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The coagulation system is comprised of both pro-coagulant and anticoagulant factors and serves an important function of maintaining the integrity of the circulatory system in the body. Under normal homoeostatic conditions, the balance between the body’s coagulation pathway and natural anticoagulants maintains blood in a state to allow unobstructed flow through the blood vessels. When there is a breach in the vasculature, the coagulation pathway is activated and fibrin clot is formed through a physiological process called hemostasis. Disorders of hemostasis can result in excessive or abnormal bleeding. On the other hand, activation of the coagulation pathway within intact blood vessels leads to pathological (as opposed to physiological) clotting or thrombosis. Thrombi can form in veins and/or arteries with possibly different mechanisms leading to thrombosis in these different vascular settings.

In this chapter, we will discuss the process of hemostasis and the approach to patients with bleeding and thrombotic disorders.


The basic components of hemostasis include vessel wall, platelets, von Willebrand factor (VWF), and the coagulation cascade. The process starts with injury to the vessel walls and includes the following three steps: (1) vascular constriction, (2) platelet plug formation (primary hemostasis), and (3) fibrin clot formation by the coagulation cascade, which stabilizes the platelet plug (secondary hemostasis). The coagulation cascade in step 3 above goes through phases of initiation, amplification, and propagation, which ultimately leads to formation of a fibrin clot. In the initiation phase, the blood vessels that are injured expose Tissue Factor (TF) on the subendothelial cells to the coagulation factors in the blood. Factor VII binds with TF to activate Factors X and XI and generate a small amount of thrombin from prothrombin. In the amplification phase, the thrombin generated in the initiation phase then interacts with the platelets at the site of injury to “activate” them. Clotting factors such as Factor V and Factor XI are also activated. The activated platelets release Factor V which cleaves Factor VIII from VWF to activate VWF. Also, Factor XI binds to activated platelets’ surfaces. Through this phase, the platelets are coated in activated coagulation factors. In propagation, eventually the factors come into play to lead to production of large amount of thrombin which converts fibrinogen into fibrin, thus stabilizing the clot along with Factor XIII.1,2


Taking a detailed and comprehensive history helps elucidate a clinical bleeding problem. The patient should be asked about bleeding events in their childhood such as umbilical stump bleeding, bleeding with loss of deciduous teeth, or bleeding with childhood trauma and surgeries. Bleeding with dental procedures should be inquired. The patient should be asked about the type of bleeding, severity of bleeding episodes, and sites where bleeding occurred. Presence of petechiae, purpura, epistaxis, gingival bleeding, menorrhagia, and/or hematuria would suggest a disorder of primary hemostasis including platelet and/or vascular ...

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