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

Answer: Juvenile osteoporosis is a condition of bone demineralization characterized by pain in the back and extremities, multiple fractures, difficulty walking, and evidence of osteoporosis. Symptoms typically develop just before puberty. Osteoporosis is rare in children and adolescents. When it does occur, it is usually caused by an underlying medical disorder or by medications used to treat the disorder. This is called secondary osteoporosis. Sometimes, however, there is no identifiable cause of osteoporosis in a child. This is known as idiopathic osteoporosis. There is no established medical or surgical therapy for juvenile osteoporosis. In some cases, treatment is not necessary, as the condition resolves spontaneously. Early diagnosis may allow for preventive steps, including physical therapy, avoidance of weight-bearing activities, use of crutches and other supportive care. A well-balanced diet rich in calcium and vitamin D is also important. In severe, long-lasting cases, medications such as bisphosphonates may be used. In most cases, complete recovery of bone occurs.
Question: What are the treatments for Buerger disease ?

Answer: How is Buerger disease treated? Currently there is not a cure for Buerger disease, however there are treatments that can help control it. The most essential part of treatment is to avoid all tobacco and nicotine products. Even one cigarette a day can worsen the disease. A doctor can help a person with Buerger disease learn about safe medications and programs to combat smoking/nicotine addiction. Continued smoking is associated with an overall amputation rate of 40 to 50 percent. The following treatments may also be helpful, but do not replace smoking/nicotine cessation: Medications to dilate blood vessels and improve blood flow (e.g., intravenous Iloprost) Medications to dissolve blood clots Treatment with calcium channel blockers Walking exercises Intermittent compression of the arms and legs to increase blood flow to your extremities Surgical sympathectomy (a controversial surgery to cut the nerves to the affected area to control pain and increase blood flow) Therapeutic angiogenesis (medications to stimulate growth of new blood vessels) Spinal cord stimulation Amputation, if infection or gangrene occurs
Question: Who is at risk for Parasites - Lice - Body Lice? ?

Answer: Body lice infestation is found worldwide but generally is limited to persons who live under conditions of crowding and poor hygiene who do not have access to regular bathing and changes of clean clothes, such as:
    
     - the homeless,
     - refugees,
     - survivors of war or natural disasters.
    
    
Infestations can spread rapidly under such conditions. Body lice infestation can occur in people of all races.
    
Body lice are spread through direct contact with a person who has body lice or through contact with articles such as clothing, beds, bed linens, or towels that have been in contact with an infested person. However, in the United States, actual infestation with body lice tends to be occur only in homeless, transient persons who do not have access to regular bathing and changes of clean clothes.
    
Body lice can transmit disease. Epidemics of typhus and louse-borne relapsing fever have been caused by body lice (typically in areas where climate, poverty, and social customs or war and social upheaval prevent regular changes and laundering of clothing).
Question: What is (are) Whipple's Disease ?

Answer: Whipple's disease is a multi-system infectious bacterial disease that interferes with the body's ability to metabolize fats. Caused by the bacterium Tropheryma whipplei, the disorder can affect any system in the body, including the brain, eyes, heart, joints, and lungs, but usually occurs in the gastrointestinal system. Neurological symptoms occur in up to 40 percent of individuals and may include dementia, abnormalities of eye and facial muscle movements, headaches, seizures, loss of muscle control, memory loss, weakness, and vision problems. Gastrointestinal symptoms may include diarrhea, weight loss, fatigue, weakness, and abdominal bleeding and pain. Fever, cough, anemia, heart and lung damage, darkening of the skin, and joint soreness may also be present. The disease is more common in men and neurological symptoms are more common in individuals who have severe abdominal disease, Rarely, neurological symptoms may appear without gastrointestinal symptoms and can mimic symptoms of almost any neurologic disease..
Question: What is (are) Fahr's Syndrome ?

Answer: Fahr's Syndrome is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement, including the basal ganglia and the cerebral cortex. Symptoms of the disorder may include deterioration of motor function, dementia, seizures, headache, dysarthria (poorly articulated speech), spasticity (stiffness of the limbs) and spastic paralysis, eye impairments, and athetosis (involuntary, writhing movements). Fahr's Syndrome can also include symptoms characteristic of Parkinson's disease such as tremors, muscle rigidity, a mask-like facial appearance, shuffling gait, and a "pill-rolling" motion of the fingers. These symptoms generally occur later in the development of the disease. More common symptoms include dystonia (disordered muscle tone) and chorea (involuntary, rapid, jerky movements). Age of onset is typically in the 40s or 50s, although it can occur at any time in childhood or adolescence.
Question: What are the genetic changes related to Duchenne and Becker muscular dystrophy ?

Answer: Mutations in the DMD gene cause the Duchenne and Becker forms of muscular dystrophy. The DMD gene provides instructions for making a protein called dystrophin. This protein is located primarily in skeletal and cardiac muscle, where it helps stabilize and protect muscle fibers. Dystrophin may also play a role in chemical signaling within cells.  Mutations in the DMD gene alter the structure or function of dystrophin or prevent any functional dystrophin from being produced. Muscle cells without enough of this protein become damaged as muscles repeatedly contract and relax with use. The damaged fibers weaken and die over time, leading to the muscle weakness and heart problems characteristic of Duchenne and Becker muscular dystrophies. Mutations that lead to an abnormal version of dystrophin that retains some function usually cause Becker muscular dystrophy, while mutations that prevent the production of any functional dystrophin tend to cause Duchenne muscular dystrophy.  Because Duchenne and Becker muscular dystrophies result from faulty or missing dystrophin, these conditions are classified as dystrophinopathies.
Question: What are the genetic changes related to systemic lupus erythematosus ?

Answer: Normal variations (polymorphisms) in many genes can affect the risk of developing SLE, and in most cases multiple genetic factors are thought to be involved. In rare cases, SLE is caused by mutations in single genes. Most of the genes associated with SLE are involved in immune system function, and variations in these genes likely affect proper targeting and control of the immune response. Sex hormones and a variety of environmental factors including viral infections, diet, stress, chemical exposures, and sunlight are also thought to play a role in triggering this complex disorder. About 10 percent of SLE cases are thought to be triggered by drug exposure, and more than 80 drugs that may be involved have been identified.  In people with SLE, cells that have undergone self-destruction (apoptosis) because they are damaged or no longer needed are not cleared away properly. The relationship of this loss of function to the cause or features of SLE is unclear. Researchers suggest that these dead cells may release substances that cause the immune system to react inappropriately and attack the body's tissues, resulting in the signs and symptoms of SLE.
Question: What is (are) Wagner syndrome ?

Answer: Wagner syndrome is a hereditary disorder that causes progressive vision loss. The eye problems that lead to vision loss typically begin in childhood, although the vision impairment might not be immediately apparent.  In people with Wagner syndrome, the light-sensitive tissue that lines the back of the eye (the retina) becomes thin and may separate from the back of the eye (retinal detachment). The blood vessels within the retina (known as the choroid) may also be abnormal. The retina and the choroid progressively break down (degenerate). Some people with Wagner syndrome have blurred vision because of ectopic fovea, an abnormality in which the part of the retina responsible for sharp central vision is out of place. Additionally, the thick, clear gel that fills the eyeball (the vitreous) becomes watery and thin. People with Wagner syndrome develop a clouding of the lens of the eye (cataract). Affected individuals may also experience nearsightedness (myopia), progressive night blindness, or a narrowing of their field of vision.  Vision impairment in people with Wagner syndrome can vary from near normal vision to complete loss of vision in both eyes.
Question: Is facioscapulohumeral muscular dystrophy inherited ?

Answer: FSHD1 is inherited in an autosomal dominant pattern, which means one copy of the shortened D4Z4 region on a "permissive" chromosome 4 is sufficient to cause the disorder. In most cases, an affected person inherits the altered chromosome from one affected parent. Other people with FSHD1 have no history of the disorder in their family. These cases are described as sporadic and are caused by a new (de novo) D4Z4 contraction on one copy of a "permissive" chromosome 4.  FSHD2 is inherited in a digenic pattern, which means that two independent genetic changes are necessary to cause the disorder. To have FSHD2, an individual must inherit a mutation in the SMCHD1 gene (which is located on chromosome 18) and, separately, they must inherit one copy of a "permissive" chromosome 4. Affected individuals typically inherit the SMCHD1 gene mutation from one parent and the "permissive" chromosome 4 from the other parent. (Because neither parent has both genetic changes in most cases, they are typically unaffected.)
Question: What is (are) malignant hyperthermia ?

Answer: Malignant hyperthermia is a severe reaction to particular drugs that are often used during surgery and other invasive procedures. Specifically, this reaction occurs in response to some anesthetic gases, which are used to block the sensation of pain, and with a muscle relaxant that is used to temporarily paralyze a person during a surgical procedure. If given these drugs, people at risk for malignant hyperthermia may experience muscle rigidity, breakdown of muscle fibers (rhabdomyolysis), a high fever, increased acid levels in the blood and other tissues (acidosis), and a rapid heart rate. Without prompt treatment, the complications of malignant hyperthermia can be life-threatening.  People at increased risk for this disorder are said to have malignant hyperthermia susceptibility. Affected individuals may never know they have the condition unless they undergo testing or have a severe reaction to anesthesia during a surgical procedure. While this condition often occurs in people without other serious medical problems, certain inherited muscle diseases (including central core disease and multiminicore disease) are associated with malignant hyperthermia susceptibility.
Question: What are the genetic changes related to myosin storage myopathy ?

Answer: Mutations in the MYH7 gene cause myosin storage myopathy. The MYH7 gene provides instructions for making a protein known as the cardiac beta ()-myosin heavy chain. This protein is found in heart (cardiac) muscle and in type I skeletal muscle fibers, one of two types of fibers that make up the muscles that the body uses for movement. Cardiac -myosin heavy chain is the major component of the thick filament in muscle cell structures called sarcomeres. Sarcomeres, which are made up of thick and thin filaments, are the basic units of muscle contraction. The overlapping thick and thin filaments attach to each other and release, which allows the filaments to move relative to one another so that muscles can contract.  Mutations in the MYH7 gene lead to the production of an altered cardiac -myosin heavy chain protein, which is thought to be less able to form thick filaments. The altered proteins accumulate in type I skeletal muscle fibers, forming the protein clumps characteristic of the disorder. It is unclear how these changes lead to muscle weakness in people with myosin storage myopathy.
Question: Is atypical hemolytic-uremic syndrome inherited ?

Answer: Most cases of atypical hemolytic-uremic syndrome are sporadic, which means that they occur in people with no apparent history of the disorder in their family. Less than 20 percent of all cases have been reported to run in families. When the disorder is familial, it can have an autosomal dominant or an autosomal recessive pattern of inheritance.  Autosomal dominant inheritance means one copy of an altered gene in each cell is sufficient to increase the risk of the disorder. In some cases, an affected person inherits the mutation from one affected parent. However, most people with the autosomal dominant form of atypical hemolytic-uremic syndrome have no history of the disorder in their family. Because not everyone who inherits a gene mutation will develop the signs and symptoms of the disease, an affected individual may have unaffected relatives who carry a copy of the mutation.  Autosomal recessive inheritance means both copies of a gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
Question: What are the genetic changes related to Ellis-van Creveld syndrome ?

Answer: Ellis-van Creveld syndrome can be caused by mutations in the EVC or EVC2 gene. Little is known about the function of these genes, although they appear to play important roles in cell-to-cell signaling during development. In particular, the proteins produced from the EVC and EVC2 genes are thought to help regulate the Sonic Hedgehog signaling pathway. This pathway plays roles in cell growth, cell specialization, and the normal shaping (patterning) of many parts of the body.  The mutations that cause Ellis-van Creveld syndrome result in the production of an abnormally small, nonfunctional version of the EVC or EVC2 protein. It is unclear how the defective proteins lead to the specific signs and symptoms of this condition. Studies suggest that they prevent normal Sonic Hedgehog signaling in the developing embryo, disrupting the formation and growth of the bones, teeth, and other parts of the body.  Together, mutations in the EVC and EVC2 genes account for more than half of all cases of Ellis-van Creveld syndrome. The cause of the remaining cases is unknown.
Question: What are the genetic changes related to anhidrotic ectodermal dysplasia with immune deficiency ?

Answer: Mutations in the IKBKG gene cause X-linked recessive EDA-ID, and mutations in the NFKBIA gene cause autosomal dominant EDA-ID. The proteins produced from these two genes regulate nuclear factor-kappa-B. Nuclear factor-kappa-B is a group of related proteins (a protein complex) that binds to DNA and controls the activity of other genes, including genes that direct the body's immune responses and inflammatory reactions. It also protects cells from certain signals that would otherwise cause them to self-destruct (undergo apoptosis).  The IKBKG and NFKBIA gene mutations responsible for EDA-ID result in the production of proteins with impaired function, which reduces activation of nuclear factor-kappa-B. These changes disrupt certain signaling pathways within immune cells, resulting in immune deficiency. It is unclear how gene mutations alter the development of the skin, teeth, sweat glands, and other tissues, although it is likely caused by abnormal nuclear factor-kappa-B signaling in other types of cells.
Question: What is (are) Kidney Stones in Children ?

Answer: Four major types of kidney stones occur in children:
                
- Calcium stones are the most common type of kidney stone and occur in two major forms: calcium oxalate and calcium phosphate. Calcium oxalate stones are more common. Calcium oxalate stone formation has various causes, which may include high calcium excretion, high oxalate excretion, or acidic urine. Calcium phosphate stones are caused by alkaline urine.  - Uric acid stones form when the urine is persistently acidic. A diet rich in purinessubstances found in animal proteins such as meats, fish, and shellfishmay cause uric acid. If uric acid becomes concentrated in the urine, it can settle and form a stone by itself or along with calcium.  - Struvite stones result from kidney infections. Eliminating infected stones from the urinary tract and staying infectionfree can prevent more struvite stones.  - Cystine stones result from a genetic disorder that causes cystine to leak through the kidneys and into the urine in high concentration, forming crystals that tend to accumulate into stones.
Question: What is (are) Gallstones ?

Answer: The biliary tract consists of the gallbladder and the bile ducts. The bile ducts carry bile and other digestive enzymes from the liver and pancreas to the duodenumthe fi rst part of the small intestine.
                
The liver produces bilea fl uid that carries toxins and waste products out of the body and helps the body digest fats and the fat-soluble vitamins A, D, E, and K. Bile mostly consists of cholesterol, bile salts, and bilirubin. Bilirubin, a reddish-yellow substance, forms when hemoglobin from red blood cells breaks down. Most bilirubin is excreted through bile.
                

                

                
The bile ducts of the biliary tract include the hepatic ducts, the common bile duct, the pancreatic duct, and the cystic duct. The gallbladder stores bile. Eating signals the gallbladder to contract and empty bile through the cystic duct and common bile duct into the duodenum to mix with food.
Question: What is (are) Diabetes, Heart Disease, and Stroke ?

Answer: If you have diabetes, you are at least twice as likely as someone who does not have diabetes to have heart disease or a stroke. People with diabetes also tend to develop heart disease or have strokes at an earlier age than other people. If you are middle-aged and have type 2 diabetes, some studies suggest that your chance of having a heart attack is as high as someone without diabetes who has already had one heart attack. Women who have not gone through menopause usually have less risk of heart disease than men of the same age. But women of all ages with diabetes have an increased risk of heart disease because diabetes cancels out the protective effects of being a woman in her child-bearing years.
                
People with diabetes who have already had one heart attack run an even greater risk of having a second one. In addition, heart attacks in people with diabetes are more serious and more likely to result in death. High blood glucose levels over time can lead to increased deposits of fatty materials on the insides of the blood vessel walls. These deposits may affect blood flow, increasing the chance of clogging and hardening of blood vessels (atherosclerosis).
Question: What are the symptoms of Psoriasis ?

Answer: Different forms of psoriasis have different symptoms. In many cases your doctor can diagnose psoriasis based on the signs seen in the physical exam as well as the symptoms you describe. Symptoms The most common symptoms of psoriasis are - patches of thick, red skin   - skin inflammation  - silvery scales  - itching  - pain. patches of thick, red skin skin inflammation silvery scales itching pain. Psoriasis most commonly affects the elbows, knees, scalp, lower back, face, palms, soles of the feet, nails, and soft tissues. Making a Diagnosis In most cases, your primary care provider can diagnose psoriasis simply by examining your skin. Because the symptoms of psoriasis may be similar to those of other skin diseases, however, sometimes the diagnosis is more difficult. You may need to see a dermatologist, a doctor who specializes in diagnosing and treating skin diseases. If your doctor isn't sure if you have psoriasis, he or she may order a biopsy. This involves removing a small sample of skin and looking at it under a microscope.
Question: Do you have information about Coronary Artery Bypass Surgery

Answer: Summary : In coronary artery disease (CAD), the arteries that supply blood and oxygen to your heart muscle grow hardened and narrowed. You may try treatments such as lifestyle changes, medicines, and angioplasty, a procedure to open the arteries. If these treatments don't help, you may need coronary artery bypass surgery.    The surgery creates a new path for blood to flow to the heart. The surgeon takes a healthy piece of vein from the leg or artery from the chest or wrist. Then the surgeon attaches it to the coronary artery, just above and below the narrowed area or blockage. This allows blood to bypass (get around) the blockage. Sometimes people need more than one bypass.    The results of the surgery usually are excellent. Many people remain symptom-free for many years. You may need surgery again if blockages form in the grafted arteries or veins or in arteries that weren't blocked before. Lifestyle changes and medicines may help prevent arteries from becoming clogged again.    NIH: National Heart, Lung, and Blood Institute
Question: What is (are) Multiple Myeloma ?

Answer: Multiple myeloma is a cancer that begins in plasma cells, a type of white blood cell. These cells are part of your immune system, which helps protect the body from germs and other harmful substances. In time, myeloma cells collect in the bone marrow and in the solid parts of bones.    No one knows the exact causes of multiple myeloma, but it is more common in older people and African Americans. It can run in families. Common symptoms may include       - Bone pain, often in the back or ribs    - Broken bones    - Weakness or fatigue    - Weight loss    - Frequent infections and fevers    - Feeling very thirsty    - Frequent urination       Doctors diagnose multiple myeloma using lab tests, imaging tests, and a bone marrow biopsy. Your treatment depends on how advanced the disease is and whether you have symptoms. If you have no symptoms, you may not need treatment right away. If you have symptoms, you may have chemotherapy, stem cell transplantation, radiation, or targeted therapy. Targeted therapy uses substances that attack cancer cells without harming normal cells.    NIH: National Cancer Institute
Question: What is (are) Sleep Apnea ?

Answer: Sleep apnea is a common disorder that causes your breathing to stop or get very shallow. Breathing pauses can last from a few seconds to minutes. They may occur 30 times or more an hour.    The most common type is obstructive sleep apnea. It causes your airway to collapse or become blocked during sleep. Normal breathing starts again with a snort or choking sound. People with sleep apnea often snore loudly. However, not everyone who snores has sleep apnea.    You are more at risk for sleep apnea if you are overweight, male, or have a family history or small airways. Children with enlarged tonsils may also get it.    Doctors diagnose sleep apnea based on medical and family histories, a physical exam, and sleep study results.    When your sleep is interrupted throughout the night, you can be drowsy during the day. People with sleep apnea are at higher risk for car crashes, work-related accidents, and other medical problems. If you have it, it is important to get treatment. Lifestyle changes, mouthpieces, surgery, and breathing devices can treat sleep apnea in many people.    NIH: National Heart, Lung, and Blood Institute