Includes vasospasm and platelet plug formation.
Platelets are the cornerstone as they adhese to exposed subendothelial collagen mediated by von Willebrand factor.
Damage to blood vessels recruits platelets to adhesive ligands, resulting in plug formation and arrest of bleeding.
Recruitment of platelets involves subendothelial von Willebrand factor and vascular collagens.
Platelet aggregation and activation leads the platelet plug formation.
Platelet accumulation at injury site exposes blood to tissue factor and leads to the formation of thrombin.
When thrombin is formed it cleaves fibrinopeptides from fibrinogen which prevents blood loss and serves as a temporary matrix for tissue healing and remodeling.
Tissue factor within the subendothelial tissue binds to factor VIIa, leading to the production of thrombin, which further activates platelets and generates fibrin.
Platelets exposed to collagen plus thrombin form coated platelets that express high levels of procoagulant proteins with factor V, fibrinogen, fibronectin, and von Willebrand factor, providing a procoagulant surface supporting further fibrin generation.
Defects include disorders of platelets and von Willebrand factor.
Binding of platelets to collagen or to von Willebrand factor leads to partial activation of platelets and the coagulation process is most effectively initiated when enough thrombin is generated on or near the tissue factor bearing cells to trigger full platelet activation and activation of coagulation cofactors on the platelet surface.