Master Coagulation Cascade Overview with Picmonic for Physician Assistant

The intrinsic pathway is also known as the contact activation pathway. This is one of two pathways the coagulation cascade can follow to form fibrin, which forms a plug with platelets to coagulate. First, activated platelets activate factor XII, which activates factor XI. Factor XI (with Ca²⁺) activates IX, which requires factor VIII (and Ca²⁺) to activate factor X. The cascade then enters the common pathway.

The intrinsic pathway can be measured by partial thromboplastin time (PTT), which can be normal, increased in hypocoagulable states, or decreased in hypercoagulable conditions. Heparin function is monitored with this test.

Heparin is an anticoagulant which activates antithrombin, decreasing fibrin formation and inactivating factor X. This affects the intrinsic pathway and is monitored with PTT.

The extrinsic pathway, also known as the tissue factor pathway, is the primary pathway for initiating coagulation. It begins with thromboplastin (tissue factor and Ca²⁺) activating factor VII. Factor VII activates factor X. The cascade then enters a common pathway.

Prothrombin time (PT) is used to measure coagulation time in the extrinsic pathway. Often it is used to monitor drugs which alter this pathway, such as warfarin (coumadin).

Warfarin, an anticoagulant, exerts its primary effects on the extrinsic pathway (specifically factor VII) and is monitored with PT.

The common pathway is the convergence of the extrinsic and intrinsic pathways. From this point on in the cascade, both pathways follow the same route: where activated factor X, in conjunction with factor V (and Ca²⁺), works to activate factor II (prothrombin to thrombin).

The main product of the coagulation cascade is thrombin (factor IIa). Thrombin then converts fibrinogen (factor I) to fibrin (factor Ia).

Factor IIa (thrombin) converts fibrinogen to fibrin (factor Ia). Fibrin, with the help of Ca²⁺ and factor XIIIa, forms a mesh.

A fibrin mesh is formed from fibrin (factor Ia), which stabilizes platelet plugs formed in primary hemostasis.