umarjan11/Medical-qna huggingface dataset:
Question: What to do for What I need to know about Hepatitis B ?

Answer: - Hepatitis B is a virus, or infection, that causes liver disease and inflammation of the liver.  - Anyone can get hepatitis B, but some people are more likely to than others.  - You could get hepatitis B through contact with an infected persons blood, semen, or other body fluid.  - Most people do not have any symptoms of hepatitis B. Adults and children ages 5 and older may have symptoms.  - See a doctor right away if you or a child in your care has symptoms of hepatitis B.  - Acute hepatitis B is a short-term infection with the hepatitis B virus.  - Chronic hepatitis B is a long-lasting infection with the hepatitis B virus. Chronic hepatitis B occurs when the body cant get rid of the hepatitis B virus.  - Children, especially infants, are more likely to get chronic hepatitis B.  - A blood test will show if you have hepatitis B.  - If you are at higher risk of getting hepatitis B, get tested. If you are pregnant, you should also get tested.  - Many people with hepatitis B do not know they are infected. Early diagnosis and treatment can help prevent liver damage.  - Hepatitis B is usually not treated unless it becomes chronic. Chronic hepatitis B is treated with medicines that slow or stop the virus from damaging the liver.  - You can avoid getting hepatitis B by receiving the hepatitis B vaccine.  - Tell your doctor and your dentist if you have hepatitis B.  - If you are pregnant and have hepatitis B, tell the doctor and staff who deliver your baby.  - See your doctor right away if you think you have been in contact with the hepatitis B virus.
Question: What are the treatments for Vesicoureteral Reflux ?

Answer: The standard treatment for primary VUR has included prompt treatment of UTIs and long-term use of antibiotics to prevent UTIs, also called antimicrobial prophylaxis, until VUR goes away on its own. Antibiotics are bacteria-fighting medications. Surgery has also been used in certain cases.
                
Several studies have raised questions about long-term use of antibiotics for prevention of UTIs. The studies found little or no effect on prevention of kidney damage. Long-term use may also make the child resistant to the antibiotic, meaning the medication does not work as well, and the child may be sicker longer and may need to take medications that are even stronger.
                
- children younger than 1 year of age continuous antibiotics should be used if a child has a history of febrile UTI or VUR grade III through V that was identified through screening  - children older than 1 year of age with BBDcontinuous antibiotics should be used while BBD is being treated  - children older than 1 year of age without BBDcontinuous antibiotics can be used at the discretion of the health care provider but is not automatically recommended; however, UTIs should be promptly treated
                
Deflux, a gellike liquid containing complex sugars, is an alternative to surgery for treatment of VUR. A small amount of Deflux is injected into the bladder wall near the opening of the ureter. This injection creates a bulge in the tissue that makes it harder for urine to flow back up the ureter. The health care provider uses a special tube to see inside the bladder during the procedure. Deflux injection is an outpatient procedure done under general anesthesia, so the child can go home the same day.
Question: What is (are) Colorectal Cancer ?

Answer: Here are some of the tools used to detect colorectal cancer. - A fecal occult blood test, or FOBT, is a test used to check for hidden blood in the stool. Sometimes cancers or polyps can bleed, and FOBT can detect small amounts of bleeding. Newer, genetically-based stool tests are proving to be more accurate than older tests. A fecal occult blood test, or FOBT, is a test used to check for hidden blood in the stool. Sometimes cancers or polyps can bleed, and FOBT can detect small amounts of bleeding. Newer, genetically-based stool tests are proving to be more accurate than older tests. - A sigmoidoscopy is an examination of the rectum and lower colon -- or sigmoid colon -- using a lighted instrument called a sigmoidoscope. A sigmoidoscopy is an examination of the rectum and lower colon -- or sigmoid colon -- using a lighted instrument called a sigmoidoscope.  - A colonoscopy is an examination of the rectum and the large intestine (but not the small intestine) using a lighted instrument called a colonoscope. A colonoscopy is an examination of the rectum and the large intestine (but not the small intestine) using a lighted instrument called a colonoscope.  - A virtual colonoscopy, which requires the same preparation as a standard colonoscopy, is done with an external scanning machine as opposed to a device inserted into the colon. The colon does need to be inflated with gas for proper scanning. A virtual colonoscopy, which requires the same preparation as a standard colonoscopy, is done with an external scanning machine as opposed to a device inserted into the colon. The colon does need to be inflated with gas for proper scanning.
Question: What are the treatments for Skin Cancer ?

Answer: Different types of treatment are available for patients with skin cancer. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. Four types of standard treatment are used: surgery, radiation therapy, chemotherapy, photodynamic therapy, and immunotherapy. Another therapy, biologic therapy, is one of many therapies currently being tested in clinical trials. These standard cancer treatments work in different ways. - Surgery removes the cancer.  - Chemotherapy uses anti-cancer drugs to kill cancer cells or stop their growth.  - Radiation therapy uses high-energy beams to kill cancer cells and shrink tumors.  - Photodynamic therapy uses a drug and a type of laser light to kill cancer cells.  - Immunotherapy, which is newer, uses the patient's own immune system to fight the cancer. Surgery removes the cancer. Chemotherapy uses anti-cancer drugs to kill cancer cells or stop their growth. Radiation therapy uses high-energy beams to kill cancer cells and shrink tumors. Photodynamic therapy uses a drug and a type of laser light to kill cancer cells. Immunotherapy, which is newer, uses the patient's own immune system to fight the cancer. In June of 2011, an important advance in treating melanoma was announced at an annual cancer meeting. A drug called ipilimumab was approved for treating the disease, and it works differently than traditional chemotherapy. It uses immunotherapy to help the immune system recognize and reject cancer cells. When its successful, immunotherapy can lead to complete reversal of even advanced disease. Some patients with stage IV metastatic disease who were treated in early immunotherapy trials after other therapies were unsuccessful are still in complete remission more than 20 years later.
Question: What are the symptoms of Pyruvate carboxylase deficiency ?

Answer: What are the signs and symptoms of Pyruvate carboxylase deficiency? The Human Phenotype Ontology provides the following list of signs and symptoms for Pyruvate carboxylase deficiency. 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) Autosomal recessive inheritance - Clonus - Congenital onset - Hepatomegaly - Hyperalaninemia - Hypoglycemia - Increased serum lactate - Increased serum pyruvate - Intellectual disability - Lactic acidosis - Muscular hypotonia - Neuronal loss in the cerebral cortex - Periventricular leukomalacia - Proximal renal tubular acidosis - Seizures - 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 Angelman syndrome ?

Answer: What causes Angelman syndrome? Angelman syndrome is caused by a loss of function of a gene called UBE3A on chromosome 15. The exact mechanism that causes this loss of function is complex. People normally inherit one copy of the UBE3A gene from each parent. Both copies of this gene are turned on (active) in many of the body's tissues. In certain areas of the brain, however, only the copy inherited from a person's mother is active. This parent-specific gene activation is known as genomic imprinting. If the maternal copy of the UBE3A gene is lost because of a chromosomal change or a gene mutation, a person will have no active copies of the gene in some parts of the brain. Several different genetic mechanisms can inactivate or delete the maternal copy of the UBE3A gene. Most cases of Angelman syndrome occur when a segment of the maternal chromosome 15 containing this gene is deleted. In other cases, Angelman syndrome is caused by a mutation in the maternal copy of the UBE3A gene. In a small percentage of cases, a person with Angelman syndrome inherits two copies of chromosome 15 from his or her father, instead of one copy from each parent. This is called paternal uniparental disomy. Rarely, Angelman syndrome can also be caused by a chromosomal rearrangement called a translocation, or by a mutation or other defect in the region of DNA that controls activation of the UBE3A gene. These genetic changes can abnormally turn off (inactivate) UBE3A or other genes on the maternal copy of chromosome 15. The cause of Angelman syndrome is unknown in 10 to 15 percent of affected individuals. Changes involving other genes or chromosomes may be responsible for the condition in these individuals.
Question: What are the symptoms of Episodic ataxia with nystagmus ?

Answer: What are the signs and symptoms of Episodic ataxia with nystagmus? The Human Phenotype Ontology provides the following list of signs and symptoms for Episodic ataxia with nystagmus. 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) Autosomal dominant inheritance - Cerebellar vermis atrophy - Diplopia - Downbeat nystagmus - Dysarthria - Dystonia - Episodic ataxia - Gaze-evoked nystagmus - Incomplete penetrance - Migraine - Muscle weakness - Myotonia - Paresthesia - Progressive cerebellar ataxia - Saccadic smooth pursuit - Tinnitus - Vertigo - Vestibular dysfunction - 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 Arthrogryposis like disorder ?

Answer: What are the signs and symptoms of Arthrogryposis like disorder? The Human Phenotype Ontology provides the following list of signs and symptoms for Arthrogryposis like disorder. 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) Gait disturbance 90% Limitation of joint mobility 90% Patellar aplasia 90% Talipes 50% Abnormal form of the vertebral bodies 7.5% Abnormality of the clavicle 7.5% Aplasia/Hypoplasia of the radius 7.5% Melanocytic nevus 7.5% Scoliosis 7.5% Autosomal recessive inheritance - Skeletal muscle atrophy - 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 genetic changes related to neuromyelitis optica ?

Answer: No genes associated with neuromyelitis optica have been identified. However, a small percentage of people with this condition have a family member who is also affected, which indicates that there may be one or more genetic changes that increase susceptibility. It is thought that the inheritance of this condition is complex and that many environmental and genetic factors are involved in the development of the condition.  The aquaporin-4 protein (AQP4), a normal protein in the body, plays a role in neuromyelitis optica. The aquaporin-4 protein is found in several body systems but is most abundant in tissues of the central nervous system. Approximately 70 percent of people with this disorder produce an immune protein called an antibody that attaches (binds) to the aquaporin-4 protein. Antibodies normally bind to specific foreign particles and germs, marking them for destruction, but the antibody in people with neuromyelitis optica attacks a normal human protein; this type of antibody is called an autoantibody. The autoantibody in this condition is called NMO-IgG or anti-AQP4.  The binding of the NMO-IgG autoantibody to the aquaporin-4 protein turns on (activates) the complement system, which is a group of immune system proteins that work together to destroy pathogens, trigger inflammation, and remove debris from cells and tissues. Complement activation leads to the inflammation of the optic nerve and spinal cord that is characteristic of neuromyelitis optica, resulting in the signs and symptoms of the condition.  The levels of the NMO-IgG autoantibody are high during episodes of neuromyelitis optica, and the levels decrease between episodes with treatment of the disorder. However, it is unclear what triggers episodes to begin or end.
Question: What are the genetic changes related to mannose-binding lectin deficiency ?

Answer: Relatively common mutations in the MBL2 gene can lead to mannose-binding lectin deficiency. This gene provides instructions for making a protein that assembles into a complex called mannose-binding lectin. Functional mannose-binding lectins are made up of two to six protein groups called trimers, which are each composed of three of the protein pieces (subunits) produced from the MBL2 gene.  Mannose-binding lectin plays an important role in the body's immune response by attaching to foreign invaders such as bacteria, viruses, or yeast and turning on (activating) the complement system. The complement system is a group of immune system proteins that work together to destroy foreign invaders (pathogens), trigger inflammation, and remove debris from cells and tissues. Mannose-binding lectin can also stimulate special immune cells to engulf and break down the attached pathogen.  Disease-associated mutations in the MBL2 gene can reduce the production of the mannose-binding lectin subunit or eliminate the subunit's ability to assemble into functional mannose-binding lectin. A decrease in the availability of the normal subunit protein may lead to a reduction of the functional mannose-binding lectin in blood. With decreased levels of mannose-binding lectin, the body does not recognize and fight foreign invaders efficiently. Consequently, infections can be more common in people with this condition.  However, not everyone with a change in the MBL2 gene has decreased levels of mannose-binding lectin, and not everyone with decreased protein levels is prone to infection. Researchers believe that a number of factors, including other genetic and environmental factors, are involved in the development of mannose-binding lectin deficiency and susceptibility to infection.
Question: What are the genetic changes related to critical congenital heart disease ?

Answer: In most cases, the cause of CCHD is unknown. A variety of genetic and environmental factors likely contribute to this complex condition.  Changes in single genes have been associated with CCHD. Studies suggest that these genes are involved in normal heart development before birth. Most of the identified mutations reduce the amount or function of the protein that is produced from a specific gene, which likely impairs the normal formation of structures in the heart. Studies have also suggested that having more or fewer copies of particular genes compared with other people, a phenomenon known as copy number variation, may play a role in CCHD. However, it is unclear whether genes affected by copy number variation are involved in heart development and how having missing or extra copies of those genes could lead to heart defects. Researchers believe that single-gene mutations and copy number variation account for a relatively small percentage of all CCHD.  CCHD is usually isolated, which means it occurs alone (without signs and symptoms affecting other parts of the body). However, the heart defects associated with CCHD can also occur as part of genetic syndromes that have additional features. Some of these genetic conditions, such as Down syndrome, Turner syndrome, and 22q11.2 deletion syndrome, result from changes in the number or structure of particular chromosomes. Other conditions, including Noonan syndrome and Alagille syndrome, result from mutations in single genes.  Environmental factors may also contribute to the development of CCHD. Potential risk factors that have been studied include exposure to certain chemicals or drugs before birth, viral infections (such as rubella and influenza) that occur during pregnancy, and other maternal illnesses including diabetes and phenylketonuria. Although researchers are examining risk factors that may be associated with this complex condition, many of these factors remain unknown.
Question: What are the symptoms of Mental retardation, X-linked, nonspecific ?

Answer: What are the signs and symptoms of Mental retardation, X-linked, nonspecific? The Human Phenotype Ontology provides the following list of signs and symptoms for Mental retardation, X-linked, nonspecific. 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) Seizures 5% Autism - Dental crowding - Hyperactivity - Hypertelorism - Intellectual disability - Intellectual disability, moderate - Joint hypermobility - Mandibular prognathia - Open mouth - Short nose - Synophrys - Tented upper lip vermilion - Uplifted earlobe - Upslanted palpebral fissure - X-linked recessive 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 Vohwinkel syndrome ?

Answer: What are the signs and symptoms of Vohwinkel syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Vohwinkel 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) Sensorineural hearing impairment 90% Abnormality of the genital system 50% Cognitive impairment 50% Abnormality of the toenails 7.5% Alopecia 7.5% Cleft palate 7.5% Ichthyosis 7.5% Osteolysis 7.5% Self-injurious behavior 7.5% Amniotic constriction ring - Autoamputation of digits - Autosomal dominant inheritance - Honeycomb palmoplantar keratoderma - 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.