umarjan11/Medical-qna huggingface dataset:
Question: What are the treatments for Childhood Interstitial Lung Disease ?

Answer: Childhood interstitial lung disease (chILD) is rare, and little research has been done on how to treat it. At this time, chILD has no cure. However, some children who have certain diseases, such as neuroendocrine cell hyperplasia of infancy, may slowly improve over time.
                
Current treatment approaches include supportive therapy, medicines, and, in the most serious cases, lung transplants.
                
Supportive Therapy
                
Supportive therapy refers to treatments that help relieve symptoms or improve quality of life. Supportive approaches used to relieve common chILD symptoms include:
                
Oxygen therapy. If your child's blood oxygen level is low, he or she may need oxygen therapy. This treatment can improve breathing, support growth, and reduce strain on the heart.
                
Bronchodilators. These medications relax the muscles around your childs airways, which helps open the airways and makes breathing easier.
                
Breathing devices. Children who have severe disease may need ventilators or other devices to help them breathe easier.
                
Extra nutrition. This treatment can help improve your child's growth and help him or her gain weight. Close monitoring of growth is especially important.
                
Techniques and devices to help relieve lung congestion. These may include chest physical therapy (CPT) or wearing a vest that helps move mucus (a sticky substance) to the upper airways so it can be coughed up. CPT may involve pounding the chest and back over and over with your hands or a device to loosen mucus in the lungs so that your child can cough it up.
                
Supervised pulmonary rehabilitation (PR). PR is a broad program that helps improve the well-being of people who have chronic (ongoing) breathing problems.
                
Medicines
                
Corticosteroids are a common treatment for many children who have chILD. These medicines help reduce lung inflammation.
                
Other medicines can help treat specific types or causes of chILD. For example, antimicrobial medicines can treat a lung infection. Acid-blocking medicines can prevent acid reflux, which can lead to aspiration.
                
Lung Transplant
                
A lung transplant may be an option for children who have severe chILD if other treatments haven't worked.
                
Currently, lung transplants are the only effective treatment for some types of chILD that have a high risk of death, such as alveolar capillary dysplasia and certain surfactant dysfunction mutations.
                
Early diagnosis of these diseases gives children the chance to receive lung transplants. So far, chILD doesn't appear to come back in patients' transplanted lungs.
                
For more information about this treatment, go to the Health Topics Lung Transplant article.
Question: What is (are) Peripheral Arterial Disease (P.A.D.) ?

Answer: Arteries Clogged With Plaque Peripheral arterial disease (P.A.D.) is a disease in which plaque (plak) builds up in the arteries that carry blood to your head, organs, and limbs. Plaque is made up of fat, cholesterol, calcium, fibrous tissue, and other substances in the blood. When plaque builds up in the body's arteries, the condition is called atherosclerosis (ATH-er-o-skler-O-sis). Over time, plaque can harden and narrow the arteries. This limits the flow of oxygen-rich blood to your organs and other parts of your body. P.A.D. usually affects the arteries in the legs, but it can also affect the arteries that carry blood from your heart to your head, arms, kidneys, and stomach. Blocked blood flow to your legs can cause pain and numbness. It also can raise your risk of getting an infection in the affected limbs. Your body may have a hard time fighting the infection. Why is P.A.D. Dangerous? Over time, the plaque may crack and cause blood clots to form. These blood clots can block arteries, causing pain, numbness, inflammation, and even permanent tissue damage in the affected part of the body. If severe enough, blocked blood flow can cause tissue death (also called gangrene.) In very serious cases, this can lead to leg amputation. P.A.D. currently affects 8 million to 12 million Americans. About 1 in every 20 Americans over the age of 50 has P.A.D. African Americans are more than twice as likely as Caucasians to have P.A.D. If you have P.A.D., your risk of coronary artery disease, heart attack, stroke, and transient ischemic attack ("mini-stroke") is much higher than in people without P.A.D. If you have coronary artery disease, you have a 1 in 3 chance of having blocked leg arteries. Although P.A.D. is serious, it is treatable. If you have the disease, it's important to see your doctor regularly and treat the underlying atherosclerosis. Other Names for Peripheral Arterial Disease -  Atherosclerotic peripheral arterial disease   -  Claudication (klaw-dih-KA-shen)   -  Hardening of the arteries   -  Leg cramps from poor circulation   -  Peripheral vascular disease   -  Poor circulation   -  Vascular disease  Atherosclerotic peripheral arterial disease Claudication (klaw-dih-KA-shen) Hardening of the arteries Leg cramps from poor circulation Peripheral vascular disease Poor circulation Vascular disease
Question: What are the symptoms of Oculoectodermal syndrome ?

Answer: What are the signs and symptoms of Oculoectodermal syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Oculoectodermal 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) Aplasia/Hypoplasia of the corpus callosum 90% Aplasia/Hypoplasia of the skin 90% Epibulbar dermoid 90% Generalized hyperpigmentation 90% Abnormality of the cardiovascular system 50% Aganglionic megacolon 50% Anteverted nares 50% Blepharophimosis 50% Brachydactyly syndrome 50% Epicanthus 50% Hearing abnormality 50% Laryngeal atresia 50% Macrocephaly 50% Muscular hypotonia 50% Polyhydramnios 50% Proptosis 50% Short nose 50% Strabismus 50% Telecanthus 50% Abnormal facial shape 7.5% Cleft eyelid 7.5% Displacement of the external urethral meatus 7.5% Arachnoid cyst 5% Astigmatism 5% Depressed nasal bridge 5% Opacification of the corneal stroma 5% Parietal bossing 5% Wide nasal bridge 5% Anisometropia - Aplasia cutis congenita - Autosomal dominant inheritance - Bladder exstrophy - Coarctation of aorta - Epidermal nevus - Growth delay - Hyperactivity - Hyperpigmentation of the skin - Lower limb asymmetry - Lymphedema - Phenotypic variability - Seizures - Transient ischemic attack - 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 is (are) Rh Incompatibility ?

Answer: Rh incompatibility is a condition that occurs during pregnancy if a woman has Rh-negative blood and her baby has Rh-positive blood.
                
"Rh-negative" and "Rh-positive" refer to whether your blood has Rh factor. Rh factor is a protein on red blood cells. If you have Rh factor, you're Rh-positive. If you don't have it, you're Rh-negative. Rh factor is inherited (passed from parents to children through the genes). Most people are Rh-positive.
                
Whether you have Rh factor doesn't affect your general health. However, it can cause problems during pregnancy.
                
Overview
                
When you're pregnant, blood from your baby can cross into your bloodstream, especially during delivery. If you're Rh-negative and your baby is Rh-positive, your body will react to the baby's blood as a foreign substance.
                
Your body will create antibodies (proteins) against the baby's Rh-positive blood. These antibodies usually don't cause problems during a first pregnancy. This is because the baby often is born before many of the antibodies develop.
                
However, the antibodies stay in your body once they have formed. Thus, Rh incompatibility is more likely to cause problems in second or later pregnancies (if the baby is Rh-positive).
                
The Rh antibodies can cross the placenta and attack the baby's red blood cells. This can lead to hemolytic anemia (HEE-moh-lit-ick uh-NEE-me-uh) in the baby.
                
Hemolytic anemia is a condition in which red blood cells are destroyed faster than the body can replace them. Red blood cells carry oxygen to all parts of the body.
                
Without enough red blood cells, your baby won't get enough oxygen. This can lead to serious problems. Severe hemolytic anemia may even be fatal to the child.
                
Outlook
                
With prompt and proper prenatal care and screening, you can prevent the problems of Rh incompatibility. Screening tests allow your doctor to find out early in your pregnancy whether you're at risk for the condition.
                
If you're at risk, your doctor will carefully check on you and your baby throughout your pregnancy and prescribe treatment as needed.
                
Injections of a medicine called Rh immune globulin can keep your body from making Rhantibodies. This medicine helps prevent the problems of Rh incompatibility. If you're Rh-negative, you'll need this medicine every time you have a baby with Rh-positive blood.
                
Other events also can expose you to Rh-positive blood, which could affect a pregnancy. Examples include a miscarriage or blood transfusion. If you're treated with Rh immune globulin right after these events, you may be able to avoid Rh incompatibility during your next pregnancy.
Question: How to diagnose Vesicoureteral Reflux ?

Answer: The most common tests used to diagnose VUR include
                
- Voiding cystourethrogram (VCUG). VCUG is an x-ray image of the bladder and urethra taken during urination, also called voiding. The bladder and urethra are filled with a special dye, called contrast medium, to make the urethra clearly visible. The x-ray machine captures a video of the contrast medium when the child urinates. The procedure is performed in a health care providers office, outpatient center, or hospital by an x-ray technician supervised by a radiologista doctor who specializes in medical imagingwho then interprets the images. Anesthesia is not needed, but sedation may be used for some children. This test can show abnormalities of the inside of the urethra and bladder.  - Radionuclide cystogram (RNC). RNC is a type of nuclear scan that involves placing radioactive material into the bladder. A scanner then detects the radioactive material as the child urinates or after the bladder is empty. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist. Anesthesia is not needed, but sedation may be used for some children. RNC is more sensitive than VCUG but does not provide as much detail of the bladder anatomy.  - Abdominal ultrasound. Ultrasound uses a device, called a transducer, that bounces safe, painless sound waves off organs to create an image of their structure. An abdominal ultrasound can create images of the entire urinary tract, including the kidneys and bladder. The procedure is performed in a health care providers office, outpatient center, or hospital by a specially trained technician, and the images are interpreted by a radiologist; anesthesia is not needed. Ultrasound may be used before VCUG or RNC if the childs family or health care provider wants to avoid exposure to x-ray radiation or radioactive material.
                
Testing is usually done on
                
- infants diagnosed during pregnancy with urine blockage affecting the kidneys  - children younger than 5 years of age with a UTI  - children with a UTI and fever, called febrile UTI, regardless of age  - males with a UTI who are not sexually active, regardless of age or fever  - children with a family history of VUR, including an affected sibling
                
More information about urine blockage in infants is provided in the NIDDK health topic, Urine Blockage in Newborns.
                
VUR is an unlikely cause of UTI in some children, so these tests are not done until other causes of UTI are ruled out for
                
- children 5 years of age and older with a UTI  - children with a UTI but no fever  - sexually active males with a UTI
Question: How to prevent Lymphocytic Choriomeningitis (LCM) ?

Answer: LCMV infection can be prevented by avoiding contact with wild mice and taking precautions when handling pet rodents (i.e. mice, hamsters, or guinea pigs). 
                
Rarely, pet rodents may become infected with LCMV from wild rodents. Breeders, pet stores, and pet owners should take measures to prevent infestations of wild rodents. Pet rodents should not come into contact with wild rodents. If you have a pet rodent, wash your hands with soap and water (or waterless alcohol-based hand rubs when soap is not available and hands are not visibly soiled) after handling rodents or their cages and bedding. 
                
If you have a rodent infestation in and around your home, take the following precautions to reduce the risk of LCMV infection: 
 
 - Seal up rodent entry holes or gaps with steel wool, lath metal, or caulk. 
 - Trap rats and mice by using an appropriate snap trap. 
 - Clean up rodent food sources and nesting sites and take precautions when cleaning rodent-infected areas: 
   
   - Use cross-ventilation when entering a previously unventilated enclosed room or dwelling prior to cleanup. 
   - Put on rubber, latex, vinyl or nitrile gloves. 
   - Do not stir up dust by vacuuming, sweeping, or any other means. 
   - Thoroughly wet contaminated areas with a bleach solution or household disinfectant. 
   - Hypochlorite (bleach) solution: Mix 1 and 1/2 cups of household bleach in 1 gallon of water. 
   - Once everything is wet, take up contaminated materials with damp towel and then mop or sponge the area with bleach solution or household disinfectant. 
   - Spray dead rodents with disinfectant and then double-bag along with all cleaning materials and throw bag out in an appropriate waste disposal system. 
   - Remove the gloves and thoroughly wash your hands with soap and water (or waterless alcohol-based hand rubs when soap is not available and hands are not visibly soiled). 
    
 
                
The geographic distributions of the rodent hosts are widespread both domestically and abroad. However, infrequent recognition and diagnosis, and historic underreporting of LCM, have limited scientists' ability to estimate incidence rates and prevalence of disease among humans. Understanding the epidemiology of LCM and LCMV infections will help to further delineate risk factors for infection and develop effective preventive strategies. Increasing physician awareness will improve disease recognition and reporting, which may lead to better characterization of the natural history and the underlying immunopathological mechanisms of disease, and stimulate future therapeutic research and development.
Question: What are the symptoms of Huntington disease ?

Answer: What are the signs and symptoms of Huntington disease? Huntington disease (HD) is a progressive disorder that causes motor, cognitive, and psychiatric signs and symptoms. On average, most people begin developing features of HD between ages 35 and 44. Signs and symptoms vary by stage and may include: Early stage: Behavioral disturbances Clumsiness Moodiness Irritability Paranoia Apathy Anxiety Hallucinations Abnormal eye movements Depression Impaired ability to detect odors Middle stage: Dystonia Involuntary movements Trouble with balance and walking Chorea with twisting and writhing motions Unsteady gait (style of walking) Slow reaction time General weakness Weight loss Speech difficulties Stubbornness Late stage: Rigidity (continual tension of the muscles) Bradykinesia (difficulty initiating and continuing movements) Severe chorea Serious weight loss Inability to speak Inability to walk Swallowing problems Inability to care for oneself There is also a less common, early-onset form of HD which begins in childhood or adolescence. For more information on this form, please visit GARD's juvenile Huntington disease Web page. The Human Phenotype Ontology provides the following list of signs and symptoms for Huntington disease. 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 movement 50% Abnormality of the voice 50% Behavioral abnormality 50% Cerebral cortical atrophy 50% Developmental regression 50% EEG abnormality 50% Hypertonia 50% Rigidity 7.5% Abnormality of eye movement - Autosomal dominant inheritance - Bradykinesia - Chorea - Dementia - Depression - Gliosis - Hyperreflexia - Neuronal loss in central nervous system - Personality changes - 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 familial erythrocytosis ?

Answer: Familial erythrocytosis can result from mutations in the EPOR, VHL, EGLN1, or EPAS1 gene. Researchers define four types of familial erythrocytosis, ECYT1 through ECYT4, based on which of these genes is altered.  The EPOR gene provides instructions for making a protein known as the erythropoietin receptor, which is found on the surface of certain blood-forming cells in the bone marrow. Erythropoietin is a hormone that directs the production of new red blood cells. Erythropoietin fits into the receptor like a key into a lock, triggering signaling pathways that lead to the formation of red blood cells. Mutations in the EPOR gene cause the erythropoietin receptor to be turned on for an abnormally long time after attaching to erythropoietin. The overactive receptor signals the production of red blood cells even when they are not needed, which results in an excess of these cells in the bloodstream. When familial erythrocytosis is caused by mutations in the EPOR gene, it is known as ECYT1.  The proteins produced from the VHL, EGLN1, and EPAS1 genes are also involved in red blood cell production; they each play a role in regulating erythropoietin. The protein produced from the EPAS1 gene is one component of a protein complex called hypoxia-inducible factor (HIF). When oxygen levels are lower than normal (hypoxia), HIF activates genes that help the body adapt, including the gene that provides instructions for making erythropoietin. Erythropoietin stimulates the production of more red blood cells to carry oxygen to organs and tissues. The proteins produced from the VHL and EGLN1 genes indirectly regulate erythropoietin by controlling the amount of available HIF. Mutations in any of these three genes can disrupt the regulation of red blood cell formation, leading to an overproduction of these cells. When familial erythrocytosis results from VHL gene mutations it is known as ECYT2; when the condition is caused by EGLN1 gene mutations it is called ECYT3; and when the condition results from EPAS1 gene mutations it is known as ECYT4.  Researchers have also described non-familial (acquired) forms of erythrocytosis. Causes of acquired erythrocytosis include long-term exposure to high altitude, chronic lung or heart disease, episodes in which breathing slows or stops for short periods during sleep (sleep apnea), and certain types of tumors. Another form of acquired erythrocytosis, called polycythemia vera, results from somatic (non-inherited) mutations in other genes involved in red blood cell production. In some cases, the cause of erythrocytosis is unknown.