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Anticoagulant Rodenticide Toxicity (view source)
Revision as of 14:13, 23 August 2010
, 14:13, 23 August 2010→Mechanism of Toxicity
===Mechanism of Toxicity===
===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, once the vessel constricts soluble fibrinogen is polymerised to fibrin which reinforces the platelet plug.
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. Aspects of the latter two stages are dependent on vitamin K and it is these which are influenced by anticoagulant rodenticide activity.
This discussion addresses only those components of the coagulation mechanism (active in the second to third phases) whose concentration in plasma is influenced by vitamin K and only those compounds which act as vitamin K antagonists.
This discussion addresses only those components of the coagulation mechanism (active in the second to third phases) whose concentration in plasma is influenced by vitamin K and only those compounds which act as vitamin K antagonists.