Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo

Coarctation of the aorta (CoA[1][2] or CoAo), also called aortic narrowing, is a congenital condition whereby the aorta is narrow, usually in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts. The word “coarctation” means narrowing. Coarctations are most common in the aortic arch. The arch may be small in babies with coarctations. Other heart defects may also occur when coarctation is present, typically occurring on the left side of the heart. When a patient has a coarctation, the left ventricle has to work harder. Since the aorta is narrowed, the left ventricle must generate a much higher pressure than normal in order to force enough blood through the aorta to deliver blood to the lower part of the body. If the narrowing is severe enough, the left ventricle may not be strong enough to push blood through the coarctation, thus resulting in lack of blood to the lower half of the body. Physiologically its complete form is manifested as interrupted aortic arch

Why is this medication prescribed? Amiodarone is used to treat and prevent certain types of serious, life-threatening ventricular arrhythmias (a certain type of abnormal heart rhythm when other medications did not help or could not be tolerated. Amiodarone is in a class of medications called antiarrhythmics. It works by relaxing overactive heart muscles. How should this medicine be used? Amiodarone comes as a tablet to take by mouth. It is usually taken once or twice a day. You may take amiodarone either with or without food, but be sure to take it the same way each time.Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take amiodarone exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.

Plantar warts are hard, grainy growths that usually appear on the heels or balls of your feet, areas that feel the most pressure. This pressure also may cause plantar warts to grow inward beneath a hard, thick layer of skin (callus). Plantar warts are caused by the human papillomavirus (HPV). The virus enters your body through tiny cuts, breaks or other weak spots on the bottom of your feet. Most plantar warts aren't a serious health concern and may not require treatment. But plantar warts can cause discomfort or pain. If self-care treatments for plantar warts don't work, you may want to see your doctor to have them removed.

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Fainting occurs when the blood supply to your brain is momentarily inadequate, causing you to lose consciousness. This loss of consciousness is usually brief. Fainting can have no medical significance, or the cause can be a serious disorder. Therefore, treat loss of consciousness as a medical emergency until the signs and symptoms are relieved and the cause is known. Discuss recurrent fainting spells with your doctor. If you feel faint Lie down or sit down. To reduce the chance of fainting again, don't get up too quickly. Place your head between your knees if you sit down. If someone else faints Position the person on his or her back. If the person is breathing, restore blood flow to the brain by raising the person's legs above heart level — about 12 inches (30 centimeters) — if possible. Loosen belts, collars or other constrictive clothing. To reduce the chance of fainting again, don't get the person up too quickly. If the person doesn't regain consciousness within one minute, call 911 or your local emergency number. Check the person's airway to be sure it's clear. Watch for vomiting. Check for signs of circulation (breathing, coughing or movement). If absent, begin CPR. Call 911 or your local emergency number. Continue CPR until help arrives or the person responds and begins to breathe.

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Thalassemia (thal-uh-SEE-me-uh) is an inherited blood disorder characterized by less hemoglobin and fewer red blood cells in your body than normal. Several types of thalassemia exist, including alpha-thalassemia, beta-thalassemia intermedia, Cooley's anemia and Mediterranean anemia. Hemoglobin is the substance in your red blood cells that allows them to carry oxygen. The low hemoglobin and fewer red blood cells of thalassemia may cause anemia, leaving you fatigued. If you have mild thalassemia, you may not need treatment. But, if you have a more severe form of thalassemia, you may need regular blood transfusions. You can also take steps on your own to cope with fatigue, such as choosing a healthy diet and exercising regularly.

Hypothyroidism is a condition in which the body lacks sufficient thyroid hormone. Since the main purpose of thyroid hormone is to "run the body's metabolism," it is understandable that people with this condition will have symptoms associated with a slow metabolism. The estimates vary, but approximately 10 million Americans have this common medical condition. In fact, as many as 10% of women may have some degree of thyroid hormone deficiency. Hypothyroidism is more common than you would believe, and millions of people are currently hypothyroid and don't know it.

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Corticosteroid Injections – Doctors sometimes inject corticosteroids directly into the knee joint for quick relief of pain and inflammation. Their benefits may last anywhere from a few days to more than six months. While the injections bring targeted relief to the joint and lack many of the side effects of oral corticosteroid medications, they are not without risks. Repeated knee injections may actually contribute to cartilage breakdown. For that reason your doctor will likely put a limit on the number of injections you can receive.

AFib is caused by abnormal electrical impulses in the atria, which are the upper chambers of the heart. The result is a rapid and irregular pumping of blood through the atria. These chambers fibrillate, or quiver, rapidly.

Rapid Algorithm Review Ventricular Fibrillation

each type of heart problem requires different treatment but may share similar warning signs. It is important to see your doctor so that you can receive a correct diagnosis and prompt treatment. Learn to recognize the symptoms that may signal heart disease. Call your doctor if you begin to have new symptoms or if they become more frequent or severe. Symptoms of Coronary Artery Disease The most common symptom of coronary artery disease is angina, or chest pain. Angina can be described as a discomfort, heaviness, pressure, aching, burning, fullness, squeezing, or painful feeling in your chest. It can be mistaken for indigestion or heartburn. Angina may also be felt in the shoulders, arms, neck, throat, jaw, or back. Other symptoms of coronary artery disease include: Shortness of breath Palpitations (irregular heart beats, or a "flip-flop" feeling in your chest) A faster heartbeat Weakness or dizziness Nausea Sweating

Lung inflation and pleural membranes anatomy

Sleep apnea is a potentially serious sleep disorder in which breathing repeatedly stops and starts. You may have sleep apnea if you snore loudly, and you feel tired even after a full night's sleep. The main types of sleep apnea are: Obstructive sleep apnea, the more common form that occurs when throat muscles relax. Central sleep apnea, which occurs when your brain doesn't send proper signals to the muscles that control breathing. Complex sleep apnea syndrome, also known as treatment-emergent central sleep apnea, occurs when someone has both obstructive sleep apnea and central sleep apnea. If you think you might have any form of sleep apnea, see your doctor. Treatment can ease your symptoms and may help prevent heart problems and other complications.

Your headache symptoms can help your doctor determine its cause and the appropriate treatment. Most headaches aren't the result of a serious illness, but some may result from a life-threatening condition requiring emergency care. Headaches are generally classified by cause: Primary headaches A primary headache is caused by overactivity of or problems with pain-sensitive structures in your head. A primary headache isn't a symptom of an underlying disease. Chemical activity in your brain, the nerves or blood vessels surrounding your skull, or the muscles of your head and neck (or some combination of these factors) can play a role in primary headaches. Some people may also carry genes that make them more likely to develop such headaches. The most common primary headaches are: Cluster headache Migraine (with and without aura) Tension headache (also known as tension-type headache) Trigeminal autonomic cephalalgia (TAC), such as cluster headache and paroxysmal hemicrania A few headache patterns also are generally considered types of primary headache, but are less common. These headaches have distinct features, such as an unusual duration or pain associated with a certain activity. Although generally considered primary, each could be a symptom of an underlying disease. They include: Chronic daily headaches (for example, chronic migraine, chronic tension-type headache, or hemicranias continua) Cough headaches Exercise headaches Sex headaches Some primary headaches can be triggered by lifestyle factors, including: Alcohol, particularly red wine Certain foods, such as processed meats that contain nitrates Changes in sleep or lack of sleep Poor posture Skipped meals Stress Secondary headaches A secondary headache is a symptom of a disease that can activate the pain-sensitive nerves of the head. Any number of conditions — varying greatly in severity — may cause secondary headaches. Possible causes of secondary headaches include: Acute sinusitis Arterial tears (carotid or vertebral dissections) Blood clot (venous thrombosis) within the brain — separate from stroke Brain aneurysm (a bulge in an artery in your brain) Brain AVM (brain arteriovenous malformation) — an abnormal formation of brain blood vessels Brain tumor Carbon monoxide poisoning Chiari malformation (structural problem at the base of your skull) Concussion Dehydration Dental problems Ear infection (middle ear) Encephalitis (brain inflammation) Giant cell arteritis (inflammation of the lining of the arteries) Glaucoma (acute angle closure glaucoma) Hangovers

Hodgkin lymphoma has characteristics that distinguish it from other diseases classified as lymphoma, including the presence of Reed-Sternberg cells. These are large, cancerous cells found in Hodgkin lymphoma tissues, named for the scientists who first identified them. Hodgkin lymphoma is one of the most curable forms of cancer. NHL represents a diverse group of diseases distinguished by the characteristics of the cancer cells associated with each disease type. Most people with NHL have a B-cell type of NHL (about 85 percent). The others have a T-cell type or an NK-cell type of lymphoma. Some patients with fast-growing NHL can be cured. For patients with slow-growing NHL, treatment may keep the disease in check for many years.

Cobalamin (vitamin B12) deficiency is particularly common in the elderly (>65 years of age), but is often unrecognized because of its subtle clinical manifestations; although they can be potentially serious, particularly from a neuropsychiatric and hematological perspective.

This video: Polycythemia vera (pol-e-sigh-THEE-me-uh VEER-uh) is a slow-growing type of blood cancer in which your bone marrow makes too many red blood cells. Polycythemia vera may also result in production of too many of the other types of blood cells — white blood cells and platelets. These excess cells thicken your blood and cause complications, such as such as a risk of blood clots or bleeding. Polycythemia vera isn't common. It usually develops slowly, and you may have it for years without noticing signs or symptoms. Often, polycythemia vera is found during a blood test done for some other reason. Without treatment, polycythemia vera can be life-threatening. However, with proper medical care, many people experience few problems related to this disease. Over time, there's a risk of progressing to more-serious blood cancers, such as myelofibrosis or acute leukemia.