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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.
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.
Primary haemostasis alone will only be temporarily beneficial unless the platelet plug is reinforced by fibrin assembled by the clotting cascade (secondary haemostsis). Secondary haemostasis is dependent on the interactions of a number of proteins (clotting factors) within the intrinsic, extrinsic and common pathways of the cascade. The clotting factors aer synthesisde in the liver. The factors circulate in the plasma in an inactive from. Fatos I, VII, IX and X are dependent upon vitamin K to become active.
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.