Platelet plug

Haemostasis is the mechanism activated after damage to the blood vessel wall that ensures that blood loss is restricted. Blood platelets are are activated and adhere to elements on the damaged lumenal surface of the vessel, eventually forming a platelet plug that stops the leakage of blood. Fibrinolytic mechanisms later produce lysis of the platelet mass when repair of the vessel has occurred. 

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. 

The red thrombus consists primarily of red cells and fibrin. It morphologically resembles the clot formed in a test tube and may form in vivo in areas of retarded blood flow or stasis (eg, veins) with or without vascular injury, or it may form at a site of injury or in an abnormal vessel in conjunction with an initiating platelet plug. 

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-... 

Enzyme systems produce prostaglandins these are substances involved with formation of platelet plugs as well as limitation of clot growth. 

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. 

Blood normally is maintained in the fluid state so that nutrients can be delivered to the various tissues of the body. When the integrity of the vascular system has been compromised, it becomes necessary for the blood to clot. As shown in Figure I, the initial response to a break in the continuity of the vasculature is the formation of the platelet plug. Platelets in the flowing blood rapidly adhere to the exposed... 

During platelet plug formation, the fibrinolytic pathway is locally activated. Plasminogen is enzymatically processed to plasmin (fibri-nolysin) by plasminogen activators present in the tissue. Plasmin interferes in clot propagation and dissolves the fibrin network as wounds heal. At present, a number of fibrinolytic enzymes are available for treatment of myocardial infarctions or pulmonary emboli (see p. 201). 

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. 

Few seconds later more platelets are deposited on the collagen fibrils and the platelets are now also sticking to each other (platelet aggregation). A growing platelet plug is formed in the lesion of the vessel wall as more platelets aggregate. At a certain stage in diis process, red blood cells are no... 

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