Coagulation of the blood can be initiation from two different pathways that both result in formation of thrombin which converts blood soluble fibrinogen into the insoluble fibrin clot at the site of injury. The intrinsic pathway is activated by trauma inside vasculature and is activated by platelets, exposed endothelium and collagen. In the liver the coagulation factors VII, IX, and X are produced there as they are vitamin K-dependent proteins. Exposed collagen from broken vessels binds to factor XII activating it to XIIa which converts prekallikrein and factor XI to kallikrein and factor XIa respectively. The extrinsic pathway is activated by the external trauma of blood escaping the vasculature system as the membrane-bound protein tissue factor (TF) is exposed to factors VII or VIIa in the plasma forming a strong activator complex. This activator complex of VIIa and TF converts factor X to the activated form. Both the intrinsic and extrinsic pathways lead to the prothrombinase complex as both pathways activate factor X, an important player in the complex. The prothrombinase complex converts prothrombin to thrombin further allowing the conversion of insoluble fibrinogen into fibrin. Fibrin at first is loose and unstable and is stabilized by coagulation factor XIIIa which cross-links them to form the fibrin clot/mesh that stops blood leaking from the vasculature system. The activated proteins are colored orange.

Coagulation References