الفهرس 
Introduction & Aim of The WorkOnly 14 pages are availabe for public view
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Abstract
The haemostatic mechanisms have two primary functions to ensure circulating blood remains fluid while in the vascular bed, and to arrest (’bleeding at the site of an injured blood vessel (NawRoth, 1986). , Normal haemostasis depends on a delicate balance and complex ’interactions between at least five components, blood vessels, platelets, lplasma coagulation proteins, inhibitors and the fibrinolytic system .,(Walker, 1985). Normal coagulation is a chain of reactions that leads to formation of ,. yfibrin clot at the site of vascular damage by the way that relatively small !(vascular stimulus activating a few initial molecules through a succession of ,tenzyme activation which is called enzyme cascade through either intrinsic f • ror extrinsic pathways. The coagulation cascade is controlled by plasma regulatory proteins ~ Including antithrombin III, protein C, its cofactor protein S, proteases and ti, T tissue-type plasaminogen activator. These factors affect protein transformation necessary for thrombus fformation, so deficiency or abnormality of these regulatory proteins will if, lead to arterial or venous thromboembolism what is called primary hypercoagulable states. Two types of 1 ry hypercoagulable states have been described, type I deficiency, in which immuno-reactive protein levels are reduced in parallel with functional activity and type II deficiency in which ( 1 )