Figure 1.

Schematic of the complex mechanism of blood vessel hemostasis. Vessel injury can lead to endothelial activation and denudation resulting in secretion and deposition of von Willebrand Factor (vWF) and exposure of collagen at the injury site, as well as, exposure of tissue factor (TF) bearing cells at the site; vWF and collagen exposure allows platelet adhesion and activation, while TF exposure allows extrinsic pathway of coagulation to propagate and produce moderate amounts of thrombin (FIIa) that activates other coagulation factors in the intrinsic pathway; activated platelets aggregate via fibrinogen (Fg) mediated interaction with platelet surface integrin GPIIb-IIIa to form a platelet plug (primary hemostasis) that staunches bleeding; the surface of aggregated active platelets exposes negatively charged phospholipids that allow co-localization and further activation of coagulation factors to form the prothrombinase (FVa + FXa + FII) complex in presence of calcium (Ca⁺⁺), leading to amplified generation of thrombin (FIIa) that breaks down fibrinogen (Fg) to fibrin; fibrin self-assembles and undergoes further crosslinking by action of FXIIIa to form a dense biopolymeric mesh that forms the hemostatic clot and arrests flow of blood components (secondary hemostasis).