic sclerosis&CREST syndrome&Progressive systemic sclerosi
+Potential signs and symptoms include:[10][11][12]
+Cardiovascular: Raynaud's phenomenon (is the presenting symptom in 30% of affected persons, occurs in 95% of affected individuals at some time during their illness); healed pitting ulcers on the fingertips; skin and mucousal telangiectasis; palpitations, irregular heart rate and fainting due to conduction abnormalities, hypertension and congestive heart failure.&Digestive: gastroesophageal reflux disease, bloating, indigestion, loss of appetite, diarrhoea alternating with constipation, sicca syndrome and its complications, loosening of teeth and hoarseness (due to acid reflux).&Pulmonary: progressive worsening of shortness of breath, chest pain (due to pulmonary artery hypertension) and dry, persistent cough due to interstitial lung disease.&Musculoskeletal: joint, muscle aches, loss of joint range of motion, carpal tunnel syndrome and muscle weakness.&Genitourinary: erectile dysfunction, dyspareunia, scleroderma renal crises and kidney failure.&Other: facial pain due to trigeminal neuralgia, hand paresthesias, headache, stroke, fatigue, calcinosis and weight loss
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DISNET disease texts/100 Original Disease Texts/Snakebite.txt

+In the developing world most snakebites occur in those who work outside such as farmers, hunters, and fishermen. They often happen when a person steps on the snake or approaches it too closely. In the United States and Europe snakebites most commonly occur in those who keep them as pets.[19]
+The type of snake that most often delivers serious bites depends on the region of the world. In Africa it is mambas, Egyptian cobras, puff adders, and carpet vipers. In the Middle East it is carpet vipers and elapids. In Central and South America it is snakes of the Bothrops and Crotalus types, the latter including rattlesnakes.[19] In North America, rattlesnakes are the primary concern, and up to 95% of all snakebite-related deaths in the United States are attributed to the western and eastern diamondback rattlesnakes.[2] In South Asia it was previously believed that Indian cobras, common kraits, Russell's viper and carpet vipers were the most dangerous; other snakes, however, may also cause significant problems in this area of the world.[19]
+The most common symptom of all snakebites is overwhelming fear, which contributes to other symptoms, including nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin.[2][14] Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and people may have unwarranted thoughts of imminent death.
+Dry snakebites and those inflicted by a non-venomous species can still cause severe injury. There are several reasons for this: a snakebite may become infected, with the snake's saliva and fangs sometimes harboring pathogenic microbial organisms, including Clostridium tetani. Infection is often reported with viper bites whose fangs are capable of deep puncture wounds. Bites may cause anaphylaxis in certain people.
+Most snakebites, whether by a venomous snake or not, will have some type of local effect. There is minor pain and redness in over 90 percent of cases, although this varies depending on the site.[2] Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within five minutes.[9] This area may also bleed and blister and can eventually lead to tissue necrosis. Other common initial symptoms of pit viper and viper bites include lethargy, bleeding, weakness, nausea, and vomiting.[2][9] Symptoms may become more life-threatening over time, developing into hypotension, tachypnea, severe tachycardia, severe internal bleeding, altered sensorium, kidney failure, and respiratory failure.[2][9]
+Bites caused by some snakes, such as the kraits, coral snake, Mojave rattlesnake, and the speckled rattlesnake, reportedly cause little or no pain despite being serious potentially life-threatening injuries.[2] Those bitten may also describe a "rubbery", "minty", or "metallic" taste if bitten by certain species of rattlesnake.[2] Spitting cobras and rinkhalses can spit venom in a person's eyes. This results in immediate pain, ophthalmoparesis, and sometimes blindness.[15][16]
+Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly healed wounds.[9] Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the skin.
+Venom emitted from elapids, including sea snakes, kraits, cobras, king cobra, mambas, and many Australian species, contain toxins which attack the nervous system, causing neurotoxicity.[2][9][18] The person may present with strange disturbances to their vision, including blurriness. Paresthesia throughout the body, as well as difficulty in speaking and breathing, may be reported.[2] Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. If not treated immediately they may die from respiratory failure.
+Venom emitted from some types of cobras, almost all vipers and some sea snakes causes necrosis of muscle tissue.[9] Muscle tissue will begin to die throughout the body, a condition known as rhabdomyolysis. Rhabdomyolysis can result in damage to the kidneys as a result of myoglobin accumulation in the renal tubules. This, coupled with hypotension, can lead to acute renal failure, and, if left untreated, eventually death.[9]
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DISNET disease texts/100 Original Disease Texts/Soy allergy.txt

+Diagnosis of soy allergy is based on the person's history of allergic reactions, skin prick test (SPT), patch test and measurement of soy protein specific serum immunoglobulin E (IgE or sIgE). A negative IgE test does not rule out non-IgE mediated allergy, also described as cell-mediated allergy.[17] SPT and sIgE have sensitivities of 55% and 83% respectively, and specificities of 68% and 38%. These numbers mean that either test may miss diagnosing an existing soy allergy, and that both can also be positive for other food allergens.[18] Confirmation is by double-blind, placebo-controlled food challenges, conducted by an allergy specialist.[17]
+Food allergies can have fast onset (from seconds to one hour) or slow onset (from hours to several days) depending on mechanism. Symptoms may include: rash, hives, itching of mouth, lips, tongue, throat, eyes, skin, or other areas, swelling of lips, tongue, eyelids, or the whole face, difficulty swallowing, runny or congested nose, hoarse voice, wheezing, shortness of breath, diarrhea, abdominal pain, lightheadedness, fainting, nausea and vomiting. Symptoms of allergies vary from person to person and may vary from incident to incident.[4] Serious danger regarding allergies can begin when the respiratory tract or blood circulation is affected. The former can be indicated by wheezing, a blocked airway and cyanosis, the latter by weak pulse, pale skin, and fainting. When these symptoms occur the allergic reaction is called anaphylaxis.[4] Anaphylaxis occurs when IgE antibodies are involved, and areas of the body that are not in direct contact with the food become affected and show severe symptoms.[4][5] Untreated, this can proceed to vasodilation, a low blood pressure situation called anaphylactic shock, and death (very rare).[5][6]
+Non-IgE mediated reactions are slower to appear, and tend to manifest as gastrointestinal symptoms, without cutaneous or respiratory symptoms.[7][8] Within non-IgE reactions, clinicians distinguish among food protein-induced enterocolitis syndrome (FPIES), food protein-induced allergic proctocolitis (FPIAP) and food protein-induced enteropathy (FPE). Common trigger foods for all are soy infant formula, and also cow's milk formula.[8][9] FPIAP is considered to be at the milder end of the spectrum, and is characterized by intermittent bloody stools. FPE is identified by chronic diarrhea which will resolve when the offending food is removed from the infant's diet. FPIES can be severe, characterized by persistent vomiting 1-4 hours after an allergen-containing food, to the point of lethargy. Watery and sometimes bloody diarrhea can develop 5-10 hours after the triggering meal, to the point of dehydration and low blood pressure. Infants reacting to soy formula may also react to cow's milk formula.[9][10] International consensus guidelines have been established for the diagnosis and treatment of FPIES.[10]
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DISNET disease texts/100 Original Disease Texts/Streptococcal pharyngitis.txt

+Strep throat is caused by group A beta-hemolytic streptococcus (GAS or S. pyogenes).[11] Other bacteria such as non–group A beta-hemolytic streptococci and fusobacterium may also cause pharyngitis.[8][10] It is spread by direct, close contact with an infected person; thus crowding, as may be found in the military and schools, increases the rate of transmission.[10][12] Dried bacteria in dust are not infectious, although moist bacteria on toothbrushes or similar items can persist for up to fifteen days.[10] Contaminated food can result in outbreaks, but this is rare.[10] Of children with no signs or symptoms, 12% carry GAS in their pharynx,[5] and, after treatment, approximately 15% of those remain positive, and are true "carriers".[13]
+Points Probability of Strep Management  headingBody  1 or fewer <10% No antibiotic or culture needed 2 11–17% Antibiotic based on culture or RADT 3 28–35% 4 or 5 52% Empiric antibiotics
+A number of scoring systems exist to help with diagnosis; however, their use is controversial due to insufficient accuracy.[14] The modified Centor criteria are a set of five criteria; the total score indicates the probability of a streptococcal infection.[8]
+One point is given for each of the criteria:[8]
+Absence of a cough&Swollen and tender cervical lymph nodes&Temperature >38.0 °C (100.4 °F)&Tonsillar exudate or swelling&Age less than 15 (a point is subtracted if age >44
+A score of one may indicated no treatment or culture is needed, or it may indicate the need to perform further testing if other high risk factors exist, such as a family member having the disease.[8]
+The Infectious Disease Society of America recommends against empirical treatment and considers antibiotics only appropriate when given after a positive test.[6] Testing is not needed in children under three as both group A strep and rheumatic fever are rare, unless a child has a sibling with the disease.[6]
+Laboratory testing => A throat culture is the gold standard[15] for the diagnosis of streptococcal pharyngitis, with a sensitivity of 90–95%.[8] A rapid strep test (also called rapid antigen detection testing or RADT) may also be used. While the rapid strep test is quicker, it has a lower sensitivity (70%) and statistically equal specificity (98%) as a throat culture.[8] In areas of the world where rheumatic fever is uncommon, a negative rapid strep test is sufficient to rule out the disease.[16]
+A positive throat culture or RADT in association with symptoms establishes a positive diagnosis in those in which the diagnosis is in doubt.[17] In adults, a negative RADT is sufficient to rule out the diagnosis. However, in children a throat culture is recommended to confirm the result.[6] Asymptomatic individuals should not be routinely tested with a throat culture or RADT because a certain percentage of the population persistently "carries" the streptococcal bacteria in their throat without any harmful results.[17]
+As the symptoms of streptococcal pharyngitis overlap with other conditions, it can be difficult to make the diagnosis clinically.[8] Coughing, nasal discharge, diarrhea, and red, irritated eyes in addition to fever and sore throat are more indicative of a viral sore throat than of strep throat.[8] The presence of marked lymph node enlargement along with sore throat, fever, and tonsillar enlargement may also occur in infectious mononucleosis.[18]
+The typical signs and symptoms of streptococcal pharyngitis are a sore throat, fever of greater than 38 °C (100 °F), tonsillar exudates (pus on the tonsils), and large cervical lymph nodes.[8]
+Other symptoms include: headache, nausea and vomiting, abdominal pain,[9] muscle pain,[10] or a scarlatiniform rash or palatal petechiae, the latter being an uncommon but highly specific finding.[8]
+Symptoms typically begin one to three days after exposure and last seven to ten days.[3][8]
+Strep throat is unlikely when any of the symptoms of red eyes, hoarseness, runny nose, or mouth ulcers are present. It is also unlikely when there is no fever.[6]
+Mouth wide open showing the throat A throat infection which on culture tested positive for group A streptococcus. Note the large tonsils with white exudate.&Mouth wide open showing the throat Note the petechiae, or small red spots, on the soft palate. This is an uncommon but highly specific finding in streptococcal pharyngitis.[8]&A set of large tonsils in the back of the throat, covered in white exudate. A culture positive case of streptococcal pharyngitis with typical tonsillar exudate in an 8-year-old
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DISNET disease texts/100 Original Disease Texts/Subdural hematoma.txt

+Subdural hematomas are most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. Subdural hematomas due to head injury are described as traumatic. Much more common than epidural hemorrhages, subdural hemorrhages generally result from shearing injuries due to various rotational or linear forces.[3][8] Subdural hemorrhage is a classic finding in shaken baby syndrome, in which similar shearing forces classically cause intra- and pre-retinal hemorrhages. Subdural hematoma is also commonly seen in the elderly and in alcoholics, who have evidence of cerebral atrophy. Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. It is also more common in patients on anticoagulants or antiplatelet drugs, such as warfarin and aspirin. Patients on these medications can have a subdural hematoma after a relatively minor traumatic event. A further cause can be a reduction in cerebral spinal fluid pressure which can create a low pressure in the subarachnoid space, pulling the arachnoid away from the dura mater and leading to a rupture of the blood vessels.
+Risk factors[edit] => Factors increasing the risk of a subdural hematoma include very young or very old age. As the brain shrinks with age, the subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears. This and the fact that the elderly have more brittle veins make chronic subdural bleeds more common in older patients.[6] Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults.[3] For this reason, subdural hematoma is a common finding in shaken baby syndrome. In juveniles, an arachnoid cyst is a risk factor for a subdural hematoma.[14]
+Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, dementia, and the presence of a cerebrospinal fluid leak.[15]
+It is important that a person receive medical assessment, including a complete neurological examination, after any head trauma. A CT scan or MRI scan will usually detect significant subdural hematomas.
+Subdural hematomas occur most often around the tops and sides of the frontal and parietal lobes.[3][8] They also occur in the posterior cranial fossa, and near the falx cerebri and tentorium cerebelli.[3] Unlike epidural hematomas, which cannot expand past the sutures of the skull, subdural hematomas can expand along the inside of the skull, creating a concave shape that follows the curve of the brain, stopping only at the dural reflections like the tentorium cerebelli and falx cerebri.
+On a CT scan, subdural hematomas are classically crescent-shaped, with a concave surface away from the skull. However, they can have a convex appearance, especially in the early stage of bleeding. This may cause difficulty in distinguishing between subdural and epidural hemorrhages. A more reliable indicator of subdural hemorrhage is its involvement of a larger portion of the cerebral hemisphere since it can cross suture lines, unlike an epidural hemorrhage. Subdural blood can also be seen as a layering density along the tentorium cerebelli. This can be a chronic, stable process, since the feeding system is low-pressure. In such cases, subtle signs of bleeding such as effacement of sulci or medial displacement of the junction between gray matter and white matter may be apparent.
+Fresh subdural bleeding is hyperdense, but becomes more hypodense over time due to dissolution of cellular elements. After somewhere between 3–14 days, the bleeding becomes isodense with brain tissue and may therefore be missed.[20] Subsequently, it will become more hypodense than brain tissue.
+Hematoma type Epidural Subdural       v t e Location Involved vessel Symptoms (depend on severity)[11] CT appearance  headingBody  Between the skull and the outer endosteal layer of the dura mater Between dura mater and arachnoid mater.[10] Temperoparietal locus (most likely) - Middle meningeal artery Frontal locus - anterior ethmoidal artery Occipital locus - transverse or sigmoid sinuses Vertex locus - superior sagittal sinus Bridging veins Lucid interval followed by unconsciousness Gradually increasing headache and confusion Biconvex lens Crescent-shaped
+Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately[12] but can be delayed as much as 2 weeks.[13] If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.[3]
+Other signs and symptoms of subdural hematoma can include any combination of the following:
+A history of recent head injury&Loss of consciousness or fluctuating levels of consciousness&Irritability&Seizures&Pain&Numbness&Headache (either constant or fluctuating)&Dizziness&Disorientation&Amnesia&Weakness or lethargy&Nausea or vomiting&Loss of appetite&Personality changes&Inability to speak or slurred speech&Ataxia, or difficulty walking&Loss of muscle control&Altered breathing patterns&Hearing loss or hearing ringing (tinnitus)&Blurred Vision&Deviated gaze, or abnormal movement of the eyes.[3
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DISNET disease texts/100 Original Disease Texts/Superior mesenteric artery syndrome.txt

+Retroperitoneal fat and lymphatic tissue normally serve as a cushion for the duodenum, protecting it from compression by the SMA. SMA syndrome is thus triggered by any condition involving an insubstantial cushion and narrow mesenteric angle. SMA syndrome can present in two forms: chronic/congenital or acute/induced.
+Patients with the chronic, congenital form of SMA syndrome predominantly have a lengthy or even lifelong history of abdominal complaints with intermittent exacerbations depending on the degree of duodenal compression. Risk factors include anatomic characteristics such as: aesthenic (very thin or "lanky") body build, an unusually high insertion of the duodenum at the ligament of Treitz, a particularly low origin of the SMA, or intestinal malrotation around an axis formed by the SMA.[12] Predisposition is easily aggravated by any of the following: poor motility of the digestive tract,[6] retroperitional tumors, loss of appetite, malabsorption, cachexia, exaggerated lumbar lordosis, visceroptosis, abdominal wall laxity, peritoneal adhesions, abdominal trauma,[13] rapid linear adolescent growth spurt, weight loss, starvation, catabolic states (as with cancer and burns), and history of neurological injury.[14]
+The acute form of SMA syndrome develops rapidly after traumatic incidents that forcibly hyper-extend the SMA across the duodenum, inducing the obstruction, or sudden weight loss for any reason. Causes include prolonged supine bed rest, scoliosis surgery, left nephrectomy, ileo-anal pouch surgery.
+It is important to note, however, that while SMA syndrome can mimic an eating disorder, distinguishing the two conditions is extremely important, as misdiagnosis in this situation can be dangerous.
+Diagnosis is very difficult, and usually one of exclusion. SMA syndrome is thus considered only after patients have undergone an extensive evaluation of their gastrointestinal tract including upper endoscopy, and evaluation for various malabsorptive, ulcerative and inflammatory instestinal conditions with a higher diagnostic frequency. Diagnosis may follow x-ray examination revealing duodenal dilation followed by abrupt constriction proximal to the overlying SMA, as well as a delay in transit of four to six hours through the gastroduodenal region. Standard diagnostic exams include abdominal and pelvic computed tomography (CT) scan with oral and IV contrast, upper gastrointestinal series (UGI), and, for equivocal cases, hypotonic duodenography. In addition, vascular imaging studies such as ultrasound and contrast angiography may be used to indicate increased bloodflow velocity through the SMA or a narrowed SMA angle.[15][16]
+Despite multiple case reports, there has been controversy surrounding the diagnosis and even the existence of SMA syndrome since symptoms do not always correlate well with radiologic findings, and may not always improve following surgical correction.[17] However, the reason for the persistence of gastrointestinal symptoms even after surgical correction in some cases has been traced to the remaining prominence of reversed peristalsis in contrast to direct peristalsis.[18]
+Since females between the ages of 10 and 30 are most frequently afflicted, it is not uncommon for physicians to initially and incorrectly assume that emaciation is a choice of the patient instead of a consequence of SMA syndrome. Patients in the earlier stages of SMA syndrome often remain unaware that they are ill until substantial damage to their health is done, since they may attempt to adapt to the condition by gradually decreasing their food intake or naturally gravitating toward a lighter and more digestible diet.
+Upper gastrointestinal series showing extreme duodenal dilation (white arrow) abruptly preceding constriction by the SMA.&Play media Ultrasound showing SMA syndrome[19]&Ultrasound showing SMA syndrome[19]&A diagram of a healthy mesenteric angle.&A diagram of a compressed duodenum due to a reduced mesenteric angle
+Signs and symptoms include early satiety, nausea, vomiting, extreme "stabbing" postprandial abdominal pain (due to both the duodenal compression and the compensatory reversed peristalsis), abdominal distention/distortion, burping (eructation), external hypersensitivity or tenderness of the abdominal area, reflux, and heartburn.[8] In infants, feeding difficulties and poor weight gain are also frequent symptoms.[9]
+In some cases of SMA syndrome, severe malnutrition accompanying spontaneous wasting may occur.[10] This, in turn, increases the duodenal compression, which worsens the underlying cause, creating a cycle of worsening symptoms.[11]
+"Food fear" is a common development among patients with the chronic form of SMA syndrome. For many, symptoms are partially relieved when in the left lateral decubitus or knee-to-chest position, or in the prone (face down) position. A Hayes maneuver (pressure applied below the umbilicus in cephalad and dorsal direction) elevates the root of the SMA, also slightly easing the constriction. Symptoms can be aggravated when leaning to the right or taking a supine (face up) position.[10]
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DISNET disease texts/100 Original Disease Texts/Taeniasis.txt

+Diagnosis of taeniasis is mainly using stool sample, particularly by identifying the eggs. However, this has limitation at the species level because tapeworms basically have similar eggs. Examination of the scolex or the gravid proglottids can resolve the exact species.[16] But body segments are not often available, therefore, laborious histological observation of the uterine branches and PCR detection of ribosomal 5.8S gene are sometimes necessary.[17][18] Ziehl–Neelsen stain is also used for T. saginata and T. solium, in most cases only the former will stain, but the method is not entirely reliable.[19] Loop-mediated isothermal amplification (LAMP) is highly sensitive (~2.5 times that of multiplex PCR), without false positives, for differentiating the taenid species from faecal samples.[20]
+To date the most relevant test for T. asiatica is by enzyme-linked immunoelectrotransfer blot (EITB). EITB can effectively identify asiatica from other taenid infections since the serological test indicates an immunoblot band of 21.5 kDa exhibited specifically by T. asiatica.[21] Even though it gives 100% sensitivity, it has not been tested with human sera for cross-reactivity, and it may show a high false positive result.
+Taeniasis is generally asymptomatic and is diagnosed when a portion of the worm is passed in the stool. It is not fatal, although cysticercosis can cause epilepsy and neurocysticercosis can be fatal.[2][3][4]
+Taenia solium[edit] => Infection by T. solium is normally asymptomatic. Heavy infection is indicated by intestinal irritation, anaemia, and indigestion.
+There are accidental consumptions of eggs of T. solium from contaminated vegetables or water. The eggs enter the intestine where they develop into larvae. The larvae enter the bloodstream and invade host tissues. This clinical condition, called cysticercosis, is the most frequent and severe disease caused by any tapeworm. It can lead to severe headaches, dizziness, occasional seizures, dementia, hypertension, lesions in the brain, blindness, tumor-like growths, and low eosinophil levels. It is the cause of major neurological problems, such as hydrocephalus, paraplegy, meningitis, convulsions, and even death.[5]
+Taenia saginata[edit] => Taenia saginata infection is asymptomatic, but heavy infection causes weight loss, dizziness, abdominal pain, diarrhea, headaches, nausea, constipation, chronic indigestion, and loss of appetite. It can cause antigen reaction that induce allergic reaction.[6] It is also a rare cause of ileus, pancreatitis, cholecystitis, and cholangitis.[7]
+Taenia asiatica[edit] => Taenia asiatica is also usually asymptomatic. The only severe case was in a 60-year-old woman at the Mackay Memorial Hospital in Taiwan. Her stomach and intestine were severely damaged with active bleeding from ulcers caused by a single tapeworm.[8][9]
+In pigs, the cysticercus can produce cysticercosis. Cysts develop in liver and lungs. (T. saginata does not cause cysticercosis.)[10] Due to its biological similarity to T. solium, which is the major cause of neurocysticercosis, T. asiatica may also cause cysticercosis.[11][12][13]
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DISNET disease texts/100 Original Disease Texts/Tetanus.txt

+Tetanus is caused by the tetanus bacterium Clostridium tetani.[22] Tetanus is an international health problem, as C. tetani spores are ubiquitous. Spores can be introduced into the body through a puncture wound (penetrating trauma). Due to C. tetani being an anaerobic bacterium, it and its endospores thrive in environments that lack oxygen, such as a puncture wound.
+The disease occurs almost exclusively in persons inadequately immunized.[23] It is more common in hot, damp climates with soil rich in organic matter. Manure-treated soils may contain spores, as they are widely distributed in the intestines and feces of many animals such as horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens.[8] In agricultural areas, a significant number of human adults may harbor the organism.
+The spores can also be found on skin surfaces and in contaminated heroin.[8] Heroin users, particularly those that inject the drug subcutaneously, appear to be at high risk of contracting tetanus.[8] Rarely, tetanus can be contracted through surgical procedures, intramuscular injections, compound fractures, and dental infections.[24] The bite of a dog can transmit tetanus.[25]
+Tetanus is often associated with rust, especially rusty nails. Although rust itself does not cause tetanus, objects that accumulate rust are often found outdoors or in places that harbour anaerobic bacteria. Additionally, the rough surface of rusty metal provides a habitat for C. tetani, while a nail affords a means to puncture skin and deliver endospores deep within the body at the site of the wound.[26] An endospore is a non-metabolizing survival structure that begins to metabolize and cause infection once in an adequate environment. Hence, stepping on a nail (rusty or not) may result in a tetanus infection, as the low-oxygen (anaerobic) environment may exist under the skin, and the puncturing object can deliver endospores to a suitable environment for growth.[27]
+There are currently no blood tests for diagnosing tetanus. The diagnosis is based on the presentation of tetanus symptoms and does not depend upon isolation of the bacterium, which is recovered from the wound in only 30% of cases and can be isolated from patients without tetanus. Laboratory identification of C. tetani can be demonstrated only by production of tetanospasmin in mice.[8] Having recently experienced head trauma may indicate cephalic tetanus if no other diagnosis has been made.
+The "spatula test" is a clinical test for tetanus that involves touching the posterior pharyngeal wall with a soft-tipped instrument and observing the effect. A positive test result is the involuntary contraction of the jaw (biting down on the "spatula") and a negative test result would normally be a gag reflex attempting to expel the foreign object. A short report in The American Journal of Tropical Medicine and Hygiene states that, in a patient research study, the spatula test had a high specificity (zero false-positive test results) and a high sensitivity (94% of infected patients produced a positive test).[28]
+Tetanus often begins with mild spasms in the jaw muscles—also known as lockjaw or trismus. The spasms can also affect the facial muscles resulting in an appearance called risus sardonicus. Chest, neck, back, abdominal muscles, and buttocks may be affected. Back muscle spasms often cause arching, called opisthotonos. Sometimes the spasms affect muscles that help with breathing, which can lead to breathing problems.[8]
+Prolonged muscular action causes sudden, powerful, and painful contractions of muscle groups, which is called "tetany". These episodes can cause fractures and muscle tears. Other symptoms include drooling, excessive sweating, fever, hand or foot spasms, irritability, difficulty swallowing, suffocation, heart attack, breathing problems, irregular heartbeat, and uncontrolled urination or defecation.[citation needed]
+Even with treatment, about 10% of people who contract tetanus die.[8] The mortality rate is higher in unvaccinated people and people over 60 years of age.[8]
+Incubation period[edit] => The incubation period of tetanus may be up to several months, but is usually about ten days.[9][10] In general, the farther the injury site is from the central nervous system, the longer the incubation period. The shorter the incubation period, the more severe the symptoms.[11] In neonatal tetanus, symptoms usually appear from 4 to 14 days after birth, averaging about 7 days. On the basis of clinical findings, four different forms of tetanus have been described.[8]
+Generalized tetanus[edit] => Generalized tetanus is the most common type of tetanus, representing about 80% of cases. The generalized form usually presents with a descending pattern. The first sign is trismus, or lockjaw, and the facial spasms called risus sardonicus, followed by stiffness of the neck, difficulty in swallowing, and rigidity of pectoral and calf muscles. Other symptoms include elevated temperature, sweating, elevated blood pressure, and episodic rapid heart rate. Spasms may occur frequently and last for several minutes with the body shaped into a characteristic form called opisthotonos. Spasms continue for up to four weeks, and complete recovery may take months.[citation needed] Sympathetic overactivity (SOA) is common in severe tetanus and manifests as labile hypertension, tachycardia, dysrhythmia, peripheral vasculature constriction, profuse sweating, fever, increased carbon dioxide output, increased catecholamine excretion and late development of hypotension. Death can occur within four days.
+Neonatal tetanus is a form of generalized tetanus that occurs in newborns, usually those born to mothers who themselves have not been vaccinated. If the mother has been vaccinated against tetanus, the infants acquire passive immunity and are thus protected.[12] It usually occurs through infection of the unhealed umbilical stump, particularly when the stump is cut with a non-sterile instrument. As of 1998 neonatal tetanus was common in many developing countries and was responsible for about 14% (215,000) of all neonatal deaths.[13] In 2010 the worldwide death toll was 58,000 newborns. As the result of a public health campaign, the death toll from neonatal tetanus was reduced by 90% between 1990 and 2010, and by 2013 the disease had been largely eliminated from all but 25 countries.[14] Neonatal tetanus is rare in developed countries.
+Local tetanus[edit] => Local tetanus is an uncommon form of the disease, in which patients have persistent contraction of muscles in the same anatomic area as the injury. The contractions may persist for many weeks before gradually subsiding. Local tetanus is generally milder; only about 1% of cases are fatal, but it may precede the onset of generalized tetanus.[citation needed]
+Cephalic tetanus[edit] => Cephalic tetanus is the rarest form of the disease (0.9–3% of cases)[15] and is limited to muscles and nerves in the head.[16] It usually occurs after trauma to the head area, including skull fracture,[17] laceration,[17] eye injury,[16] dental extraction,[18] and otitis media,[19] but it has been observed from injuries to other parts of the body.[20] Paralysis of the facial nerve is most frequently implicated, which may cause lockjaw, facial palsy, or ptosis, but other cranial nerves can also be affected.[18][21] Cephalic tetanus may progress to a more generalized form of the disease.[15][21] Due to its rarity, clinicians may be unfamiliar with the clinical presentation and may not suspect tetanus as the illness.[16] Treatment can be complicated as symptoms may be concurrent with the initial injury that caused the infection.[17] Cephalic tetanus is more likely than other forms of tetanus to be fatal, with the progression to generalized tetanus carrying a 15–30% case fatality rate.[15][17][21]
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DISNET disease texts/100 Original Disease Texts/Tethered spinal cord syndrome.txt

+Tethered spinal cord can be caused by various conditions but the main cause is when tissue attachments limit the movement of the spinal cord in the spinal column which causes abnormal stretching of the cord. The tethered spinal cord syndrome is correlated with having the causes:
+Spina bifida Occulta Mylomeningocele Meningocele&Occulta&Mylomeningocele&Meningocele&History of spinal trauma&History of spinal surgery&Tumor(s) in the spinal column&Thickened and/or tight filum terminale&Lipoma(s) in the spinal column&Dermal Sinus Tract (congenital deformity)&Diastematomyelia (split spinal cord)[5
+Tethered spinal cord is a disorder and not a mechanism so it does not spread to other people and there are no measures that can be done to prevent it beforehand. The only preventative measure that is successful is to surgically untether the spinal cord though there might already be irreversible damage.[6]
+Tethered spinal cord and spina bifida[edit] => In tethered spinal cord cases spina bifida can be accompanied by tethering of the spinal cord but in rare cases with Spina bifida occulta. Tethering of the spinal cord tends to occur in the cases of Spina bifida with mylomeningocele. In a normal person the spine grows faster than the spinal cord during development which causes the end of the spinal cord to appear to rise relative to the bony spine next to it. By the time of birth the spinal cord is located between L1 and L2. In a baby with Spina bifida the spinal cord is still attached to the skin around it preventing it from rising properly. This occurs because the spinal cord in a child with Spina bifida is low lying and tethered at the bottom. At the time of birth the mylomeningocele is separated from the skin but the spinal cord is still stuck in the same place. As the child begins to grow the spinal cord remains in the same place becoming stretched out causing the tight cord and the tethering at the end. With this type of tethering there is an interference with the blood supply to the nerves and body which can then cause the deterioration of the body causing orthopedic, neurological, and urological problems. With milder forms of Spina bifida such as Occulta, may be related to the degree of strain on the cord which can become worse with physical activity, injury, pregnancy, bone spurs, or spinal stenosis. The tethered cord in this case might not be diagnosed until adulthood when it worsens and can still cause neurological, orthopedic, and urological dysfunctions.[6]
+For children younger than eight weeks of age (and possibly in utero), a tethered cord may be observed using ultrasonography. Ultrasonography may still be useful through age 5 in limited circumstances. [7]
+MRI imaging appears to be the gold standard for diagnosing a tethered cord.[8][9]
+A tethered cord is often diagnosed as a "low conus." The conus medullaris (or lower termination of the spinal cord) normally terminates at or above the L1-2 disk space (where L1 is the first, or topmost lumbar vertebra). After about 3 months of age, a conus below the L1-2 disk space may indicate a tethered cord and termination below L3-4 is unmistakably tethered. "Cord tethering is often assumed when the conus is below the normal L2-3 level.
+TCS, however, is a clinical diagnosis that should be based on "neurological and musculoskeletal signs and symptoms. Imaging features are in general obtained to support rather than make the diagnosis."[10] Clinical evaluation may include a simple rectal examination and may also include invasive or non-invasive urological examination.[11][12] "Bladder dysfunction occurs in ~40% of patients affected by tethered cord syndrome. ... [I]t may be the earliest sign of the syndrome." [13]
+In children, symptoms may include:
+Lesions, hairy patches, dimples, or fatty tumours on the lower back&Foot and spinal deformities[3]&Weakness in the legs[3] (loss of muscle strength and tone)&Change in or abnormal gait including awkwardness while running or wearing the tips or side of one shoe[3]&Low back pain[3]&Scoliosis[3] (abnormal curvature of the spine to the left or right)&Urinary irregularities (incontinence or retention)[3
+Tethered spinal cord syndrome may go undiagnosed until adulthood, when sensory, motor, bowel, and bladder control issues emerge. This delayed presentation of symptoms relates to the degree of strain on the spinal cord over time.
+Tethering may also develop after spinal cord injury. Scar tissue can block the flow of fluids around the spinal cord. Fluid pressure may cause cysts to form in the spinal cord, a condition called syringomyelia. This can lead to additional loss of movement or feeling, or the onset of pain or autonomic nervous system symptoms.
+In adults, onset of symptoms typically include:
+Severe pain (in the lower back and radiating into the legs, groin, and perineum)&Bilateral muscle weakness and numbness&Loss of feeling and movement in lower extremities&Urinary irregularities (incontinence or retention)&Bowel control issue
+Neurological symptoms can include a mixed picture of upper and lower motor neuron findings, such as amyotrophy, hyperreflexia, and pathologic plantar response, occurring in the same limb. Profound sensory changes, such as loss of pain, temperature, and proprioceptive sensations, are common. Last, progressive symptoms of a neuropathic bladder are noted on over 70% of adult patients, versus only 20% to 30% of children. These symptoms include urinary frequency and urgency, feeling of incomplete voiding, poor voluntary control, and urge and stress incontinence. Chronic recurrent infections are common and occasionally lead to nephrolithiasis (kidney stones), renal failure, or renal transplantation. Female patients also give a history of ineffective labor and postpartum rectal prolapse, presumably due to an atonic pelvic floor.[4]
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DISNET disease texts/100 Original Disease Texts/Thyroid storm.txt

+The transition from hyperthyroidism to thyroid storm is typically triggered by a non-thyroidal insult including, but not limited to fever, sepsis, dehydration, myocardial infarction, and psychiatric diseases.[vague][9][8] Individuals are at higher risk of thyroid storm if their hyperthyroidism is incompletely treated or if their anti-thyroid drugs are discontinued. Many of these individuals have underlying primary causes of hyperthyroidism (Graves disease, toxic multi-nodular goiter, solitary toxic adenoma). However, thyroid storm can occur in individuals with unrecognized thyrotoxicosis experiencing non-thyroid surgery, labor, infection, or exposure to certain medications and radiocontrast dyes.
+The diagnosis of thyroid storm is based on the presence of symptoms consistent with severe hyperthyroidism, as outlined in the Signs and symptoms section above.[6] Multiple approaches have been proposed to calculate the probability of thyroid storm based on clinical criteria, however, none have been universally adopted by clinicians. For instance, Burch and Wartofsky published the Burch-Wartofsky point scale (BWPS) in 1993, assigning a numerical value based on the presence of specific signs and symptoms organized within the following categories: temperature, cardiovascular dysfunction (including heart rate and presence of atrial fibrillation or congestive heart failure), central nervous system (CNS) dysfunction, gastrointestinal or liver dysfunction and presence of a precipitating event.[6][10] A Burch-Wartofsky score below 25 is not suggestive of thyroid storm whereas 25 to 45 suggests impending thyroid storm and greater than 45 suggests current thyroid storm.[11] Alternatively, the Japanese Thyroid Association (JTA) criteria, derived from a large cohort of patients with thyroid storm in Japan and published in 2012, provide a qualitative method to determine the probability of thyroid storm. The JTA criteria separate the diagnosis of thyroid storm into definite versus suspected based on the specific combination of signs and symptoms a patient exhibits and require elevated free triiodothyronine (T3) or free thyroxine (T4) for definite thyroid storm.[12]
+Temperature Score Heart Rate Score Symptoms of Heart Failure Score Presence of Atrial Fibrillation Score Symptoms of CNS Dysfunction Score Gastrointestinal or Liver Dysfunction Score Presence of Precipitating Event Score  headingBody  99.0 to 99.9 5 90 to109 5 None 0 Absent 0 None 0 None 0 None 0 100.0 to 100.9 10 110 to 119 10 Mild (i.e. pedal edema) 5 Present 10 Mild (e.g. showing signs of agitation) 10 Moderate (e.g. diarrhea, nausea, vomiting or abdominal pain) 10 Present 10 101.0 to 101.9 15 120 to 129 15 Moderate (i.e. bibasilar rales) 10   Moderate (e.g. delirium, psychosis, lethargy) 20 Severe (i.e. unexplained jaundice) 20   102.0 to 102.9 20 130 to 139 20 Severe (i.e. pulmonary edema) 15   Severe (e.g. seizure or coma) 30     103 to 103.9 25 Greater than or equal to 140 25           Greater than or equal to 104 30
+Laboratory findings[edit] => As with hyperthyroidism, TSH is suppressed. Both free and serum (or total) T3 and T4 are elevated.[4] An elevation in thyroid hormone levels is suggestive of thyroid storm when accompanied by signs of severe hyperthyroidism but is not diagnostic as it may also correlate with uncomplicated hyperthyroidism.[6][10] Moreover, serum T3 may be normal in critically ill patients due to decreased conversion of T4 to T3.[6] Other potential abnormalities include the following:[6][10]
+Hyperglycemia likely due to catecholamine-mediated effects on insulin release and metabolism as well as increased glycogenolysis, evolving into hypoglycemia when glycogen stores are depleted&Elevated aspartate aminotransferase (AST), bilirubin and lactate dehydrogenase (LDH)&Hypercalcemia and elevated alkaline phosphatase due to increased bone resorption&Elevated white blood cell count
+Thyroid storm is characterized by an acute onset of symptoms of hyperthyroidism (fast heart rate, restlessness, agitation) accompanied by other features such as fever (temperatures often above 40 °C/104 °F), mental status changes, diarrhea, and vomiting.[4]
+Individuals can exhibit varying signs of organ dysfunction. Patients may experience liver dysfunction, and yellow discoloration of the skin is considered a poor prognostic sign. Heart (cardiac) symptoms include abnormal heart rhythms, decreased blood flow to the heart and heart attacks, and congestive heart failure, which may lead to cardiovascular collapse. Mortality can be as high as 20-30%.[5]
+In some situations, individuals may not experience the classic signs of restlessness and agitation, but instead present with apathetic signs of weakness and confusion.[4]
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DISNET disease texts/100 Original Disease Texts/Thyrotoxic periodic paralysis.txt

+Genetics[edit] => Genetic mutations in the L-type calcium channel α1-subunit (Cav1.1) have been described in Southern Chinese with TPP. The mutations are located in a different part of the gene from those described in the related condition familial periodic paralysis. In TPP, the mutations described are single-nucleotide polymorphisms located in the hormone response element responsive to thyroid hormone, implying that transcription of the gene and production of ion channels may be altered by increased thyroid hormone levels. Furthermore, mutations have been reported in the genes coding for potassium voltage-gated channel, Shaw-related subfamily, member 4 (Kv3.4) and sodium channel protein type 4 subunit alpha (Na41.4).[1]
+Of people with TPP, 33% from various populations were demonstrated to have mutations in KCNJ18, the gene coding for Kir2.6, an inward-rectifier potassium ion channel. This gene, too, harbors a thyroid response element.[3]
+Certain forms of human leukocyte antigen (HLA)—especially B46, DR9, DQB1*0303, A2, Bw22, AW19, B17, and DRW8—are more common in TPP. Linkage to particular forms of HLA, which plays a central role in the immune response, might imply an immune system cause, but it is uncertain whether this directly causes TPP or whether it increases the susceptibility to Graves' disease, a known autoimmune disease.[1]
+Thyroid disease[edit] => The most common underlying form of thyroid disease associated with TPP is Graves' disease, a syndrome due to an autoimmune reaction that leads to overproduction of thyroid hormone.[6] TPP has also been described in people with other thyroid problems such as thyroiditis, toxic nodular goiter, toxic adenoma, TSH-producing pituitary adenoma, excessive ingestion of thyroxine or iodine,[1] and amiodarone-induced hyperthyroidism.[2]
+Hypokalemia (low blood potassium levels) commonly occurs during attacks; levels below 3.0 mmol/l are typically encountered. Magnesium and phosphate levels are often found to be decreased. Creatine kinase levels are elevated in two thirds of cases, usually due to a degree of muscle injury; severe elevations suggestive of rhabdomyolysis (muscle tissue destruction) are rare.[1][2] Electrocardiography (ECG/EKG) may show tachycardia (a fast heart rate) due to the thyroid disease, abnormalities due to cardiac arrhythmia (atrial fibrillation, ventricular tachycardia), and conduction changes associated with hypokalemia (U waves, QRS widening, QT prolongation, and T wave flattening).[2] Electromyography shows changes similar to those encountered in myopathies (muscle diseases), with a reduced amplitude of the compound muscle action potentials (CMAPs);[4] they resolve when treatment has commenced.[1]
+TPP is distinguished from other forms of periodic paralysis (especially hypokalemic periodic paralysis) with thyroid function tests on the blood. These are normal in the other forms, and in thyrotoxicosis the levels of thyroxine and triiodothyronine are elevated, with resultant suppression of TSH production by the pituitary gland.[1][6] Various other investigations are usually performed to separate the different causes of hyperthyroidism.[6]
+An attack often begins with muscle pain, cramping, and stiffness.[5] This is followed by weakness or paralysis that tends to develop rapidly, usually in late evening or the early hours of the morning. The weakness is usually symmetrical;[5] the limb muscles closer to the trunk (proximal) are predominantly affected, and weakness tends to start in the legs and spread to the arms. Muscles of the mouth and throat, eyes, and breathing are usually not affected, but occasionally weakness of the respiratory muscles can cause life-threatening respiratory failure. Attacks typically resolve within several hours to several days, even in the absence of treatment.[1][2][5] On neurological examination during an attack, flaccid weakness of the limbs is noted; reflexes are usually diminished, but the sensory system is unaffected.[1][5] Mental status is not affected.[5]
+Attacks may be brought on by physical exertion, drinking alcohol, or eating food high in carbohydrates or salt. This may explain why attacks are more common in summer, when more people drink sugary drinks and engage in exercise. Exercise-related attacks tend to occur during a period of rest immediately after exercise; exercise may therefore be recommended to abort an attack.[1]
+There may be symptoms of thyroid overactivity, such as weight loss, a fast heart rate, tremor, and perspiration;[1][2] but such symptoms occur in only half of all cases.[5] The most common type of hyperthyroidism, Graves' disease, may additionally cause eye problems (Graves' ophthalmopathy) and skin changes of the legs (pretibial myxedema).[6] Thyroid disease may also cause muscle weakness in the form of thyrotoxic myopathy, but this is constant rather than episodic.[5]
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DISNET disease texts/100 Original Disease Texts/Tonsillitis.txt

+The most common cause is viral infection and includes adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus.[10][11][12][13] It can also be caused by Epstein-Barr virus, herpes simplex virus, cytomegalovirus, or HIV.[10][11][12][13] The second most common cause is bacterial infection of which the predominant is Group A β-hemolytic streptococcus (GABHS), which causes strep throat.[10][11][12][13] Less common bacterial causes include: Staphylococcus aureus (including methicillin resistant Staphylococcus aureus or MRSA ),[16] Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae, Bordetella pertussis, Fusobacterium sp., Corynebacterium diphtheriae, Treponema pallidum, and Neisseria gonorrhoeae.[10][11][12][13]
+Anaerobic bacteria have been implicated in tonsillitis and a possible role in the acute inflammatory process is supported by several clinical and scientific observations.[17]
+Under normal circumstances, as viruses and bacteria enter the body through the nose and mouth, they are filtered in the tonsils.[18][19] Within the tonsils, white blood cells of the immune system destroy the viruses or bacteria by producing inflammatory cytokines like phospholipase A2,[20] which also lead to fever.[18][19] The infection may also be present in the throat and surrounding areas, causing inflammation of the pharynx.[21]
+Sometimes, tonsillitis is caused by an infection of spirochaeta and treponema, in this case called Vincent's angina or Plaut-Vincent angina.[22]
+The diagnosis of group A beta-hemolytic streptococcus (GABHS) tonsillitis can be confirmed by culture of samples obtained by swabbing both tonsillar surfaces and the posterior pharyngeal wall and plating them on sheep blood agar medium. The isolation rate can be increased by incubating the cultures under anaerobic conditions and using selective growth media. A single throat culture has a sensitivity of 90–95% for the detection of GABHS (which means that GABHS is actually present 5–10% of the time culture suggests that it is absent). This small percentage of false-negative results are part of the characteristics of the tests used but are also possible if the patient has received antibiotics prior to testing. Identification requires 24 to 48 hours by culture but rapid screening tests (10–60 minutes), which have a sensitivity of 85–90%, are available. Older antigen tests detect the surface Lancefield group A carbohydrate. Newer tests identify GABHS serotypes using nucleic acid (DNA) probes or polymerase chain reaction. Bacterial culture may need to be performed in cases of a negative rapid streptococcal test.[23]
+True infection with GABHS, rather than colonization, is defined arbitrarily as the presence of >10 colonies of GABHS per blood agar plate. However, this method is difficult to implement because of the overlap between carriers and infected patients. An increase in antistreptolysin O (ASO) streptococcal antibody titer 3–6 weeks following the acute infection can provide retrospective evidence of GABHS infection[24] and is considered definitive proof of GABHS infection.
+Increased values of secreted phospholipase A2[20] and altered fatty acid metabolism[25] in patients with tonsillitis may have diagnostic utility.
+Common signs and symptoms include:[10][11][12][13]
+sore throat&red, swollen tonsils&pain when swallowing&high temperature (fever)&headache&tiredness&chills&a general sense of feeling unwell (malaise)&white pus-filled spots on the tonsils&swollen lymph nodes (glands) in the neck&pain in the ears or neck&weight loss&difficulty ingesting and swallowing meal/liquid intake&difficulty sleepin
+Less common symptoms include:
+nausea&fatigue&stomach ache&vomiting&furry tongue&bad breath (halitosis)&voice changes&difficulty opening the mouth (trismus)&loss of appetite&anxiety/fear of chokin
+In cases of acute tonsillitis, the surface of the tonsil may be bright red and with visible white areas or streaks of pus.[14]
+Tonsilloliths occur in up to 10% of the population frequently due to episodes of tonsillitis.[15]
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DISNET disease texts/100 Original Disease Texts/Trichinosis.txt

+The classical agent is T. spiralis (found worldwide in many carnivorous and omnivorous animals, both domestic and sylvatic), but there are also seven primarily sylvatic species of Trichinella now recognized:
+T. spiralis is most adapted to swine, most pathogenic in humans and is cosmopolitan in distribution.&T. britovi is the second most common species to infect humans; it is distributed throughout Europe, Asia, and northern and western Africa, usually in wild carnivores, wild boar and domesticated pigs.&T. murrelli also infects humans, especially from black bear meat; it is distributed among wild carnivores in North America.&T. nativa, which has a high resistance to freezing, is found in the Arctic and subarctic regions; reservoir hosts include polar bears, Arctic foxes, walruses and other wild game.&T. nelsoni, found in east African predators and scavengers, has been documented to cause a few human cases.&T. papuae infects both mammals and reptiles, including crocodiles, humans, wild pigs and domestic pigs; this species, found in Papua New Guinea and Thailand, is also nonencapsulated.[15]&T. pseudospiralis infects birds and mammals, and has demonstrated infection in humans;[16] it is a nonencapsulated species.&T. zimbabwensis can infect mammals, and possibly humans; this nonencapsulated species was detected in crocodiles in Africa.[1
+Taxonomy[edit] => Kingdom: Animalia&Phylum: Nematoda&Class: Adenophorea&Order: Trichurida&Family: Trichinellidae&Genus: Trichinell
+The typical life cycle for T. spiralis involves humans, pigs, and rodents. A pig becomes infected when it eats infectious cysts in raw meat, often porcine carrion or a rat (sylvatic cycle). A human becomes infected by consuming raw or undercooked infected pork (domestic cycle). In the stomach, the cysts from infected undercooked meat are acted on by pepsin and hydrochloric acid, which help release the larvae from the cysts into the stomach.[9] The larvae then migrate to the small intestine, and burrow into the intestinal mucosa, where they molt four times before becoming adults.[9]
+Thirty to 34 hours after the cysts were originally ingested, the adults mate, and within five days produce larvae.[9] Adult worms can only reproduce for a limited time, because the immune system will eventually expel them from the small intestine.[9] The larvae then use their piercing mouthpart, called the "stylet", to pass through the intestinal mucosa and enter the lymphatic vessels, and then enter the bloodstream.[17]
+The larvae travel by capillaries to various organs, such as the retina, myocardium, or lymph nodes; however, only larvae that migrate to skeletal muscle cells survive and encyst.[13] The larval host cell becomes a nurse cell, in which the larva will be encapsulated, potentially for the life of the host. The development of a capillary network around the nurse cell completes encystation of the larva. Trichinosis is not soil-transmitted, as the parasite does not lay eggs, nor can it survive long outside a host.[5][18]
+Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, and laboratory testing.
+Exposure history[edit] => An epidemiological investigation can be done to determine a patient's exposure to raw infected meat. Often, an infection arises from home-preparation of contaminated meat, in which case microscopy of the meat may be used to determine the infection. Exposure determination does not have to be directly from a laboratory-confirmed infected animal. Indirect exposure criteria include the consumption of products from a laboratory-confirmed infected animal, or sharing of a common exposure with a laboratory-confirmed infected human.[13]
+Clinical diagnosis[edit] => Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness, splinter hemorrhage, nonspecific gastroenteritis, and muscle pain.[13] The case definition for trichinosis at the European Center for Disease Control states "at least three of the following six: fever, muscle soreness and pain, gastrointestinal symptoms, facial edema, eosinophilia, and subconjuctival, subungual, and retinal hemorrhages."[13]
+Laboratory testing[edit] => Blood tests and microscopy can be used to aid in the diagnosis of trichinosis. Blood tests include a complete blood count for eosinophilia, creatine phosphokinase activity, and various immunoassays such as ELISA for larval antigens.[13]
+The great majority of trichinosis infections have either minor or no symptoms and no complications.[8] There are two main phases for the infection: enteral (affecting the intestines) and parenteral (outside the intestines). The symptoms vary depending on the phase, species of Trichinella, quantity of encysted larvae ingested, age, sex, and host immunity.[9]
+Enteral phase[edit] => A large burden of adult worms in the intestines promotes symptoms such as nausea, heartburn, dyspepsia, and diarrhea from two to seven days after infection, while small worm burdens generally are asymptomatic. Eosinophilia presents early and increases rapidly.[10]
+Parenteral phase[edit] => The severity of symptoms caused by larval migration from the intestines depends on the number of larvae produced. As the larvae migrate through tissue and vessels, the body's inflammatory response results in edema, muscle pain, fever, and weakness. A classic sign of trichinosis is periorbital edema, swelling around the eyes, which may be caused by vasculitis. Splinter hemorrhage in the nails is also a common symptom.[11]
+They may very rarely cause enough damage to produce serious neurological deficits (such as ataxia or respiratory paralysis) from worms entering the central nervous system. The CNS is compromised by trichinosis in 10–24% of reported cases of cerebral venous sinus thrombosis, a very rare form of stroke (3-4 cases per million annual incidence in adults).[12] Trichinosis can be fatal depending on the severity of the infection; death can occur 4–6 weeks after the infection,[13] and is usually caused by myocarditis, encephalitis, or pneumonia.[14]
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DISNET disease texts/100 Original Disease Texts/Tropical sprue.txt

+The cause of tropical sprue is not known.[1] It may be caused by persistent bacterial, viral, amoebal, or parasitic infections.[5] Folic acid deficiency, effects of malabsorbed fat on intestinal motility, and persistent small intestinal bacterial overgrowth may combine to cause the disorder.[6] A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved in the aetiology of post-infectious IBS.[7]
+Diagnosis of tropical sprue can be complicated because many diseases have similar symptoms. The following investigation results are suggestive:
+Abnormal flattening of villi and inflammation of the lining of the small intestine, observed during an endoscopic procedure.&Presence of inflammatory cells (most often lymphocytes) in the biopsy of small intestine tissue.&Low levels of vitamins A, B12, E, D, and K, as well as serum albumin, calcium, and folate, revealed by a blood test.&Excess fat in the feces (steatorrhoea).&Thickened small bowel folds seen on imaging
+Tropical sprue is largely limited to within about 30 degrees north and south of the equator. Recent travel to this region is a key factor in diagnosing this disease in residents of countries outside of that geographical region.[1]
+Other conditions which can resemble tropical sprue need to be differentiated.[4] Coeliac disease (also known as coeliac sprue or gluten sensitive enteropathy), has similar symptoms to tropical sprue, with the flattening of the villi and small intestine inflammation and is caused by an autoimmune disorder in genetically susceptible individuals triggered by ingested gluten. Malabsorption can also be caused by protozoan infections, tuberculosis, HIV/AIDS, immunodeficiency, chronic pancreatitis and inflammatory bowel disease.[1] Environmental enteropathy is a less severe, subclinical condition similar to tropical sprue.[1]
+The illness usually starts with an attack of acute diarrhoea, fever and malaise following which, after a variable period, the patient settles into the chronic phase of diarrhoea, steatorrhoea, weight loss, anorexia, malaise, and nutritional deficiencies.[1][3] The symptoms of tropical sprue are:
+Diarrhoea&Steatorrhoea or fatty stool (often foul-smelling and whitish in colour)&Indigestion&Cramps&Weight loss and malnutrition&Fatigu
+Left untreated, nutrient and vitamin deficiencies may develop in patients with tropical sprue.[1] These deficiencies may have these symptoms:
+Vitamin A deficiency: hyperkeratosis or skin scales&Vitamin B12 and folic acid deficiencies: anaemia&Vitamin D and calcium deficiencies: spasm, bone pain, numbness, and tingling sensation&Vitamin K deficiency: bruise
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DISNET disease texts/100 Original Disease Texts/Typhoid fever.txt

+The bacterium that causes typhoid fever may be spread through poor hygiene habits and public sanitation conditions, and sometimes also by flying insects feeding on feces. Public education campaigns encouraging people to wash their hands after defecating and before handling food are an important component in controlling spread of the disease. According to statistics from the United States Centers for Disease Control and Prevention (CDC), the chlorination of drinking water has led to dramatic decreases in the transmission of typhoid fever in the United States.
+Bacteria[edit] => The cause is the bacterium Salmonella Typhi, also known as Salmonella enterica serotype Typhi.[17]
+There are two main types of Typhi namely the ST1 and ST2 based on MLST subtyping scheme, which are currently widespread globally.[18]
+Diagnosis is made by any blood, bone marrow or stool cultures and with the Widal test (demonstration of antibodies against Salmonella antigens O-somatic and H-flagellar). In epidemics and less wealthy countries, after excluding malaria, dysentery, or pneumonia, a therapeutic trial time with chloramphenicol is generally undertaken while awaiting the results of the Widal test and cultures of the blood and stool.[19]
+The Widal test is time-consuming, and prone to significant false positive results. The test may be also falsely negative in the early course of illness. However, unlike Typhidot test Widal test quantifies the specimen with titres.
+Typhidot is a medical test consisting of a dot ELISA kit that detects IgM and IgG antibodies against the outer membrane protein (OMP) of the Salmonella typhi. The typhidot test becomes positive within 2–3 days of infection and separately identifies IgM and IgG antibodies. The test is based on the presence of specific IgM and IgG antibodies to a specific 50Kd OMP antigen, which is impregnated on nitrocellulose strips. IgM shows recent infection whereas IgG signifies remote infection. The most important limitation of this test is that it is not quantitative and result is only positive or negative.
+The term 'enteric fever' is a collective term that refers to severe typhoid and paratyphoid.[20]
+Classically, the course of untreated typhoid fever is divided into four distinct stages, each lasting about a week. Over the course of these stages, the patient becomes exhausted and emaciated.[15]
+In the first week, the body temperature rises slowly, and fever fluctuations are seen with relative bradycardia (Faget sign), malaise, headache, and cough. A bloody nose (epistaxis) is seen in a quarter of cases, and abdominal pain is also possible. A decrease in the number of circulating white blood cells (leukopenia) occurs with eosinopenia and relative lymphocytosis; blood cultures are positive for Salmonella Typhi or S. paratyphi. The Widal test is usually negative in the first week.[16]&In the second week, the person is often too tired to get up, with high fever in plateau around 40 °C (104 °F) and bradycardia (sphygmothermic dissociation or Faget sign), classically with a dicrotic pulse wave. Delirium is frequent, often calm, but sometimes agitated. This delirium gives to typhoid the nickname of "nervous fever". Rose spots appear on the lower chest and abdomen in around a third of patients. Rhonchi are heard in lung bases.&The abdomen is distended and painful in the right lower quadrant, where borborygmi can be heard. Diarrhea can occur in this stage: six to eight stools in a day, green, comparable to pea soup, with a characteristic smell. However, constipation is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender, and liver transaminases are elevated. The Widal test is strongly positive, with antiO and antiH antibodies. Blood cultures are sometimes still positive at this stage.&(The major symptom of this fever is that the fever usually rises in the afternoon up to the first and second week.)&In the third week of typhoid fever, a number of complications can occur: Intestinal haemorrhage due to bleeding in congested Peyer's patches; this can be very serious, but is usually not fatal. Intestinal perforation in the distal ileum: this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicaemia or diffuse peritonitis sets in. Encephalitis Respiratory diseases such as pneumonia and acute bronchitis Neuropsychiatric symptoms (described as "muttering delirium" or "coma vigil"), with picking at bedclothes or imaginary objects. Metastatic abscesses, cholecystitis, endocarditis, and osteitis The fever is still very high and oscillates very little over 24 hours. Dehydration ensues, and the patient is delirious (typhoid state). One-third of affected individuals develop a macular rash on the trunk. Platelet count goes down slowly and risk of bleeding rises.&Intestinal haemorrhage due to bleeding in congested Peyer's patches; this can be very serious, but is usually not fatal.&Intestinal perforation in the distal ileum: this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicaemia or diffuse peritonitis sets in.&Encephalitis&Respiratory diseases such as pneumonia and acute bronchitis&Neuropsychiatric symptoms (described as "muttering delirium" or "coma vigil"), with picking at bedclothes or imaginary objects.&Metastatic abscesses, cholecystitis, endocarditis, and osteitis&The fever is still very high and oscillates very little over 24 hours. Dehydration ensues, and the patient is delirious (typhoid state). One-third of affected individuals develop a macular rash on the trunk.&Platelet count goes down slowly and risk of bleeding rises.&By the end of third week, the fever starts subsidin
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DISNET disease texts/100 Original Disease Texts/Upper respiratory tract infection.txt

+In terms of pathophysiology, rhino virus infection resembles the immune response. The viruses do not cause damage to the cells of the upper respiratory tract but rather cause changes in the tight junctions of epithelial cells. This allows the virus to gain access to tissues under the epithelial cells and initiate the innate and adaptive immune responses.[7]
+Up to 15% of acute pharyngitis cases may be caused by bacteria, most commonly Streptococcus pyogenes, a group A streptococcus in streptococcal pharyngitis ("strep throat").[8] Other bacterial causes are Streptococcus pneumoniae, Haemophilus influenzae, Corynebacterium diphtheriae, Bordetella pertussis, and Bacillus anthracis[citation needed].
+Sexually transmitted infections have emerged as causes of oral and pharyngeal infections.[9]
+Symptoms Allergy URI Influenza  headingBody  Itchy, watery eyes Common Rare (conjunctivitis may occur with adenovirus) Soreness behind eyes, sometimes conjunctivitis Nasal discharge Common Common[4] Common Nasal congestion Common Common Sometimes Sneezing Very common Very common[4] Sometimes Sore throat Sometimes (post-nasal drip) Very common[4] Sometimes Cough Sometimes Common (mild to moderate, hacking)[4] Common (dry cough, can be severe) Headache Uncommon Rare Common Fever Never Rare in adults, possible in children[4] Very common 100–102 °F (or higher in young children), lasting 3–4 days; may have chills Malaise Sometimes Sometimes Very common Fatigue, weakness Sometimes Sometimes Very common (can last for weeks, extreme exhaustion early in course) Muscle pain Never Slight[4] Very common (often severe)
+In uncomplicated colds, cough and nasal discharge may persist for 14 days or more even after other symptoms have resolved.[4] Acute upper respiratory tract infections include rhinitis, pharyngitis/tonsillitis and laryngitis often referred to as a common cold, and their complications: sinusitis, ear infection and sometimes bronchitis (though bronchi are generally classified as part of the lower respiratory tract.) Symptoms of URTIs commonly include cough, sore throat, runny nose, nasal congestion, headache, low-grade fever, facial pressure and sneezing.
+Symptoms of rhinovirus in children usually begin 1–3 days after exposure. The illness usually lasts 7–10 more days.[4]
+Color or consistency changes in mucous discharge to yellow, thick, or green are the natural course of viral upper respiratory tract infection and not an indication for antibiotics.[4]
+Group A beta hemolytic streptococcal pharyngitis/tonsillitis (strep throat) typically presents with a sudden onset of sore throat, pain with swallowing and fever. Strep throat does not usually cause runny nose, voice changes, or cough.
+Pain and pressure of the ear caused by a middle ear infection (otitis media) and the reddening of the eye caused by viral conjunctivitis are often associated with upper respiratory infections.
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DISNET disease texts/100 Original Disease Texts/Vascular dementia.txt

+Vascular dementia can be caused by ischemic or hemorrhagic infarcts affecting multiple brain areas, including the anterior cerebral artery territory, the parietal lobes, or the cingulate gyrus. On rare occasion, infarcts in the hippocampus or thalamus are the cause of dementia.[6] Brain vascular lesions can also be the result of diffuse cerebrovascular disease, such as small vessel disease.
+Risk factors for vascular dementia include age, hypertension, smoking, hypercholesterolemia, diabetes mellitus, cardiovascular disease, and cerebrovascular disease. Other risk factors include geographic origin, genetic predisposition, and prior strokes.[7]
+Vascular dementia can sometimes be triggered by cerebral amyloid angiopathy, which involves accumulation of beta amyloid plaques in the walls of the cerebral arteries, leading to breakdown and rupture of the vessels. Since amyloid plaques are a characteristic feature of Alzheimer's Disease, vascular dementia may occur as a consequence. Cerebral amyloid angiopathy can, however, appear in people with no prior dementia condition. Some beta amyloid plaques are often present in cognitively normal elderly persons[citation needed].
+Several specific diagnostic criteria can be used to diagnose vascular dementia,[8] including the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria, the International Classification of Diseases, Tenth Edition (ICD-10) criteria, the National Institute of Neurological Disorders and Stroke criteria, Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN) criteria,[9] the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski Ischemic Score (after Vladimir Hachinski).[10]
+The recommended investigations for cognitive impairment include: blood tests (for anemia, vitamin deficiency, thyrotoxicosis, infection, etc.), chest X-Ray, ECG, and neuroimaging, preferably a scan with a functional or metabolic sensitivity beyond a simple CT or MRI. When available as a diagnostic tool, single photon emission computed tomography (SPECT) and positron emission tomography (PET) neuroimaging may be used to confirm a diagnosis of multi-infarct dementia in conjunction with evaluations involving mental status examination.[11] In a person already having dementia, SPECT appears to be superior in differentiating multi-infarct dementia from Alzheimer's disease, compared to the usual mental testing and medical history analysis.[12] Advances have led to the proposal of new diagnostic criteria.[13][14]
+The screening blood tests typically include full blood count, liver function tests, thyroid function tests, lipid profile, erythrocyte sedimentation rate, C reactive protein, syphilis serology, calcium serum level, fasting glucose, urea, electrolytes, vitamin B-12, and folate. In selected patients, HIV serology and certain autoantibody testing may be done.
+Mixed dementia is diagnosed when people have evidence of Alzheimer's disease and cerebrovascular disease, either clinically or based on neuro-imaging evidence of ischemic lesions.
+Pathology[edit] => Gross examination of the brain may reveal noticeable lesions and damage to blood vessels. Accumulation of various substances such as lipid deposits and clotted blood appear on microscopic views. The white matter is most affected, with noticeable atrophy (tissue loss), in addition to calcification of the arteries. Microinfarcts may also be present in the gray matter (cerebral cortex), sometimes in large numbers. Although atheroma of the major cerebral arteries is typical in vascular dementia, smaller vessels and arterioles are mainly affected.
+Differentiating the different dementia syndromes can be challenging, due to the frequently overlapping clinical features and related underlying pathology. In particular, Alzheimer's dementia often co-occurs with vascular dementia.[3]
+People with vascular dementia present with progressive cognitive impairment, acutely or subacutely as in mild cognitive impairment, frequently step-wise, after multiple cerebrovascular events (strokes). Some people may appear to improve between events and decline after more silent strokes. A rapidly deteriorating condition may lead to death from a stroke, heart disease, or infection.[4]
+Signs and symptoms are cognitive, motor, behavioral, and for a significant proportion of patients also affective. These changes typically occur over a period of 5–10 years. Signs are typically the same as in other dementias, but mainly include cognitive decline and memory impairment of sufficient severity as to interfere with activities of daily living, sometimes with presence of focal neurologic signs, and evidence of features consistent with cerebrovascular disease on brain imaging (CT or MRI).[5] The neurologic signs localizing to certain areas of the brain that can be observed are hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, as well as gait and swallowing difficulties. People have patchy deficits in terms of cognitive testing. They tend to have better free recall and fewer recall intrusions when compared with patients with Alzheimer's disease. In the more severely affected patients, or patients affected by infarcts in Wernicke's or Broca's areas, specific problems with speaking called dysarthrias and aphasias may be present.
+In small vessel disease, the frontal lobes are often affected. Consequently, patients with vascular dementia tend to perform worse than their Alzheimer's disease counterparts in frontal lobe tasks, such as verbal fluency, and may present with frontal lobe problems: apathy, abulia, problems with attention, orientation, and urinary incontinence. They tend to exhibit more perseverative behavior. VaD patients may also present with general slowing of processing ability, difficulty shifting sets, and impairment in abstract thinking. Apathy early in the disease is more suggestive of vascular dementia.
+Rare genetic disorders which result in vascular lesions in the brain have other patterns of presentation. As a rule, they tend to present earlier in life and have a more aggressive course. In addition, infectious disorders, such as syphilis, can lead to arterial damage, strokes, and bacterial inflammation of the brain.
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DISNET disease texts/100 Original Disease Texts/Waterhouse–Friderichsen syndrome.txt

+Multiple species of bacteria can be associated with the condition:
+Meningococcus is another term for the bacterial species Neisseria meningitidis; blood infection with said species usually underlies WFS. While many infectious agents can infect the adrenals, an acute, selective infection is usually meningococcus.&Pseudomonas aeruginosa can also cause WFS.[3]&WFS can also be caused by Streptococcus pneumoniae infections, a common bacterial pathogen typically associated with meningitis in the adult and elderly population.[2]&Mycobacterium tuberculosis could also cause WFS. Tubercular invasion of the adrenal glands could cause hemorrhagic destruction of the glands and cause mineralocorticoid deficiency.&Staphylococcus aureus has recently also been implicated in pediatric WFS.[4]&It can also be associated with Haemophilus influenzae.[5][6
+Viruses may also be implicated in adrenal problems:
+Cytomegalovirus can cause adrenal insufficiency,[7] especially in the immunocompromised.&Ebola virus infection may also cause similar acute adrenal failure.[citation needed
+Leukocytosis Acidosis Hyperkalemia Hyponatremia Abnormal complete blood count Acute kidney injury C reactive protein Acth test TFT
+Waterhouse-Friderichsen Syndrome can be caused by a number of different organisms (see below). When caused by Neisseria meningitidis, WFS is considered the most severe form of meningococcal sepsis. The onset of the illness is nonspecific with fever, rigors, vomiting, and headache. Soon a rash appears; first macular, not much different from the rose spots of typhoid, and rapidly becoming petechial and purpuric with a dusky gray color. Low blood pressure (hypotension) develops and rapidly leads to septic shock. The cyanosis of extremities can be extreme and the patient is very prostrated or comatose. In this form of meningococcal disease, meningitis generally does not occur. Low levels of blood glucose and sodium, high levels of potassium in the blood, and the ACTH stimulation test demonstrate the acute adrenal failure. Leukocytosis need not be extreme and in fact leukopenia may be seen and it is a very poor prognostic sign. C-reactive protein levels can be elevated or almost normal. Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of disseminated intravascular coagulation (DIC). Acidosis and acute kidney failure can be seen as in any severe sepsis. Meningococci can be readily cultured from blood or cerebrospinal fluid, and can sometimes be seen in smears of cutaneous lesions. Difficulty swallowing, atrophy of the tongue, and cracks at the corners of the mouth are also characteristic features.[citation needed]
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DISNET disease texts/100 Original Disease Texts/Weight loss.txt

+Disease-related => Disease-related malnutrition can be considered in four categories:[29]
+Problem Cause  headingBody  Impaired intake Poor appetite can be a direct symptom of an illness, or an illness could make eating painful or induce nausea. Illness can also cause food aversion. Inability to eat can result from: diminished consciousness or confusion, or physical problems affecting the arm or hands, swallowing or chewing. Eating restrictions may also be imposed as part of treatment or investigations. Lack of food can result from: poverty, difficulty in shopping or cooking, and poor quality meals. Impaired digestion &/or absorption This can result from conditions that affect the digestive system. Altered requirements Changes to metabolic demands can be caused by illness, surgery and organ dysfunction. Excess nutrient losses Losses from the gastrointestinal can occur because of symptoms such as vomiting or diarrhea, as well as fistulae and stomas. There can also be losses from drains, including nasogastric tubes. Other losses: Conditions such as burns can be associated with losses such as skin exudates.
+Weight loss issues related to specific diseases include:
+As chronic obstructive pulmonary disease (COPD) advances, about 35% of patients experience severe weight loss called pulmonary cachexia, including diminished muscle mass.[31] Around 25% experience moderate to severe weight loss, and most others have some weight loss.[31] Greater weight loss is associated with poorer prognosis.[31] Theories about contributing factors include appetite loss related to reduced activity, additional energy required for breathing, and the difficulty of eating with dyspnea (labored breathing).[31]&Cancer, a very common and sometimes fatal cause of unexplained (idiopathic) weight loss. About one-third of unintentional weight loss cases are secondary to malignancy. Cancers to suspect in patients with unexplained weight loss include gastrointestinal, prostate, hepatobilary (hepatocellular carcinoma, pancreatic cancer), ovarian, hematologic or lung malignancies.&People with HIV often experience weight loss, and it is associated with poorer outcomes.[35] Wasting syndrome is an AIDS-defining condition.[35]&Gastrointestinal disorders are another common cause of unexplained weight loss – in fact they are the most common non-cancerous cause of idiopathic weight loss.[citation needed] Possible gastrointestinal etiologies of unexplained weight loss include: celiac disease, peptic ulcer disease, inflammatory bowel disease (crohn's disease and ulcerative colitis), pancreatitis, gastritis, diarrhea and many other GI conditions.&Infection. Some infectious diseases can cause weight loss. Fungal illnesses, endocarditis, many parasitic diseases, AIDS, and some other subacute or occult infections may cause weight loss.&Renal disease. Patients who have uremia often have poor or absent appetite, vomiting and nausea. This can cause weight loss.&Cardiac disease. Cardiovascular disease, especially congestive heart failure, may cause unexplained weight loss.&Connective tissue disease&Neurologic disease, including dementia[36]&Oral, taste or dental problems (including infections) can reduce nutrient intake leading to weight loss.[27
+Therapy-related => Medical treatment can directly or indirectly cause weight loss, impairing treatment effectiveness and recovery that can lead to further weight loss in a vicious cycle.[25]
+Many patients will be in pain and have a loss of appetite after surgery.[25] Part of the body's response to surgery is to direct energy to wound healing, which increases the body's overall energy requirements.[25] Surgery affects nutritional status indirectly, particularly during the recovery period, as it can interfere with wound healing and other aspects of recovery.[25][29] Surgery directly affects nutritional status if a procedure permanently alters the digestive system.[25] Enteral nutrition (tube feeding) is often needed.[25] However a policy of 'nil by mouth' for all gastrointestinal surgery has not been shown to benefit, with some suggestion it might hinder recovery.[37]
+Early post-operative nutrition is a part of Enhanced Recovery After Surgery protocols.[38] These protocols also include carbohydrate loading in the 24 hours before surgery, but earlier nutritional interventions have not been shown to have a significant impact.[38]
+Some medications can cause weight loss,[39] while others can cause weight gain.[40][41]
+Social conditions => Social conditions such as poverty, social isolation and inability to get or prepare preferred foods can cause unintentional weight loss, and this may be particularly common in older people.[42] Nutrient intake can also be affected by culture, family and belief systems.[27] Ill-fitting dentures and other dental or oral health problems can also affect adequacy of nutrition.[27]
+Loss of hope, status or social contact and spiritual distress can cause depression, which may be associated with reduced nutrition, as can fatigue.[27]
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DISNET disease texts/100 Original Disease Texts/Whipple's disease.txt

+Common clinical signs and symptoms of Whipple's disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms.[7] Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of non-destructive seronegative arthritis, often of large joints.[8]
+Diagnosis is made by biopsy, usually by duodenal endoscopy, which reveals PAS-positive macrophages in the lamina propria containing non-acid-fast gram-positive bacilli.[4] Immunohistochemical staining for antibodies against T. whipplei has been used to detect the organism in a variety of tissues, and a PCR-based assay is also available.[4] PCR can be confirmatory if performed on blood, vitreous fluid, synovial fluid, heart valves, or cerebrospinal fluid.[9] PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipple's disease, but that a negative PCR is most likely indicative of a healthy individual.[4]
+Endoscopy of the duodenum and jejunum can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipple's disease, and small bowel X-rays may show some thickened folds. Other pathological findings may include enlarged mesenteric lymph nodes, hypercellularity of lamina propria with "foamy macrophages", and a concurrent decreased number of lymphocytes and plasma cells, per high power field view of the biopsy.
+A D-Xylose test can be performed, which is where the patient will consume 4.5g of D-xylose, a sugar, by mouth. The urine excretion of D-Xylose is then measured after 5 hours. The majority of D-Xylose is absorbed normally, and should be found in the urine. If the D-Xylose is found to be low in the urine, this suggests an intestinal malabsorption problem such as bacterial overgrowth of the proximal small intestine, Whipple's Disease, or an autoimmune with diseases such as Celiac's Disease (allergy to gluten) or Crohn's Disease (autoimmune disease affecting the small intestine). With empiric antibiotic treatment after an initial positive D-Xylose test, and if a follow-up D-Xylose test is positive (decreased urine excretion) after antibiotic therapy, then this would signify it is not bacterial overgrowth of the proximal small intestine. Since Whipple's disease is so rare, a follow-up positive D-Xylose test more likely indicates a non-infectious etiology and more likely an autoimmune etiology. Clinical correlation is recommended to rule out Whipple's disease.
+The most common symptoms are diarrhea, abdominal pain, weight loss, and joint pains. The joint pains may be due to migratory non-deforming arthritis, which may occur many years before any digestive tract symptoms develop; they tend to involve the large joints but can occur in any pattern and tend not to damage the joint surface to the point that the joint becomes deformed. Fever and chills occur in a small proportion of people.[4]
+In its more advanced form, malabsorption (insufficient absorption of nutrients from the diet) leads to wasting and the enlargement of lymph nodes in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing steatorrhea (fatty, offensive stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of albumin, a blood protein, which may lead to peripheral edema caused by the lowered oncotic pressures.[4]
+Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as uveitis, may occur; this is typically associated with deteriorating vision and pain in the affected eye. Endocarditis (infection of the heart valve) has been reported in a small number of cases, sometimes in people with no other symptoms of Whipple's disease; this is typically noticed as breathlessness and leg swelling due to fluid accumulation as the heart is unable to pump fluid through the body.[4]
+Of those affected by Whipple's disease, 10–40% of people have problems related to the involvement of the brain; the symptoms relate to the part of the brain that is affected. The most common problems are dementia, memory loss, confusion, and decreased level of consciousness. Eye movement disturbances and myorhythmia (rapidly repetitive movements of the muscles) of the face, together referred to as oculomasticatory myorhythmia, are highly characteristic for Whipple's disease. Weakness and poor coordination of part of the body, headaches, seizures, as well as a number of more uncommon neurological features, are present in some cases.[4]
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DISNET disease texts/100 Original Disease Texts/Xerostomia.txt

+A diagnosis of hyposalivation is based predominantly on the clinical signs and symptoms.[1] There is little correlation between symptoms and objective tests of salivary flow,[18] such as sialometry. This test is simple and noninvasive, and involves measurement of all the saliva a patient can produce during a certain time, achieved by dribbling into a container. Sialometery can yield measures of stimulated salivary flow or unstimulated salivary flow. Stimulated salivary flow rate is calculated using a stimulant such as 10% citric acid dropped onto the tongue, and collection of all the saliva that flows from one of the parotid papillae over five or ten minutes. Unstimulated whole saliva flow rate more closely correlates with symptoms of xerostomia than stimulated salivary flow rate.[1] Sialography involves introduction of radio-opaque dye such as iodine into the duct of a salivary gland.[1] It may show blockage of a duct due to a calculus. Salivary scintiscanning using technetium is rarely used. Other medical imaging that may be involved in the investigation include chest x-ray (to exclude sarcoidosis), ultrasonography and magnetic resonance imaging (to exclude Sjögren's syndrome or neoplasia).[1] A minor salivary gland biopsy, usually taken from the lip,[19] may be carried out if there is a suspicion of organic disease of the salivary glands.[1] Blood tests and urinalysis may be involved to exclude a number of possible causes.[1] To investigate xerophthalmia, the Schirmer test of lacrimal flow may be indicated.[1] Slit-lamp examination may also be carried out.[1]
+True hyposalivation may give the following signs and symptoms:
+Dental caries (xerostomia related caries) – Without the anticariogenic actions of saliva, tooth decay is a common feature and may progress much more aggressively than it would otherwise ("rampant caries"). It may affect tooth surfaces that are normally spared, e.g., cervical caries and root surface caries. This is often seen in patients who have had radiotherapy involving the major salivary glands, termed radiation-induced caries.[9] Therefore it's important that any products used in managing dry mouth symptoms are sugar-free, as the presence of sugars in the mouth support the growth of oral bacteria, resulting in acid production and development of dental caries [8].&Acid erosion. Saliva acts as a buffer and helps to prevent demineralization of teeth.[10]&Oral candidiasis – A loss of the antimicrobial actions of saliva may also lead to opportunistic infection with Candida species.[9]&Ascending (suppurative) sialadenitis – an infection of the major salivary glands (usually the parotid gland) that may be recurrent.[3] It is associated with hyposalivation, as bacteria are able to enter the ductal system against the diminished flow of saliva.[7] There may be swollen salivary glands even without acute infection, possibly caused by autoimmune involvement.[3]&Dysgeusia – altered taste sensation (e.g., a metallic taste)[1] and dysosmia, altered sense of smell.[3]&Intraoral halitosis[1] – possibly due to increased activity of halitogenic biofilm on the posterior dorsal tongue (although dysgeusia may cause a complaint of nongenuine halitosis in the absence of hyposalivation).&Oral dysesthesia – a burning or tingling sensation in the mouth.[1][3]&Saliva that appears thick or ropey.[9]&Mucosa that appears dry.[9]&A lack of saliva pooling in the floor of the mouth during examination.[1]&Dysphagia – difficulty swallowing and chewing, especially when eating dry foods. Food may stick to the tissues during eating.[9]&The tongue may stick to the palate,[7] causing a clicking noise during speech, or the lips may stick together.[1]&Gloves or a dental mirror may stick to the tissues.[9]&Fissured tongue with atrophy of the filiform papillae and a lobulated, erythematous appearance of the tongue.[1][9]&Saliva cannot be "milked" (expressed) from the parotid duct.[1]&Difficulty wearing dentures, e.g., when swallowing or speaking.[1] There may be generalized mucosal soreness and ulceration of the areas covered by the denture.[3]&Mouth soreness and oral mucositis.[1][3]&Lipstick or food may stick to the teeth.[1]&A need to sip drinks frequently while talking or eating.[3]&Dry, sore, and cracked lips and angles of mouth.[3]&Thirst.[3
+However, sometimes the clinical findings do not correlate with the symptoms experienced.[9] E.g., a person with signs of hyposalivation may not complain of xerostomia. Conversely a person who reports experiencing xerostomia may not show signs of reduced salivary secretions (subjective xerostomia).[8] In the latter scenario, there are often other oral symptoms suggestive of oral dysesthesia ("burning mouth syndrome").[3] Some symptoms outside the mouth may occur together with xerostomia.
+These include:
+Xerophthalmia (dry eyes).[1]&Inability to cry.[1]&Blurred vision.[1]&Photophobia (light intolerance).[1]&Dryness of other mucosae, e.g., nasal, laryngeal, and/or genital.[1]&Burning sensation.[1]&Itching or grittiness.[1]&Dysphonia (voice changes).[1
+There may also be other systemic signs and symptoms if there is an underlying cause such as Sjögren's syndrome,[1] for example, joint pain due to associated rheumatoid arthritis.
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