shaneperry0101/health-chatbot huggingface dataset:
Question: What are the symptoms of Vasculitis ?
Answer: The signs and symptoms of vasculitis vary. They depend on the type of vasculitis you have, the organs involved, and the severity of the condition. Some people may have few signs and symptoms. Other people may become very sick.
Sometimes the signs and symptoms develop slowly, over months. Other times, the signs and symptoms develop quickly, over days or weeks.
Systemic Signs and Symptoms
Systemic signs and symptoms are those that affect you in a general or overall way. Common systemic signs and symptoms of vasculitis are:
Fever
Loss of appetite
Weight loss
Fatigue (tiredness)
General aches and pains
Organ- or Body System-Specific Signs and Symptoms
Vasculitis can affect specific organs and body systems, causing a range of signs and symptoms.
Skin
If vasculitis affects your skin, you may notice skin changes. For example, you may have purple or red spots or bumps, clusters of small dots, splotches, bruises, or hives. Your skin also may itch.
Joints
If vasculitis affects your joints, you may ache or develop arthritis in one or more joints.
Lungs
If vasculitis affects your lungs, you may feel short of breath. You may even cough up blood. The results from a chest x ray may show signs that suggest pneumonia, even though that may not be what you have.
Gastrointestinal Tract
If vasculitis affects your gastrointestinal tract, you may get ulcers (sores) in your mouth or have stomach pain.
In severe cases, blood flow to the intestines can be blocked. This can cause the wall of the intestines to weaken and possibly rupture (burst). A rupture can lead to serious problems or even death.
Sinuses, Nose, Throat, and Ears
If vasculitis affects your sinuses, nose, throat, and ears, you may have sinus or chronic (ongoing) middle ear infections. Other symptoms include ulcers in the nose and, in some cases, hearing loss.
Eyes
If vasculitis affects your eyes, you may develop red, itchy, burning eyes. Your eyes also may become sensitive to light, and your vision may blur. Rarely, certain types of vasculitis may cause blindness.
Brain
If vasculitis affects your brain, symptoms may include headaches, problems thinking clearly, changes in mental function, or stroke-like symptoms, such as muscle weakness and paralysis (an inability to move).
Nerves
If vasculitis affects your nerves, you may have numbness, tingling, and weakness in various parts of your body. You also may have a loss of feeling or strength in your hands and feet and shooting pains in your arms and legs.
Question: What are the treatments for Vasculitis ?
Answer: Treatment for vasculitis will depend on the type of vasculitis you have, which organs are affected, and the severity of the condition.
People who have severe vasculitis are treated with prescription medicines. Rarely, surgery may be done. People who have mild vasculitis may find relief with over-the-counter pain medicines, such as acetaminophen, aspirin, ibuprofen, or naproxen.
The main goal of treating vasculitis is to reduce inflammation in the affected blood vessels. This usually is done by reducing or stopping the immune response that caused the inflammation.
Types of Treatment
Common prescription medicines used to treat vasculitis include corticosteroids and cytotoxic medicines.
Corticosteroids help reduce inflammation in your blood vessels. Examples of corticosteroids are prednisone, prednisolone, and methylprednisolone.
Doctors may prescribe cytotoxic medicines if vasculitis is severe or if corticosteroids don't work well. Cytotoxic medicines kill the cells that are causing the inflammation. Examples of these medicines are azathioprine, methotrexate, and cyclophosphamide.
Your doctor may prescribe both corticosteroids and cytotoxic medicines.
Other treatments may be used for certain types of vasculitis. For example, the standard treatment for Kawasaki disease is high-dose aspirin and immune globulin. Immune globulin is a medicine thats injected into a vein.
Certain types of vasculitis may require surgery to remove aneurysms that have formed as a result of the condition. (An aneurysm is an abnormal bulge in the wall of a blood vessel.)
Question: How to prevent Vasculitis ?
Answer: You can't prevent vasculitis. However, treatment can help prevent or delay the complications of vasculitis.
People who have severe vasculitis are treated with prescription medicines. Rarely, surgery may be done. People who have mild vasculitis may find relief with over-the-counter pain medicines, such as acetaminophen, aspirin, ibuprofen, or naproxen.
For more information about vasculitis treatments, go to "How Is Vasculitis Treated?"
Question: What is (are) Alpha-1 Antitrypsin Deficiency ?
Answer: Alpha-1 antitrypsin (an-tee-TRIP-sin) deficiency, or AAT deficiency, is a condition that raises your risk for lung disease (especially if you smoke) and other diseases.
Some people who have severe AAT deficiency develop emphysema (em-fi-SE-ma)often when they're only in their forties or fifties. Emphysema is a serious lung disease in which damage to the airways makes it hard to breathe.
A small number of people who have AAT deficiency develop cirrhosis (sir-RO-sis) and other serious liver diseases.
Cirrhosis is a disease in which the liver becomes scarred. The scarring prevents the organ from working well. In people who have AAT deficiency, cirrhosis and other liver diseases usually occur in infancy and early childhood.
A very small number of people who have AAT deficiency have a rare skin disease called necrotizing panniculitis (pa-NIK-yu-LI-tis). This disease can cause painful lumps under or on the surface of the skin.
This article focuses on AAT deficiency as it relates to lung disease.
Overview
Alpha-1 antitrypsin, also called AAT, is a protein made in the liver. Normally, the protein travels through the bloodstream. It helps protect the body's organs from the harmful effects of other proteins. The lungs are one of the main organs that the AAT protein protects.
AAT deficiency occurs if the AAT proteins made in the liver aren't the right shape. They get stuck inside liver cells and can't get into the bloodstream.
As a result, not enough AAT proteins travel to the lungs to protect them. This increases the risk of lung disease. Also, because too many AAT proteins are stuck in the liver, liver disease can develop.
Severe AAT deficiency occurs if blood levels of the AAT protein fall below the lowest amount needed to protect the lungs.
AAT deficiency is an inherited condition. "Inherited" means it's passed from parents to children through genes.
Doctors don't know how many people have AAT deficiency. Many people who have the condition may not know they have it. Estimates of how many people have AAT deficiency range from about 1 in every 1,600 people to about 1 in every 5,000 people.
Outlook
People who have AAT deficiency may not have serious complications, and they may live close to a normal lifespan.
Among people with AAT deficiency who have a related lung or liver disease, about 3percent die each year.
Smoking is the leading risk factor for life-threatening lung disease if you have AAT deficiency. Smoking or exposure to tobacco smoke increases the risk of earlier lung-related symptoms and lung damage. If you have severe AAT deficiency, smoking can shorten your life by as much as 20 years.
AAT deficiency has no cure, but treatments are available. Treatments often are based on the type of disease you develop.
Question: What causes Alpha-1 Antitrypsin Deficiency ?
Answer: Alpha-1 antitrypsin (AAT) deficiency is an inherited disease. "Inherited" means it's passed from parents to children through genes.
Children who have AAT deficiency inherit two faulty AAT genes, one from each parent. These genes tell cells in the body how to make AAT proteins.
In AAT deficiency, the AAT proteins made in the liver aren't the right shape. Thus, they get stuck in the liver cells. The proteins can't get to the organs in the body that they protect, such as the lungs. Without the AAT proteins protecting the organs, diseases can develop.
The most common faulty gene that can cause AAT deficiency is called PiZ. If you inherit two PiZ genes (one from each parent), you'll have AAT deficiency.
If you inherit a PiZ gene from one parent and a normal AAT gene from the other parent, you won't have AAT deficiency. However, you might pass the PiZ gene to your children.
Even if you inherit two faulty AAT genes, you may not have any related complications. You may never even realize that you have AAT deficiency.
Question: Who is at risk for Alpha-1 Antitrypsin Deficiency? ?
Answer: Alpha-1 antitrypsin (AAT) deficiency occurs in all ethnic groups. However, the condition occurs most often in White people of European descent.
AAT deficiency is an inherited condition. "Inherited" means the condition is passed from parents to children through genes.
If you have bloodline relatives with known AAT deficiency, you're at increased risk for the condition. Even so, it doesn't mean that you'll develop one of the diseases related to the condition.
Some risk factors make it more likely that you'll develop lung disease if you have AAT deficiency. Smoking is the leading risk factor for serious lung disease if you have AAT deficiency. Your risk for lung disease also may go up if you're exposed to dust, fumes, or other toxic substances.
Question: What are the symptoms of Alpha-1 Antitrypsin Deficiency ?
Answer: The first lung-related symptoms of alpha-1 antitrypsin (AAT) deficiency may include shortness of breath, less ability to be physically active, and wheezing. These signs and symptoms most often begin between the ages of 20 and 40.
Other signs and symptoms may include repeated lung infections, tiredness, a rapid heartbeat upon standing, vision problems, and weight loss.
Some people who have severe AAT deficiency develop emphysema (em-fi-SE-ma)often when they're only in their forties or fifties. Signs and symptoms of emphysema include problems breathing, wheezing, and a chronic (ongoing) cough.
At first, many people who have AAT deficiency are diagnosed with asthma. This is because wheezing also is a symptom of asthma. Also, people who have AAT deficiency respond well to asthma medicines.
Question: How to diagnose Alpha-1 Antitrypsin Deficiency ?
Answer: Alpha-1 antitrypsin (AAT) deficiency usually is diagnosed after you develop a lung or liver disease that's related to the condition.
Your doctor may suspect AAT deficiency if you have signs or symptoms of a serious lung condition, especially emphysema, without any obvious cause. He or she also may suspect AAT deficiency if you develop emphysema when you're 45 years old or younger.
Specialists Involved
Many doctors may be involved in the diagnosis of AAT deficiency. These include primary care doctors, pulmonologists (lung specialists), and hepatologists (liver specialists).
To diagnose AAT deficiency, your doctor will:
Ask about possible risk factors. Risk factors include smoking and exposure to dust, fumes, and other toxic substances.
Ask about your medical history. A common sign of AAT deficiency is if you have a lung or liver disease without any obvious causes or risk factors. Another sign is if you have emphysema at an unusually early age (45 years or younger).
Ask about your family's medical history. If you have bloodline relatives who have AAT deficiency, you're more likely to have the condition.
Diagnostic Tests
Your doctor may recommend tests to confirm a diagnosis of AAT deficiency. He or she also may recommend tests to check for lung- or liver-related conditions.
A genetic test is the most certain way to check for AAT deficiency. This test will show whether you have faulty AAT genes.
A blood test also may be used. This test checks the level of AAT protein in your blood. If the level is a lot lower than normal, it's likely that you have AAT deficiency.
Lung-Related Tests
If you have a lung disease related to AAT deficiency, your doctor may recommend lung function tests and high-resolution computed tomography (to-MOG-rah-fee) scanning, also called CT scanning.
Lung function tests measure how much air you can breathe in and out, how fast you can breathe air out, and how well your lungs deliver oxygen to your blood. These tests may show how severe your lung disease is and how well treatment is working.
High-resolution CT scanning uses x rays to create detailed pictures of parts of the body. A CT scan can show whether you have emphysema or another lung disease and how severe it is.
Question: What are the treatments for Alpha-1 Antitrypsin Deficiency ?
Answer: Alpha-1 antitrypsin (AAT) deficiency has no cure, but its related lung diseases have many treatments. Most of these treatments are the same as the ones used for a lung disease called COPD (chronic obstructive pulmonary disease).
If you have symptoms related to AAT deficiency, your doctor may recommend:
Medicines called inhaled bronchodilators (brong-ko-di-LA-tors) and inhaled steroids. These medicines help open your airways and make breathing easier. They also are used to treat asthma and COPD.
Flu and pneumococcal (noo-mo-KOK-al) vaccines to protect you from illnesses that could make your condition worse. Prompt treatment of lung infections also can help protect your lungs.
Pulmonary rehabilitation (rehab). Rehab involves treatment by a team of experts at a special clinic. In rehab, you'll learn how to manage your condition and function at your best.
Extra oxygen, if needed.
A lung transplant. A lung transplant may be an option if you have severe breathing problems. If you have a good chance of surviving the transplant surgery, you may be a candidate for it.
Augmentation (og-men-TA-shun) therapy is a treatment used only for people who have AAT-related lung diseases. This therapy involves getting infusions of the AAT protein. The infusions raise the level of the protein in your blood and lungs.
Not enough research has been done to show how well this therapy works. However, some research suggests that this therapy may slow the development of AAT deficiency in people who don't have severe disease.
People who have AAT deficiency and develop related liver or skin diseases will be referred to doctors who treat those diseases.
Future Treatments
Researchers are working on possible treatments that will target the faulty AAT genes and replace them with healthy genes. These treatments are in the early stages of development.
Researchers also are studying therapies that will help misshapen AAT proteins move from the liver into the bloodstream. They're also studying a type of augmentation therapy in which the AAT protein is inhaled instead of injected into a vein.
If you're interested in new treatments, ask your doctor about ongoing clinical trials for AAT deficiency.
Question: How to prevent Alpha-1 Antitrypsin Deficiency ?
Answer: You can't prevent alpha-1 antitrypsin (AAT) deficiency because the condition is inherited (passed from parents to children through genes).
If you inherit two faulty AAT genes, you'll have AAT deficiency. Even so, you may never develop one of the diseases related to the condition.
You can take steps to prevent or delay lung diseases related to AAT deficiency. One important step is to quit smoking. If you don't smoke, don't start.
Talk with your doctor about programs and products that can help you quit smoking. If you have trouble quitting smoking on your own, consider joining a support group. Many hospitals, workplaces, and community groups offer classes to help people quit smoking.
For more information about how to quit smoking, go to the Health Topics Smoking and Your Heart article and the National Heart, Lung, and Blood Institute's "Your Guide to a Healthy Heart." Although these resources focus on heart health, they include basic information about how to quit smoking.
Also, try to avoid secondhand smoke and places with dust, fumes, or other toxic substances that you may inhale.
Check your living and working spaces for things that may irritate your lungs. Examples include flower and tree pollen, ash, allergens, air pollution, wood burning stoves, paint fumes, and fumes from cleaning products and other household items.
If you have a lung disease related to AAT deficiency, ask your doctor whether you might benefit from augmentation therapy. This is a treatment in which you receive infusions of AAT protein.
Augmentation therapy raises the level of AAT protein in your blood and lungs. (For more information, go to "How Is Alpha-1 Antitrypsin Deficiency Treated?")
Question: What causes Cystic Fibrosis ?
Answer: A defect in the CFTR gene causes cystic fibrosis (CF). This gene makes a protein that controls the movement of salt and water in and out of your body's cells. In people who have CF, the gene makes a protein that doesn't work well. This causes thick, sticky mucus and very salty sweat.
Research suggests that the CFTR protein also affects the body in other ways. This may help explain other symptoms and complications of CF.
More than a thousand known defects can affect the CFTR gene. The type of defect you or your child has may affect the severity of CF. Other genes also may play a role in the severity of the disease.
How Is Cystic Fibrosis Inherited?
Every person inherits two CFTR genesone from each parent. Children who inherit a faulty CFTR gene from each parent will have CF.
Children who inherit one faulty CFTR gene and one normal CFTR gene are "CF carriers." CF carriers usually have no symptoms of CF and live normal lives. However, they can pass the faulty CFTR gene to their children.
The image below shows how two parents who are both CF carriers can pass the faulty CFTR gene to their children.
Example of an Inheritance Pattern for Cystic Fibrosis
Question: Who is at risk for Cystic Fibrosis? ?
Answer: Cystic fibrosis (CF) affects both males and females and people from all racial and ethnic groups. However, the disease is most common among Caucasians of Northern European descent.
CF also is common among Latinos and American Indians, especially the Pueblo and Zuni. The disease is less common among African Americans and Asian Americans.
More than 10 million Americans are carriers of a faulty CF gene. Many of them don't know that they're CF carriers.
Question: How to diagnose Cystic Fibrosis ?
Answer: Doctors diagnose cystic fibrosis (CF) based on the results from various tests.
Newborn Screening
All States screen newborns for CF using a genetic test or a blood test. The genetic test shows whether a newborn has faulty CFTR genes. The blood test shows whether a newborn's pancreas is working properly.
Sweat Test
If a genetic test or blood test suggests CF, a doctor will confirm the diagnosis using a sweat test. This test is the most useful test for diagnosing CF. A sweat test measures the amount of salt in sweat.
For this test, the doctor triggers sweating on a small patch of skin on an arm or leg. He or she rubs the skin with a sweat-producing chemical and then uses an electrode to provide a mild electrical current. This may cause a tingling or warm feeling.
Sweat is collected on a pad or paper and then analyzed. The sweat test usually is done twice. High salt levels confirm a diagnosis of CF.
Other Tests
If you or your child has CF, your doctor may recommend other tests, such as:
Genetic tests to find out what type of CFTR defect is causing your CF.
A chest x ray. This test creates pictures of the structures in your chest, such as your heart, lungs, and blood vessels. A chest x ray can show whether your lungs are inflamed or scarred, or whether they trap air.
A sinus x ray. This test may show signs of sinusitis, a complication of CF.
Lung function tests. These tests measure how much air you can breathe in and out, how fast you can breathe air out, and how well your lungs deliver oxygen to your blood.
A sputum culture. For this test, your doctor will take a sample of your sputum (spit) to see whether bacteria are growing in it. If you have bacteria called mucoid Pseudomonas, you may have more advanced CF that needs aggressive treatment.
Prenatal Screening
If you're pregnant, prenatal genetic tests can show whether your fetus has CF. These tests include amniocentesis (AM-ne-o-sen-TE-sis) and chorionic villus (ko-re-ON-ik VIL-us) sampling (CVS).
In amniocentesis, your doctor inserts a hollow needle through your abdominal wall into your uterus. He or she removes a small amount of fluid from the sac around the baby. The fluid is tested to see whether both of the baby's CFTR genes are normal.
In CVS, your doctor threads a thin tube through the vagina and cervix to the placenta. The doctor removes a tissue sample from the placenta using gentle suction. The sample is tested to see whether the baby has CF.
Cystic Fibrosis Carrier Testing
People who have one normal CFTR gene and one faulty CFTR gene are CF carriers. CF carriers usually have no symptoms of CF and live normal lives. However, carriers can pass faulty CFTR genes on to their children.
If you have a family history of CF or a partner who has CF (or a family history of it) and you're planning a pregnancy, you may want to find out whether you're a CF carrier.
A genetics counselor can test a blood or saliva sample to find out whether you have a faulty CF gene. This type of testing can detect faulty CF genes in 9 out of 10 cases.
Question: What is (are) Peripheral Artery Disease ?
Answer: Peripheral artery disease (P.A.D.) is a disease in which plaque builds up in the arteries that carry blood to your head, organs, and limbs. Plaque is made up of fat, cholesterol, calcium, fibrous tissue, and other substances in the blood.
When plaque builds up in the body's arteries, the condition is called atherosclerosis. Over time, plaque can harden and narrow the arteries. This limits the flow of oxygen-rich blood to your organs and other parts of your body.
P.A.D. usually affects the arteries in the legs, but it also can affect the arteries that carry blood from your heart to your head, arms, kidneys, and stomach. This article focuses on P.A.D. that affects blood flow to the legs.
Normal Artery and Artery With Plaque Buildup
Overview
Blocked blood flow to your legs can cause pain and numbness. It also can raise your risk of getting an infection in the affected limbs. Your body may have a hard time fighting the infection.
If severe enough, blocked blood flow can cause gangrene (tissue death). In very serious cases, this can lead to leg amputation.
If you have leg pain when you walk or climb stairs, talk with your doctor. Sometimes older people think that leg pain is just a symptom of aging. However, the cause of the pain could be P.A.D. Tell your doctor if you're feeling pain in your legs and discuss whether you should be tested for P.A.D.
Smoking is the main risk factor for P.A.D. If you smoke or have a history of smoking, your risk of P.A.D. increases. Other factors, such as age and having certain diseases or conditions, also increase your risk of P.A.D.
Outlook
P.A.D. increases your risk of coronary heart disease, heart attack, stroke, and transient ischemic attack("mini-stroke").Although P.A.D. is serious, it's treatable. If you have the disease, see your doctor regularly and treat the underlying atherosclerosis.P.A.D. treatment may slow or stop disease progress and reduce the risk of complications. Treatments include lifestyle changes, medicines, and surgery or procedures. Researchers continue to explore new therapies for P.A.D.
Question: What causes Peripheral Artery Disease ?
Answer: The most common cause of peripheral arterydisease (P.A.D.) is atherosclerosis. Atherosclerosis is a disease in which plaque builds up in your arteries. The exact cause of atherosclerosis isn't known.
The disease may start if certain factors damage the inner layers of the arteries. These factors include:
Smoking
High amounts of certain fats and cholesterol in the blood
High blood pressure
High amounts of sugar in the blood due to insulin resistance or diabetes
When damage occurs, your body starts a healing process. The healing may cause plaque to build up where the arteries are damaged.
Eventually, a section of plaque can rupture (break open), causing a blood clot to form at the site. The buildup of plaque or blood clots can severely narrow or block the arteries and limit the flow of oxygen-rich blood to your body.