Changes

Anticoagulant rodenticide toxiticy is one of the most common causes of acquired coagulopathy in small animals. Warfarin itself has a short half-life and a fairly low toxicity in non-rodent species, so unless large or repeated doses are consumed clinical bleeding is rare. However, the second generation anticoagulant rodenticides are far more potent, with  tendency to accumulate in the liver and a long half life (4-6 days) owing to high levels of plasma protein binding^{2, 3}. These newer drugs are therefore more commonly implicated in cases of poisoning³, and it is possible for a domestic animal to acquire secondary poisoning by ingesting a killed rodent².

Anticoagulant rodenticide toxiticy is one of the most common causes of acquired coagulopathy in small animals. Warfarin itself has a short half-life and a fairly low toxicity in non-rodent species, so unless large or repeated doses are consumed clinical bleeding is rare. However, the second generation anticoagulant rodenticides are far more potent, with  tendency to accumulate in the liver and a long half life (4-6 days) owing to high levels of plasma protein binding^{2, 3}. These newer drugs are therefore more commonly implicated in cases of poisoning³, and it is possible for a domestic animal to acquire secondary poisoning by ingesting a killed rodent².

 

The coumarin derivatives exert interaction of

The coumarin derivatives exert interaction of

their anticoagulant eftect by inhibiting the enzyme, vitamin K epoxide reductase (see box on page 63). This enizymiie is a component of

their anticoagulant eftect by inhibiting the enzyme, vitamin K epoxide reductase (see box on page 63). This enizymiie is a component of