A. The Clot and Serum: Clotted blood consists of 2 parts:
(1) the clot, or thrombus, which includes the formed elements and some of the proteins previously dissolved in the plasma, and
(2) the serum, a clear yellow liquid that is similar to plasma except that it lacks fibrinogen and contains more serotonin.
B. Clotting Factors: Clotting involves a cascade of molecular interactions among several plasma proteins and ions (clotting factors I-XIII). The cascade can be initiated by 2 converging pathways, each of which results in the conversion of fibrinogen to fibrin by the enzyme thrombin. In the intrinsic pathway, initiation of the cascade occurs when factor XII is activated by contact with collagen underlying the endothelium (indicating damage to the endothelial lining of a vessel). In the extrinsic pathway, cells in a damaged vessel wall or the surrounding tissue release an ill-defined clot-promoting substance termed thromboplastin (factor III), which com bines with blood calcium and factor VII to activate factor X, a plasma protein. Factor X is a point of convergence of the 2 pathways and, in its activated form, promotes the conversion of prothrombin (factor II) to thrombin. Both factor X and prothrombin are synthesized by the liver and require vitamin K as a cofactor in their synthesis. Thrombin enzymatically converts plasma fibrinogen (factor I, released into plasma by platelets and by the liver) into fibrin; this explains the lower concentration of fibrinogen in serum than in plasma. Other factors act as promoters and accelerators of the clotting process or help stabilize the fibrin once it has formed. An inherited abnormality in factor VIII (whose precise role in the clotting process is uncertain) results in the clotting disorder known as hemophilia.
(1) the clot, or thrombus, which includes the formed elements and some of the proteins previously dissolved in the plasma, and
(2) the serum, a clear yellow liquid that is similar to plasma except that it lacks fibrinogen and contains more serotonin.
B. Clotting Factors: Clotting involves a cascade of molecular interactions among several plasma proteins and ions (clotting factors I-XIII). The cascade can be initiated by 2 converging pathways, each of which results in the conversion of fibrinogen to fibrin by the enzyme thrombin. In the intrinsic pathway, initiation of the cascade occurs when factor XII is activated by contact with collagen underlying the endothelium (indicating damage to the endothelial lining of a vessel). In the extrinsic pathway, cells in a damaged vessel wall or the surrounding tissue release an ill-defined clot-promoting substance termed thromboplastin (factor III), which com bines with blood calcium and factor VII to activate factor X, a plasma protein. Factor X is a point of convergence of the 2 pathways and, in its activated form, promotes the conversion of prothrombin (factor II) to thrombin. Both factor X and prothrombin are synthesized by the liver and require vitamin K as a cofactor in their synthesis. Thrombin enzymatically converts plasma fibrinogen (factor I, released into plasma by platelets and by the liver) into fibrin; this explains the lower concentration of fibrinogen in serum than in plasma. Other factors act as promoters and accelerators of the clotting process or help stabilize the fibrin once it has formed. An inherited abnormality in factor VIII (whose precise role in the clotting process is uncertain) results in the clotting disorder known as hemophilia.
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