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This is how Paraumbilical hernia looks like and how it is examined although it looks very simple but in exam it can be very difficult to perform all steps in small amount of time. This can be short case or even long of #cpsp #fcps #mbbs #medicalstudent #mbbsexams #plab2 #plab #plab1 and MS #genernalknowledge #surgery exams

#para-umbilical hernia
#umbilical hernia #paraumbilical #hernia repair#laparoscopic paraumbilical hernia repair. #umbilical defect, #vetral hernia surgery. #herniatreatment #herniatreatment #ventral hernia hernia,#laparoscopic ventral hernia repair,umbilicus,carl lowe jr,hernia repair,training,north carolina,hernia repair surgery,charlotte,operation,laparoscopic,bulge,surgery,surgeon,dr. lowe,ipom repair,live surgery,mesh,
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Most babies will move into delivery position a few weeks prior to birth, with the head moving closer to the birth canal. When this fails to happen, the baby’s buttocks and/or feet will be positioned to be delivered first. This is referred to as “breech presentation.”

Triplet C-section

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Watch that video to know the Female Genital Infections Causes and treatments.

Volar Slab Splint for Forearm and Wrist Fractures and Sprains

Labia minoraplasty is an elective procedure that can reduce the size and reshape the inner vaginal lips. Large or asymmetrical labia minora can leave you feeling self-conscience in tight clothing or during intimacy. Long labia may result in rubbing, irritation or discomfort during intercourse and exercise. Certain skin conditions can cause increased sensitivity or tearing of the labia minora. In some cases, the labia minora may be fused with tissue in the labia majora and require medical correction.

Part 1: from Loyola Medical School, Chicago showing clinical examination of the neurological system.

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An untreated hepatic abscess is nearly uniformly fatal as a result of complications that include sepsis, empyema, or peritonitis from rupture into the pleural or peritoneal spaces, and retroperitoneal extension. Treatment should include drainage, either percutaneous or surgical. Antibiotic therapy as a sole treatment modality is not routinely advocated, though it has been successful in a few reported cases. It may be the only alternative in patients too ill to undergo invasive procedures or in those with multiple abscesses not amenable to percutaneous or surgical drainage. In these instances, patients are likely to require many months of antimicrobial therapy with serial imaging and close monitoring for associated complications.

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Mouth ulcers are sores that appear in the mouth, often on the inside of the cheeks. Mouth ulcers, also known as aphthous ulcers, can be painful when eating, drinking or brushing teeth. Occasional mouth ulcers are usually harmless and clear up on their own. Seek medical advice if they last longer than 3 weeks or keep coming back. Mouth ulcers cannot be caught from someone else. Up to 1 in 5 people get recurrent mouth ulcers.

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

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Lysis of E. Coli bacteria with penicillin

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.