RT Book, Section A1 Freeman, Brian S. A1 Berger, Jeffrey S. SR Print(0) ID 1204770349 T1 Anticoagulants T2 Anesthesiology Core Review: Part One: BASIC Exam, 2nd Edition YR 2024 FD 2024 PB McGraw-Hill Education PP New York, NY SN 9781264285518 LK accessanesthesiology.mhmedical.com/content.aspx?aid=1204770349 RD 2025/03/21 AB When tissue injury occurs, platelets gather around the injured site to form the primary hemostatic plug. This step in turn activates other platelets and releases additional cellular and humoral components of hemostasis. Furthermore, exposed tissue factors promote thrombin generation during the coagulation phase of hemostasis to stabilize the weak platelet hemostatic plug. This process leads to a cascade of protease activation that foster the formation of a fibrin clot localized to the injury (Figure 189-1). Further fibrin clot formation is limited due to a series of inhibitors balancing out the coagulation. Normal hemostasis is a balance between procoagulant and anticoagulant mechanisms. When there is an imbalance, a hypercoagulable state can lead to unwanted arterial or venous thrombosis. This can give rise to devastating injury and leave the patient disabled with an increase in mortality.