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The coagulation cascade and platelet function represent the two primary, interconnected components of the hemostatic system responsible for preventing blood loss following vascular injury [1, 8]. The platelet function arm involves the rapid adhesion, activation, and aggregation of platelets to form a primary hemostatic plug, while the coagulation cascade consists of a series of proteolytic reactions involving clotting factors that culminate in the generation of thrombin and the formation of a stable fibrin mesh [4, 8]. Dysregulation of these processes can lead to either pathological thrombosis, such as myocardial infarction or stroke, or severe bleeding disorders like hemophilia [3, 6]. Consequently, this system is a major focus of pharmacological intervention, with drugs targeting various enzymes (e.g., Factor Xa, Thrombin) and receptors (e.g., P2Y12, GP IIb/IIIa) to modulate clot formation and maintain vascular patency [2, 12].
Inhibition of specific coagulation factors (e.g., Thrombin, Factor Xa) or platelet activation pathways (e.g., COX-1 inhibition, P2Y12 antagonism, GP IIb/IIIa blockade) to prevent or treat thrombosis [8, 12].
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