Coagulation consists of three pathways, the extrinsic, intrinsic, and common pathways, that interact together to form a stable blood clot. The extrinsic and intrinsic coagulation pathways both lead into the final common pathway by independently activating factor X. The extrinsic pathway involves initiation by factor III (i.e., tissue factor) and its interaction with factor VII. Whereas, factors XII, XI, IX, and VIII are utilized in the intrinsic pathway. Then, the common pathway uses factors X, V, II, I, and XIII. The extrinsic pathway begins when there is injury to the endothelial tissue (i.e., skin tissue), exposing tissue factor (factor III) to the blood. Tissue factor then becomes bound with calcium and factor VIIa to activate factor X. Factor VII is present in the blood and requires vitamin K to be activated. Meanwhile, the intrinsic pathway begins when factor XII or the Hageman factor is exposed to collagen, kallikrein, and high molecular weight kininogen (HMWK) and is subsequently activated. Factor XIIa activates factor XI into XIa. With a calcium ion, factor XIa activates factor IX. Then, factor IXa, factor VIIIa, and calcium form a complex to activate factor X. Factor VIII is found in the blood and is often activated by thrombin (factor IIa). The common pathway may result after the activation of factor X at the end of either pathway. The common pathway begins when factor Xa, Va, and calcium bind together, forming a prothrombinase complex. The prothrombinase complex then activates prothrombin (factor II) into thrombin (factor IIa). Next, thrombin cleaves fibrinogen (factor I) into fibrin (factor Ia). Afterwards, thrombin cleaves the stabilizing factor (factor XIII) into XIIIa. Factor XIIIa binds with calcium to then create fibrin crosslinks to stabilize the clot. Thrombin has several functions, including activating platelets (cell fragments involved in clot formation) and activating factors V, VIII, and IX.