umarjan11/Medical-qna huggingface dataset:
Question: Do you have information about HPV

Answer: Summary : Human papillomaviruses (HPV) are common viruses that can cause warts. There are more than 100 types of HPV. Most are harmless, but about 30 types put you at risk for cancer. These types affect the genitals and you get them through sexual contact with an infected partner. They can be either low-risk or high-risk. Low-risk HPV can cause genital warts. High-risk HPV can lead to cancers of the cervix, vulva, vagina, and anus in women. In men, it can lead to cancers of the anus and penis.    Although some people develop genital warts from HPV infection, others have no symptoms. Your health care provider can treat or remove the warts. In women, Pap tests can detect changes in the cervix that might lead to cancer. Both Pap and HPV tests are types of cervical cancer screening.    Correct usage of latex condoms greatly reduces, but does not eliminate, the risk of catching or spreading HPV. Vaccines can protect against several types of HPV, including some that can cause cancer.    NIH: National Institute of Allergy and Infectious Diseases
Question: What is (are) Head Lice ?

Answer: Head lice are parasitic wingless insects. They live on people's heads and feed on their blood. An adult louse is about the size of a sesame seed. The eggs, called nits, are even smaller - about the size of a knot in thread. Lice and nits are found on or near the scalp, most often at the neckline and behind the ears.    Lice spread by close person-to-person contact. It is possible, but not common, to get lice by sharing personal belongings such as hats or hairbrushes. Children ages 3-11 and their families get head lice most often. Personal hygiene has nothing to do with getting head lice. Head lice do not spread disease.    Symptoms are        - Tickling feeling in the hair    - Frequent itching    - Sores from scratching    - Irritability and difficulty sleeping. Head lice are most active in the dark.       Treatment is recommended for people who have an active infestation of head lice. All household members and other close contacts should be checked and treated if necessary. Some experts also recommend treating anyone who shares a bed with an infested person. It is important to treat everyone at the same time.    Centers for Disease Control and Prevention
Question: What is (are) E. Coli Infections ?

Answer: E. coli is the name of a type of bacteria that lives in your intestines. Most types of E. coli are harmless. However, some types can make you sick and cause diarrhea. One type causes travelers' diarrhea. The worst type of E. coli causes bloody diarrhea, and can sometimes cause kidney failure and even death. These problems are most likely to occur in children and in adults with weak immune systems.     You can get E. coli infections by eating foods containing the bacteria. Symptoms of infection include       - Nausea or vomiting    - Severe abdominal cramps    - Watery or very bloody diarrhea    - Fatigue    - Fever       To help avoid food poisoning and prevent infection, handle food safely. Cook meat well, wash fruits and vegetables before eating or cooking them, and avoid unpasteurized milk and juices. You can also get the infection by swallowing water in a swimming pool contaminated with human waste.    Most cases of E. coli infection get better without treatment in 5 to 10 days.    NIH: National Institute of Allergy and Infectious Diseases
Question: What is (are) Dry Mouth ?

Answer: Dry mouth is the feeling that there is not enough saliva in your mouth. Everyone has a dry mouth once in a while - if they are nervous, upset or under stress. But if you have a dry mouth all or most of the time, it can be uncomfortable and can lead to serious health problems.    Symptoms of dry mouth include       - A sticky, dry feeling in the mouth    - Trouble chewing, swallowing, tasting, or speaking    - A burning feeling in the mouth    - A dry feeling in the throat    - Cracked lips    - A dry, rough tongue    - Mouth sores    - An infection in the mouth       Dry mouth is not a normal part of aging. Causes include some medicines, radiation therapy, chemotherapy, and nerve damage. Salivary gland diseases, Sjogren's syndrome, HIV/AIDS, and diabetes can also cause dry mouth. Treatment depends on the cause. Things you can do include sipping water, avoiding drinks with caffeine, tobacco, and alcohol, and chewing sugarless gum or sucking on sugarless hard candy.    NIH: National Institute of Dental and Craniofacial Research
Question: How to diagnose Cowden syndrome ?

Answer: How is Cowden syndrome diagnosed? A diagnosis of Cowden syndrome is based on the presence of characteristic signs and symptoms. Genetic testing for a change (mutation) in the PTEN gene can then be ordered to confirm the diagnosis. If a mutation in PTEN is not identified, genetic testing for the other genes known to cause Cowden syndrome can be considered. GeneReviews offers more detailed information regarding the diagnosis of Cowden syndrome including the clinical diagnostic criteria. Click here to view this resource. The PTEN Cleveland Clinic Risk Calculator can be used to estimate the chance of finding a PTEN mutation in children and adults with signs and symptoms of Cowden syndrome. Is genetic testing available for Cowden syndrome? Yes, genetic testing is available for many of the genes known to cause Cowden syndrome. Carrier testing for at-risk relatives and prenatal testing are possible if the disease-causing mutation in the family is known. The Genetic Testing Registry (GTR) is a centralized online resource for information about genetic tests. The intended audience for the GTR is health care providers and researchers. Patients and consumers with specific questions about a genetic test should contact a health care provider or a genetics professional.
Question: What are the treatments for Parkes Weber syndrome ?

Answer: How might Parkes Weber syndrome be treated? For capillary malformations (such as port wine stains) that are of cosmetic concern, individuals may be referred to a dermatologist. For arteriovenous malformations (AVMs) and arteriovenous fistulas (AVFs), the risks and benefits of intervention (i,e, embolization versus surgery) may be considered, usually with input from a multi-disciplinary team (e.g., specialists in interventional radiology, neurosurgery, surgery, cardiology, and dermatology). For risks associated with heart failure, referral to a cardiologist may be warranted. Hypertrophy (overgrowth) of the limb and/or difference in size between limbs may be treated surgically by an orthopedist. Supportive care may include compression garments (tight-fitting pieces of clothing on the affected limb to reduce pain and swelling); these may also protect the limb from bumps and scrapes, which can cause bleeding. Heel inserts may be used if the legs are different lengths, which can aid in walking normally. Various pain medications and antibiotic medications may be prescribed as needed.
Question: What causes Congenital diaphragmatic hernia ?

Answer: What causes congenital diaphragmatic hernia? Congenital diaphragmatic hernia (CDH) can occur as an isolated finding, as part of a genetic syndrome or chromosome abnormality, or as part of a complex but nonsyndromic set of findings. Currently, about 15%-20% of individuals with CDH have an identifiable cause for their diaphragm defect. These individuals are classified as having syndromic CDH either resulting from a recognized chromosome abnormality or as a single gene disorder. In the remaining 80%-85% of individuals with CDH, the cause is not known. Potential causes in these individuals may include: a currently undetectable chromosomal microdeletion (tiny loss of genetic material) or microduplication (an extra copy of genetic material) a mutation in a major gene important for diaphragm development combined effects of multiple minor genetic mutations or variants (polygenic inheritance) effects of gene-environment interactions (multifactorial inheritance) effects of non-genetic factors (e.g. epigenetic or teratogenic) GeneReviews has more detailed information about causes of CDH; this information can be viewed by clicking here.
Question: What is (are) Spinocerebellar ataxia 11 ?

Answer: Spinocerebellar ataxia type 11 (SCA11) is characterized by progressive cerebellar ataxia (difficulty walking and balance) and abnormal eye signs (jerky pursuit, horizontal and vertical movements (nystagmus), pyramidal features (increased muscular tonus, increased reflexes and an abnormal reflex known as Babinski sign and inability to make to perform fine movements), peripheral neuropathy with numbness, weakness or pain in the feet or hands or other places of the body and dystonia. It is a very rare disease and very few patients have been reported to date. In them, age of onset ranged from the early teens to the second decade of life and life span was normal. Diagnosis is based on signs and symptoms and with a genetic exam showing an alteration (mutation) in the TTBK2 gene. It is inherited in an autosomal dominant manner. Treatment may include speech and language therapy for talking and swallowing problems, occupational therapy, including home adaptations, physiotherapy and use of assistive walking devices and ankle-foot orthotics (AFOs) for those with neuropathy.
Question: What are the treatments for Endocarditis ?

Answer: Infective endocarditis (IE) is treated with antibiotics and sometimes with heart surgery.
                
Antibiotics
                
Antibiotics usually are given for 2 to 6 weeks through an intravenous (IV) line inserted into a vein. You're often in a hospital for at least the first week or more of treatment. This allows your doctor to make sure the medicine is helping.
                
If you're allowed to go home before the treatment is done, the antibiotics are almost always continued by vein at home. You'll need special care if you get IV antibiotic treatment at home. Before you leave the hospital, your medical team will arrange for you to receive home-based care so you can continue your treatment.
                
You also will need close medical followup, usually by a team of doctors. This team often includes a doctor who specializes in infectious diseases, a cardiologist (heart specialist), and a heart surgeon.
                
Surgery
                
Sometimes surgery is needed to repair or replace a damaged heart valve or to help clear up IE. For example, IE caused by fungi often requires surgery. This is because this type of IE is harder to treat than IE caused by bacteria.
Question: What is (are) Migraine ?

Answer: The pain of a migraine headache is often described as an intense pulsing or throbbing pain in one area of the head. However, it is much more; the International Headache Society diagnoses a migraine by its pain and number of attacks (at least 5, lasting 4-72 hours if untreated), and additional symptoms including nausea and/or vomiting, or sensitivity to both light and sound. Migraine is three times more common in women than in men and affects more than 10 percent of people worldwide. Roughly one-third of affected individuals can predict the onset of a migraine because it is preceded by an "aura," visual disturbances that appear as flashing lights, zig-zag lines or a temporary loss of vision. People with migraine tend to have recurring attacks triggered by a number of different factors, including stress, anxiety, hormonal changes, bright or flashing lights, lack of food or sleep, and dietary substances. Migraine in some women may relate to changes in hormones and hormonal levels during their menstrual cycle. For many years, scientists believed that migraines were linked to the dilation and constriction of blood vessels in the head. Investigators now believe that migraine has a genetic cause.
Question: What are the genetic changes related to 5-alpha reductase deficiency ?

Answer: Mutations in the SRD5A2 gene cause 5-alpha reductase deficiency. The SRD5A2 gene provides instructions for making an enzyme called steroid 5-alpha reductase 2. This enzyme is involved in processing androgens, which are hormones that direct male sexual development. Specifically, the enzyme is responsible for a chemical reaction that converts the hormone testosterone to DHT. DHT is essential for the normal development of male sex characteristics before birth, particularly the formation of the external genitalia.  Mutations in the SRD5A2 gene prevent steroid 5-alpha reductase 2 from effectively converting testosterone to DHT in the developing reproductive tissues. These hormonal factors underlie the changes in sexual development seen in infants with 5-alpha reductase deficiency.  During puberty, the testes produce more testosterone. Researchers believe that people with 5-alpha reductase deficiency develop secondary male sex characteristics in response to higher levels of this hormone. Some affected people also retain a small amount of 5-alpha reductase 2 activity, which may produce DHT and contribute to the development of secondary sex characteristics during puberty.
Question: What are the genetic changes related to spondyloepimetaphyseal dysplasia, Strudwick type ?

Answer: Spondyloepimetaphyseal dysplasia, Strudwick type is one of a spectrum of skeletal disorders caused by mutations in the COL2A1 gene. This gene provides instructions for making a protein that forms type II collagen. This type of collagen is found mostly in the clear gel that fills the eyeball (the vitreous) and cartilage. Cartilage is a tough, flexible tissue that makes up much of the skeleton during early development. Most cartilage is later converted to bone, except for the cartilage that continues to cover and protect the ends of bones and is present in the nose and external ears. Type II collagen is essential for the normal development of bones and other connective tissues that form the body's supportive framework.  Most mutations in the COL2A1 gene that cause spondyloepimetaphyseal dysplasia, Strudwick type interfere with the assembly of type II collagen molecules. Abnormal collagen prevents bones and other connective tissues from developing properly, which leads to the signs and symptoms of spondyloepimetaphyseal dysplasia, Strudwick type.
Question: What are the genetic changes related to hereditary hemorrhagic telangiectasia ?

Answer: Mutations in the ACVRL1, ENG, and SMAD4 genes cause hereditary hemorrhagic telangiectasia.  Hereditary hemorrhagic telangiectasia type 1 is caused by mutations in the gene ENG. Type 2 is caused by mutations in the gene ACVRL1. Juvenile polyposis/hereditary hemorrhagic telangiectasia syndrome is caused by mutations in the gene SMAD4. All these genes provide instructions for making proteins that are found in the lining of the blood vessels. These proteins interact with growth factors that control blood vessel development. The gene involved in hereditary hemorrhagic telangiectasia type 3 is not known, but is believed to be located on chromosome 5.  Mutations in these genes generally prevent the production of the associated protein, or result in the production of a defective protein that cannot fulfill its function. An individual with a mutated gene will therefore have a reduced amount of the functional protein available in the tissue lining the blood vessels. This deficiency is believed to result in the signs and symptoms of hereditary hemorrhagic telangiectasia.
Question: What are the genetic changes related to Lennox-Gastaut syndrome ?

Answer: Researchers have not identified any genes specific to Lennox-Gastaut syndrome, although the disorder likely has a genetic component. About two-thirds of cases are described as symptomatic, which means that they are related to an existing neurological problem. Symptomatic Lennox-Gastaut syndrome can be associated with brain injuries that occur before or during birth, problems with blood flow in the developing brain, brain infections, or other disorders affecting the nervous system. The condition can also result from a brain malformation known as cortical dysplasia or occur as part of a genetic disorder called tuberous sclerosis complex. Many people with Lennox-Gastaut syndrome have a history of recurrent seizures beginning in infancy (infantile spasms) or a related condition called West syndrome.  In about one-third of cases, the cause of Lennox-Gastaut syndrome is unknown. When the disorder occurs without an apparent underlying reason, it is described as cryptogenic. Individuals with cryptogenic Lennox-Gastaut syndrome have no history of epilepsy, neurological problems, or delayed development prior to the onset of the disorder.
Question: What are the genetic changes related to spondyloperipheral dysplasia ?

Answer: Spondyloperipheral dysplasia is one of a spectrum of skeletal disorders caused by mutations in the COL2A1 gene. This gene provides instructions for making a protein that forms type II collagen. This type of collagen is found mostly in the clear gel that fills the eyeball (the vitreous) and in cartilage. Cartilage is a tough, flexible tissue that makes up much of the skeleton during early development. Most cartilage is later converted to bone, except for the cartilage that continues to cover and protect the ends of bones and is present in the nose and external ears. Type II collagen is essential for the normal development of bones and other connective tissues that form the body's supportive framework.  Mutations in the COL2A1 gene interfere with the assembly of type II collagen molecules, reducing the amount of this type of collagen in the body. Instead of forming collagen molecules, the abnormal COL2A1 protein builds up in cartilage cells (chondrocytes). These changes disrupt the normal development of bones and other connective tissues, leading to the signs and symptoms of spondyloperipheral dysplasia.
Question: What are the genetic changes related to intrauterine growth restriction, metaphyseal dysplasia, adrenal hypoplasia congenita, and genital anomalies ?

Answer: IMAGe syndrome is caused by mutations in the CDKN1C gene. This gene provides instructions for making a protein that helps control growth before birth. The mutations that cause IMAGe syndrome alter the structure and function of the CDKN1C protein, which inhibits normal growth starting in the early stages of development before birth. Researchers are working to determine how these genetic changes underlie the bone abnormalities, adrenal gland underdevelopment, and other signs and symptoms of this condition.  People inherit one copy of most genes from their mother and one copy from their father. For most genes, both copies are fully turned on (active) in cells. The CDKN1C gene, however, is most active when it is inherited from a person's mother. The copy of CDKN1C inherited from a person's father is active at much lower levels in most tissues. This sort of parent-specific difference in gene activation is caused by a phenomenon called genomic imprinting. When genomic imprinting reduces the activity of the copy of a gene inherited from the father, that gene is said to be paternally imprinted.
Question: What are the genetic changes related to benign chronic pemphigus ?

Answer: Benign chronic pemphigus results from mutations in the ATP2C1 gene. This gene provides instructions for producing a protein called hSPCA1, which is found in many types of cells. The hSPCA1 protein helps cells store calcium until it is needed. Calcium has several critical functions in cells, including regulating cell growth and division and helping cells stick to one another (cell adhesion). The hSPCA1 protein appears to be particularly important for the normal function of cells called keratinocytes, which are found in the outer layer of the skin (the epidermis).  Mutations in the ATP2C1 gene reduce the amount of functional hSPCA1 protein in cells. This abnormality impairs cells' ability to store calcium normally. For unknown reasons, this abnormal calcium storage affects keratinocytes more than other types of cells. The abnormal regulation of calcium impairs many cell functions, including cell adhesion. As a result, keratinocytes do not stick tightly to one another, which causes the epidermis to become fragile and less resistant to minor trauma. Because the skin is easily damaged, it develops raw, blistered areas, particularly in skin folds where there is moisture and friction.
Question: What are the complications of Prostate Enlargement: Benign Prostatic Hyperplasia ?

Answer: The complications of benign prostatic hyperplasia may include
                
- acute urinary retention  - chronic, or long lasting, urinary retention  - blood in the urine  - urinary tract infections (UTIs)  - bladder damage  - kidney damage  - bladder stones
                
Most men with benign prostatic hyperplasia do not develop these complications. However, kidney damage in particular can be a serious health threat when it occurs.
                

                
When to Seek Medical Care   A person may have urinary symptoms unrelated to benign prostatic hyperplasia that are caused by bladder problems, UTIs, or prostatitisinflammation of the prostate. Symptoms of benign prostatic hyperplasia also can signal more serious conditions, including prostate cancer.   Men with symptoms of benign prostatic hyperplasia should see a health care provider.   Men with the following symptoms should seek immediate medical care:   - complete inability to urinate   - painful, frequent, and urgent need to urinate, with fever and chills   - blood in the urine   - great discomfort or pain in the lower abdomen and urinary tract
Question: What is (are) Hemochromatosis ?

Answer: Hemochromatosis is a disease in which too much iron builds up in your body. Your body needs iron but too much of it is toxic. If you have hemochromatosis, you absorb more iron than you need. Your body has no natural way to get rid of the extra iron. It stores it in body tissues, especially the liver, heart, and pancreas. The extra iron can damage your organs. Without treatment, it can cause your organs to fail.    There are two types of hemochromatosis. Primary hemochromatosis is an inherited disease. Secondary hemochromatosis is usually the result of something else, such as anemia, thalassemia, liver disease, or blood transfusions.    Many symptoms of hemochromatosis are similar to those of other diseases. Not everyone has symptoms. If you do, you may have joint pain, fatigue, general weakness, weight loss, and stomach pain.    Your doctor will diagnose hemochromatosis based on your medical and family histories, a physical exam, and the results from tests and procedures. Treatments include removing blood (and iron) from your body, medicines, and changes in your diet.    NIH: National Heart, Lung, and Blood Institute
Question: What is (are) Anaphylaxis ?

Answer: Anaphylaxis is a serious allergic reaction. It can begin very quickly, and symptoms may be life-threatening. The most common causes are reactions to foods (especially peanuts), medications, and stinging insects. Other causes include exercise and exposure to latex. Sometimes no cause can be found.    It can affect many organs:       - Skin - itching, hives, redness, swelling    - Nose - sneezing, stuffy nose, runny nose    - Mouth - itching, swelling of the lips or tongue    - Throat - itching, tightness, trouble swallowing, swelling of the back of the throat    - Chest - shortness of breath, coughing, wheezing, chest pain or tightness    - Heart - weak pulse, passing out, shock    - Gastrointestinal tract - vomiting, diarrhea, cramps    - Nervous system - dizziness or fainting       If someone is having a serious allergic reaction, call 9-1-1. If an auto-injector is available, give the person the injection right away.    NIH: National Institute of Allergy and Infectious Diseases