Blood coagulation is an extremely complex system. A wide variety of mechanisms ensure that, when a blood vessel is injured, uncontrolled blood loss does not occur. Haemostasis is a vital process that stops bleeding caused by injuries to blood vessels.
Primary, cellular haemostasis (also known as blood clotting) involves thrombocytes (platelets), the endothelial cells and smooth muscle cells of the affected blood vessel, as well as the tissue outside the vessel. In secondary, plasma haemostasis (also known as blood coagulation), this still loose seal of the vessel is reinforced by the formation of fibrin strands. In this process, coagulation factors and the formation of fibrin from fibrinogen play an important role.
The plasma coagulation cascade is further divided into an intrinsic and an extrinsic system. However, increasing overlap between the two systems is being observed. Put simply, the intrinsic pathway involves damage to the vascular system without involvement of surrounding tissue and proceeds via factors XII, XI, IX and VIII to the common final pathway. In the extrinsic pathway, the triggering factor is usually damaged endothelium due to external trauma and blood escaping from the vascular system. Here, activation of factor VII leads into the common final pathway. Following the separate course of both systems, coagulation then proceeds via the common final pathway with activation of factor X, involving factors V, II and I.
