Info

reaction

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

Was this article helpful?

0 0

Post a comment