Shekswess/llama3_medquad_instruct_dataset huggingface dataset:
Question: What are the symptoms of Thrombotic Thrombocytopenic Purpura ?
Answer: Blood clots, a low platelet count, and damaged red blood cells cause the signs and symptoms of thrombotic thrombocytopenic purpura (TTP).
                
The signs and symptoms include:
                
Purplish bruises on the skin or mucous membranes (such as in the mouth). These bruises, called purpura, are caused by bleeding under the skin.
                
Pinpoint-sized red or purple dots on the skin. These dots, called petechiae, often are found in groups and may look like a rash. Bleeding under the skin causes petechiae.
                
Paleness or jaundice (a yellowish color of the skin or whites of the eyes).
                
Fatigue (feeling very tired and weak).
                
Fever.
                
A fast heart rate or shortness of breath.
                
Headache, speech changes, confusion, coma, stroke, or seizure.
                
A low amount of urine, or protein or blood in the urine.
                
If you've had TTP and have any of these signs or symptoms, you may be having a relapse (flareup). Ask your doctor when to call him or her or seek emergency care.
Question: What are the treatments for Thrombotic Thrombocytopenic Purpura ?
Answer: Thrombotic thrombocytopenic purpura (TTP) can be fatal or cause lasting damage, such as brain damage or a stroke, if it's not treated right away.
                
In most cases, TTP occurs suddenly and lasts for days or weeks, but it can go on for months. Relapses (flareups) can occur in up to 60 percent of people who have acquired TTP. Flareups also occur in most people who have inherited TTP.
                
Plasma treatments are the most common way to treat TTP. Other treatments include medicines and surgery. Treatments are done in a hospital.
                
Plasma Therapy
                
Plasma is the liquid part of your blood. It carries blood cells, hormones, enzymes, and nutrients to your body.
                
TTP is treated with plasma therapy. This includes:
                
Fresh frozen plasma for people who have inherited TTP
                
Plasma exchange for people who have acquired TTP
                
Plasma therapy is started in the hospital as soon as TTP is diagnosed or suspected.
                
For inherited TTP, fresh frozen plasma is given through an intravenous (IV) line inserted into a vein. This is done to replace the missing or changed ADAMTS13 enzyme.
                
Plasma exchange (also called plasmapheresis) is used to treat acquired TTP. This is a lifesaving procedure. It removes antibodies (proteins) from the blood that damage your ADAMTS13 enzyme. Plasma exchange also replaces the ADAMTS13 enzyme.
                
If plasma exchange isn't available, you may be given fresh frozen plasma until it is available.
                
During plasma exchange, an IV needle or tube is placed in a vein in your arm to remove blood. The blood goes through a cell separator, which removes plasma from the blood. The nonplasma part of the blood is saved, and donated plasma is added to it.
                
Then, the blood is put back into you through an IV line inserted into one of your blood vessels. The time required to complete the procedure varies, but it often takes about 2hours.
                
Treatments of fresh frozen plasma or plasma exchange usually continue until your blood tests results and signs and symptoms improve. This can take days or weeks, depending on your condition. You'll stay in the hospital while you recover.
                
Some people who recover from TTP have flareups. This can happen in the hospital or after you go home. If you have a flareup, your doctor will restart plasma therapy.
                
Other Treatments
                
Other treatments are used if plasma therapy doesn't work well or if flareups occur often.
                
For acquired TTP, medicines can slow or stop antibodies to the ADAMTS13 enzyme from forming. Medicines used to treat TTP include glucocorticoids, vincristine, rituximab, and cyclosporine A.
                
Sometimes surgery to remove the spleen (an organ in the abdomen) is needed. This is because cells in the spleen make the antibodies that block ADAMTS13 enzyme activity.
Question: How to prevent Thrombotic Thrombocytopenic Purpura ?
Answer: Both inherited and acquired thrombotic thrombocytopenic purpura (TTP) occur suddenly with no clear cause. You can't prevent either type.
                
If you've had TTP, watch for signs and symptoms of a relapse (flareup). (For more information, go to "Living With Thrombotic Thrombocytopenic Purpura.")
                
Ask your doctor about factors that may trigger TTP or a flareup, including:
                
Some diseases or conditions, such as pregnancy, cancer, HIV, lupus, or infections.
                
Some medical procedures, such as surgery and blood and marrow stem cell transplant.
                
Some medicines, such as ticlopidine, clopidogrel, cyclosporine A, chemotherapy, and hormone therapy and estrogens. If you take any of these medicines, your doctor may prescribe a different medicine.
                
Quinine, which is a substance often found in tonic water and nutritional health products.
Question: What causes Atherosclerosis ?
Answer: The exact cause of atherosclerosis isn't known. However, studies show that atherosclerosis is a slow, complex disease that may start in childhood. It develops faster as you age.
                
Atherosclerosis may start when 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
                
Plaque may begin to build up where the arteries are damaged. Over time, plaque hardens and narrows the arteries. Eventually, an area of plaque can rupture (break open).
                
When this happens, blood cell fragments called platelets (PLATE-lets) stick to the site of the injury. They may clump together to form blood clots. Clots narrow the arteries even more, limiting the flow of oxygen-rich blood to your body.
                
Depending on which arteries are affected, blood clots can worsen angina (chest pain) or cause a heart attack or stroke.
                
Researchers continue to look for the causes of atherosclerosis. They hope to find answers to questions such as:
                
Why and how do the arteries become damaged?
                
How does plaque develop and change over time?
                
Why does plaque rupture and lead to blood clots?
Question: How to prevent Atherosclerosis ?
Answer: Taking action to control your risk factors can help prevent or delay atherosclerosis and its related diseases. Your risk for atherosclerosis increases with the number of risk factors youhave.
                
One step you can take is to adopt a healthy lifestyle, which can include:
                
Heart-Healthy Eating. Adopt heart-healthy eating habits, which include eating different fruits and vegetables (including beans and peas), whole grains, lean meats, poultry without skin, seafood, and fat-free or low-fat milk and dairy products. A heart-healthy diet is low in sodium, added sugar, solid fats, and refined grains. Following a heart-healthy diet is an important part of a healthy lifestyle.
                
Physical Activity. Be as physically active as you can. Physical activity can improve your fitness level and your health. Ask your doctor what types and amounts of activity are safe for you. Read more about Physical Activity and Your Heart.
                
Quit Smoking. If you smoke, quit. Smoking can damage and tighten blood vessels and raise your risk for atherosclerosis. Talk with your doctor about programs and products that can help you quit. Also, try to avoid secondhand smoke. Read more about Smoking and Your Heart.
                
Weight Control. If youre overweight or obese, work with your doctor to create a reasonable weight-loss plan. Controlling your weight helps you control risk factors foratherosclerosis.
                
Other steps that can prevent or delay atherosclerosis include knowing your family history of atherosclerosis. If you or someone in your family has an atherosclerosis-related disease, be sure to tell your doctor.
                
If lifestyle changes arent enough, your doctor may prescribe medicines to control your atherosclerosis risk factors. Take all of your medicines as your doctor advises.
Question: What causes Sickle Cell Disease ?
Answer: Abnormal hemoglobin, called hemoglobin S, causes sickle cell disease (SCD).
                
The problem in hemoglobin S is caused by a small defect in the gene that directs the production of the beta globin part of hemoglobin. This small defect in the beta globin gene causes a problem in the beta globin part of hemoglobin, changing the way that hemoglobin works. (See Overview.)
                

                
How Is Sickle Cell Disease Inherited?
                
When the hemoglobin S gene is inherited from only one parent and a normal hemoglobin gene is inherited from the other, a person will have sickle cell trait. People with sickle cell trait are generally healthy.
                
Only rarely do people with sickle cell trait have complications similar to those seen in people with SCD. But people with sickle cell trait are carriers of a defective hemoglobin S gene. So, they can pass it on when they have a child.
                
If the childs other parent also has sickle cell trait or another abnormal hemoglobin gene (like thalassemia, hemoglobin C, hemoglobin D, hemoglobin E), that child has a chance of having SCD.
                
Example of an Inheritance Pattern
                

                
In the image above, each parent has one hemoglobin A gene and one hemoglobin S gene, and each of their children has:
                
A 25 percent chance of inheriting two normal genes: In this case the child does not have sickle cell trait or disease. (Case 1)
                
A 50 percent chance of inheriting one hemoglobin A gene and one hemoglobin S gene: This child has sickle cell trait. (Cases 2 and 3)
                
A 25 percent chance of inheriting two hemoglobin S genes: This child has sickle cell disease. (Case 4)
                
It is important to keep in mind that each time this couple has a child, the chances of that child having sickle cell disease remain the same. In other words, if the first-born child has sickle cell disease, there is still a 25 percent chance that the second child will also have the disease. Both boys and girls can inherit sickle cell trait, sickle cell disease, or normal hemoglobin.
                
If a person wants to know if he or she carries a sickle hemoglobin gene, a doctor can order a blood test to find out.
Question: Who is at risk for Sickle Cell Disease? ?
Answer: In the United States, most people with sickle cell disease (SCD) are of African ancestry or identify themselves as black.
                
About 1 in 13 African American babies is born with sickle cell trait.
                
About 1 in every 365 black children is born with sickle cell disease.
                
There are also many people with this disease who come from Hispanic, southern European, Middle Eastern, or Asian Indian backgrounds.
                
Approximately 100,000 Americans have SCD.
Question: How to diagnose Sickle Cell Disease ?
Answer: Screening Tests
                
People who do not know whether they make sickle hemoglobin (hemoglobin S) or another abnormal hemoglobin (such as C,  thalassemia, E) can find out by having their blood tested. This way, they can learn whether they carry a gene (i.e., have the trait) for an abnormal hemoglobin that they could pass on to a child.
                
When each parent has this information, he or she can be better informed about the chances of having a child with some type of sickle cell disease (SCD), such as hemoglobin SS, SC, S thalassemia, or others.
                
Newborn Screening
                
When a child has SCD, it is very important to diagnose it early to better prevent complications.
                
Every state in the United States, the District of Columbia, and the U.S. territories require that every baby is tested for SCD as part of a newborn screening program.
                
In newborn screening programs, blood from a heel prick is collected in spots on a special paper. The hemoglobin from this blood is then analyzed in special labs.
                
Newborn screening results are sent to the doctor who ordered the test and to the childs primary doctor.
                
If a baby is found to have SCD, health providers from a special follow-up newborn screening group contact the family directly to make sure that the parents know the results. The child is always retested to be sure that the diagnosis is correct.
                
Newborn screening programs also find out whether the baby has an abnormal hemoglobin trait. If so, parents are informed, and counseling is offered.
                
Remember that when a child has sickle cell trait or SCD, a future sibling, or the childs own future child, may be at risk. These possibilities should be discussed with the primary care doctor, a blood specialist called a hematologist, and/or a genetics counselor.
                
Prenatal Screening
                
Doctors can also diagnose SCD before a baby is born. This is done using a sample of amniotic fluid, the liquid in the sac surrounding a growing embryo, or tissue taken from the placenta, the organ that attaches the umbilical cord to the mothers womb.
                
Testing before birth can be done as early as 810 weeks into the pregnancy. This testing looks for the sickle hemoglobin gene rather than the abnormal hemoglobin.
Question: How to prevent Sickle Cell Disease ?
Answer: People who do not know whether they carry an abnormal hemoglobin gene can ask their doctor to have their blood tested.
                
Couples who are planning to have children and know that they are at risk of having a child with sickle cell disease (SCD) may want to meet with a genetics counselor. A genetics counselor can answer questions about the risk and explain the choices that are available.
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.