Medical/Science Study World

  Sulfhemoglobin:      What is SulfHb? SulfHb is a rare complication of exposure of heme groups to sulfur.  A rare abnormal form of hemoglobin   that can't carry oxygen. It causes the irreversible bonding of sulfur to the heme moiety, with resultant cyanosis as SulfHb does not bind oxygen. The clinical presentation is similar to that of MetHb, but it does not respond to treatment with methylene blue or ascorbic acid. It may result from certain medicines such as dapsone, metoclopramide, nitrates or sulfonamides.      How do you get sulfhemoglobinemia ? Sulfhemoglobinemia is caused by   excessive exposure to sulphur-containing compounds , like medications that contain sulfonamides (such as sumatriptan or furosemide), nitrate fertilizer, or the overconsumption of nitrogenous vegetables like spinach (usually only in infants)    

 Screening coagulation tests for Bleeding Time  Definition A bleeding time test determines how quickly your blood clots to stop bleeding. The test involves making small punctures in your skin. The test is a basic assessment of how well your blood platelets work to form clots. Platelets are tiny cell fragments that circulate in your blood. They’re the first cells to react to a blood vessel injury. They seal off the wound to prevent more blood from escaping. Determination of bleeding time recognizes vascular defect and platelet disorder . The latter is further confirmed through other tests described later. Prolonged bleeding time is generally found with thrombocytopaenia (platelet count <50000 platelets/ µL ) and where there is a platelet dysfunction. In case of von Willebrand’s disease, which is caused by a platelet defect combined with factor VIII deficiency, bleeding time is high with a normal platelet count. Normal Range Duke Method :  1 to  5  minutes. Ivy Method    :  5

Extrinsic and intrinsic pathways: Two partially independent pathways were identified in 1960s for the triggering of a blood clot: The extrinsic pathway   is a rapid clotting system activated when blood vessels are ruptured and tissues are damaged.   The intrinsic pathway   is activated when the inner walls of blood vessels become damaged or irregular. Damaged tissue triggers the extrinsic pathway, which initiates blood clotting by the release of thromboplastin, known in this form as tissue factor. (A somewhat different form of thromboplastin is at work at the site of ruptured vessels, triggered by the disintegration of platelets). Tissue factor combines with a mixture of enzymes and the phospholipids from damaged cell membranes released by the injured tissue to produce a substance called pro-thrombin activator. At this point, the extrinsic system merges with the intrinsic system to activate yet another mechanism (called the common pathway) that actually produces the clot. The

Definition Clotting factors are circulating plasma proteins. The final coagulation product, the clot, results from the interaction of clotting factors through an enzymatic cascade. In vivo, many of these interactions take place on lipid surfaces, the most abundant of which are provided by platelets. In contrast, in vitro, the cascade can be dissected into three pathways: intrinsic, extrinsic, and common. Although to some extent artificial, this distinction remains useful for performing and understanding the tests of coagulation. For instance, PT reflects the extrinsic and common pathway, whereas PTT reflects the intrinsic and common pathway. Fibrinogen, the penultimate step in the generation of clots, is the target of the common pathway, being changed by   thrombin   into fibrin; finally, fibrin is consolidated by factor XIII to generate a stable clot, essential for achieving hemostasis through clotting. (Primary hemostasis through activation of platelets and the von Willebrand factor