Blood Coagulation
Blood coagulation is the process whereby the components of the liquid blood are transformed into a semisolid material called a blood clot.
The purpose of coagulation is obvious - to plug up ruptured vessels so as to stop bleeding and prevent loss of vital body fluid.
The blood clot is made up mainly of blood cells entrapped in a meshwork of fibrin. Fibrin is formed from proteins in the plasma as the result of a complex series of reactions. At least 12 clotting factors are involved in the reaction that forms fibrin.
The blood-coagulation mechanism presumably consists of a series of chemical reactions that take place in a definite and rapid sequence. When tissue is injured, it starts the first of these changes that initiate blood clotting.
The trigger that starts it is the appearance of a "rough" spot in the lining of a blood vessel. Within a matter of 1 or 2 seconds, clumps of platelets adhere to any portion of a blood vessel that loses its normal, perfectly smooth quality and releases a variety of substances.
After the platelets release its substances, a series of chemical reactions take place in a rapid-fire succession. Some of these substances that accelerate coagulation are Factors VII, VIII, IX, X, XI, and XII. Factor XII is also referred to as the Hageman factor (after a patient named John Hageman).
The sequence of events that leads to the generation of thrombin and the formation of a fibrin clot is a biochemical cascade and consists of two distinct pathways, extrinsic (coming from outside) and intrinsic (coming from within, not dependent on externals).
In the intrinsic pathway, Factor XII is activated during the contact phase of blood clotting, followed by the sequential activation of factors IX, X, and XI, and prothrombin.
The extrinsic pathway is also activated. This is the initial blood clotting mechanism and is the only known time when Factor XII affects coagulation.
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