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How does injury inside a blood vessel activate the intrinsic pathway of coagulation?

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Fibrin in blood clotting — bleeding and blood clotting Red blood cells (erythrocytes) trapped in a mesh of fibrin threads. Fibrin, a tough, insoluble protein formed after injury to the blood vessels, is an essential component of blood clots.

The intrinsic pathway of coagulation is initiated by injury occurring within a blood vessel, which exposes internal surfaces to the circulating blood.1

When blood comes into contact with these injured internal surfaces, it triggers the activation of factor XII (also known as Hageman factor). This activation is facilitated by the presence of certain negatively charged surfaces exposed by the injury, as well as by proteins such as high-molecular-weight kininogen and prekallikrein. Once factor XII is converted to its active enzyme form, factor XIIa, it initiates a cascade of reactions involving other clotting factors—specifically factor XI, factor IX, and factor VIII—that ultimately leads to the activation of factor X and the subsequent formation of a fibrin clot.213