TAILIEUCHUNG - Chapter 110. Coagulation Disorders (Part 8)

The central mechanism of DIC is the uncontrolled generation of thrombin by exposure of the blood to pathologic levels of tissue factor (Fig. 110-3). Simultaneous suppression of physiologic anticoagulant mechanisms and abnormal fibrinolysis further accelerate the process. Together these abnormalities contribute to systemic fibrin deposition in small and mid-sized vessels. The duration and intensity of the fibrin deposition can compromise the blood supply of many organs, especially the lung, kidney, liver, and brain, with consequent organ failure. The sustained activation of coagulation results in consumption of clotting factors and platelets, which in turn leads to systemic bleeding. This is. | Chapter 110. Coagulation Disorders Part 8 The central mechanism of DIC is the uncontrolled generation of thrombin by exposure of the blood to pathologic levels of tissue factor Fig. 110-3 . Simultaneous suppression of physiologic anticoagulant mechanisms and abnormal fibrinolysis further accelerate the process. Together these abnormalities contribute to systemic fibrin deposition in small and mid-sized vessels. The duration and intensity of the fibrin deposition can compromise the blood supply of many organs especially the lung kidney liver and brain with consequent organ failure. The sustained activation of coagulation results in consumption of clotting factors and platelets which in turn leads to systemic bleeding. This is further aggravated by secondary hyperfibrinolysis. Studies in animals demonstrate that the fibrinolytic system is indeed suppressed at the time of maximal activation of coagulation. Interestingly in patients with APL a severe hyperfibrinolytic state often occurs in addition to the coagulation activation. The release of several proinflammatory cytokines such as interleukin 6 and tumor necrosis factor a play central roles in mediating the coagulation defects in DIC and symptoms associated with systemic inflammatory response syndrome. Figure 110-3 The pathophysiology of disseminated intravascular coagulation DIC . Interactions between coagulation and fibrinolytic pathways result in bleeding and thrombosis in the microcirculation in patients with DIC. Clinical manifestations of DIC are related to the magnitude of the imbalance of hemostasis to the underlying disease or to both. The most common findings are bleeding ranging from oozing from venipuncture sites petechiae and ecchymoses to severe hemorrhage from the gastrointestinal tract or lung or into the central nervous system. In chronic DIC the bleeding symptoms are discreet and restricted to skin or mucosal surfaces. The hypercoagulability of DIC manifests as the occlusion of vessels in the .

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