Graft versus host disease
• Excessive generation of thrombin is triggered by thromboplastin release (endothelial cells, placenta, leukemic cells [promyelocytes or monoblasts], tumors).
• Simultaneous enzymatic conversion of fibrinogen to fibrin occurs.
• Plasmin generation simultaneously degrades fibrinogen/fibrin into FDPs; excess FDPs are formed.
• FDPs have affinity for fibrin monomers but fail to polymerize properly; excess FDPs have an anticoagulant effect.
• Plasmin causes inactivation of factors V VIII, XI, and XII.
• Hemorrhage occurs as soluble fibrin monomers are formed; platelets are inactivated and clotting factors are inactivated as both are coated by the soluble monomers.
• Clots that are formed are not stable.
Although the body attempts to minimize damage once a DIC event occurs, the physiological inhibitors protein C, protein S, and thrombomodulin are each inactivated. A disorder related to DIC is primary fibri-nolysis: activation of plasmin within the circulation by sources other than thrombin activation. In this rare condition, plasmin acts on fibrinogen and fibrin indiscriminately, therefore hemorrhage is inevitable. Since
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