Continuing education course #2: current understanding of hemostasis

Abstract

The goal of this review is to briefly summarize the two primary pathways of hemostasis, primary hemostasis and secondary hemostasis, as well as to summarize anticoagulant mechanisms and fibrinolysis. In addition, this review will discuss pathologies of hemostasis and the mechanisms of the various drugs that are available to impact these pathways to prevent either thrombosis or bleeding. While many of the main drugs that are used to treat disorders of hemostasis have been used for decades, greater understanding of hemostasis has led to development of various new drugs that have come onto the market recently or are close to coming onto the market. Thus, improved understanding of hemostasis continues to lead to benefits for patients.

Figure 1

Primary hemostasis; the platelet response. Platelet aggregation at the site of injury is mediated by platelet receptors, platelet-derived agonists, platelet-derived adhesive proteins and plasma-derived adhesive proteins. Fibrin deposition around the resulting platelet plug is generated by the coagulation cascade (Figure 2). ADP = adenosine diphosphate, TXA2 = thromboxane A2 and VWF = von Willebrand factor.

Figure 2

Secondary hemostasis; the coagulation cascade. At the site of injury, tissue factor (TF) initiates the coagulation cascade that results in the formation of the serine protease thrombin. Thrombin performs multiple functions, including fibrin generation, platelet activation, positive feedback activation of the intrinsic pathway, and negative feedback activation of the activated protein C pathway. Procoagulant reactions are shown in blue, and anticoagulant reactions are shown in pink. APC = activated protein C, FV = factor V, PS = protein S and TM = thrombomodulin.