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

Answer: Hepatitis B is not usually treated unless it becomes chronic. Chronic hepatitis B is treated with medicines that slow or stop the virus from damaging the liver.
                
Medicines for Chronic Hepatitis B
                
Your doctor will choose medicines or a combination of medicines that are likely to work for you. The doctor will closely watch your symptoms and schedule regular blood tests to make sure treatment is working.
                
Medicines given by shots include
                
- interferon  - peginterferon
                
Medicines taken by mouth include
                
- adefovir  - entecavir  - lamivudine  - telbivudine  - tenofovir
                
The length of treatment varies. Talk with your doctor before taking other prescription medicines and over-the-counter medicines.
                
Liver Transplant
                
A liver transplant may be necessary if chronic hepatitis B causes severe liver damage that leads to liver failure. Symptoms of severe liver damage include the symptoms of hepatitis B and
                
- generalized itching  - a longer than usual amount of time for bleeding to stop  - easy bruising  - swollen stomach or ankles  - spiderlike blood vessels, called spider angiomas, that develop on the skin
                
Liver transplant is surgery to remove a diseased or injured liver and replace it with a healthy one from another person, called a donor. If your doctors tell you that you need a transplant, you should talk with them about the long-term demands of living with a liver transplant.
                
A team of surgeonsdoctors who specialize in surgeryperforms a liver transplant in a hospital. You will learn how to take care of yourself after you go home and about the medicines youll need to take to protect your new liver. Medicines taken after liver transplant surgery can prevent hepatitis B from coming back.
                
Testing for Liver Cancer
                
Having hepatitis B increases your risk for getting liver cancer, so your doctor may suggest an ultrasound test of the liver every 6 to 12 months. Finding cancer early makes it more treatable. Ultrasound is a machine that uses sound waves to create a picture of your liver. Ultrasound is performed at a hospital or radiology center by a specially trained technician. The image, called a sonogram, can show the livers size and the presence of cancerous tumors.
Question: What is (are) Diabetic Retinopathy ?

Answer: Can Cause Vision Loss, Blindness Diabetic retinopathy is a complication of diabetes and a leading cause of blindness. It occurs when diabetes damages the tiny blood vessels inside the retina in the back of the eye. A healthy retina is necessary for good vision. If you have diabetic retinopathy, at first you may notice no changes to your vision. But over time, diabetic retinopathy can get worse and cause vision loss. Diabetic retinopathy usually affects both eyes. Four Stages The four stages of diabetic retinopathy are - mild nonproliferative retinopathy  - moderate nonproliferative retinopathy  - severe nonproliferative retinopathy  - proliferative retinopathy. mild nonproliferative retinopathy moderate nonproliferative retinopathy severe nonproliferative retinopathy proliferative retinopathy. The first stage is mild nonproliferative retinopathy. At this earliest stage, there are small areas of balloon-like swelling in the retina's tiny blood vessels. The second stage is moderate nonproliferative retinopathy. As the disease progresses, some blood vessels that nourish the retina are blocked. The third stage is severe nonproliferative retinopathy. Many more blood vessels are blocked, depriving several areas of the retina of their blood supply. These areas send signals to the body to grow new blood vessels for nourishment. The fourth stage is proliferative retinopathy. At this advanced stage, the signals sent by the retina for nourishment cause the growth of new blood vessels. These new blood vessels are abnormal and fragile. The new blood vessels grow along the retina and along the surface of the clear, vitreous gel that fills the inside of the eye. By themselves, these blood vessels do not cause symptoms or vision loss. However, they have thin, fragile walls. If they leak blood, severe vision loss and even blindness can result. Other Diabetic Eye Diseases In addition to diabetic retinopathy, other diabetic eye diseases that people with diabetes may face are cataract and glaucoma. See this graphic for a quick overview of diabetic eye disease, including how many people it affects, whos at risk, what to do if you have it, and how to learn more.
Question: What are the symptoms of Orofaciodigital syndrome 3 ?

Answer: What are the signs and symptoms of Orofaciodigital syndrome 3? The Human Phenotype Ontology provides the following list of signs and symptoms for Orofaciodigital syndrome 3. 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 the pupil 90% Cleft palate 90% Cognitive impairment 90% Increased number of teeth 90% Kyphosis 90% Pectus excavatum 90% Postaxial hand polydactyly 90% Abnormal nasal morphology 50% Abnormality of eye movement 50% Abnormality of the fingernails 50% Abnormality of the nipple 50% Abnormality of the tragus 50% EEG abnormality 50% Frontal bossing 50% Hypertelorism 50% Hypertonia 50% Low-set, posteriorly rotated ears 50% Muscular hypotonia 50% Prominent occiput 50% Round face 50% Abnormality of the macula 7.5% Autosomal recessive inheritance - Bifid uvula - Bulbous nose - Hyperconvex nail - Intellectual disability - Low-set ears - Microdontia - Myoclonus - Postaxial foot polydactyly - Short sternum - Tongue nodules - 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 IVIC syndrome ?

Answer: What are the signs and symptoms of IVIC syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for IVIC 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) Hearing impairment 90% Limitation of joint mobility 90% Short stature 90% Strabismus 90% Abnormal dermatoglyphics 50% Aplasia/Hypoplasia of the thumb 50% Radioulnar synostosis 50% Scoliosis 50% Synostosis of carpal bones 50% Triphalangeal thumb 50% Abnormality of the clavicle 7.5% Arrhythmia 7.5% Leukocytosis 7.5% Preaxial hand polydactyly 7.5% Thrombocytopenia 7.5% Urogenital fistula 7.5% Absent thumb - Anal atresia - Autosomal dominant inheritance - Carpal bone hypoplasia - Carpal synostosis - External ophthalmoplegia - Hypoplasia of deltoid muscle - Hypoplasia of the radius - Intestinal malrotation - Limited elbow movement - Limited interphalangeal movement - Limited wrist movement - Pectoralis major hypoplasia - Phenotypic variability - Rectovaginal fistula - Short 1st metacarpal - Small thenar eminence - 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 dihydropyrimidinase deficiency ?

Answer: Dihydropyrimidinase deficiency is caused by mutations in the DPYS gene, which provides instructions for making an enzyme called dihydropyrimidinase. This enzyme is involved in the breakdown of molecules called pyrimidines, which are building blocks of DNA and its chemical cousin RNA. The dihydropyrimidinase enzyme is involved in the second step of the three-step process that breaks down pyrimidines. This step opens the ring-like structures of molecules called 5,6-dihydrothymine and 5,6-dihydrouracil so that these molecules can be further broken down.  The DPYS gene mutations that cause dihydropyrimidinase deficiency greatly reduce or eliminate dihydropyrimidinase enzyme function. As a result, the enzyme is unable to begin the breakdown of 5,6-dihydrothymine and 5,6-dihydrouracil. Excessive amounts of these molecules accumulate in the blood and in the fluid that surrounds and protects the brain and spinal cord (the cerebrospinal fluid or CSF) and are released in the urine.  The relationship between the inability to break down 5,6-dihydrothymine and 5,6-dihydrouracil and the specific features of dihydropyrimidinase deficiency is unclear. Failure to complete this step in the breakdown of pyrimidines also impedes the final step of the process, which produces molecules called beta-aminoisobutyric acid and beta-alanine. Both of these molecules are thought to protect the nervous system and help it function properly. Reduced production of beta-aminoisobutyric acid and beta-alanine may impair the function of these molecules in the nervous system, leading to neurological problems in some people with dihydropyrimidinase deficiency. Because fluoropyrimidine drugs are broken down by the same three-step process as pyrimidines, deficiency of the dihydropyrimidinase enzyme could lead to the drug buildup that causes fluoropyrimidine toxicity.  It is unknown why some people with dihydropyrimidinase deficiency do not develop health problems related to the condition; other genetic and environmental factors likely help determine the effects of this disorder.
Question: What are the genetic changes related to Diamond-Blackfan anemia ?

Answer: Diamond-Blackfan anemia can be caused by mutations in the RPL5, RPL11, RPL35A, RPS7, RPS10, RPS17, RPS19, RPS24, and RPS26 genes. These genes provide instructions for making several of the approximately 80 different ribosomal proteins, which are components of cellular structures called ribosomes. Ribosomes process the cell's genetic instructions to create proteins.  Each ribosome is made up of two parts (subunits) called the large and small subunits. The RPL5, RPL11, and RPL35A genes provide instructions for making ribosomal proteins that are among those found in the large subunit. The ribosomal proteins produced from the RPS7, RPS10, RPS17, RPS19, RPS24, and RPS26 genes are among those found in the small subunit.  The specific functions of each ribosomal protein within these subunits are unclear. Some ribosomal proteins are involved in the assembly or stability of ribosomes. Others help carry out the ribosome's main function of building new proteins. Studies suggest that some ribosomal proteins may have other functions, such as participating in chemical signaling pathways within the cell, regulating cell division, and controlling the self-destruction of cells (apoptosis).  Mutations in any of the genes listed above are believed to affect the stability or function of the ribosomal proteins. Studies indicate that a shortage of functioning ribosomal proteins may increase the self-destruction of blood-forming cells in the bone marrow, resulting in anemia. Abnormal regulation of cell division or inappropriate triggering of apoptosis may contribute to the other health problems that affect some people with Diamond-Blackfan anemia.  Approximately 25 percent of individuals with Diamond-Blackfan anemia have identified mutations in the RPS19 gene. About another 25 to 35 percent of individuals with this disorder have identified mutations in the RPL5, RPL11, RPL35A, RPS7, RPS10, RPS17, RPS24, or RPS26 genes. In the remaining 40 to 50 percent of cases, the cause of the condition is unknown. Researchers suspect that other genes may also be associated with Diamond-Blackfan anemia.
Question: What to do for What I need to know about Physical Activity and Diabetes ?

Answer: - Starting a physical activity program can help you lose weight or keep a healthy weight and keep your blood glucose levels on target.  - Always talk with your health care team before you start a new physical activity program.  - Ask your health care team if you need to change the amount of medicine you take or the food you eat before any physical activity.  - Talk with your health care team about what types of physical activity are safe for you, such as walking, weightlifting, or housework.  - To make sure you stay active, find activities you like to do. Ask a friend or family member to be your exercise buddy.  - Write down your blood glucose levels and when and how long you are physically active in a record book.  - Doctors suggest that you aim for 30 to 60 minutes of moderate to vigorous physical activity most days of the week.  - Children and adolescents with type 2 diabetes who are 10 to 17 years old should aim for 60 minutes of moderate to vigorous activity every day.  - Not all physical activity has to take place at the same time. For example, you might take a walk for 20 minutes, lift hand weights for 10 minutes, and walk up and down the stairs for 5 minutes.  - Doing moderate to vigorous aerobic exercise for 30 to 60 minutes a day most days of the week provides many benefits. You can even split up these minutes into several parts.  - Start exercising slowly, with 5 to 10 minutes a day, and add a little more time each week. Try walking briskly, hiking, or climbing stairs.  - Whether youre a man or a woman, you can do strength training with hand weights, elastic bands, or weight machines two to three times a week.  - Stretching exercises are a light to moderate physical activity that both men and women can do. When you stretch, you increase your flexibility, lower your stress, and help prevent sore muscles.  - Increase daily activity by spending less time watching TV or at the computer.  - Try these simple ways to add light, moderate, or vigorous physical activities in your life every day:      - Walk around while you talk on the phone.    - Take a walk through your neighborhood.    - Do chores, such as work in the garden or rake leaves, clean the house, or wash the car.    - If you have type 1 diabetes, try not to do vigorous physical activity when you have ketones in your blood or urine.
Question: What are the symptoms of ADULT syndrome ?

Answer: What are the signs and symptoms of ADULT syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for ADULT 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) Abnormality of the eye 90% Abnormality of the fingernails 90% Abnormality of the toenails 90% Dry skin 90% Fine hair 90% Finger syndactyly 90% Freckling 90% Melanocytic nevus 90% Skin ulcer 90% Split foot 90% Thin skin 90% Toe syndactyly 90% Abnormality of dental morphology 50% Aplasia/Hypoplasia of the nipples 50% Breast aplasia 50% Prominent nasal bridge 7.5% Absent nipple - Adermatoglyphia - Autosomal dominant inheritance - Breast hypoplasia - Conjunctivitis - Cutaneous photosensitivity - Dermal atrophy - Ectodermal dysplasia - Eczema - Fair hair - Hypodontia - Hypoplastic nipples - Microdontia - Nail pits - Nasolacrimal duct obstruction - Oligodontia - Oral cleft - Premature loss of permanent teeth - Sparse axillary hair - Sparse scalp hair - Split hand - Wide intermamillary distance - 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 Baraitser-Winter syndrome ?

Answer: What are the signs and symptoms of Baraitser-Winter syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Baraitser-Winter 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) Duplication of phalanx of hallux 5% Highly arched eyebrow 5% Microphthalmia 5% Oral cleft 5% Retrognathia 5% Ventriculomegaly 5% Abnormality of metabolism/homeostasis - Agenesis of corpus callosum - Anteverted nares - Aortic valve stenosis - Autosomal dominant inheritance - Autosomal recessive inheritance - Bicuspid aortic valve - Chorioretinal coloboma - Cryptorchidism - Hypertelorism - Intellectual disability - Iris coloboma - Lissencephaly - Long palpebral fissure - Long philtrum - Low posterior hairline - Low-set ears - Microcephaly - Micropenis - Muscular hypotonia - Overfolded helix - Pachygyria - Patent ductus arteriosus - Pointed chin - Postnatal growth retardation - Prominent epicanthal folds - Ptosis - Seizures - Sensorineural hearing impairment - Short neck - Short nose - Short stature - Trigonocephaly - Wide mouth - Wide nasal bridge - 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 Chromosome 17q deletion ?

Answer: What are the signs and symptoms of Chromosome 17q deletion? The Human Phenotype Ontology provides the following list of signs and symptoms for Chromosome 17q deletion. 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 form of the vertebral bodies 90% Abnormality of the cardiac septa 90% Abnormality of the hip bone 90% Abnormality of the metacarpal bones 90% Abnormality of the philtrum 90% Aplasia/Hypoplasia of the thumb 90% Aplasia/Hypoplasia of the uvula 90% Asymmetric growth 90% Deviation of finger 90% Hepatomegaly 90% Hypertelorism 90% Low-set, posteriorly rotated ears 90% Melanocytic nevus 90% Microcephaly 90% Micromelia 90% Narrow mouth 90% Optic atrophy 90% Patent ductus arteriosus 90% Premature birth 90% Prominent metopic ridge 90% Respiratory insufficiency 90% Short palm 90% Short stature 90% Short thorax 90% Single transverse palmar crease 90% Upslanted palpebral fissure 90% 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.