ABSTRACT
Introduction 71 Platelets 71 Blood coagulation 75 The fibrinolytic system and thrombosis 80 Effect of increased endogenous estrogens (pregnancy)
on blood coagulation and thrombotic risk 80
Effect of exogenous oral estrogens (combined oral contraceptives and hormone replacement therapy) on blood coagulation and thrombotic risk 80
References 80
Hemostasis is the arrest of blood loss following blood vessel injury. Initial vasoconstriction is followed by formation of a platelet-fibrin hemostatic plug. Thrombosis has been described as ‘hemostasis in the wrong place’.1 Pathologic, pharmacologic, and epidemiologic studies have established that the interaction of blood platelets and coagulation factors with the blood vessel wall is important not only in hemostasis, but also in both arterial and venous thrombosis.2-4 The aims of this chapter are to:
● outline the interactions of blood platelets and coagulation factors (and their inhibitors) with the blood vessel wall in hemostasis and thrombosis
● summarize epidemiologic studies of the associations of hemostatic variables with venous and arterial thrombosis
● to inform, and link to, subsequent chapters in this book on thrombophilias and hemophilias (Chapters 7-9), antithrombotic drugs (Chapters 11 and 12), hemostatic and thrombotic problems in reproduction (Section 2), and the thrombotic problems of oral contraceptives, hormone replacement therapy (HRT)
Platelets are anuclear cell fragments, (1-3 m in diameter), which are derived from bone marrow megakaryocytes, and circulate in human blood at a concentration of 150-450 109/L. They play a key role in hemostasis. Disruption of the vessel wall exposes circulating platelets to subendothelial collagen, and to products of cellular injury including adenosine diphosphate (ADP) and thrombin. These substances activate platelets through interaction with specific platelet membrane receptors, resulting in platelet activation through several biochemical pathways (Fig. 6.1). Activated platelets adhere to vascular subendothelium and aggregate, forming a hemostatic plug (Fig. 6.2). This is subsequently stabilized by strands of fibrin formed from circulating fibrinogen by thrombin, which is formed by the interaction of circulating coagulation factors upon the surface of activated platelets (Fig. 6.2).
