Intrinsic Pathway for Initiating Clotting
The second mechanism for initiating formation of prothrombin activator, and therefore for initiating clotting, begins with trauma to the blood or exposure of the blood to collagen from a traumatized blood vessel wall. Then the process continues through the series of cascading reactions shown in Figure 37-6. 1. Blood trauma causes (1) activation of factor XII and (2) release of platelet phospholipids. Trauma to the blood or exposure of the blood to vascular wall collagen alters two important clotting factors in the blood: factor XII and the platelets. When factor XII is disturbed, such as by coming into contact with collagen or with a wettable surface such as glass, it takes on a new molecular configuration that converts it into a proteolytic enzyme called activated factor XII. Simultaneously, the blood trauma also damages the platelets because of adherence to collagen or to a wettable surface (or by damage in other ways); this releases platelet phospholipids that contain the lipoprotein called platelet factor 3, which also plays a role in subsequent clotting reactions.
Activation of factor X—role of factor VIII. The activated factor IX, acting in concert with activated factor VIII and the platelet phospholipids and factor III from the traumatized platelets, activates factor X. It is clear that when either factor VIII or platelets are in short supply, this step is deficient. Factor VIII is the factor that is missing in a person who has classic hemophilia, so it is called antihemophilic factor. Platelets are the clotting factor that is lacking in the bleeding disease called thrombocytopenia.
