Cholelithiasis involves the presence of gallstones (see the image below), which are concretions that form in the biliary tract, usually in the gallbladder. Choledocholithiasis refers to the presence of 1 or more gallstones in the common bile duct (CBD).

This video shows the heart transplant surgery

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Foramen Magnum Neurofibroma Complete surgical removal.No Deficit

This video is designed for my introductory A&P course to study the endocrine system. This tutorial will take you through the various endocrine organs, hormones produced, and effects at each tissue. Prolactin is one of the 5 hormones we are studying of the anterior pituitary. SHOW MORE

Pulmonary fibrosis is a condition in which the tissue deep in your lungs becomes scarred over time. This tissue gets thick and stiff. That makes it hard for you to catch your breath, and your blood may not get enough oxygen. Causes of pulmonary fibrosis include environmental pollutants, some medicines, some connective tissue diseases, and interstitial lung disease. Interstitial lung disease is the name for a large group of diseases that inflame or scar the lungs. In most cases, the cause cannot be found. This is called idiopathic pulmonary fibrosis

Grape Jelly Abscess on the Butt

Anterior Release Test

A video showing breast examination after breast implants

Watch Spinal Stenosis Videos Spinal stenosis occurs when the spinal cord in the neck (cervical spine) or the spinal nerve roots in the lower back (lumbar spine) are compressed. Symptoms of lumbar stenosis often include leg pain (sciatica) and leg tingling, weakness, or numbness. Arm pain is a typical symptom of cervical spinal stenosis. For cervical spinal stenosis with myelopathy, difficulty with coordination often occurs. Stenosis treatment may include non-surgical options (exercise, anti-inflammatory medication, epidural injections, and activity modification) or back surgery.

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What combines research opportunities, intellectual challenge, and international collaboration in the study of a disease which affects many organs of the body and all sectors of society? And demands that specialists from many different backgrounds work together to crack sometimes intractable problems? It is, of course, oncology. As a career choice, it's demanding; it takes passion coupled with a willingness to put in the hours and to learn how to discuss death honestly and sensitively. But for the right person, it can be immensely rewarding.

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

Throughout the body, there are several points at which blood vessels unite. The junctions are termed anastomoses. In the simplest sense, an anastomosis is any connection (made surgically or occurring naturally) between tube-like structures. Naturally occurring arterial anastomoses provide an alternative blood supply to target areas in cases where the primary arterial pathway is obstructed. They are most abundant in regions of the body where the blood supply may can be easily damaged or blocked (such as the joints or intestines). This article focuses on the arterial anastomotic networks of the upper limb.

This is a surgical video that shows the removal of a volar ganglion cyst. This is a common surgical procedure and this video may help you better understand the steps that occur during the procedure.

A doctor pops a giant cyst on a boy's eye and films the whole thing. As the big cyst pops, puss oozes out.