Blood clotting results from the interaction between blood vessels, platelets and coagulation factors. Coagulation factors circulate in the blood in their inactive form to prevent coagulation from occurring when it’s not necessary. When there’s an injury, coagulation factor VII binds to the cells of the exposed vessel wall, triggering the activation of the coagulation cascade. This allows the subsequent activation of the rest of the clotting factors, which ultimately leads to the formation of thrombin (factor II). Thrombin converts fibrinogen into fibrin (factor I), which forms a tightly connected mesh that stabilizes the platelet plug.  To limit the formation of clots to the site of injury and prevent them from growing too big, the coagulation cascade is regulated by different anticoagulant mechanisms. Protein C, along with protein S, form a complex that inactivates factors V and VIII. On the other hand, antithrombin III directly decreases the production of thrombin and inactivates factor X.  Any condition that causes an imbalance between thrombogenic and antithrombogenic mechanisms predisposes an individual to either an increased risk of bleeding or a hypercoagulable state.