Platelets normal hemostasis

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. 

Normal hemostasis is a balance between excessive and inadequate blood clotting. Overactive blood clotting is harmful because of the tendency for thrombus formation and occlusion of arteries and veins. Vessels may become directly blocked by the thrombus, or a portion of the thrombus may break off and create an embolism that lodges elsewhere in the vascular system. The tendency for excessive thrombus formation in the venous system is usually treated with anticoagulant drugs such as heparin and warfarin. Platelet inhibitors such as aspirin help prevent arterial thrombogenesis. Thrombolytic drugs (streptokinase, t-PA) that facilitate the dissolution of harmful clots may successfully reopen... 

The platelet is central to normal hemostasis and to all thromboembolic disease. A white thrombus forms initially in high-pressure arteries by adherence of circulating platelets to areas of abnormal endothelium as described above. The growing thrombus of aggregated platelets reduces arterial flow. This localized stasis triggers fibrin formation, and a red thrombus forms around the nidal white thrombus. 

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. 

The intetaction of proteolytically-active a-tfarombin with platelets and other cells of the vasculature, such as endothelial cells and smooth muscle cells, plays a major role in both normal hemostasis and atherosclerosis. Despite extensive studies in numerous laboratories extending back over thirty years, major questions regarding the mechanism of these interactions remain uruesolved. Furthermore, since dirombin can also induce chemotaxis and adhesion of inflammatory cells, and fibroblast mitogenesis, the importance of elucidating the nature of its receptor, or receptors, extends r beyond its role in platelet activation. However, this review will be restricted mainly to considerations of thrombin receptors in human platelets. 

Platelets are the formed elements of the blood which participate in hemostasis. Platelets are enucleated, discoid fragments which arise from mature megakaryocytes in the bone marrow. Under normal circumstances, platelets do not adhere to endothelial surfaces of blood vessels. However, platelets can adhere to damaged areas of blood vessels and become activated in such a way that they can also bind fibrinogen. 

Little intravascular coagulation of blood occurs in normal physiological conditions. Hemostasis involves the interplay of three procoagulant phases vascular, platelet, and coagulation) that promote blood clotting to prevent blood loss (Fig. 22.1). The fibrinolytic system prevents propagation of clotting beyond the site of vascular injury and is involved in clot dissolution, or lysis (Fig. 22.2). 

Platelets are actively involved in the process of hemostasis, by which any break in the vascular endothelium is rapidly repaired without compromising the fluidity of the blood. In response to injury, platelets adhere to the subendothelial matrix of a damaged vessel, spread over the surface, and recruit additional platelets within a developing platelet aggregate or thrombus. Whereas hemostasis is a normal physiological response to endothelial wound repair, improper regulation or overreactivity of this system can lead to the pathological condition of thrombosis. 

Upon activation, platelets release several factors, which are normally involved in hemostasis and coagulation, and are also implicated in TCIPA (Honn et al., 1992b).These factors can be recovered from activated platelets and tested on tumor cells. 

In conclusion, PAF is a unique and potent endogenous lipid mediator which activates platelets. Increases or decreases in PAF levels in vivo can profoundly influence vascular hemostasis. PAF activates multiple signaling pathways in platelets but the molecular properties of platelet PAF receptor and its regulation are poorly understood. Similarly the expression of PAF receptor in megakaryocyte development in normal and disease states would also be a topic of interest in the feture. 

Castillo R, Escolar G, Monteagudo J, Aznar-Salatti J, Reverter JC, Ordinas A Hemostasis in patients with severe von Willebrand disease improves after normal platelet transftisicm and mormalizes with further correction of the plasma defect. Transfusion 37 785-790,1997. 

Platelets are the smallest cellular elements of blood of 2.5 pm in average normal diameter. They fulfill an essential role in hemostasis and thrombosis. Thrombosis is a complex phenomenon, involving interaction of endothelial cells and blood cellular elements like platelets, leukocytes and red blood cells. Moreover, platelets influence both thrombosis formation and fibrinolysis. 

Coagulation disorders Blood products (PPF, platelets), vitamin K CBC, prothrombin time, platelet count Normalize PT time, maintain/improve hemostasis... 

This rapid platelet aggregation and thrombus formation at the site of vascular injury is the main mechanism of hemostasis (stoppage of bleeding, a normal process of wound healing). When platelets are activated on the ruptured atherosclerotic plaques or in regions of restricted blood flow, however, it can lead to thromboembolic... 

Results indicate that even at supratherapeutic doses, celecoxib will not interfere with normal mechanisms of platelet aggregation and hemostasis. Patients treated with celecoxib experienced fewer decreases in... 

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