Abstract
Physiological haemostasis is the process by which blood is maintained in a fluid state in the absence of vascular injury, but is able to rapidly form thrombus if a breach in vascular integrity occurs. Multiple components, both circulating in the intravascular compartment and located in the sub-endothelial matrix, contribute to the haemostatic process. Proteins and cells involved in haemostasis circulate in a resting or unactivated state in the presence of an intact endothelium. Exposure to components of the subendothelium leads to activation of platelets and the coagulation system, resulting in thrombus formation. Primary haemostasis, resulting from interaction between platelets and subendothelial adhesive proteins (von Willebrand factor and collagen), results in the sequential occurrence of platelet adhesion, activation and ultimately aggregation. This enables a stable platelet plug to be formed. Secondary haemostasis then follows, resulting from activation of the enzymes of the coagulation cascade that leads to the formation of a cross-linked fibrin network. This process is kept in check by numerous inhibitory proteins, localizing the haemostatic response to areas of vascular injury and preventing widespread clot formation. Once haemostasis is intact, the fibrinolytic system is responsible for the removal of fibrin leading to restoration of vessel patency.
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Further Reading
Hoffman M, Monroe DM. A Cell-based Model of Hemostasis. Thromb Haemost. 2001;85:958–65.
Jackson S. The growing complexity of platelet aggregation. Blood. 2007;109:5087.
O’Donnell JS, O’Sullivan JM, Preston RJS. Advances in understanding the molecular mechanisms that maintain normal haemostasis. Brit J Haematol. 2019;186:24–36.
Ruggeri ZM. Structure and function of von Willebrand factor. Thromb Haemost. 1999;82:576–84.
Ware JA, Heistad DD. Seminars in medicine of the Beth Israel Hospital, Boston. Platelet-endothelium interactions. N Engl J Med. 1993;328:628–35.
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McRae, S. (2020). Physiological Haemostasis. In: Fitridge, R. (eds) Mechanisms of Vascular Disease. Springer, Cham. https://doi.org/10.1007/978-3-030-43683-4_9
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DOI: https://doi.org/10.1007/978-3-030-43683-4_9
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