INTRODUCTION

The mechanisms that lead to the formation of hemostatic plugs or pathologic thrombi are complex, and both seem to involve the same underlying biochemical mechanisms. Hemostatic plugs always form at sites of vessel wall damage, but this is not always true of pathologic thrombi, especially those that form in veins. Both processes involve a complex interplay between platelets and the coagulation system, with lesser contributions from other blood cells and the endothelium. It is abundantly clear from centuries of clinical experience that both platelets and the coagulation proteins are vital for normal hemostasis, the relative importance of one system over the other depending on the site of injury and the flow characteristics in the blood vessel, among other factors. For example, although congenital deficiencies of both platelet adhesion molecules and clotting factors are capable of causing severe hemostatic defects, the two manifest in very different ways. Mucocutaneous bleeding is more prominent in platelet defects than in hemophilia, whereas joint bleeding is a prominent feature of hemophilia but not usually seen with platelet defects. The aim of this chapter is to highlight some of the ways in which platelets and the coagulation system collaborate and influence each other in the formation of blood clots.

EFFECTS OF PLATELETS AND THEIR PRODUCTS ON COAGULATION

Platelets affect coagulation at several steps: by producing substances that stimulate the synthesis of blood clotting proteins, localizing clotting reactions to sites of blood vessel injury, providing the anionic surface on which the complexes of the coagulation form, and secreting or synthesizing clotting proteins that form parts of those complexes [e.g. factor Va and tissue factor (TF)] or that are essential components of the final thrombus (fibrinogen) (Fig. 5.1).