umarjan11/Medical-qna huggingface dataset:
Question: What are the symptoms of Dandy-Walker cyst with Renal-Hepatic-Pancreatic dysplasia ?

Answer: What are the signs and symptoms of Dandy-Walker cyst with Renal-Hepatic-Pancreatic dysplasia? The Human Phenotype Ontology provides the following list of signs and symptoms for Dandy-Walker cyst with Renal-Hepatic-Pancreatic dysplasia. 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) Dandy-Walker malformation 90% Multicystic kidney dysplasia 90% Abnormality of the liver 50% Abnormality of the pancreas 50% Aplasia/Hypoplasia of the lungs 50% Intestinal malrotation 50% Oligohydramnios 50% Polyhydramnios 50% Bile duct proliferation - 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 Autoimmune hepatitis ?

Answer: What are the signs and symptoms of Autoimmune hepatitis? Symptoms of autoimmune hepatitis range from mild to severe. Fatigue is probably the most common symptom of autoimmune hepatitis. Other symptoms include: an enlarged liver jaundice itching skin rashes joint pain abdominal discomfort spider angiomas, or abnormal blood vessels, on the skin nausea vomiting loss of appetite dark urine pale or gray-colored stools People in advanced stages of the disease are more likely to have symptoms related to chronic liver disease, such as fluid in the abdomenalso called ascitesand mental confusion. Women may stop having menstrual periods. The Human Phenotype Ontology provides the following list of signs and symptoms for Autoimmune hepatitis. 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) Autoimmune antibody positivity - 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 Hypomagnesemia primary ?

Answer: What are the signs and symptoms of Hypomagnesemia primary? The Human Phenotype Ontology provides the following list of signs and symptoms for Hypomagnesemia primary. 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) Abdominal pain - Astigmatism - Autosomal recessive inheritance - Chronic kidney disease - Failure to thrive - Feeding difficulties in infancy - Hematuria - Hypercalciuria - Hypermagnesiuria - Hypermetropia - Hyperuricemia - Hypocitraturia - Hypomagnesemia - Juvenile onset - Myopia - Nephrocalcinosis - Nephrolithiasis - Nystagmus - Polydipsia - Polyuria - Recurrent urinary tract infections - Renal calcium wasting - Renal magnesium wasting - Renal tubular acidosis - Seizures - Strabismus - Tetany - 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 Sea-Blue histiocytosis ?

Answer: What are the signs and symptoms of Sea-Blue histiocytosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Sea-Blue histiocytosis. 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) Abnormality of coagulation 90% Blepharitis 90% Edema 90% Hepatomegaly 90% Mediastinal lymphadenopathy 90% Splenomegaly 90% Subcutaneous hemorrhage 90% Thrombocytopenia 90% Pulmonary infiltrates 50% Irregular hyperpigmentation 7.5% Retinopathy 7.5% Abnormality of the eye - Absent axillary hair - Autosomal recessive inheritance - Cirrhosis - Sea-blue histiocytosis - 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: Who is at risk for Parasites - Babesiosis? ?

Answer: People can get infected with Babesia parasites in several ways:
    
     - The main way is through the bite of an infected tick—during outdoor activities in areas where babesiosis is found (see below).
     - A less common way is by getting a transfusion from a blood donor who has a Babesia infection but does not have any symptoms. (No tests have been licensed yet for screening blood donors for Babesia.)
     - Rare cases of congenital transmission—from an infected mother to her baby (during pregnancy or delivery)—have been reported.
    
    
Babesia parasites are not transmitted from person-to-person like the flu or the common cold.
    
Many different species (types) of Babesia parasites have been found in animals, only a few of which have been found in people. Babesia microti—which usually infects white-footed mice and other small mammals—is the main species that has been found in people in the United States. Occasional (sporadic) cases of babesiosis caused by other Babesia species have been detected.
    
     
    
    
Babesia microti is transmitted in nature by Ixodes scapularis ticks (also called blacklegged ticks or deer ticks).
    
     - Tickborne transmission primarily occurs in the Northeast and upper Midwest, especially in parts of New England, New York state, New Jersey, Wisconsin, and Minnesota.
     - The parasite typically is spread by the young nymph stage of the tick, which is most apt to be found (seeking or "questing" for a blood meal) during warm months (spring and summer), in areas with woods, brush, or grass.
     - Infected people might not recall a tick bite because I. scapularis nymphs are very small (about the size of a poppy seed).
Question: How to prevent Marburg hemorrhagic fever (Marburg HF) ?

Answer: Preventive measures against Marburg virus infection are not well defined, as transmission from wildlife to humans remains an area of ongoing research. However, avoiding fruit bats, and sick non-human primates in central Africa, is one way to protect against infection. 
 
Measures for prevention of secondary, or person-to-person, transmission are similar to those used for other hemorrhagic fevers. If a patient is either suspected or confirmed to have Marburg hemorrhagic fever, barrier nursing techniques should be used to prevent direct physical contact with the patient. These precautions include wearing of protective gowns, gloves, and masks; placing the infected individual in strict isolation; and sterilization or proper disposal of needles, equipment, and patient excretions. 
 
In conjunction with the World Health Organization, CDC has developed practical, hospital-based guidelines, titled: Infection Control for Viral Haemorrhagic Fevers In the African Health Care Setting. The manual can help health-care facilities recognize cases and prevent further hospital-based disease transmission using locally available materials and few financial resources. 
 
Marburg hemorrhagic fever is a very rare human disease. However, when it occurs, it has the potential to spread to other people, especially health care staff and family members who care for the patient. Therefore, increasing awareness in communities and among health-care providers of the clinical symptoms of patients with Marburg hemorrhagic fever is critical. Better awareness can lead to earlier and stronger precautions against the spread of Marburg virus in both family members and health-care providers. Improving the use of diagnostic tools is another priority. With modern means of transportation that give access even to remote areas, it is possible to obtain rapid testing of samples in disease control centers equipped with Biosafety Level 4 laboratories in order to confirm or rule out Marburg virus infection.
Question: What is (are) tyrosine hydroxylase deficiency ?

Answer: Tyrosine hydroxylase (TH) deficiency is a disorder that primarily affects movement, with symptoms that may range from mild to severe.  The mild form of this disorder is called TH-deficient dopa-responsive dystonia (DRD). Symptoms usually appear during childhood. Affected individuals may exhibit unusual limb positioning and a lack of coordination when walking or running. In some cases, people with TH-deficient DRD have additional movement problems such as shaking when holding a position (postural tremor) or involuntary upward-rolling movements of the eyes. The movement difficulties may slowly increase with age but almost always get better with medical treatment.  The severe forms of TH deficiency are called infantile parkinsonism and progressive infantile encephalopathy. These forms of the disorder appear soon after birth and are more difficult to treat effectively.  Babies with infantile parkinsonism have delayed development of motor skills such as sitting unsupported or reaching for a toy. They may have stiff muscles, especially in the arms and legs; unusual body positioning; droopy eyelids (ptosis); and involuntary upward-rolling eye movements. The autonomic nervous system, which controls involuntary body functions, may also be affected. Resulting signs and symptoms can include constipation, backflow of stomach acids into the esophagus (gastroesophageal reflux), and difficulty regulating blood sugar, body temperature, and blood pressure. People with the infantile parkinsonism form of the disorder may have intellectual disability, speech problems, attention deficit disorder, and psychiatric conditions such as depression, anxiety, or obsessive-compulsive behaviors.  Progressive infantile encephalopathy is an uncommon severe form of TH deficiency. It is characterized by brain dysfunction and structural abnormalities leading to profound physical and intellectual disability.
Question: What is (are) centronuclear myopathy ?

Answer: Centronuclear myopathy is a condition characterized by muscle weakness (myopathy) and wasting (atrophy) in the skeletal muscles, which are the muscles used for movement. The severity of centronuclear myopathy varies among affected individuals, even among members of the same family.  People with centronuclear myopathy begin experiencing muscle weakness at any time from birth to early adulthood. The muscle weakness slowly worsens over time and can lead to delayed development of motor skills, such as crawling or walking; muscle pain during exercise; and difficulty walking. Some affected individuals may need wheelchair assistance as the muscles atrophy and weakness becomes more severe. In rare instances, the muscle weakness improves over time.  Some people with centronuclear myopathy experience mild to severe breathing problems related to the weakness of muscles needed for breathing. People with centronuclear myopathy may have droopy eyelids (ptosis) and weakness in other facial muscles, including the muscles that control eye movement. People with this condition may also have foot abnormalities, a high arch in the roof of the mouth (high-arched palate), and abnormal side-to-side curvature of the spine (scoliosis). Rarely, individuals with centronuclear myopathy have a weakened heart muscle (cardiomyopathy), disturbances in nerve function (neuropathy), or intellectual disability.  A key feature of centronuclear myopathy is the displacement of the nucleus in muscle cells, which can be viewed under a microscope. Normally the nucleus is found at the edges of the rod-shaped muscle cells, but in people with centronuclear myopathy the nucleus is located in the center of these cells. How the change in location of the nucleus affects muscle cell function is unknown.
Question: What is (are) alpha-1 antitrypsin deficiency ?

Answer: Alpha-1 antitrypsin deficiency is an inherited disorder that may cause lung disease and liver disease. The signs and symptoms of the condition and the age at which they appear vary among individuals.  People with alpha-1 antitrypsin deficiency usually develop the first signs and symptoms of lung disease between ages 20 and 50. The earliest symptoms are shortness of breath following mild activity, reduced ability to exercise, and wheezing. Other signs and symptoms can include unintentional weight loss, recurring respiratory infections, fatigue, and rapid heartbeat upon standing. Affected individuals often develop emphysema, which is a lung disease caused by damage to the small air sacs in the lungs (alveoli). Characteristic features of emphysema include difficulty breathing, a hacking cough, and a barrel-shaped chest. Smoking or exposure to tobacco smoke accelerates the appearance of emphysema symptoms and damage to the lungs.  About 10 percent of infants with alpha-1 antitrypsin deficiency develop liver disease, which often causes yellowing of the skin and whites of the eyes (jaundice). Approximately 15 percent of adults with alpha-1 antitrypsin deficiency develop liver damage (cirrhosis) due to the formation of scar tissue in the liver. Signs of cirrhosis include a swollen abdomen, swollen feet or legs, and jaundice. Individuals with alpha-1 antitrypsin deficiency are also at risk of developing a type of liver cancer called hepatocellular carcinoma.  In rare cases, people with alpha-1 antitrypsin deficiency develop a skin condition called panniculitis, which is characterized by hardened skin with painful lumps or patches. Panniculitis varies in severity and can occur at any age.
Question: What are the genetic changes related to nemaline myopathy ?

Answer: Mutations in one of many genes can cause nemaline myopathy. These genes provide instructions for producing proteins that play important roles in skeletal muscles. Within skeletal muscle cells, these proteins are found in structures called sarcomeres. Sarcomeres are necessary for muscles to tense (contract). Many of the proteins associated with nemaline myopathy interact within the sarcomere to facilitate muscle contraction. When the skeletal muscle cells of people with nemaline myopathy are stained and viewed under a microscope, these cells usually appear abnormal. These abnormal muscle cells contain rod-like structures called nemaline bodies.  Most cases of nemaline myopathy with a known genetic cause result from mutations in one of two genes, NEB or ACTA1. NEB gene mutations account for about 50 percent of all cases of nemaline myopathy and ACTA1 gene mutations account for 15 to 25 percent of all cases. When nemaline myopathy is caused by NEB gene mutations, signs and symptoms are typically present at birth or beginning in early childhood. When nemaline myopathy is caused by ACTA1 gene mutations, the condition's severity and age of onset vary widely. Mutations in the other genes associated with nemaline myopathy each account for only a small percentage of cases.  Mutations in any of the genes associated with nemaline myopathy lead to disorganization of the proteins found in the sarcomeres of skeletal muscles. The disorganized proteins cannot interact normally, which disrupts muscle contraction. Inefficient muscle contraction leads to muscle weakness and the other features of nemaline myopathy.  Some individuals with nemaline myopathy do not have an identified mutation. The genetic cause of the disorder is unknown in these individuals.
Question: How to prevent Prevent diabetes problems: Keep your heart and blood vessels healthy ?

Answer: You can do a lot to prevent heart disease and stroke.
                
- Keep your blood glucose under control. You can see if your blood glucose is under control by having an A1C test at least twice a year. The A1C test tells you your average blood glucose for the past 2 to 3 months. The target for most people with diabetes is below 7. In some people with heart disease or other special circumstances, their doctor may recommend slightly higher levels of A1C.  - Keep your blood pressure under control. Have it checked at every doctor visit. The target for most people with diabetes is below 140/80, unless their doctor sets a different target.  - Keep your cholesterol under control. Have it checked at least once a year. The targets for most people with diabetes are      - LDLbadcholesterol: below 100    - HDLgoodcholesterol: above 40 in men and above 50 in women    - triglyceridesanother type of fat in the blood: below 150    - Make sure the foods you eat are "heart-healthy." Include foods high in fiber, such as oat bran, oatmeal, whole-grain breads and cereals, fruits, and vegetables. Cut back on foods high in saturated fat or cholesterol, such as meats, butter, dairy products with fat, eggs, shortening, lard, and foods with palm oil or coconut oil. Limit foods with trans fat, such as snack foods and commercial baked goods.  - If you smoke, quit. Your doctor can tell you about ways to help you quit smoking.  - Ask your doctor whether you should take an aspirin every day. Studies have shown that taking a low dose of aspirin every day can help reduce your risk of heart disease and stroke.  - Take your medicines as directed.
Question: What to do for Gallstones ?

Answer: - Gallstones are hard particles that develop in the gallbladder.  - Imbalances in the substances that make up bile cause gallstones. Gallstones may form if bile contains too much cholesterol, too much bilirubin, or not enough bile salts. Scientists do not fully understand why these imbalances occur.   - Women, people over age 40, people with a family history of gallstones, American Indians, and Mexican Americans have a higher risk of developing gallstones.   - Many people with gallstones do not have symptoms. Gallstones that do not cause symptoms are called asymptomatic, or silent, gallstones.  - If gallstones block the bile ducts, pressure increases in the gallbladder, causing a gallbladder attack.  - Gallbladder attacks often follow heavy meals, and they usually occur in the evening or during the night.  - Gallstone symptoms may be similar to those of other conditions.   - If gallstones are not causing symptoms, treatment is usually not needed. However, if a person has a gallbladder attack or other symptoms, a health care provider will usually recommend treatment.   - The usual treatment for gallstones is surgery to remove the gallbladder. If a person cannot undergo surgery, nonsurgical treatments may be used to dissolve cholesterol gallstones. A health care provider may use endoscopic retrograde cholangiopancreatography (ERCP) to remove stones in people who cannot undergo surgery or to remove stones from the common bile duct in people who are about to have gallbladder removal surgery.   - The gallbladder is not an essential organ, which means a person can live normally without a gallbladder. Once the gallbladder is removed, bile  flows out of the liver through the hepatic and common bile ducts and directly into the duodenum, instead of being stored in the gallbladder.
Question: What is (are) Breast Cancer ?

Answer: Key Points
                    - Breast cancer is a disease in which malignant (cancer) cells form in the tissues of the breast.    - Breast cancer is the second leading cause of death from cancer in American women.    -  Different factors increase or decrease the risk of breast cancer.
                
                
                    Breast cancer is a disease in which malignant (cancer) cells form in the tissues of the breast.
                    The breast is made up of lobes and ducts. Each breast has 15 to 20 sections called lobes, which have many smaller sections called lobules. Lobules end in dozens of tiny bulbs that can produce milk. The lobes, lobules, and bulbs are linked by thin tubes called ducts.     Each breast also contains blood vessels and lymph vessels. The lymph vessels carry an almost colorless fluid called lymph. Lymph vessels lead to organs called lymph nodes. Lymph nodes are small bean-shaped structures that are found throughout the body. They filter substances in lymph and help fight infection and disease. Clusters of lymph nodes are found near the breast in the axilla (under the arm), above the collarbone, and in the chest.   See the following PDQ summaries for more information about breast cancer:         -  Breast Cancer Prevention     -  Breast Cancer Treatment     -  Genetics of Breast and Gynecologic Cancers
                
                
                    Breast cancer is the second leading cause of death from cancer in American women.
                    Women in the United States get breast cancer more than any other type of cancer except for skin cancer. Breast cancer is second only to lung cancer as a cause of cancer death in women.    Breast cancer occurs more often in white women than in black women. However, black women are more likely than white women to die from the disease.   Breast cancer occurs in men also, but the number of cases is small.