Chapter 4: Hemostasis

Hemostasis is the complex interaction of proteins, cells, and blood vessels with a goal of arresting hemorrhage. Blood clot formation occurs at the site of vascular injury and this must occur quickly, remain localized, and be tightly controlled. With an imbalance or dysfunction at any level of the hemostatic process, excessive bleeding or clotting may occur, both of which can be life-threatening. In health, a balance is maintained so that animals experience neither hemorrhaging nor thrombosis through hypocoagulation or hypercoagulation, respectively. This balance is maintained in several ways: intact blood vessel endothelium is anticoagulant, whereas, injured endothelium is procoagulant; many of the coagulation factors must be first activated in order to participate in clotting; and potent anticoagulants are present both in the peripheral blood and bound to vascular endothelium. The normal sequence of events when vascular injury occurs is: vasoconstriction, platelet plug formation, and coagulation, followed by clot retraction and fibrinolysis (Figs 4.1 and 4.6). There is clinical relevance in distinguishing between primary hemostasis (vasoconstriction and platelet plug formation) and secondary hemostasis (coagulation), although both are closely associated and often occur simultaneously, depending on the degree of injury.

Figure 4.1 Hemostasis. A. Normal undamaged blood vessel. B. Transient vasoconstriction occurs at site of vascular injury through the action of endothelin and similar molecules as well as neural factors. C. Platelets adhere to damaged endothelium/subendothelium. Adhesion is strengthened through subendothelial/collagen-bound von Willebrand factor (vWF) binding to its receptor on the platelet surface. Platelets undergo shape change, release of granule contents, and aggregation, forming the primary hemostatic plug.D. Tissue factor is released and other coagulation factors are activated. Ultimately, this results in formation of the secondary/stable hemostatic plug through fibrin deposition and polymerization on local phospholipid surfaces (mainly platelet surfaces, but also other cells that have been incorporated into the hemostatic plug). ECM=extracellular matrix.
Figure 4.1 Hemostasis. A. Normal undamaged blood vessel. B. Transient vasoconstriction occurs at site of vascular injury through the action of endothelin and similar molecules as well as neural factors. C. Platelets adhere to damaged endothelium/subendothelium. Adhesion is strengthened through subendothelial/collagen-bound von Willebrand factor (vWF) binding to its receptor on the platelet surface. Platelets undergo shape change, release of granule contents, and aggregation, forming the primary hemostatic plug. D. Tissue factor is released and other coagulation factors are activated. Ultimately, this results in formation of the secondary/stable hemostatic plug through fibrin deposition and polymerization on local phospholipid surfaces (mainly platelet surfaces, but also other cells that have been incorporated into the hemostatic plug). ECM=extracellular matrix.
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Veterinary Clinical Pathology: An Introduction Copyright © by Marion Jackson; Beverly Kidney; and Nicole Fernandez is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, except where otherwise noted.

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