Physiological And Pathological Thrombosis

Normal hemostasis refers to the body's physiological response to vascular injury. Normal clot formation and clot dissolution is accomplished by interaction among five major components: vascular system, platelets, coagulation system, fibrinolytic system, and inhibitors. These components must be in the functional state for normal hemostasis to occur. Imbalance in any of the above components will tilt the hemostatic scale in favor of bleeding or thrombosis. There are two systems of hemostasis: the primary and secondary hemostatic systems. Primary hemostasis refers to the process by which the platelet plug is formed at the site of injury, while secondary hemostasis is defined as the interaction of coagulation factors to generate a cross-linked fibrin clot to stabilize the platelet plug to form physiological thrombosis.

Physiological thrombosis results from the body's natural response to vascular injury. It is localized and is formed to prevent excess blood loss. Pathological thrombosis includes deep venous thrombosis, arterial thrombosis, and pulmonary embolism. Pathological thrombosis may be caused by acquired or inherited conditions. Arterial thrombosis is primarily composed of platelets with small amounts of fibrin and red and white cells. This clot may be also referred to as the

"white clot." Complications associated with arterial thrombosis are occlusions of the vascular system leading to infarction of tissues.1 Factors causing arterial thrombosis are hypertension, hyper viscosity, qualitative platelet abnormalities, and atherosclerosis.

Venous thrombosis is composed of large amounts of fibrin and red cells resembling the blood clot formed in the test tube. Venous thrombosis is associated with slow blood flow, activation of coagulation, impairment of the fibrinolytic system, and deficiency of physiological inhibitors. The most serious complication associated with venous thrombosis is demobilization of the clot. This occurs when a clot is dislodged from the site of origin and filtered out in the pulmonary circulation.

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