Pathophysiology
Clinical meaning
The cell-based model of coagulation has replaced the traditional cascade model. Initiation occurs on tissue factor-bearing cells where TF-VIIa generates small amounts of thrombin. Amplification occurs on activated platelet surfaces where thrombin activates factors V, VIII, XI, and platelets. Propagation involves tenase (IXa-VIIIa) and prothrombinase (Xa-Va) complexes on platelet surfaces generating a thrombin burst sufficient for stable fibrin clot formation. Natural anticoagulants include: antithrombin III (heparin cofactor; inhibits IIa, Xa, IXa), protein C pathway (thrombomodulin-thrombin activates protein C, which with protein S inactivates Va/VIIIa), and TFPI (limits TF-VIIa). Fibrinolysis: plasminogen is converted to plasmin by tPA, degrading fibrin into D-dimers and fibrin degradation products.