Coagulation platelet plug

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,... 

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-... 

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) ... 

Hemostasis begins with the formation of the platelet plug, followed by activation of the clotting cascade, and propagation of the clot. One of the major multicomponent complexes in the coagulation cascade consists of activated factor IX (factor IXa) as the protease, activated factor VIII (factor Villa), calcium, and phospholipids as the cofactors, and factor X as the substrate. Factor IXa can be generated by either factor Xa activation of the intrinsic pathway or by the tissue factor/factor Vila complex. 

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. 

Formation of fibrin (coagulation), which stabilises the platelet plug... 

In addition to their role in coagulation, platelets are of the utmost importance in the hemostatic and thrombotic processes. The structure of an arterial thrombus resembles that of a hemostatic platelet plug. 

Physical trauma to the vascular system, such as a puncture or cut, initiates a complex series of interactions between platelets, endothelial cells, and the coagulation cascade. This results in the formation of a platelet-fibrin plug. The creation of an unwanted thrombus involves many of the same steps, except that the triggering stimulus is a pathologic condition in the vascular system rather than physical trauma. 

Role of fibrin Local stimulation of the coagulation cascade by factors released from the injured tissue and platelets results in the formation of thrombin (Factor II). In turn, thrombin, a serine protease, catalyzes the conversion of fibrinogen to fibrin, which is incorporated into the plug. Subsequent cross-linking of the fibrin strands stabilizes the clot and forms a hemostatic plug. 

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