Blood coagulation plug formation

Primary hemostasis is the first phase of hemostasis consisting of platelet plug formation at the site of injury. It occurs within seconds and stops blood loss from capillaries, arterioles, and venules. Secondary hemostasis, in contrast, requires several minutes to be complete and involves the formation of fibrin through the coagulation cascade. 

Following endothelial injury, vessel-wall response involves vasoconstriction, platelet plug formation, coagulation, and fibrinolysis regulation. In normal circumstances, platelets circulate in the blood in an inactive form. After injury, platelets undergo activation, which consists of (1) adhesion to the subendothelium,... 

Platelets play a role in each of the mechanisms of normal hemostasis vasoconstriction, formation of the platelet plug, and blood coagulation. However, they are also involved in pathological processes that lead to atherosclerosis and thrombosis (formation of a blood clot within the vascular system). Antiplatelet drugs interfere with platelet function and are used to prevent the development of atherosclerosis and formation of arterial thrombi. 

Blood coagulation. The third major step in hemostasis is coagulation, or the formation of a blood clot. This complex process involves a series of reactions that result in formation of a protein fiber meshwork that stabilizes the platelet plug. Three essential steps lead to clotting (see Figure 16.1) ... 

The damage of a blood vessel results in the formation of a hemostatic plug, which is achieved by several differ-entmechanisms including vascular spasm, formation of a platelet plug, blood coagulation, and growth of fibrous tissue into the blood clot. 

Injury to the endothelium and exposure of tissue factor on the subendothelial layer to plasma proteins also activate the blood coagulation cascade, which ultimately activates thrombin and Factor XIII Factor XIII cross-links strands of polymerized fibrin monomers to form a stable clot (the secondary hemostatic plug). The blood coagulation cascade consists of a series of enzymes (such as Factor X), which are inactive until proteolytically cleaved by the preceding enzyme in the cascade. Other proteins (Factor V and Factor VIII) serve as binding proteins, which assemble factor complexes at the site of injury. Ca and y-carboxyglutamate residues in the proteins (formed by a vitamin K-dependent process in the liver) attach the factor complexes to phosphoUpids exposed on platelet membranes. Consequently, thrombus formation is rapidly accelerated and localized to the site of injury. 

Hemostasis is the process that stops bleeding in a blood vessel. Normal hemostasis involves a complex process of extrinsic and intrinsic factors. Figure 44-1 shows the coagulation pathway and factors involved. The copulation cascade is so named because as each factor is activated it acts as a catalyst that enhances the next reaction, with the net result being a large collection of fibrin that forms a plug in the vessel. Fibrin is the insoluble protein that is essential to clot formation. 

Within the intact blood vessel, coagulation factors circulate as inactive zymogens. The formation of a platelet plug to arrest bleeding from a ruptured blood ves-... 

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