umarjan11/Medical-qna huggingface dataset:
Question: What causes Merkel cell carcinoma ?

Answer: What causes Merkel cell carcinoma? The exact underlying cause of Merkel cell carcinoma (MCC) is unknown, but several risk factors have been associated with the development of MCC. Having one or more risk factors does not mean that a person will develop MCC; most individuals with risk factors will not develop MCC. Risk factors include:     -being over 50 years of age     -having fair skin     -having a history of extensive sun exposure (natural or artificial)     -having chronic immune suppression, such as after organ transplantation or having HIV Researchers have also found that a virus called Merkel cell polyomavirus (MCPyV) is frequently involved in the development of MCC. MCPyV is found in about 80% of tumor cells tested. This virus is thought to alter the DNA in such a way that influences tumor development.
Question: What causes Mnire's disease ?

Answer: What causes Mnire's disease? The underlying cause of Mnire's disease is unknown, although it probably results from a combination of environmental and genetic factors. Possible factors that have been studied include viral infections; trauma to the middle ear; middle ear infection (otitis media); head injury; a hereditary predisposition; syphilis; allergies; abnormal immune system responses; migraines; and noise pollution. The symptoms of Mnire's disease are thought to relate to changes in fluid volume in the inner ear, which contains structures necessary for normal hearing and balance. Changes in fluid volume may disrupt signals sent from the inner ear to the brain, or may lead to tears or ruptures of the structures that affect hearing and balance. More detailed information about the causes of symptoms associated with Mnire's disease is available on NIDCD's Web site.
Question: What is (are) Spinocerebellar ataxia 13 ?

Answer: Spinocerebellar ataxia 13 (SCA13) is a rare sub-type of spinocerebellar ataxias, a group of neurological conditions characterized by degeneration of the brain and spinal cord. Signs and symptoms of SCA13 appear to vary among affected people and range from childhood-onset, slowly progressive gait ataxia and dysarthria (often with intellectual disability and occasional seizures) to adult-onset progressive ataxia. Life expectancy is normal. SCA13 is caused by mutations in the KCNC3 gene and is inherited in an autosomal dominant manner. Treatment may include anti-seizure medications; assistive devices (such as a canes and walkers); and/or speech therapy and communication devices.
Question: What are the treatments for Esthesioneuroblastoma ?

Answer: How is esthesioneuroblastoma usually treated? Various treatment regimens for esthesioneuroblastoma have been used through the years. Early treatment included using either surgery or radiation therapy, but, for the most part, these regimens resulted in high rates of recurrence. Subsequently, multimodality therapy with surgery and radiation therapy has been more frequently administered, and some institutions recommend trimodality therapy, with the addition of chemotherapy to surgery and radiation therapy. Most patients are initially treated with surgical removal if possible. Radiation therapy is most commonly administered after surgical removal of the tumor. The role of chemotherapy for esthesioneuroblastoma remains poorly defined. Many institutions incorporate chemotherapy into the treatment regimen, especially for stage C disease, whereas others have not noted any substantial clinical response to chemotherapy.
Question: What is (are) Dextrocardia with situs inversus ?

Answer: Dextrocardia with situs inversus is a condition that is characterized by abnormal positioning of the heart and other internal organs. In people affected by dextrocardia, the tip of the heart points towards the right side of the chest instead of the left side. Situs inversus refers to the mirror-image reversal of the organs in the chest and abdominal cavity. Some affected people have no obvious signs or symptoms. However, a small percentage of people also have congenital heart defects, usually transposition of the great vessels. Dextrocardia with situs inversus can also be associated with primary ciliary dyskinesia (also known as Kartagener syndrome). Treatment typically depends on the heart or physical problems the person may have in addition to dextrocardia with situs inversus.
Question: What is (are) 15q11.2 microdeletion ?

Answer: 15q11.2 microdeletion refers to a chromosome abnormality in which a tiny piece of genetic material on the long arm of chromosome 15 (at a location designated q11.2) is missing (deleted). The features of people with a 15q11.2 microdeletion vary widely. The most common features include developmental, motor, and language delays; behavior and emotional problems; attention deficit disorders; and autism spectrum disorder. Other features may include birth defects and seizures. However, some people have no apparent physical, learning, or behavior problems. A 15q11.2 microdeletion may occur randomly for the first time in an affected person, or it may be inherited from a parent. Treatment depends on the signs and symptoms in each person.
Question: Is Cutaneous mastocytosis inherited ?

Answer: Is cutaneous mastocytosis inherited? Most cases of cutaneous mastocytosis are not inherited. They occur spontaneously in families with no history of the condition and are due to somatic changes (mutations) in the KIT gene. Somatic mutations occur after conception and are only present in certain cells. Because they are not present in the germ cells (egg and sperm), they are not passed on to the next generation. Cutaneous mastocytosis can rarely affect more than one family member. In these cases, the condition is typically inherited in an autosomal dominant manner. This means that to be affected, a person only needs a change (mutation) in one copy of the responsible gene in each cell. A person with familial cutaneous mastocytosis has a 50% chance with each pregnancy of passing along the altered gene to his or her child.
Question: What is (are) WAGR syndrome ?

Answer: WAGR syndrome is a genetic syndrome in which there is a predisposition to several conditions, including certain malignancies, distinctive eye abnormalities, and/or mental retardation. WAGR is an acronym for Wilms tumor, Aniridia, Genitourinary anomalies (such as undescended testicles or hypospadias in males, or internal genital or urinary anomalies in females), mental Retardation syndrome. A combination of two or more of these conditions is usually present in most individuals with WAGR syndrome. The syndrome is due to a microdeletion in the 11p13 region of chromosome 11. In most cases, this genetic change occurs spontaneously during early embryonic development (de novo) for unknown reasons (sporadic). Only rarely is the mutation inherited.
Question: What is (are) Common variable immunodeficiency ?

Answer: Common variable immunodeficiency (CVID) is a group of disorders in which the immune system cannot make antibodies against agents that cause infection (such as bacteria). CVID is characterized by low levels of most or all of the immunoglobulin (Ig) classes. This causes affected people to get frequent infections, particularly in the sinuses, lungs, and digestive tract. Symptoms most commonly begin in early adulthood but have been found in children as young as age two. While in most cases the cause of CVID is unknown, it has been associated with changes (mutations) in at least 10 genes. About 10% of cases are due to mutations in the TNFRSF13B gene. Treatment for CVID includes Ig replacement therapy, which stops the cycle of recurrent infections.
Question: What is (are) Von Hippel-Lindau disease ?

Answer: Von Hippel-Lindau (VHL) disease is an inherited disorder characterized by the abnormal growth of both benign and cancerous tumors and cysts in many parts of the body. Tumors usually first appear in young adulthood. The types of tumors associated with VHL disease include hemangioblastomas (slow-growing tumors of the central nervous system); kidney cysts and clear cell renal cell carcinoma; pancreatic neuroendocrine tumors; pheochromocytomas (noncancerous tumors of the adrenal glands); and endolymphatic sac tumors. VHL disease is caused by a mutation in the VHL gene and is inherited in an autosomal dominant manner. Early detection and treatment of VHL disease is important, and usually involves surgical removal of tumors.
Question: What is (are) Pretibial epidermolysis bullosa ?

Answer: Pretibial epidermolysis bullosa is a rare form of epidermolysis bullosa, a condition characterized by fragile skin that blisters easily in response to minor injury or friction. In the pretibial form, specifically, the characteristic blisters and skin erosions develop predominantly on the front of the lower legs (known as the "pretibial region"). In some affected people, the feet, hands and/or nails may also be affected. Healing of the blisters is generally associated with hypertrophic scarring. Pretibial epidermolysis bullosa is caused by changes (mutations) in the COL7A1 gene and can be inherited in an autosomal dominant or autosomal recessive manner. Treatment is based on the signs and symptoms present in each person.
Question: What is (are) Celiac artery compression syndrome ?

Answer: Celiac artery compression syndrome is a rare disorder characterized by chronic, recurrent abdominal pain related to compression of the celiac artery (which supplies blood to the upper abdominal organs) by the median arcuate ligament (a muscular fibrous band of the diaphragm). It usually presents with symptoms of abdominal pain, weight loss, and an abdominal bruit (abnormal sound of a blood vessel when blocked or narrowed). The cause is not fully understood; however, it is suspected that there could be a combination of vascular (blood supply) and neurogenic (neurological) components involved. Diagnosis is usually confirmed with imaging such as CT angiography, MRI, ultrasound, and arteriography.Surgery is currently the only treatment option and involves releasing the ligament.
Question: What is (are) Acquired pure red cell aplasia ?

Answer: Acquired pure red cell aplasia (PRCA) is a bone marrow disorder characterized by a reduction of red blood cells (erythrocytes) produced by the bone marrow. Signs and symptoms may include fatigue, lethargy, and/or abnormal paleness of the skin (pallor) due to the anemia the caused by the disorder. In most cases, the cause of acquired PRCA is unknown (idiopathic). In other cases it may occur secondary to autoimmune disorders, tumors of the thymus gland (thymomas), hematologic cancers, solid tumors, viral infections, or certain drugs. Treatment depends on the cause of the condition (if known) but often includes transfusions for individuals who are severely anemic and have cardiorespiratory failure.
Question: What are the symptoms of Complex regional pain syndrome ?

Answer: What are the signs and symptoms of complex regional pain syndrome? Complex regional pain syndrome (CRPS) usually develops after an injury, surgery, stroke or heart attack. The key symptom of CRPS is continuous, intense pain that is out of proportion to the severity of the injury. The pain gets worse over time. CRPS most often affects one of the arms, legs, hands, or feet, and the pain often spreads throughout the entire affected arm or leg. Other signs and symptoms may include: sensitivity to touch or cold swelling of the painful area changes in skin temperature, color, and/or texture joint stiffness and swelling muscle weakness and/or muscle spasms Symptoms may change over time and vary from person to person. In some people, signs and symptoms of go away on their own. In others, symptoms can persist for months to years.
Question: What is (are) Primary Familial Brain Calcification ?

Answer: Primary familial brain calcification (PFBC) is a neurodegenerative disorder characterized by calcium deposits in the basal ganglia, a part of the brain that helps start and control movement. The first symptoms often include clumsiness, fatigue, unsteady walking (gait), slow or slurred speech, difficulty swallowing (dysphagia) and dementia. Migraines and seizures frequently occur. Symptoms typically start in an individual's 30's to 40's but may begin at any age.The neuropsychiatric symptoms and movement disorders worsen over time. Mutations in the SLC20A2, PDGFRB, and PDGFB genes have been found to cause PFBC. This condition is inherited in an autosomal dominant manner.
Question: What is (are) Weill-Marchesani syndrome ?

Answer: Weill-Marchesani syndrome is an inherited connective tissue disorder that mainly affects the bones and eyes. People with this condition have short stature; short fingers; and limited joint movement, especially of the hands. Weill-Marchesani syndrome also causes abnormalities of the lens of the eye that lead to severe nearsightedness, and it can also cause glaucoma. Occasionally patients with this condition have heart defects. In some families this condition is inherited in an autosomal recessive pattern and caused by mutations in the ADAMTS10 or LTPBP2 genes. Weill-Marchesani syndrome can also have autosomal dominant inheritance, and a FBN1 gene mutation has been found in one family. People with this condition usually need regular eye exams and sometimes need eye surgery.
Question: How to prevent Parasites - Ascariasis ?

Answer: The best way to prevent ascariasis is to always:
    
     - Avoid ingesting soil that may be contaminated with human feces, including where human fecal matter ("night soil") or wastewater is used to fertilize crops.
     - Wash your hands with soap and warm water before handling food.
     - Teach children the importance of washing hands to prevent infection.
     - Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.
    
    
More on: Handwashing
    
Transmission of infection to others can be prevented by
    
     - Not defecating outdoors.
     - Effective sewage disposal systems.
    
    
More on: Handwashing
Question: How to prevent Parasites - Fascioliasis (Fasciola Infection) ?

Answer: No vaccine is available to protect people against Fasciola infection.
    
In some areas of the world where fascioliasis is found (endemic), special control programs are in place or are planned. The types of control measures depend on the setting (such as epidemiologic, ecologic, and cultural factors). Strict control of the growth and sale of watercress and other edible water plants is important.
    
Individual people can protect themselves by not eating raw watercress and other water plants, especially from endemic grazing areas. As always, travelers to areas with poor sanitation should avoid food and water that might be contaminated (tainted). Vegetables grown in fields that might have been irrigated with polluted water should be thoroughly cooked, as should viscera from potentially infected animals.
Question: Who is at risk for Kyasanur Forest Disease (KFD)? ?

Answer: KFD has historically been limited to the western and central districts of Karnataka State, India. However, in November 2012, samples from humans and monkeys tested positive for KFDV in the southernmost district of the State which neighbors Tamil Nadu State and Kerala State, indicating the possibility of wider distribution of KFDV. Additionally, a virus very similar to KFD virus (Alkhurma hemorrhagic fever virus) has been described in Saudi Arabia. 
                
People with recreational or occupational exposure to rural or outdoor settings (e.g., hunters, herders, forest workers, farmers) within Karnataka State are potentially at risk for infection by contact with infected ticks. Seasonality is another important risk factor as more cases are reported during the dry season, from November through June.
Question: What is the outlook for Acute Disseminated Encephalomyelitis ?

Answer: Corticosteroid therapy typically helps hasten recovery from most ADEM symptoms. The long-term prognosis for individuals with ADEM is generally favorable. For most individuals, recovery begins within days, and within six months the majority of ADEM patients will have total or near total recoveries. Others may have mild to moderate lifelong impairment ranging from cognitive difficulties, weakness, loss of vision, or numbness. Severe cases of ADEM can be fatal but this is a very rare occurrence. ADEM can recur, usually within months of the initial diagnosis, and is treated by restarting corticosteroids. A small fraction of individuals who are initially diagnosed as having ADEM can go on to develop MS, but there is currently no method or known risk factors to predict whom those individuals will be.
Question: What are the genetic changes related to mitochondrial membrane protein-associated neurodegeneration ?

Answer: Mutations in the C19orf12 gene cause MPAN. The protein produced from this gene is found in the membrane of cellular structures called mitochondria, which are the energy-producing centers of the cell. Although its function is unknown, researchers suggest that the C19orf12 protein plays a role in the maintenance of fat (lipid) molecules, a process known as lipid homeostasis.  The gene mutations that cause this condition lead to an altered C19orf12 protein that likely has little or no function. It is unclear how these genetic changes lead to the neurological problems associated with MPAN. Researchers are working to determine whether there is a link between problems with lipid homeostasis and brain iron accumulation and how these abnormalities might contribute to the features of this disorder.
Question: What are the treatments for esophageal atresia/tracheoesophageal fistula ?

Answer: These resources address the diagnosis or management of EA/TEF:  - Boston Children's Hospital: Esophageal Atresia  - Children's Hospital of Wisconsin  - Gene Review: Gene Review: Esophageal Atresia/Tracheoesophageal Fistula Overview  - Genetic Testing Registry: Tracheoesophageal fistula  - MedlinePlus Encyclopedia: Tracheoesophageal Fistula and Esophageal Atresia Repair  - University of California, San Francisco (UCSF) Medical Center   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care
Question: What are the genetic changes related to Bowen-Conradi syndrome ?

Answer: Bowen-Conradi syndrome is caused by a mutation in the EMG1 gene. This gene provides instructions for making a protein that is involved in the production of cellular structures called ribosomes, which process the cell's genetic instructions to create new proteins. Ribosomes are assembled in a cell compartment called the nucleolus.  The particular EMG1 gene mutation known to cause Bowen-Conradi syndrome is thought to make the protein unstable, resulting in a decrease in the amount of EMG1 protein that is available in the nucleolus. A shortage of this protein in the nucleolus would impair ribosome production, which may reduce cell growth and division (proliferation); however, it is unknown how EMG1 gene mutations lead to the particular signs and symptoms of Bowen-Conradi syndrome.
Question: Is phosphoribosylpyrophosphate synthetase superactivity inherited ?

Answer: This condition is inherited in an X-linked pattern. The gene associated with this condition is located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), a mutation in the only copy of the gene in each cell causes the disorder. In females (who have two X chromosomes), a mutation in one of the two copies of the gene in each cell sometimes causes the disorder.  In most reported cases, affected individuals have inherited the mutation from a parent who carries an altered copy of the PRPS1 gene. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons. PRS superactivity may also result from new mutations in the PRPS1 gene and can occur in people with no history of the disorder in their family.
Question: What are the treatments for Alport syndrome ?

Answer: These resources address the diagnosis or management of Alport syndrome:  - Gene Review: Gene Review: Alport Syndrome and Thin Basement Membrane Nephropathy  - Genetic Testing Registry: Alport syndrome  - Genetic Testing Registry: Alport syndrome, X-linked recessive  - Genetic Testing Registry: Alport syndrome, autosomal dominant  - Genetic Testing Registry: Alport syndrome, autosomal recessive  - MedlinePlus Encyclopedia: Alport Syndrome  - MedlinePlus Encyclopedia: End-Stage Kidney Disease   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care
Question: What is (are) dystonia 6 ?

Answer: Dystonia 6 is one of many forms of dystonia, which is a group of conditions characterized by involuntary movements, twisting (torsion) and tensing of various muscles, and unusual positioning of affected body parts. Dystonia 6 can appear at any age from childhood through adulthood; the average age of onset is 18.  The signs and symptoms of dystonia 6 vary among affected individuals. The disorder usually first impacts muscles of the head and neck, causing problems with speaking (dysarthria) and eating (dysphagia). Eyelid twitching (blepharospasm) may also occur. Involvement of one or more limbs is common, and in some cases occurs before the head and neck problems. Dystonia 6 gradually gets worse, and it may eventually involve most of the body.
Question: What are the treatments for Ectopic Kidney ?

Answer: No treatment for an ectopic kidney is needed if urinary function is normal and no blockage of the urinary tract is present.
                
If tests show an obstruction, surgery may be needed to correct the position of the kidney to allow for better drainage of urine. Reflux can be corrected by surgery to alter the ureter or injection of a gellike liquid into the bladder wall near the opening of the ureter.
                
If extensive kidney damage has occurred, surgery may be needed to remove the kidney. As long as the other kidney is working properly, losing one kidney should have no adverse health effects. More information is provided in the NIDDK health topic, Solitary Kidney.
                
With the right testing and treatment, if needed, an ectopic kidney should cause no serious long-term health problems.
Question: What are the symptoms of Dumping Syndrome ?

Answer: The symptoms of early and late dumping syndrome are different and vary from person to person. Early dumping syndrome symptoms may include
                
- nausea  - vomiting  - abdominal pain and cramping  - diarrhea  - feeling uncomfortably full or bloated after a meal  - sweating  - weakness  - dizziness  - flushing, or blushing of the face or skin  - rapid or irregular heartbeat
                
- hypoglycemia  - sweating  - weakness  - rapid or irregular heartbeat  - flushing  - dizziness
                
About 75 percent of people with dumping syndrome report symptoms of early dumping syndrome and about 25 percent report symptoms of late dumping syndrome. Some people have symptoms of both types of dumping syndrome.1
Question: What are the symptoms of High Blood Pressure and Kidney Disease ?

Answer: Most people with high blood pressure do not have symptoms. In rare cases, high blood pressure can cause headaches.
                
Kidney disease also does not have symptoms in the early stages. A person may have swelling called edema, which happens when the kidneys cannot get rid of extra fluid and salt. Edema can occur in the legs, feet, or ankles and less often in the hands or face. Once kidney function decreases further, symptoms can include
                
- appetite loss  - nausea  - vomiting  - drowsiness or feeling tired  - trouble concentrating  - sleep problems  - increased or decreased urination  - generalized itching or numbness  - dry skin  - headaches  - weight loss  - darkened skin  - muscle cramps  - shortness of breath  - chest pain