Pathology notes

Apr 16th, 2015
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DISSEMINATEDINTRAVASCULARCOAGULOPATHYBy Rebecca Lusaka. Acute, sub acute or chronic thrombohemorrhagic disorder. Secondary complication in a variety of diseases. Caused by systemic activation of coagulation pathways leading toformation of thrombi throughout microcirculation. Consequentially theres consumption of platelets & coagulationfactors & secondarily activation of fibrinolysis. Can give rise to either tissue hypoxia & micro infarcts caused by alarge no. of micro thrombi or bleeding disorder related topathologic activation of fibrinolysis & depletion of the elementsrequired for hemostasis ( consumptive coagulopathy)ETIOLOGY & PATHOGENESIS 2 major mechanisms trigger DIC; release of tissue factor & thromboplasticsubstances into circulation. AND widespread endothelial cell damage. Thromboplastic substances can be released into circulation by e.g.placenta in obstetric complications Carcinomas can also produce procoagulant substances Some tumors express tissue factor on cell membrane. In gram-ve & +ve sepsis, endotoxins & exotoxins cause increasedsynthesis, surface expression & release of tissue factor from monocytes Activated monocytes release IL-1 &TNF, which increase expression oftissue factor on endothelial cells and simultaneously decrease expressionof thrombomodulin which activates prot C an anticoagulant. Endothelial damage can unleash procoagulant activity by stimulatingincreased tissue factor expre

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