Coagulation is a complex network of interactions involving vessels, platelets, and factors. The ability to form and to remove a clot is truly a system dependent on many synergistic forces. Hemostasis depends on a system of checks and balances between thrombosis and hemorrhage that includes both procoagulants and anticoagulants. This scale needs to be kept in balance. Thrombosis is an activation of the hemostatic system at an inappropriate time in a vessel. Thrombi formed in this fashion are pathologic and beyond the normal hemostatic mechanism. If physiological anticoagulants are decreased in the circulation there will be a clot. If procoagulants or clotting factors are decreased, the scale will tip toward bleeding. Hemorrhage or excessive bleeding may be due to blood vessel disease, rupture, platelet abnormalities, and acquired or congenital abnormalities. Hemostasis is comprised of the vascular system, platelets, and a series of enzymatic reactions of the coagulation factors. The role of hemostasis is to arrest bleeding from a vessel wall defect, while at the same time maintaining fluidity within circulation. Under physiological conditions, fluidity is maintained by the anticoagulant, profibrinolytic, and antiplatelet properties of the normal endothelium.3
Coagulation is divided into two major systems: the primary and secondary systems of hemostasis. The pri-
mary system comprises platelet function and vasoconstriction. The secondary system involves coagulation proteins and a series of enzymatic reactions. Once the coagulation proteins become involved, fibrin is formed and this reinforces platelet plug formation until healing is complete. The product of the coagulation cascade is the conversion of soluble fibrinogen into an insoluble fibrin clot. This is accomplished by the action of a powerful coagulant, thrombin. Thrombin is formed by a precursor circulating protein, prothrombin. Dissolution of the platelet plug is achieved by the fibrinolytic process.
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