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.
Fibrin is formed by the action of the protease thrombin on fibrinogen, which causes it to polymerize.
The polymerized fibrin, together with platelets, forms a hemostatic plug or clot over a wound site.
When the lining of a blood vessel is broken, platelets are attracted, forming a platelet plug. These platelets have thrombin receptors on their surfaces that bind serum thrombin molecules, which in turn convert soluble fibrinogen in the serum into fibrin at the wound site.
Fibrin forms long strands of tough insoluble protein that are bound to the platelets.
Factor XIII completes the cross-linking of fibrin so that it hardens and contracts.
The cross-linked fibrin forms a mesh atop the platelet plug that completes the clot.
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.