umarjan11/Medical-qna huggingface dataset:
Question: What causes Systemic scleroderma ?

Answer: What causes systemic scleroderma? The exact, underlying cause of systemic sclerosis is unknown. The cause appears to involve some injury to the cells that line blood vessels, resulting in excessive activation of dermal connective tissue cells, called fibroblasts. Fibroblasts normally produce collagen and other proteins. Build-up of collagen in the skin and other organs causes the signs and symptoms of the condition. It is suspected that scleroderma may develop from a variety of factors, which may include: Abnormal immune or inflammatory activity Genetic susceptibility: while no specific genes are thought to cause scleroderma, certain genes (or combination of genes) may increase a person's risk to be affected. However, the condition is not passed directly from parents to children. Environmental triggers: suspected triggers may include infections; injury; drugs (e.g. vitamin K, cocaine, penicillamine, appetite suppressants and some chemotherapeutic agents); and chemicals (e.g. silica, organic solvents, pesticides, aliphatic hydrocarbons and epoxy resin). Hormones: because women develop scleroderma more often than men, researchers suspect that hormones may play a role. However, the role of female hormones has not been proven. Widespread scleroderma can also occur in association with other autoimmune diseases, including systemic lupus erythematosus and polymyositis.
Question: What is (are) Primary orthostatic hypotension ?

Answer: Primary orthostatic hypotension is a rare type of orthostatic hypotension. It is not a disease per se, but a condition caused by several disorders that affect a specific part of the autonomic nervous system, such as multiple system atrophy, young-onset Parkinsons disease, pure autonomic failure, dopamine beta-hydroxylase deficiency, familial dysautonomia, and pure autonomic failure among others. The autonomic nervous system is the part of the nervous system that regulates certain involuntary body functions such as heart rate, blood pressure, sweating, and bowel and bladder control. Orthostatic hypotension is a form of low blood pressure that happens when standing-up from sitting or lying down. Common symptoms may include dizziness, lightheadedness, generalized weakness, leg buckling, nausea, blurry vision, fatigue, and headaches. Additional symptoms can include chest pain (angina), head and neck pain (often affecting neck and shoulders with a coat hanger distribution), decline in cognitive functioning such as difficulty concentrating, temporary loss of consciousness or blackout. Some people with primary orthostatic hypotension may also have high blood pressure when lying down. The treatment depends upon several factors including the specific underlying cause including The treatment depends upon several factors including the specific underlying cause and may include physical counter-maneuvers like lying down, sitting down, squatting clenching buttocks, leg crossing, and support garment and medication.
Question: What are the symptoms of Dermoids of cornea ?

Answer: What are the signs and symptoms of Dermoids of cornea? The Human Phenotype Ontology provides the following list of signs and symptoms for Dermoids of cornea. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Opacification of the corneal stroma 90% Visual impairment 90% Abnormality of the pupil 50% Abnormality of the eye - X-linked inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
Question: What causes Disseminated Intravascular Coagulation ?

Answer: Some diseases and conditions can disrupt the body's normal blood clotting process and lead to disseminated intravascular coagulation (DIC). These diseases and conditions include:
                
Sepsis (an infection in the bloodstream)
                
Surgery and trauma
                
Cancer
                
Serious complications of pregnancy and childbirth
                
Examples of less common causes of DIC are bites from poisonous snakes (such as rattlesnakes and other vipers), frostbite, and burns.
                
The two types of DIC are acute and chronic. Acute DIC begins with clotting in the small blood vessels and quickly leads to serious bleeding. Chronic DIC causes blood clotting, but it usually doesn't lead to bleeding. Cancer is the most common cause of chronic DIC.
                
Similar Clotting Conditions
                
Two other conditions cause blood clotting in the small blood vessels. However, their causes and treatments differ from those of DIC.
                
These conditions are thrombotic thrombocytopenic purpura (throm-BOT-ik throm-bo-cy-toe-PEE-nick PURR-purr-ah), or TTP, and hemolytic-uremic syndrome (HUS). HUS is more common in children than adults. It's also more likely to cause kidney damage than TTP.
Question: what research (or clinical trials) is being done for Arteriovenous Malformation ?

Answer: The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. The NINDS has established an Arteriovenous Study Group to learn more about the natural causes of AVMs and to improve surgical treatment of these lesions. An NINDS study at Columbia University, A Randomized Trial of Unruptured Brain AVMs (ARUBA), showed that medical management alone is superior to medical management and interventional therapy (conventional surgery, endovascular procedures, and radiosurgery) for improving the long-term outcome of individuals with unruptured brain arteriovenous malformations. Data from a recently closed observational phase will show if the disparities continued over the additional five years of follow-up.
                
Among other NINDS-funded research, scientists are testing a class of drugs called beta-blockers to see if they may lead to the development of new treatments for people with vascular malformations. Other NINDS-funded investigators hope to develop biomarkers (signs that may indicate risk of a disease) for AVM that may improve risk assessment and aid in the choice of therapy that may provide maximize benefit with minimal risk to the individual. Additional NINDS-funded research hopes to determine molecular pathways fundamental to the formation of brain AVMs.
Question: What is (are) Cerebral Arteriosclerosis ?

Answer: Cerebral arteriosclerosis is the result of thickening and hardening of the walls of the arteries in the brain. Symptoms of cerebral arteriosclerosis include headache, facial pain, and impaired vision.
                
Cerebral arteriosclerosis can cause serious health problems. If the walls of an artery are too thick, or a blood clot becomes caught in the narrow passage, blood flow to the brain can become blocked and cause an ischemic stroke. When the thickening and hardening is uneven, arterial walls can develop bulges (called aneurysms). If a bulge ruptures, bleeding in the brain can cause a hemorrhagic stroke. Both types of stroke can be fatal.
                
Cerebral arteriosclerosis is also related to a condition known as vascular dementia, in which small, symptom-free strokes cause cumulative damage and death to neurons (nerve cells) in the brain. Personality changes in the elderly, such as apathy, weeping, transient befuddlement, or irritability, might indicate that cerebral arteriosclerosis is present in the brain. Computer tomography (CT) and magnetic resonance imaging (MRI) of the brain can help reveal the presence of cerebral arteriosclerosis before ischemic strokes, hemorrhagic strokes, or vascular dementia develop.
Question: What are the genetic changes related to Shprintzen-Goldberg syndrome ?

Answer: Shprintzen-Goldberg syndrome is often caused by mutations in the SKI gene. This gene provides instructions for making a protein that regulates the transforming growth factor beta (TGF-) signaling pathway. The TGF- pathway regulates many processes, including cell growth and division (proliferation), the process by which cells mature to carry out special functions (differentiation), cell movement (motility), and the self-destruction of cells (apoptosis). By attaching to certain proteins in the pathway, the SKI protein blocks TGF- signaling. The SKI protein is found in many cell types throughout the body and appears to play a role in the development of many tissues, including the skull, other bones, skin, and brain.  SKI gene mutations involved in Shprintzen-Goldberg syndrome alter the SKI protein. The altered protein is no longer able to attach to proteins in the TGF- pathway and block signaling. As a result, the pathway is abnormally active. Excess TGF- signaling changes the regulation of gene activity and likely disrupts development of many body systems, including the bones and brain, resulting in the wide range of signs and symptoms of Shprintzen-Goldberg syndrome.  Not all cases of Shprintzen-Goldberg syndrome are caused by mutations in the SKI gene. Other genes may be involved in this condition, and in some cases, the genetic cause is unknown.
Question: What are the genetic changes related to complement component 2 deficiency ?

Answer: Complement component 2 deficiency is caused by mutations in the C2 gene. This gene provides instructions for making the complement component 2 protein, which helps regulate a part of the body's immune response known as the complement system. The complement system is a group of proteins that work together to destroy foreign invaders, trigger inflammation, and remove debris from cells and tissues. The complement component 2 protein is involved in the pathway that turns on (activates) the complement system when foreign invaders, such as bacteria, are detected.  The most common C2 gene mutation, which is found in more than 90 percent of people with complement component 2 deficiency, prevents the production of complement component 2 protein. A lack of this protein impairs activation of the complement pathway. As a result, the complement system's ability to fight infections is diminished. It is unclear how complement component 2 deficiency leads to an increase in autoimmune disorders. Researchers speculate that the dysfunctional complement system is unable to distinguish what it should attack, and it sometimes attacks normal tissues, leading to autoimmunity. Alternatively, the dysfunctional complement system may perform partial attacks on invading molecules, which leaves behind foreign fragments that are difficult to distinguish from the body's tissues, so the complement system sometimes attacks the body's own cells. It is likely that other factors, both genetic and environmental, play a role in the variability of the signs and symptoms of complement component 2 deficiency.
Question: What is (are) Diabetes ?

Answer: People with diabetes should - do aerobic activities,  such as brisk walking, which use the bodys large muscles to make the heart beat faster. The large muscles are those of the upper and lower arms and legs and those that control head, shoulder, and hip movements.  - do activities to strengthen muscles and bone, such as sit-ups or lifting weights. Aim for two times a week.  - stretch to increase flexibility, lower stress, and help prevent muscle soreness after physical activity.  do aerobic activities,  such as brisk walking, which use the bodys large muscles to make the heart beat faster. The large muscles are those of the upper and lower arms and legs and those that control head, shoulder, and hip movements. do activities to strengthen muscles and bone, such as sit-ups or lifting weights. Aim for two times a week. stretch to increase flexibility, lower stress, and help prevent muscle soreness after physical activity. Try to exercise almost every day for a total of about 30 minutes. If you haven't exercised lately, begin slowly. Start with 5 to 10 minutes, and then add more time. Or exercise for 10 minutes, three times a day. (Tip: you dont need to get your exercise in all at one time.) For more information on exercise and older adults, see Exercises To Try or visit  Go4Life, the exercise and physical activity campaign from the National Institute on Aging. Always talk with a doctor before starting a new physical activity program.
Question: What is (are) Testicular Cancer ?

Answer: Key Points
                    - Testicular cancer is a disease in which malignant (cancer) cells form in the tissues of one or both testicles.    - Testicular cancer is the most common cancer in men aged 15 to 34 years.    - Testicular cancer can usually be cured.    - A condition called cryptorchidism (an undescended testicle) is a risk factor for testicular cancer.
                
                
                    Testicular cancer is a disease in which malignant (cancer) cells form in the tissues of one or both testicles.
                    The testicles are 2 egg-shaped glands inside the scrotum (a sac of loose skin that lies directly below the penis). The testicles are held within the scrotum by the spermatic cord. The spermatic cord also contains the vas deferens and vessels and nerves of the testicles.     The testicles are the male sex glands and make testosterone and sperm. Germ cells in the testicles make immature sperm. These sperm travel through a network of tubules (tiny tubes) and larger tubes into the epididymis (a long coiled tube next to the testicles). This is where the sperm mature and are stored.   Almost all testicular cancers start in the germ cells. The two main types of testicular germ cell tumors are seminomas and nonseminomas.    See the PDQ summary on Testicular Cancer Treatment for more information about testicular cancer.
Question: What is (are) Chikungunya ?

Answer: Chikungunya is a virus that spread by the same kinds of mosquitoes that spread dengue and Zika virus. Rarely, it can spread from mother to newborn around the time of birth. It may also possibly spread through infected blood. There have been outbreaks of chikungunya virus in Africa, Asia, Europe, the Indian and Pacific Oceans, the Caribbean, and Central and South America.    Most people who are infected will have symptoms, which can be severe. They usually start 3-7 days after being bitten by an infected mosquito. The most common symptoms are fever and joint pain. Other symptoms may include headache, muscle pain, joint swelling, and rash.    Most people feel better within a week. In some cases, however, the joint pain may last for months. People at risk for more severe disease include newborns, older adults, and people with diseases such as high blood pressure, diabetes, or heart disease.    A blood test can show whether you have chikungunya virus. There are no vaccines or medicines to treat it. Drinking lots of fluids, resting, and taking non-aspirin pain relievers might help.    The best way to prevent chikungunya infection is to avoid mosquito bites:       - Use insect repellent    - Wear clothes that cover your arms, legs, and feet    - Stay in places that have air conditioning or that use window and door screens       Centers for Disease Control and Prevention
Question: What is (are) Kidney Cysts ?

Answer: A cyst is a fluid-filled sac. There are two types of kidney cysts.     Polycystic kidney disease (PKD) runs in families. In PKD, the cysts take the place of the normal tissue. They enlarge the kidneys and make them work poorly, leading to kidney failure. When PKD causes kidneys to fail - which usually happens after many years - people need dialysis or kidney transplantation. About half of people with the most common type of PKD end up with kidney failure. PKD also causes cysts in other parts of the body, such as the liver.     Symptoms of PKD include       - Pain in the back and lower sides    - Headaches    - Urinary tract infections    - Blood in the urine       Doctors diagnose PKD with imaging tests and family history. Treatments include medications, and, when people with PKD develop kidney failure, dialysis or kidney transplants.    Acquired cystic kidney disease (ACKD) usually happens in people who are on dialysis. Unlike PKD, the kidneys are normal sized, and cysts do not form in other parts of the body. People with ACKD already have chronic kidney disease when they develop cysts. ACKD often has no symptoms. In most cases, the cysts are harmless and do not need treatment.     NIH: National Institute of Diabetes and Digestive and Kidney Diseases
Question: What are the symptoms of Gupta Patton syndrome ?

Answer: What are the signs and symptoms of Gupta Patton syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Gupta Patton syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Anotia - Aplasia/Hypoplasia of the middle ear - Autosomal recessive inheritance - Conductive hearing impairment - Facial asymmetry - Microtia - Wide mouth - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
Question: What are the symptoms of Cone-rod dystrophy X-linked 2 ?

Answer: What are the signs and symptoms of Cone-rod dystrophy X-linked 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Cone-rod dystrophy X-linked 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Cone/cone-rod dystrophy - Progressive cone degeneration - X-linked inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
Question: What are the symptoms of ABCD syndrome ?

Answer: What are the signs and symptoms of ABCD syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for ABCD syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal auditory evoked potentials - Aganglionic megacolon - Albinism - Autosomal recessive inheritance - Hearing impairment - Hypopigmentation of the fundus - Large for gestational age - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
Question: What are the symptoms of Melanoma astrocytoma syndrome ?

Answer: What are the signs and symptoms of Melanoma astrocytoma syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Melanoma astrocytoma syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Medulloblastoma 50% Meningioma 50% Astrocytoma - Autosomal dominant inheritance - Cutaneous melanoma - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.