Endothelial injury releases glycoprotein tissue factor (factor III) that drives the coagulation process and activates platelets. Adjacent intact endothelium generates prostacyclin (PGI2 ) via arachidonic acid metabolism to inhibit clot propagation beyond where it is needed. PGI2 and nitric oxide are powerful vasodilators and inhibitors of platelet aggregation. This limits thrombus formation just to the area of injury. Glycoprotein IIb/IIIa, which induces shape change; phospholipid, which binds fibrinogen and calcium; and platelet-activating factor are procoagulants that drive thrombosis and platelet activation. Tissue-type plasminogen activator promotes fibrinolytic activity after a thrombus has formed. Thrombomodulin binds to thrombin to form an anticoagulant that activates protein C, which then cleaves activated factor V and factor VIII. Thromboxane is generated via arachidonic acid metabolism in platelets to promote platelet activation and vasoconstriction.