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

Answer: Espaol
                
Varicose (VAR-i-kos) veins are swollen, twisted veins that you can see just under the surface of the skin. These veins usually occur in the legs, but they also can form in other parts of the body.
                
Varicose veins are a common condition. They usually cause few signs and symptoms. Sometimes varicose veins cause mild to moderate pain, blood clots, skin ulcers (sores), or other problems.
                
Overview
                
Veins are blood vessels that carry blood from your body's tissues to your heart. Your heart pumps the blood to your lungs to pick up oxygen. The oxygen-rich blood then is pumped to your body through blood vessels called arteries.
                
From your arteries, the blood flows through tiny blood vessels called capillaries, where it gives up its oxygen to the body's tissues. Your blood then returns to your heart through your veins to pick up more oxygen. For more information about blood flow, go to the Health Topics How the Heart Works article.
                
Veins have one-way valves that help keep blood flowing toward your heart. If the valves are weak or damaged, blood can back up and pool in your veins. This causes the veins to swell, which can lead to varicose veins.
                
Many factors can raise your risk for varicose veins. Examples of these factors include family history, older age, gender, pregnancy, overweight or obesity, lack of movement, and leg trauma.
                
Varicose veins are treated with lifestyle changes and medical procedures. The goals of treatment are to relieve symptoms, prevent complications, and improve appearance.
                
Outlook
                
Varicose veins usually don't cause medical problems. If they do, your doctor may simply suggest making lifestyle changes.
                
Sometimes varicose veins cause pain, blood clots, skin ulcers, or other problems. If this happens, your doctor may recommend one or more medical procedures. Some people choose to have these procedures to improve the way their veins look or to relieve pain.
                
Many treatments for varicose veins are quick and easy and don't require a long recovery.
Question: What are the treatments for Pericarditis ?

Answer: Most cases of pericarditis are mild; they clear up on their own or with rest and simple treatment. Other times, more intense treatment is needed to prevent complications. Treatment may include medicines and, less often, procedures or surgery.
                
The goals of treatment include:
                
Reducing pain and inflammation
                
Treating the underlying cause, if it's known
                
Checking for complications
                
Specific Types of Treatment
                
As a first step in your treatment, your doctor may advise you to rest until you feel better and have no fever. He or she may tell you to take over-the-counter, anti-inflammatory medicines to reduce pain and inflammation. Examples of these medicines include aspirin and ibuprofen.
                
You may need stronger medicine if your pain is severe. If your pain continues to be severe, your doctor may prescribe a medicine called colchicine and, possibly, prednisone (a steroid medicine).
                
If an infection is causing your pericarditis, your doctor will prescribe an antibiotic or other medicine to treat the infection.
                
You may need to stay in the hospital during treatment for pericarditis so your doctor can check you for complications.
                
The symptoms of acute pericarditis can last from a few days to 3 weeks. Chronic pericarditis may last several months.
                
Other Types of Treatment
                
You may need treatment for complications of pericarditis. Two serious complications are cardiac tamponade and chronic constrictive pericarditis.
                
Cardiac tamponade is treated with a procedure called pericardiocentesis (per-ih-KAR-de-o-sen-TE-sis). A needle or tube (called a catheter) is inserted into the chest wall to remove excess fluid in the pericardium. This procedure relieves pressure on the heart.
                
The only cure for chronic constrictive pericarditis is surgery to remove the pericardium. This is known as a pericardiectomy (PER-i-kar-de-EK-to-me).
                
The treatments for these complications require hospital stays.
Question: What are the genetic changes related to mucolipidosis II alpha/beta ?

Answer: Mutations in the GNPTAB gene cause mucolipidosis II alpha/beta. This gene provides instructions for making part of an enzyme called GlcNAc-1-phosphotransferase. This enzyme helps prepare certain newly made enzymes for transport to lysosomes. Lysosomes are compartments within the cell that use digestive enzymes to break down large molecules into smaller ones that can be reused by cells. GlcNAc-1-phosphotransferase is involved in the process of attaching a molecule called mannose-6-phosphate (M6P) to specific digestive enzymes. Just as luggage is tagged at the airport to direct it to the correct destination, enzymes are often "tagged" after they are made so they get to where they are needed in the cell. M6P acts as a tag that indicates a digestive enzyme should be transported to the lysosome.  Mutations in the GNPTAB gene that cause mucolipidosis II alpha/beta prevent the production of any functional GlcNAc-1-phosphotransferase. Without this enzyme, digestive enzymes cannot be tagged with M6P and transported to lysosomes. Instead, they end up outside the cell and have increased digestive activity. The lack of digestive enzymes within lysosomes causes large molecules to accumulate there. Conditions that cause molecules to build up inside lysosomes, including mucolipidosis II alpha/beta, are called lysosomal storage disorders. The signs and symptoms of mucolipidosis II alpha/beta are most likely caused by the lack of digestive enzymes within lysosomes and the effects these enzymes have outside the cell.  Mutations in the GNPTAB gene can also cause a similar but milder disorder called mucolipidosis III alpha/beta. Instead of preventing the production of any enzyme, these mutations reduce the activity of GlcNAc-1-phosphotransferase. Mucolipidosis III alpha/beta and mucolipidosis II alpha/beta represent two ends of a spectrum of disease severity.
Question: What are the treatments for Depression ?

Answer: Medications called antidepressants work to normalize brain chemicals called neurotransmitters, notably serotonin, norepinephrine, and dopamine. Scientists studying depression have found that these chemicals, and possibly others, are involved in regulating mood, but they are unsure of exactly how they work.  Newer Antidepressants. The newest and most popular types of antidepressant medications are called selective serotonin reuptake inhibitors (SSRIs). They include fluoxetine (Prozac), citalopram (Celexa) and several others. Similar to SSRIs are serotonin and norepinephrine reuptake inhibitors (SNRIs) and include venlafaxine (Effexor) and duloxetine (Cymbalta). Another newer antidepressant bupropion (Wellbutrin) is neither an SSRI nor an SNRI but is popular as well.  Older Antidepressants.  Older antidepressants, called tricyclics and monoamine oxidase inhibitors (MAOIs), are still used sometimes, too. However, these older antidepressants are not as popular as the newer ones because they tend to have more side effects. However, medications affect everyone differently so talk with your doctor to decide which type is best for you.  Practical Considerations. People taking MAOIs must follow strict food and medicine restrictions to avoid potentially serious interactions. If you take an MAOI, your doctor should give you a complete list of foods, medicines, and substances to avoid. MAOIs can also react with SSRIs to produce a serious condition called "serotonin syndrome," which can cause confusion, hallucinations, increased sweating, muscle stiffness, seizures, changes in blood pressure or heart rhythm, and other potentially life threatening conditions. MAOIs should not be taken with SSRIs. Caution is required when combining any serotonergic medication (not just MAOIs) with SSRIs. For example, in 2006 the FDA issued specific warnings against using triptans that are commonly-prescribed to treat migraine headaches together with SSRIs or SNRIs. Using these medications together can cause serotonin syndrome.
Question: What are the treatments for Dry Eye ?

Answer: Dry eye can be a temporary or ongoing condition, so treatments can be short term or may extend over long periods of time. The goal of treatment is to keep the eyes moist and relieve symptoms. Talk to your doctor to rule out other conditions that can cause dry eye, such as Sjgren's syndrome. You may need to treat these conditions. If dry eye results from taking a medication, your doctor may recommend switching to a medication that does not cause dry eye as a side effect. Here are treatments for dry eye. Medication. Cyclosporine, an anti-inflammatory medication, is a prescription eye drop available to treat certain kinds of dry eye. In people with certain kinds of dry eye, it may decrease damage to the cornea, increase basic tear production, and reduce symptoms of dry eye. It may take three to six months of twice-a-day dosages for the medication to work. Some patients with severe dry eye may need to use corticosteroid eye drops that decrease inflammation under close observation by an eye care professional.  Nutritional Supplements. In some patients with dry eye, supplements of omega-3 fatty acids (especially DHA and EPA) may decrease symptoms of irritation. Talk with your eye care professional or your primary medical doctor about whether this is an option for you. Lenses. If dry eye is a result of wearing contact lens for too long, your eye care practitioner may recommend another type of lens or reducing the number of hours you wear your lenses. In the case of severe dry eye, your eye care professional may advise you not to wear contact lenses at all. Punctal plugs. Another option to increase the available tears on the eye surface is to plug the drainage holes, small circular openings at the inner corners of the eyelids where tears drain from the eye into the nose. Lacrimal plugs, also called punctal plugs, can be inserted painlessly by an eye care professional. These plugs are made of silicone or collagen. These plugs can be temporary or permanent. Punctal cautery. In some cases, a simple surgery called punctal cautery is recommended to permanently close the drainage holes. The procedure works similarly to installing punctal plugs, but cannot be reversed.
Question: What are the genetic changes related to cone-rod dystrophy ?

Answer: Mutations in approximately 30 genes are known to cause cone-rod dystrophy. Approximately 20 of these genes are associated with the form of cone-rod dystrophy that is inherited in an autosomal recessive pattern. Mutations in the ABCA4 gene are the most common cause of autosomal recessive cone-rod dystrophy, accounting for 30 to 60 percent of cases. At least 10 genes have been associated with cone-rod dystrophy that is inherited in an autosomal dominant pattern. Mutations in the GUCY2D and CRX genes account for about half of these cases. Changes in at least two genes cause the X-linked form of the disorder, which is rare.  The genes associated with cone-rod dystrophy play essential roles in the structure and function of specialized light receptor cells (photoreceptors) in the retina. The retina contains two types of photoreceptors, rods and cones. Rods are needed for vision in low light, while cones provide vision in bright light, including color vision.  Mutations in any of the genes associated with cone-rod dystrophy lead to a gradual loss of rods and cones in the retina. The progressive degeneration of these cells causes the characteristic pattern of vision loss that occurs in people with cone-rod dystrophy. Cones typically break down before rods, which is why sensitivity to light and impaired color vision are usually the first signs of the disorder. (The order of cell breakdown is also reflected in the condition name.) Night vision is disrupted later, as rods are lost.  Some of the genes associated with cone-rod dystrophy are also associated with other eye diseases, including a group of related eye disorders called rod-cone dystrophy. Rod-cone dystrophy has signs and symptoms similar to those of cone-rod dystrophy. However, rod-cone dystrophy is characterized by deterioration of the rods first, followed by the cones, so night vision is affected before daylight and color vision. The most common form of rod-cone dystrophy is a condition called retinitis pigmentosa.
Question: What is (are) thrombotic thrombocytopenic purpura ?

Answer: Thrombotic thrombocytopenic purpura is a rare disorder that causes blood clots (thrombi) to form in small blood vessels throughout the body. These clots can cause serious medical problems if they block vessels and restrict blood flow to organs such as the brain, kidneys, and heart. Resulting complications can include neurological problems (such as personality changes, headaches, confusion, and slurred speech), fever, abnormal kidney function, abdominal pain, and heart problems.  Blood clots normally form to prevent excess blood loss at the site of an injury. In people with thrombotic thrombocytopenic purpura, clots develop in blood vessels even in the absence of injury. Blood clots are formed from clumps of cell fragments called platelets, which circulate in the blood and assist with clotting. Because a large number of platelets are used to make clots in people with thrombotic thrombocytopenic purpura, fewer platelets are available in the bloodstream. A reduced level of circulating platelets is known as thrombocytopenia. Thrombocytopenia can lead to small areas of bleeding just under the surface of the skin, resulting in purplish spots called purpura.  This disorder also causes red blood cells to break down (undergo hemolysis) prematurely. As blood squeezes past clots within blood vessels, red blood cells can break apart. A condition called hemolytic anemia occurs when red blood cells are destroyed faster than the body can replace them. This type of anemia leads to paleness, yellowing of the eyes and skin (jaundice), fatigue, shortness of breath, and a rapid heart rate.  There are two major forms of thrombotic thrombocytopenic purpura, an acquired (noninherited) form and a familial form. The acquired form usually appears in late childhood or adulthood. Affected individuals may have a single episode of signs and symptoms, or they may recur over time. The familial form of this disorder is much rarer and typically appears in infancy or early childhood. In people with the familial form, signs and symptoms often recur on a regular basis.
Question: What is (are) STING-associated vasculopathy with onset in infancy ?

Answer: STING-associated vasculopathy with onset in infancy (SAVI) is a disorder involving abnormal inflammation throughout the body, especially in the skin, blood vessels, and lungs. Inflammation normally occurs when the immune system sends signaling molecules and white blood cells to a site of injury or disease to fight microbial invaders and help with tissue repair. Excessive inflammation damages the body's own cells and tissues. Disorders such as SAVI that result from abnormally increased inflammation are known as autoinflammatory diseases.  The signs and symptoms of SAVI begin in the first few months of life, and most are related to problems with blood vessels (vasculopathy) and damage to the tissues that rely on these vessels for their blood supply. Affected infants develop areas of severely damaged skin (lesions), particularly on the face, ears, nose, fingers, and toes. These lesions begin as rashes and can progress to become wounds (ulcers) and dead tissue (necrosis). The skin problems, which worsen in cold weather, can lead to complications such as scarred ears, a hole in the tissue that separates the two nostrils (nasal septum perforation), or fingers or toes that require amputation. Individuals with SAVI also have a purplish skin discoloration (livedo reticularis) caused by abnormalities in the tiny blood vessels of the skin. Affected individuals may also experience episodes of Raynaud phenomenon, in which the fingers and toes turn white or blue in response to cold temperature or other stresses. This effect occurs because of problems with the small vessels that carry blood to the extremities.  In addition to problems affecting the skin, people with SAVI have recurrent low-grade fevers and swollen lymph nodes. They may also develop widespread lung damage (interstitial lung disease) that can lead to the formation of scar tissue in the lungs (pulmonary fibrosis) and difficulty breathing; these respiratory complications can become life-threatening. Rarely, muscle inflammation (myositis) and joint stiffness also occur.
Question: What are the genetic changes related to Fanconi anemia ?

Answer: Mutations in at least 15 genes can cause Fanconi anemia. Proteins produced from these genes are involved in a cell process known as the FA pathway. The FA pathway is turned on (activated) when the process of making new copies of DNA, called DNA replication, is blocked due to DNA damage. The FA pathway sends certain proteins to the area of damage, which trigger DNA repair so DNA replication can continue.  The FA pathway is particularly responsive to a certain type of DNA damage known as interstrand cross-links (ICLs). ICLs occur when two DNA building blocks (nucleotides) on opposite strands of DNA are abnormally attached or linked together, which stops the process of DNA replication. ICLs can be caused by a buildup of toxic substances produced in the body or by treatment with certain cancer therapy drugs.  Eight proteins associated with Fanconi anemia group together to form a complex known as the FA core complex. The FA core complex activates two proteins, called FANCD2 and FANCI. The activation of these two proteins brings DNA repair proteins to the area of the ICL so the cross-link can be removed and DNA replication can continue.  Eighty to 90 percent of cases of Fanconi anemia are due to mutations in one of three genes, FANCA, FANCC, and FANCG. These genes provide instructions for producing components of the FA core complex. Mutations in any of the many genes associated with the FA core complex will cause the complex to be nonfunctional and disrupt the entire FA pathway. As a result, DNA damage is not repaired efficiently and ICLs build up over time. The ICLs stall DNA replication, ultimately resulting in either abnormal cell death due to an inability make new DNA molecules or uncontrolled cell growth due to a lack of DNA repair processes. Cells that divide quickly, such as bone marrow cells and cells of the developing fetus, are particularly affected. The death of these cells results in the decrease in blood cells and the physical abnormalities characteristic of Fanconi anemia. When the buildup of errors in DNA leads to uncontrolled cell growth, affected individuals can develop acute myeloid leukemia or other cancers.
Question: What are the symptoms of Gout ?

Answer: Attacks Usually Start at Night Gout is a form of arthritis that causes sudden onset of intense pain and swelling in the joints, which also may be warm and red. Gout typically attacks one joint at a time, and the attacks usually begin at night. Where Gout Usually Occurs Gout normally attacks joints in the lower part of the body, such as the knee, ankle or big toe. For many people, the joints in the big toe are the first to be attacked. In fact, sometime during the course of the disease, many people will develop gout in the big toe. Other Signs and Symptoms These can include - hyperuricemia -- high levels of uric acid in the body  hyperuricemia -- high levels of uric acid in the body -  the presence of uric acid crystals in joint fluid  the presence of uric acid crystals in joint fluid -  more than one attack of acute arthritis more than one attack of acute arthritis -  arthritis that develops in a day, producing a swollen, red, and warm joint  arthritis that develops in a day, producing a swollen, red, and warm joint -  an attack of arthritis in only one joint, often the toe, ankle, or knee. an attack of arthritis in only one joint, often the toe, ankle, or knee. Diagnosis May Be Difficult Gout may be difficult for doctors to diagnose because the symptoms can be vague, and gout often mimics other conditions. Although most people with gout have hyperuricemia at some time during the course of their disease, it may not be present during an acute attack. In addition, having hyperuricemia alone does not mean that a person will get gout. In fact, most people with hyperuricemia do not develop the disease. Testing for Gout To confirm a diagnosis of gout, the doctor inserts a needle into the inflamed joint and draws a sample of synovial fluid, the substance that lubricates a joint. A laboratory technician places some of the fluid on a slide and looks for monosodium urate crystals under a microscope. If crystals are found in the joint fluid, the person usually has gout.
Question: What are the symptoms of Dry Eye ?

Answer: Symptoms of Dry Eye Dry eye symptoms may include any of the following. - stinging or burning of the eye   - a sandy or gritty feeling as if something is in the eye   - episodes of excess tears following very dry eye periods   - a stringy discharge from the eye   - pain and redness of the eye   - episodes of blurred vision  - heavy eyelids   - inability to cry when emotionally stressed   - uncomfortable contact lenses   - decreased ability to read, work on the computer, or do any activity that requires you to use your eyes for long periods of time   - eye fatigue.  stinging or burning of the eye a sandy or gritty feeling as if something is in the eye episodes of excess tears following very dry eye periods a stringy discharge from the eye pain and redness of the eye episodes of blurred vision heavy eyelids inability to cry when emotionally stressed uncomfortable contact lenses decreased ability to read, work on the computer, or do any activity that requires you to use your eyes for long periods of time eye fatigue. If you have symptoms that you think could result from dry eye, consult an eye care professional to get an accurate diagnosis of the condition and begin treatment.  Diagnosing Dry Eye Diagnosis of dry eye requires a comprehensive eye evaluation. Your eye care professional will ask you about your symptoms, your health (conditions for which you are treated, medications that you take), your eye history (use of contact lenses, past refractive or other eye surgery), and aspects of your daily environment (exposure to environmental allergens or occupational hazards). He or she will test your vision, check your eye pressure, examine your eyelids and front eye structures, and, if necessary, may dilate the pupils to examine the inside of the eye. Your eye care professional may order a tearing test to find out if you are making enough tears to keep your eyes moist. In one type of test, called a Schirmers test, the doctor may measure your tear production by placing strips of blotting paper under your lower eyelids, usually done after numbing the eye with anesthetic drops. After a few minutes, the doctor removes the strips and measures the amount of tear production.