umarjan11/Medical-qna huggingface dataset:
Question: What is (are) Meningitis ?

Answer: Meningitis is inflammation of the thin tissue that surrounds the brain and spinal cord, called the meninges. There are several types of meningitis. The most common is viral meningitis, which you get when a virus enters the body through the nose or mouth and travels to the brain. Bacterial meningitis is rare, but can be deadly. It usually starts with bacteria that cause a cold-like infection. It can block blood vessels in the brain and lead to stroke and brain damage. It can also harm other organs. Pneumococcal infections and meningococcal infections can cause bacterial meningitis.    Anyone can get meningitis, but it is more common in people whose bodies have trouble fighting infections. Meningitis can progress rapidly. You should seek medical care quickly if you have       - A sudden fever     - A severe headache     - A stiff neck        Early treatment can help prevent serious problems, including death. Vaccines can prevent some of the bacterial infections that cause meningitis. Parents of adolescents and students living in college dorms should talk to a doctor about the vaccination.     NIH: National Institute of Neurological Disorders and Stroke
Question: What is (are) Childhood Leukemia ?

Answer: Leukemia is cancer of the white blood cells. It is the most common type of childhood cancer. Your blood cells form in your bone marrow. White blood cells help your body fight infection. In leukemia, the bone marrow produces abnormal white blood cells. These cells crowd out the healthy blood cells, making it hard for blood to do its work.    Leukemia can develop quickly or slowly. Acute leukemia is a fast growing type while chronic leukemia grows slowly. Children with leukemia usually have one of the acute types.     Symptoms include       - Infections    - Fever    - Loss of appetite    - Tiredness    - Easy bruising or bleeding    - Swollen lymph nodes    - Night sweats    - Shortness of breath    - Pain in the bones or joints       Risk factors for childhood leukemia include having a brother or sister with leukemia, having certain genetic disorders and having had radiation or chemotherapy. Treatment often cures childhood leukemia. Treatment options include chemotherapy, other drug therapy and radiation. In some cases bone marrow and blood stem cell transplantation might help.     NIH: National Cancer Institute
Question: What is (are) 15q13.3 microdeletion syndrome ?

Answer: 15q13.3 microdeletion syndrome is a type of contiguous gene deletion syndrome. Individuals with this microdeletion may have very different signs and symptoms from other affected individuals (even within the same family), or no symptoms at all. Features of the condition may include mild to moderate mental retardation, learning difficulties, or normal intelligence; autism; epilepsy (recurring seizures); and mental illness (such as schizophrenia or bipolar disorder). Various dysmorphic (abnormally formed) features have been reported, but there are no consistent physical features among individuals who have the condition. It is caused by a tiny deletion (microdeletion) on the long arm of chromosome 15 that spans at least 6 genes; the features of the syndrome are caused by the absence of these genes, which are usually necessary for normal growth and development. It can be inherited in an autosomal dominant manner with reduced penetrance, or can occur as a new (de novo) deletion. Treatment typically focuses on individual signs and symptoms (such as medication for seizures) when possible.
Question: What causes Alport syndrome ?

Answer: What causes Alport syndrome? Alport syndrome may be caused by mutations in either the COL4A3, COL4A4, or COL4A5 genes. These genes each provide instructions for making one component of a protein called type IV collagen, which plays an important role in the glomeruli of the kidneys. Glomeruli are clusters of specialized blood vessels that remove water and waste products from the blood and create urine. Mutations in the genes mentioned above result in abnormalities of the type IV collagen in glomeruli, which prevents the kidneys from properly filtering the blood. As a result, blood and protein pass into the urine. Over time, the kidneys become scarred and many people with Alport syndrome develop kidney failure. Type IV collagen is also an important component of the organ of Corti, an inner ear structure that transforms sound waves into nerve impulses for the brain. Alterations in type IV collagen may result in abnormal inner ear function, which can lead to hearing loss. In addition, type IV collagen plays a role in the eye, where it helps maintain the shape of the lens and the normal color of the retina. Mutations found in Alport syndrome may affect the shape of the lenses and the color of the retina.
Question: What are the treatments for Cold agglutinin disease ?

Answer: How might cold agglutinin disease be treated? The treatment of cold agglutinin disease depends on many factors including the severity of the condition, the signs and symptoms present in each person, and the underlying cause. For example, in those affected by secondary cold agglutinin disease, it is important to diagnose and treat the underlying condition which may include certain types of cancer; bacterial, viral, or parasitic infections; and/or other autoimmune disease. People with few symptoms and/or mild anemia may not require any specific treatment. These cases are often managed by simply avoiding exposure to the cold. In severe cases, medical interventions may be necessary. Rituximab (an antibody that selectively reduces specific types of immune cells) may be recommended either alone or in combination with other medications for people with severe hemolysis. Plasmapheresis, which involves filtering blood to remove antibodies, and/or blood transfusions may be an option for temporary relief of severe symptoms. Other therapies exist; however, they have been used with variable success. Medscape Reference's Web site offers more specific information about these alternative treatments. Please click on the link to access this resource.
Question: What is (are) Granulomatous Amebic Encephalitis ?

Answer: Granulomatous amebic encephalitis is a life-threatening infection of the brain caused by the free-living amoebae Acanthamoeba spp., Balamuthia mandrillaris and Sappinia pedata. Acanthamoeba species, are commonly found in lakes, swimming pools, tap water, and heating and air conditioning units. The disease affects immunocompromised peple and is very serious. Symptoms include mental status changes, loss of coordination, fever, muscular weakness or partial paralysis affecting one side of the body, double vision, sensitivity to light and other neurologic problems. The diagnosis is difficult and is often made at advanced stages. Tests useful in the diagnosis include brain scans, biopsies, or spinal taps and in disseminated disease, biopsy of the involved sites and testing by the laboratory experts. Early diagnosis is important for the prognosis. No single drug is effective; hence multiple antibiotics are needed for successful treatment. A combination of surgical and medical interventions involving multiple specialty experts is required to prevent death and morbidity in survivors.
Question: What is (are) Chiari malformation type 2 ?

Answer: Chiari malformation type 2 (CM type II) is a type of Chiari malformation in which both the cerebellum and brain stem tissue extend into the foramen magnum (the hole at the skull base for passing of the spinal cord). This form is often accompanied by a type of spina bifida called myelomeningocele, and can also be accompanied by syringomyelia, hydrocephalus, or other abnormalities. Symptoms in infants may include stridor (wheezing sound); difficulty swallowing (dysphagia); feeding difficulties; hypotonia; and weak cry. Symptoms in children and/or adults may include headache; fatigue; loss of vision; tingling extremities; nausea; dysphagia; dizziness; muscle weakness; and ataxia. Adults and adolescents who previously had no symptoms may begin to have symptoms later in life. The exact cause of the condition is not known but it appears to be due to a developmental failure of the brain stem and upper spine. The term Arnold-Chiari malformation is technically specific to type II but may sometimes be used to describe other types of Chiari malformations.
Question: What is the outlook for Traumatic Brain Injury ?

Answer: Approximately half of severely head-injured patients will need surgery to remove or repair hematomas (ruptured blood vessels) or contusions (bruised brain tissue). Disabilities resulting from a TBI depend upon the severity of the injury, the location of the injury, and the age and general health of the individual. Some common disabilities include problems with cognition (thinking, memory, and reasoning), sensory processing (sight, hearing, touch, taste, and smell), communication (expression and understanding), and behavior or mental health (depression, anxiety, personality changes, aggression, acting out, and social inappropriateness). More serious head injuries may result in stupor, an unresponsive state, but one in which an individual can be aroused briefly by a strong stimulus, such as sharp pain; coma, a state in which an individual is totally unconscious, unresponsive, unaware, and unarousable; vegetative state, in which an individual is unconscious and unaware of his or her surroundings, but continues to have a sleep-wake cycle and periods of alertness; and a persistent vegetative state (PVS), in which an individual stays in a vegetative state for more than a month.
Question: What is the outlook for Alzheimer's Disease ?

Answer: In very few families, people develop AD in their 30s, 40s, and 50s. This is known as "early onset" AD. These individuals have a mutation in one of three different inherited genes that causes the disease to begin at an earlier age. More than 90 percent of AD develops in people older than 65. This form of AD is called "late-onset" AD, and its development and pattern of damage in the brain is similar to that of early-onset AD. The course of this disease varies from person to person, as does the rate of decline. In most people with AD, symptoms first appear after age 65.
                
We don't yet completely understand the causes of late-onset AD, but they probably include genetic, environmental, and lifestyle factors. Although the risk of developing AD increases with age, AD and dementia symptoms are not a part of normal aging. There are also some forms of dementia that aren't related to brain diseases such as AD, but are caused by systemic abnormalities such as metabolic syndrome, in which the combination of high blood pressure, high cholesterol, and diabetes causes confusion and memory loss.
Question: Is Allan-Herndon-Dudley syndrome inherited ?

Answer: This condition is inherited in an X-linked recessive pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation must be present in both copies of the gene to cause the disorder. Males are affected by X-linked recessive disorders much more frequently than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.  In X-linked recessive inheritance, a female with one altered copy of the gene in each cell is called a carrier. She can pass on the mutated gene, but usually does not experience signs and symptoms of the disorder. Carriers of SLC16A2 mutations have normal intelligence and do not experience problems with movement. Some carriers have been diagnosed with thyroid disease, a condition which is relatively common in the general population. It is unclear whether thyroid disease is related to SLC16A2 gene mutations in these cases.
Question: What is (are) desmosterolosis ?

Answer: Desmosterolosis is a condition that is characterized by neurological problems, such as brain abnormalities and developmental delay, and can also include other signs and symptoms.  Children with desmosterolosis have delayed speech and motor skills (such as sitting and walking). Later in childhood, some affected individuals are able to walk with support; verbal communication is often limited to a few words or phrases. Common brain abnormalities in desmosterolosis include malformation of the tissue that connects the left and right halves of the brain (the corpus callosum) and loss of white matter, which consists of nerve fibers covered by a fatty substance called myelin.  People with desmosterolosis commonly have muscle stiffness (spasticity) and stiff, rigid joints (arthrogryposis) affecting their hands and feet. Other features seen in some affected individuals include short stature, abnormal head size (either larger or smaller than normal), a small lower jaw (micrognathia), an opening in the roof of the mouth (cleft palate), involuntary eye movements (nystagmus) or eyes that do not look in the same direction (strabismus), heart defects, and seizures.
Question: What are the treatments for megalencephalic leukoencephalopathy with subcortical cysts ?

Answer: These resources address the diagnosis or management of megalencephalic leukoencephalopathy with subcortical cysts:  - Gene Review: Gene Review: Megalencephalic Leukoencephalopathy with Subcortical Cysts  - Genetic Testing Registry: Megalencephalic leukoencephalopathy with subcortical cysts  - Genetic Testing Registry: Megalencephalic leukoencephalopathy with subcortical cysts 1  - Genetic Testing Registry: Megalencephalic leukoencephalopathy with subcortical cysts 2a  - Genetic Testing Registry: Megalencephalic leukoencephalopathy with subcortical cysts 2b, remitting, with or without mental retardation  - MedlinePlus Encyclopedia: Myelin   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care
Question: What are the genetic changes related to KBG syndrome ?

Answer: KBG syndrome is caused by mutations in the ANKRD11 gene. The protein produced from this gene enables other proteins to interact with each other and helps control gene activity. The ANKRD11 protein is found in nerve cells (neurons) in the brain. It plays a role in the proper development of the brain and may be involved in the ability of neurons to change and adapt over time (plasticity), which is important for learning and memory. ANKRD11 may function in other cells in the body and appears to be involved in normal bone development.  Most of the ANKRD11 gene mutations involved in KBG syndrome lead to an abnormally short ANKRD11 protein, which likely has little or no function. Reduction of this protein's function is thought to underlie the signs and symptoms of the condition. Because ANKRD11 is thought to play an important role in neurons and brain development, researchers speculate that a partial loss of its function may lead to developmental delay and intellectual disability in KBG syndrome. However, the mechanism is not fully known. It is also unclear how loss of ANKRD11 function leads to the skeletal features of the condition.
Question: What is (are) white sponge nevus ?

Answer: White sponge nevus is a condition characterized by the formation of white patches of tissue called nevi (singular: nevus) that appear as thickened, velvety, sponge-like tissue. The nevi are most commonly found on the moist lining of the mouth (oral mucosa), especially on the inside of the cheeks (buccal mucosa). Affected individuals usually develop multiple nevi. Rarely, white sponge nevi also occur on the mucosae (singular: mucosa) of the nose, esophagus, genitals, or anus. The nevi are caused by a noncancerous (benign) overgrowth of cells.  White sponge nevus can be present from birth but usually first appears during early childhood. The size and location of the nevi can change over time. In the oral mucosa, both sides of the mouth are usually affected. The nevi are generally painless, but the folds of extra tissue can promote bacterial growth, which can lead to infection that may cause discomfort. The altered texture and appearance of the affected tissue, especially the oral mucosa, can be bothersome for some affected individuals.
Question: Is Cornelia de Lange syndrome inherited ?

Answer: When Cornelia de Lange syndrome is caused by mutations in the NIPBL, RAD21, or SMC3 gene, the condition is considered to have an autosomal dominant pattern of inheritance. Autosomal dominant inheritance means one copy of the altered gene in each cell is sufficient to cause the disorder. Most cases result from new gene mutations and occur in people with no history of the condition in their family.  When Cornelia de Lange syndrome is caused by mutations in the HDAC8 or SMC1A gene, the condition has an X-linked dominant pattern of inheritance. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. Studies of X-linked Cornelia de Lange syndrome indicate that one copy of the altered gene in each cell may be sufficient to cause the condition. Unlike X-linked recessive conditions, in which males are more frequently affected or experience more severe symptoms than females, X-linked dominant Cornelia de Lange syndrome appears to affect males and females similarly. Most cases result from new mutations in the HDAC8 or SMC1A gene and occur in people with no history of the condition in their family.
Question: What are the treatments for What I need to know about My Child's Urinary Tract Infection ?

Answer: Bacteria-fighting medicines called antibiotics are used to treat a UTI. While the lab is doing the urine culture, the health care provider may begin treatment with an antibiotic that treats the bacteria most likely to be causing the infection. Once culture results are known, the health care provider may switch your child to a different antibiotic that targets the specific type of bacteria.
                
Your child will need to take antibiotics for at least 3 to 5 days and maybe as long as several weeks. Be sure your child takes every pill or every dose of liquid. Your child should feel better after a couple of days, but the infection might come back if your child stops taking the antibiotic too early.
                
You should let your child drink as much as your child wants. But dont force your child to drink large amounts of fluid. Call your childs health care provider if your child doesnt want to or isnt able to drink. Also, talk with your childs health care provider if your child needs medicine for the pain of a UTI. The health care provider can recommend an over-the-counter pain medicine. A heating pad on the back or abdomen may also help.
Question: Who is at risk for Proteinuria? ?

Answer: People with diabetes, hypertension, or certain family backgrounds are at risk for proteinuria. In the United States, diabetes is the leading cause of ESRD.1 In both type 1 and type 2 diabetes, albumin in the urine is one of the first signs of deteriorating kidney function. As kidney function declines, the amount of albumin in the urine increases.
                
Another risk factor for developing proteinuria is hypertension, or high blood pressure. Proteinuria in a person with high blood pressure is an indicator of declining kidney function. If the hypertension is not controlled, the person can progress to full kidney failure.
                
African Americans are more likely than Caucasians to have high blood pressure and to develop kidney problems from it, even when their blood pressure is only mildly elevated. In fact, African Americans are six times more likely than Caucasians to develop hypertension-related kidney failure.2
                
Other groups at risk for proteinuria are American Indians, Hispanics/Latinos, Pacific Islander Americans, older adults, and overweight people. These at-risk groups and people who have a family history of kidney disease should have their urine tested regularly.
Question: How to prevent High Blood Pressure and Kidney Disease ?

Answer: The best way to slow or prevent kidney disease from high blood pressure is to take steps to lower blood pressure. These steps include a combination of medication and lifestyle changes, such as
                
- healthy eating  - physical activity  - maintaining a healthy weight  - quitting smoking  - managing stress
                
No matter what the cause of the kidney disease, high blood pressure can increase damage to the kidneys. People with kidney disease should keep their blood pressure below 140/90.4
                
Medication
                
Medications that lower blood pressure can also significantly slow the progression of kidney disease. Two types of blood pressure-lowering medications, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), have been shown effective in slowing the progression of kidney disease. Many people require two or more medications to control their blood pressure. In addition to an ACE inhibitor or an ARB, a health care provider may prescribe a diuretica medication that helps the kidneys remove fluid from the blood. A person may also need beta blockers, calcium channel blockers, and other blood pressure medications.
Question: What causes Quitting Smoking for Older Adults ?

Answer: Yes. Smoking is the leading cause of cancer in the United States, and it increases the risk of many types of cancer, including -  lung cancer  - throat cancer  -  mouth cancer  -  nasal cavity cancer (cancer in the airways of the nose)  - esophageal cancer (cancer of the esophagus)  - stomach cancer  -  pancreatic cancer (cancer of the pancreas)  -  kidney cancer   - bladder cancer  -  cervical cancer (cancer of the cervix)  -  acute myeloid leukemia (blood cancer).  lung cancer throat cancer  mouth cancer  nasal cavity cancer (cancer in the airways of the nose) esophageal cancer (cancer of the esophagus) stomach cancer  pancreatic cancer (cancer of the pancreas)  kidney cancer  bladder cancer  cervical cancer (cancer of the cervix)  acute myeloid leukemia (blood cancer). If you smoke, you are up to 10 times more likely to get cancer than a person who has never smoked. This depends on how much and how long you smoked.
Question: Do you have information about HIV/AIDS Medicines

Answer: Summary : In the early 1980s, when the HIV/AIDS epidemic began, patients rarely lived longer than a few years. But today, there are many effective medicines to fight the infection, and people with HIV have longer, healthier lives.    There are five major types of medicines:       - Reverse transcriptase (RT) inhibitors - interfere with a critical step during the HIV life cycle and keep the virus from making copies of itself    - Protease inhibitors - interfere with a protein that HIV uses to make infectious viral particles    - Fusion inhibitors - block the virus from entering the body's cells    - Integrase inhibitors - block an enzyme HIV needs to make copies of itself    - Multidrug combinations - combine two or more different types of drugs into one       These medicines help people with HIV, but they are not perfect. They do not cure HIV/AIDS. People with HIV infection still have the virus in their bodies. They can still spread HIV to others through unprotected sex and needle sharing, even when they are taking their medicines.    NIH: National Institute of Allergy and Infectious Diseases