The Principles of Laparoscopic Suturing

Clean hands can help prevent the spread of infectious diseases, such as flu. This podcast explains the proper way to wash your hands.

An Echocardiography showing an Acute Pulmonary Embolism

CDC's Dr. Joe Bresee describes how to prevent giving and getting novel H1N1 flu.

This minimally invasive procedure employs two small cuts rather than a long incision before fusing two vertebra together. The result is less pain, as well as quicker recovery. ~ Detroit Medical Center

Endotracheal Intubation Sample Animation

Tummy Tuck Surgery Video

USMLE Step 2 CS - Dysphagia This is just preview video. To get full access please visit our website : www.usmletutoring.com

ROTIGS medical device by Honolulu inventor Dr. Brad NaPier makes difficult airway intubations easier for medical professionals.

Histology of Spinal Cord

Histology of Secretory Endometrium

Surgical Glove Flip How To

Meningeococcal Bacterial Maningitis Introduction

Congestive Heart Failure 3D Animation

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

Prostatitis is an infection or inflammation of the prostate gland that presents as several syndromes with varying clinical features. The term prostatitis is defined as microscopic inflammation of the tissue of the prostate gland and is a diagnosis that spans a broad range of clinical conditions. The National Institutes of Health (NIH) has recognized and defined a classification system for prostatitis in 1999.[1] The 4 syndromes of prostatitis are as follows: I - Acute bacterial prostatitis II - Chronic bacterial prostatitis III - Chronic prostatitis and chronic pelvic pain syndrome (CPPS; further classified as inflammatory or noninflammatory) IV - Asymptomatic inflammatory prostatitis

IV Dose Calculations

Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Vitamin D promotes the absorption of calcium and phosphorus from the gastrointestinal tract. A deficiency of vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets. Adding vitamin D or calcium to the diet generally corrects the bone problems associated with rickets. When rickets are due to another underlying medical problem, your child may need additional medications or other treatment. Some skeletal deformities caused by rickets may require corrective surgery.

The most frequent incision utilized to open the abdomen for liver surgery is called a chevron incision. In this incision a cut is made on the abdomen below the rib cage. The cut starts under the armpit below the ribs on the right side of the abdomen and continues all the way across the abdomen to the opposite arm pit thereby the whole width of the abdomen is cut to provide access to the liver. The average length of the incision is approximately 24 to 30 inches. This is one of the longest incisions is utilized in abdominal surgery. The incision is frequently associated with significant discomfort after the surgery and in some patients the discomfort can continue for many months, particularly when some of the nerves in the abdominal wall have been cut during the surgery. Laparoscopic surgery provides advantages over open surgery for the liver since the chevron incision is completely avoided and the surgery is performed through tiny incisions. As a consequence the duration of stay in hospital, the amount and duration of post operative discomfort, and the length of recovery is much shorter after the laparoscopic procedure compared to open surgery

Absence of a woman's monthly menstrual period is called amenorrhea. Secondary amenorrhea is when a woman who has been having normal menstrual cycles stops getting her periods for 6 months or longer. Causes Secondary amenorrhea can occur due to natural changes in the body. For example, the most common cause of secondary amenorrhea is pregnancy. Breastfeeding and menopause are also common, but natural, causes. Women who take birth control pills or who receive hormone shots such as Depo-Provera may not have any monthly bleeding. When they stop taking these hormones, their periods may not return for more than 6 months. You are more likely to have absent periods if you: Are obese Exercise too much and for long periods of time Have very low body fat (less than 15 to 17%) Have severe anxiety or emotional distress Lose a lot of weight suddenly (for example, from strict or extreme diets or after gastric bypass surgery) Other causes include: Brain (pituitary) tumors Drugs for cancer treatment Drugs to treat schizophrenia or psychosis Overactive thyroid gland Polycystic ovarian syndrome Reduced function of the ovaries