Heat stroke

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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