Hemostasis 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. 

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. 

Platelet participation in normal hemostasis. The hemostatic plug is the specific response to external vessel lesion and depends on the extent of vessel wall damage, the specific interaction between endothelial cells and activated platelets, release of the contents of platelets intracellular granules in response to activation, the conjoint activity of activated factor Vll and platelet agonists, and the open conditions of blood flow. After activation, platelets also produce the external ization of membrane phosphatidylserine through the flip-flop mechanism that will support the function of the prothrombinase complex ending in thrombin generation and local clot formation. 

Several hematologists are of the view that the primary step in hemostasis is the adhesion of platelets to exposed collagen fibers. " It has been proposed that the adhesion is due to the formation of an enzyme-acceptor complex between the incomplete carbohydrate chains (galactosyl residues) of collagen and an enzyme of the platelet membrane (glycosyl transferase). Platelets in contact with collagen fibers contract and release adenosine diphosphate (ADP) as well as other platelet constituents. ADP causes more platelets to adhere and the autocatalytic reaction proceeds towards the formation of a hemostatic plug. 

Hemostasis in small capillaries is particularly intriguing. It can no longer be explained by capillary constriction or platelet formation. No capillary plugs are observed. 

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