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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
A vaginoplasty is a surgical procedure that tightens the vagina. This is done by removing excess vaginal lining and tightening the surrounding soft tissues and muscles. During delivery of a baby the vagina and surrounding tissues and muscles become stretched. After delivery the vagina may return to a more “normal” size, but it often fails to return to its’ pre pregnancy diameter. Generally, the more vaginal deliveries, the worse the condition gets. Many women will complain of decreased sensation and sexual satisfaction during intercourse. Commonly this is due to a lack of friction. Often their partner may notice a change although he may say nothing. Kegel exercises are often recommended but rarely succeed in restoring vaginal tightness.
An excellent video demonstrating how a laparoscopy is performed to evaluate the uterus (note a small fibroid appearing as a bulge in the uterus), fallopian tubes and ovaries. Blue dye is injected into the uterus, entering the fallopian tubes and spilling from the end of the tubes into the abdominal cavity, confirming that both tubes are open
High blood pressure is a common condition in which the long-term force of the blood against your artery walls is high enough that it may eventually cause health problems, such as heart disease. Blood pressure is determined both by the amount of blood your heart pumps and the amount of resistance to blood flow in your arteries. The more blood your heart pumps and the narrower your arteries, the higher your blood pressure. You can have high blood pressure (hypertension) for years without any symptoms. Even without symptoms, damage to blood vessels and your heart continues and can be detected. Uncontrolled high blood pressure increases your risk of serious health problems, including heart attack and stroke. High blood pressure generally develops over many years, and it affects nearly everyone eventually. Fortunately, high blood pressure can be easily detected. And once you know you have high blood pressure, you can work with your doctor to control it.
Calcium channel blockers prevent calcium from entering cells of the heart and blood vessel walls, resulting in lower blood pressure. Calcium channel blockers, also called calcium antagonists, relax and widen blood vessels by affecting the muscle cells in the arterial walls. Some calcium channel blockers have the added benefit of slowing your heart rate, which can further reduce blood pressure, relieve chest pain (angina) and control an irregular heartbeat. Examples of calcium channel blockers Some calcium channel blockers are available in short-acting and long-acting forms. Short-acting medications work quickly, but their effects last only a few hours. Long-acting medications are slowly released to provide a longer lasting effect. Several calcium channel blockers are available. Which one is best for you depends on your health and the condition being treated. Examples of calcium channel blockers include: Amlodipine (Norvasc) Diltiazem (Cardizem, Tiazac, others) Felodipine Isradipine Nicardipine Nifedipine (Adalat CC, Afeditab CR, Procardia) Nisoldipine (Sular) Verapamil (Calan, Verelan) In some cases, your doctor might prescribe a calcium channel blocker with other high blood pressure medications or with cholesterol-lowering drugs such as statins.
Acute kidney injury is common entity in medical practice. The present definition is based on a serum creatinine rise of more 0.3 mg/dl in 48 hours or less, a 50% increase from the baseline over a period of 07 days or a urine output of less than 0.5 ml/kg/hour for more than 06 hours. The main causes of acute kidney injury may be classified into pre renal, intrinsic or post renal causes. Rapid diagnosis and prompt treatment is essential to prevent mortality or morbidity. This presentation discusses in detail the causes of all three mechanisms, pre-renal, post renal and intrinsic.
How Does a Bone Heal? All broken bones go through the same healing process. This is true whether a bone has been cut as part of a surgical procedure or fractured through an injury. The bone healing process has three overlapping stages: inflammation, bone production and bone remodeling. Inflammation starts immediately after the bone is fractured and lasts for several days. When the bone is fractured, there is bleeding into the area, leading to inflammation and clotting of blood at the fracture site. This provides the initial structural stability and framework for producing new bone. Diagram of inflammation in a fractured bone Bone production begins when the clotted blood formed by inflammation is replaced with fibrous tissue and cartilage (known as soft callus). As healing progresses, the soft callus is replaced with hard bone (known as hard callus), which is visible on x-rays several weeks after the fracture. Bone remodeling, the final phase of bone healing, goes on for several months. In remodeling, bone continues to form and becomes compact, returning to its original shape. In addition, blood circulation in the area improves. Once adequate bone healing has occurred, weightbearing (such as standing or walking) encourages bone remodeling.
Vasectomy is a minor surgical procedure wherein the vasa deferentia of a man are severed, and then tied or sealed in a manner such to prevent sperm from entering the seminal stream (ejaculate). Typically done in an outpatient setting, a traditional vasectomy involves numbing (local anesthetic) of the scrotum after which 1 (or 2) small incisions are made, allowing a surgeon to gain access to the vas deferens.