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Anticoagulant Rodenticide Toxicity (view source)
Revision as of 14:25, 23 August 2010
, 14:25, 23 August 2010→Mechanism of Toxicity
Normally, haemostastis is maintained by three key events<sup>4</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>4</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.
Two simultaneous cascades are activated to achieve coagulation: the intrinsic and extrinsic pathways. These converge at the common pathway, which eventually results in the formation of fibrin from fibrinogen. The factors involved in the intrinsic pathway are
Two simultaneous cascades are activated to achieve coagulation: the intrinsic and extrinsic pathways. The intrinsic pathway is activated by contact with collagen and involves the clotting factors XII, XI, IX and VIII. The extrinsic pathway is triggered by trauma and contact with "tissue factor", and involves the factor VII. These pathways progress independently before converging at the common pathway, which involves the factors X, V, II and I and ultimately results in the formation of fibrin from fibrinogen.
Within each independent (intrinsic, extrinsic) pathway and in the common pathway, at least one coagulation (clotting) factor that depends on the action of vitamin K for its synthesis is involved. When vitamin K is deficient or inhibited, the flow of the cascade is interrupted, preventing eventual formation of the insoluble fibrin polymer.
Within each independent (intrinsic, extrinsic) pathway and in the common pathway, at least one coagulation (clotting) factor that depends on the action of vitamin K for its synthesis is involved. When vitamin K is deficient or inhibited, the flow of the cascade is interrupted, preventing eventual formation of the insoluble fibrin polymer.