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Haemostasis is a complex process involving blood vessels, platelets and coagultion proteins. It is divided into a vascular/platelet phase (primary haemostasis) and a subsequent coagulation phase (secondary haemostasis). The end product of haemostasis is a solid clot composed of fused platelest enclosed in a mesh of fibrin strands. Excessive clot formation is prevented by the fibrinolytic system, which acts to breakdown fibrin within blood clots.
Haemostasis is a complex process involving blood vessels, platelets and coagultion proteins. It is divided into a vascular/platelet phase (primary haemostasis) and a subsequent coagulation phase (secondary haemostasis). The end product of haemostasis is a solid clot composed of fused platelest enclosed in a mesh of fibrin strands. Excessive clot formation is prevented by the fibrinolytic system, which acts to breakdown fibrin within blood clots.
Primary haemostasis starts with vasoconstriction triggered by vessel injury, and continues until vessel integrity is restored and bleeding stops. As well as lacerations, vascular damage may result from trauma, excessive turbulense, indwelling catheters, or inflammation (endocarditis). Plates respond to vessel injusry be adhhereing to vascular subendothelium (adhesion) and to other platelets (primary aggreggation), changing shape and releaseing substances which promote vasoconstriction and activate more platelets (the relsease reaction). Platelet contraction and aaggregation triggered by the substances released by the platelets (secondary aggregation) continue until the injusty is sealed by a fragile platelet plug.
Normally, haemostastis is maintained by three key events<sup>3</sup>. Firstly, platelets are activated, adhere to endothelial connective tissue and aggregate to form a platelet plug. Next, substances are released that trigger coagulation and vasoconstriction. Finally, fibrinogen is polymerised to fibrin which reinforces the platelet plug. Some components of the coagulation and fibrin formation stages are dependent on vitamin K, and it is these which are influenced by anticoagulant rodenticide activity.
Normally, haemostastis is maintained by three key events<sup>3</sup>. Firstly, platelets are activated, adhere to endothelial connective tissue and aggregate to form a platelet plug. Next, substances are released that trigger coagulation and vasoconstriction. Finally, fibrinogen is polymerised to fibrin which reinforces the platelet plug. Some components of the coagulation and fibrin formation stages are dependent on vitamin K, and it is these which are influenced by anticoagulant rodenticide activity.