The mechanism of blood coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot. It potentially results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion, and aggregation of platelets, as well as deposition and maturation of fibrin¹. Coagulation begins almost instantly after an injury to the endothelium lining a blood vessel.

Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial tissue factor to plasma factor VII, which ultimately leads to cross-linked fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: additional coagulation (clotting) factors beyond factor VII (listed below) respond in a cascade to form fibrin strands, which strengthen the platelet plug.

Disorders of coagulation are disease states which can result in problems with hemorrhage, bruising, or thrombosis. Coagulation is highly conserved throughout biology. In all mammals, coagulation involves both cellular components (platelets) and proteinaceous components (here, coagulation factors). The pathway in humans has been the most extensively researched and is the best understood.