الفهرس 
Intrinsic Pathway of coagulation
General risk factorsOnly 14 pages are availabe for public view
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Abstract
Normal physiological haemostasis relies on the careful equilibrium between ability to form clot and the retention of the fluid phase. This is achieved by a balance between platelet adhesion and aggregation on vascular endothelium, activation of coagulation cascade (including procoagulant and anticoagulant pathways) and fibrinolysis. Subtle disruptions to this complex can result in the pathological states of thrombosis or bleeding (Lim et al., 2022). Under physiological conditions, intact endothelium acts as a non-adhesive, negatively charged surface with various anticoagulant properties which inhibit intra-vascular thrombus formation and platelet activation (Wang et al., 2018). The negatively charged glycosaminoglycan layer, which forms the glycocalyx lining the luminal endothelial surface, inhibits thrombin generation through interactions with circulating endogenous anticoagulants (such as anti-thrombin) and also inhibits adhesion of leucocytes and platelets (Weissgerber et al., 2019). Constitutive endothelial generation of substances such as nitric oxide and prostacyclin also serves to limit coagulation activation by inhibiting platelet activation and by opposing vasoconstriction. Moreover, the physiological endothelial expressions of anticoagulant proteins such as thrombomodulin (TM), the endothelial protein C receptor (EPCR) and substances such as tissue plasminogen activator (tPA) are key to the activity of the APC and fibrinolytic systems (Wang et al., 2018).