umarjan11/Medical-qna huggingface dataset:
Question: What are the treatments for Vasculitis ?

Answer: Treatment for vasculitis will depend on the type of vasculitis you have, which organs are affected, and the severity of the condition.
                
People who have severe vasculitis are treated with prescription medicines. Rarely, surgery may be done. People who have mild vasculitis may find relief with over-the-counter pain medicines, such as acetaminophen, aspirin, ibuprofen, or naproxen.
                
The main goal of treating vasculitis is to reduce inflammation in the affected blood vessels. This usually is done by reducing or stopping the immune response that caused the inflammation.
                
Types of Treatment
                
Common prescription medicines used to treat vasculitis include corticosteroids and cytotoxic medicines.
                
Corticosteroids help reduce inflammation in your blood vessels. Examples of corticosteroids are prednisone, prednisolone, and methylprednisolone.
                
Doctors may prescribe cytotoxic medicines if vasculitis is severe or if corticosteroids don't work well. Cytotoxic medicines kill the cells that are causing the inflammation. Examples of these medicines are azathioprine, methotrexate, and cyclophosphamide.
                
Your doctor may prescribe both corticosteroids and cytotoxic medicines.
                
Other treatments may be used for certain types of vasculitis. For example, the standard treatment for Kawasaki disease is high-dose aspirin and immune globulin. Immune globulin is a medicine thats injected into a vein.
                
Certain types of vasculitis may require surgery to remove aneurysms that have formed as a result of the condition. (An aneurysm is an abnormal bulge in the wall of a blood vessel.)
Question: What are the genetic changes related to mucolipidosis III gamma ?

Answer: Mutations in the GNPTG gene cause mucolipidosis III gamma. This gene provides instructions for making one part (subunit) of an enzyme called GlcNAc-1-phosphotransferase. This enzyme helps prepare certain newly made enzymes for transport to lysosomes. Lysosomes are compartments within the cell that use digestive enzymes to break down large molecules into smaller ones that can be reused by cells. GlcNAc-1-phosphotransferase is involved in the process of attaching a molecule called mannose-6-phosphate (M6P) to specific digestive enzymes. Just as luggage is tagged at the airport to direct it to the correct destination, enzymes are often "tagged" after they are made so they get to where they are needed in the cell. M6P acts as a tag that indicates a digestive enzyme should be transported to the lysosome.  Mutations in the GNPTG gene that cause mucolipidosis III gamma result in reduced activity of GlcNAc-1-phosphotransferase. These mutations disrupt the tagging of digestive enzymes with M6P, which prevents many enzymes from reaching the lysosomes. Digestive enzymes that do not receive the M6P tag end up outside the cell, where they have increased activity. The shortage of digestive enzymes within lysosomes causes large molecules to accumulate there. Conditions that cause molecules to build up inside lysosomes, including mucolipidosis III gamma, are called lysosomal storage disorders. The signs and symptoms of mucolipidosis III gamma are most likely due to the shortage of digestive enzymes inside lysosomes and the effects these enzymes have outside the cell.
Question: What is (are) Donohue syndrome ?

Answer: Donohue syndrome is a rare disorder characterized by severe insulin resistance, a condition in which the body's tissues and organs do not respond properly to the hormone insulin. Insulin normally helps regulate blood sugar levels by controlling how much sugar (in the form of glucose) is passed from the bloodstream into cells to be used as energy. Severe insulin resistance leads to problems with regulating blood sugar levels and affects the development and function of organs and tissues throughout the body.  Severe insulin resistance underlies the varied signs and symptoms of Donohue syndrome. Individuals with Donohue syndrome are unusually small starting before birth, and affected infants experience failure to thrive, which means they do not grow and gain weight at the expected rate. Additional features that become apparent soon after birth include a lack of fatty tissue under the skin (subcutaneous fat); wasting (atrophy) of muscles; excessive body hair growth (hirsutism); multiple cysts on the ovaries in females; and enlargement of the nipples, genitalia, kidneys, heart, and other organs. Most affected individuals also have a skin condition called acanthosis nigricans, in which the skin in body folds and creases becomes thick, dark, and velvety. Distinctive facial features in people with Donohue syndrome include bulging eyes, thick lips, upturned nostrils, and low-set ears. Affected individuals develop recurrent, life-threatening infections beginning in infancy.  Donohue syndrome is one of a group of related conditions described as inherited severe insulin resistance syndromes. These disorders, which also include Rabson-Mendenhall syndrome and type A insulin resistance syndrome, are considered part of a spectrum. Donohue syndrome represents the most severe end of the spectrum; most children with this condition do not survive beyond age 2.
Question: What is (are) craniometaphyseal dysplasia ?

Answer: Craniometaphyseal dysplasia is a rare condition characterized by progressive thickening of bones in the skull (cranium) and abnormalities at the ends of long bones in the limbs (metaphyseal dysplasia). Except in the most severe cases, the lifespan of people with craniometaphyseal dysplasia is normal.  Bone overgrowth in the head causes many of the signs and symptoms of craniometaphyseal dysplasia. Affected individuals typically have distinctive facial features such as a wide nasal bridge, a prominent forehead, wide-set eyes (hypertelorism), and a prominent jaw. Excessive new bone formation (hyperostosis) in the jaw can delay teething (dentition) or result in absent (non-erupting) teeth. Infants with this condition may have breathing or feeding problems caused by narrow nasal passages. In severe cases, abnormal bone growth can compress the nerves that emerge from the brain and extend to various areas of the head and neck (cranial nerves). Compression of the cranial nerves can lead to paralyzed facial muscles (facial nerve palsy), blindness, or deafness.  The x-rays of individuals with craniometaphyseal dysplasia show unusually shaped long bones, particularly the large bones in the legs. The ends of these bones (metaphyses) are wider and appear less dense in people with this condition.  There are two types of craniometaphyseal dysplasia, which are distinguished by their pattern of inheritance. They are known as the autosomal dominant and autosomal recessive types. Autosomal recessive craniometaphyseal dysplasia is typically more severe than the autosomal dominant form.
Question: What are the genetic changes related to distal hereditary motor neuropathy, type II ?

Answer: Mutations in the HSPB1 and HSPB8 genes cause distal hereditary motor neuropathy, type II. These genes provide instructions for making proteins called heat shock protein beta-1 and heat shock protein beta-8. Heat shock proteins help protect cells under adverse conditions such as infection, inflammation, exposure to toxins, elevated temperature, injury, and disease. They block signals that lead to programmed cell death. In addition, they appear to be involved in activities such as cell movement (motility), stabilizing the cell's structural framework (the cytoskeleton), folding and stabilizing newly produced proteins, and repairing damaged proteins. Heat shock proteins also appear to play a role in the tensing of muscle fibers (muscle contraction).  Heat shock protein beta-1 and heat shock protein beta-8 are found in cells throughout the body and are abundant in nerve cells. In nerve cells, heat shock protein beta-1 helps to organize a network of molecular threads called neurofilaments that maintain the diameter of specialized extensions called axons. Maintaining proper axon diameter is essential for the efficient transmission of nerve impulses. The function of heat shock protein beta-8 is not well understood, but studies have shown that it interacts with heat shock protein beta-1.  The HSPB1 and HSPB8 gene mutations that cause distal hereditary motor neuropathy, type II change single protein building blocks (amino acids) in the protein sequence. If either protein is altered, they may be more likely to cluster together and form clumps (aggregates). Aggregates of heat shock proteins may block the transport of substances that are essential for the proper function of nerve axons. The disruption of other cell functions in which these proteins are involved may also contribute to the signs and symptoms of distal hereditary motor neuropathy, type II.
Question: What are the treatments for Treatment Methods for Kidney Failure: Peritoneal Dialysis ?

Answer: Your health care team will perform several tests to tell if your dialysis exchanges are removing enough wastes. These tests are especially important during the first weeks of treatment to determine whether your schedule is adequate.
                
Peritoneal Equilibration Test
                
For a peritoneal equilibration test, a dialysis nurse takes samples of your blood and dialysis solution during a 4-hour exchange. The peritoneal equilibration test measures how much dextrose your body absorbs from a bag of dialysis solution. The peritoneal equilibration test also measures how much urea and creatininewaste products of normal muscle and protein breakdownmove from your blood into the dialysis solution.
                
Clearance Test
                
For a clearance test, you will collect the used dialysis solution from a 24-hour period. A dialysis nurse takes a blood sample during the same 24-hour period. Your doctor or nurse compares the amount of urea in the used solution with the amount in your blood to see how much urea was removed. For the first months or even years of peritoneal dialysis treatment, you may still produce small amounts of urine. If you produce more than 100 milliliters (3 ounces) of urine per day, you will also collect your urine to measure its urea content.
                
From the measurements of used solution, blood, and, if available, urine, your health care team can determine your urea clearancea measurement doctors call your Kt/Vand your creatinine clearance rate. These measurements will show whether you are using the right peritoneal dialysis schedule and doses. If your dialysis schedule is not removing enough wastes, your doctor will make adjustments. More information is provided in the NIDDK health topic, Peritoneal Dialysis Dose and Adequacy.
Question: What to do for Viral Gastroenteritis ?

Answer: - Viral gastroenteritis is inflammation of the lining of the stomach, small intestine, and large intestine. Several different viruses can cause viral gastroenteritis, which is highly contagious and extremely common.  - The main symptoms of viral gastroenteritis are watery diarrhea and vomiting.  - Dehydration is the most common complication of viral gastroenteritis.  - When someone does not drink enough fluids to replace those that are lost through vomiting and diarrhea, dehydration can result. Signs of dehydration in adults are excessive thirst, infrequent urination, dark-colored urine, dry skin, and lethargy, dizziness, or faintness.  - Infants, young children, older adults, and people with weak immune systems have the greatest risk of becoming dehydrated.  - Viral gastroenteritis is transmitted from person to person.  - Diagnosis of viral gastroenteritis is usually based on symptoms alone.  - Most cases of viral gastroenteritis resolve over time without specific treatment. Antibiotics are not effective against viral infections. The primary goal of treatment is to reduce symptoms.  - Adults with viral gastroenteritis should drink plenty of liquids such as fruit juices, sports drinks, caffeine-free soft drinks, and broths to replace fluids and electrolytes.  - Children with viral gastroenteritis should be given oral rehydration solutions to prevent dehydration.  - People can reduce their chances of getting or spreading viral gastroenteritis if they wash their hands thoroughly with soap and warm water for 20 seconds after using the bathroom or changing diapers and before eating or handling food, disinfect contaminated surfaces, and avoid foods or liquids that might be contaminated.
Question: What are the treatments for Glaucoma ?

Answer: Although open-angle glaucoma cannot be cured, it can usually be controlled. While treatments may save remaining vision, they do not improve sight already lost from glaucoma. The most common treatments for glaucoma are medication and surgery. Medications  Medications for glaucoma may be either in the form of eye drops or pills. Some drugs reduce pressure by slowing the flow of fluid into the eye. Others help to improve fluid drainage. (Watch the video to learn more about coping with glaucoma. To enlarge the video, click the brackets in the lower right-hand corner. To reduce the video, press the Escape (Esc) button on your keyboard.) For most people with glaucoma, regular use of medications will control the increased fluid pressure. But, these drugs may stop working over time. Or, they may cause side effects. If a problem occurs, the eye care professional may select other drugs, change the dose, or suggest other ways to deal with the problem.  Read or listen to ways some patients are coping with glaucoma. Surgery Laser surgery is another treatment for glaucoma. During laser surgery, a strong beam of light is focused on the part of the anterior chamber where the fluid leaves the eye. This results in a series of small changes that makes it easier for fluid to exit the eye. Over time, the effect of laser surgery may wear off. Patients who have this form of surgery may need to keep taking glaucoma drugs. Researching Causes and Treatments Through studies in the laboratory and with patients, NEI is seeking better ways to detect, treat, and prevent vision loss in people with glaucoma. For example, researchers have discovered genes that could help explain how glaucoma damages the eye. NEI also is supporting studies to learn more about who is likely to get glaucoma, when to treat people who have increased eye pressure, and which treatment to use first.
Question: What is (are) Heart Failure ?

Answer: In heart failure, the heart cannot pump enough blood to meet the body's needs. In some cases, the heart cannot fill with enough blood. In other cases, the heart can't pump blood to the rest of the body with enough force. Some people have both problems. Heart failure develops over time as the pumping action of the heart gets weaker. It can affect either the right, the left, or both sides of the heart. Heart failure does not mean that the heart has stopped working or is about to stop working. When heart failure affects the left side of the heart, the heart cannot pump enough oxygen-rich blood to the rest of the body. When heart failure affects the right side, the heart cannot pump enough blood to the lungs, where it picks up oxygen. The Heart's Pumping Action In normal hearts, blood vessels called veins bring oxygen-poor blood from the body to the right side of the heart. It is then pumped through the pulmonary artery to the lungs, picking up oxygen. From there, the blood returns to the left side of the heart. Then it is pumped through a large artery called the aorta that distributes blood throughout the body. When the heart is weakened by heart failure, blood and fluid can back up into the lungs, and fluid builds up in the feet, ankles, and legs. People with heart failure often experience tiredness and shortness of breath. Heart Failure is Serious Heart failure is a serious and common condition. Scientists estimate that 5 million people in the U.S. have heart failure and that number is growing. It contributes to 300,000 deaths each year. Heart failure is most common in those age 65 and older and it is the number one reason older people are hospitalized. Other Names for Heart Failure Heart failure can also be called congestive heart failure, systolic heart failure, diastolic heart failure, left-sided heart failure, or right-sided heart failure.
Question: What are the symptoms of Ectodermal dysplasia skin fragility syndrome ?

Answer: What are the signs and symptoms of Ectodermal dysplasia skin fragility syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Ectodermal dysplasia skin fragility 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 blistering of the skin 90% Abnormality of the eyebrow 90% Abnormality of the nail 90% Alopecia 90% Palmoplantar keratoderma 90% Skin ulcer 90% Blepharitis 50% Dry skin 50% Furrowed tongue 50% Malabsorption 50% Pruritus 50% Woolly hair 7.5% Ectodermal dysplasia - Fragile skin - 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 Steatocystoma multiplex ?

Answer: What are the signs and symptoms of Steatocystoma multiplex? Signs and symptoms of steatocystoma multiplex include multiple cysts on the skin. The cysts are often 1 to 2 centimeter wide. They frequently occur on the trunk of the body, upper arms, legs, and face; however, they can develop on other parts of the body as well.The cysts are typically filled with a yellowish to white, oily fluid, and occasionally have hair within them. The cysts can become infected and may cause pain and scarring. The Human Phenotype Ontology provides the following list of signs and symptoms for Steatocystoma multiplex. 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) Adenoma sebaceum 90% Nephrolithiasis 7.5% Autosomal dominant inheritance - Steatocystoma multiplex - 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 Laryngeal cleft ?

Answer: What are the signs and symptoms of Laryngeal cleft? The symptoms of laryngeal clefts range from mild stridor to significant difficulties with breathing and swallowing.  Severity of symptoms depends on the severity of the cleft.  Swallowing problems, a husky cry and feeding difficulties are common.  Feeding often causes stridor, coughing, choking, gagging, cyanosis, regurgitation, and frequent respiratory infections.  Many individuals with laryngeal clefts develop chronic lung disease. The Human Phenotype Ontology provides the following list of signs and symptoms for Laryngeal cleft. 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) Laryngomalacia 90% Abnormality of the voice - Aspiration - Cyanosis - Laryngeal stridor - 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 Conductive deafness with malformed external ear ?

Answer: What are the signs and symptoms of Conductive deafness with malformed external ear? The Human Phenotype Ontology provides the following list of signs and symptoms for Conductive deafness with malformed external ear. 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) Conductive hearing impairment 90% Low-set, posteriorly rotated ears 90% Abnormality of the palate 50% Cognitive impairment 50% Overfolded helix 50% Atresia of the external auditory canal 7.5% Hernia of the abdominal wall 7.5% Preauricular skin tag 7.5% Sensorineural hearing impairment 7.5% Abnormality of the middle ear ossicles - Autosomal recessive inheritance - Hypogonadism - Intellectual disability - 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.