The coagulation system results in the formation of insoluble fibrin clot from the soluble precursor, fibrinogen, found in plasma. The coagulation cascade is a complex interaction of clotting factors and sequential activation of a series of proenzymes. There are two mechanisms, the intrinsic mechanism that involves the activation of Factor XII by collagen after blood vessel injury and the extrinsic mechanism that involves activation of Factor VII by thromboplastin release from damaged tissue. Both mechanisms are required for normal haemostasis. These two pathways interact and share a common pathway after activation of Factor X.
The intrinsic mechanism proceeds spontaneously and is slow. It requires 5 to 20 minutes for visible fibrin formation. A specific lipoprotein, Thromboplastin, is contained in all tissues and accelerates the rate at which blood clots. The placenta as well as the lung and the brain are particularly rich in tissue factor, which will produce fibrin formation in 12 seconds. This acceleration of coagulation is brought about by bypassing the reactions involved in the intrinsic system.
Powerful control mechanisms must act to prevent dissemination of coagulation beyond the site of trauma. The action of thrombin in vivo is controlled by its absorption into the locally formed fibrin and by the presence of a potent inhibitor, anti-thrombin III, an a2-globulin, which destroys thrombin activity.
Normal pregnancy is accompanied by major changes in the coagulation system with increases in levels of Factors VII, VIII, and X and, particularly, a marked increase in the level of plasma fibrinogen. The effects of pregnancy on the coagulation system can be seen as early as the third month of pregnancy. In late pregnancy, the level of fib-rinogen is at least double that of the non-pregnant state.
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