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Anticoagulant Rodenticide Toxicity (view source)
Revision as of 12:31, 23 August 2010
, 12:31, 23 August 2010→Description
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==Description==
==Description==
+One of the most common causes of an acquired coagulopathy
+in dogs is the accidental ingestion of an anticoagulant
+rodenticide. The first generatlion
+coumarin-derivative anticoagulant,
+warfarin. has a short half-life
+of about 12 hours and a relatively
+low toxicity in non-target species.
+Therefore, repeated or massive exposure
+would generally be required to
+produce clinical bleeding in a dog.
+The second generation coumarin
+derivatives (bromadiolone and brodifacoum)
+and indandione rodenticides
+(pindone and diaphacinone), developed
+in response to wartarin resistance
+in target species, are tar more
+potent than warfarin. They have much
+longer lasting etfects (half-lives of
+four to six days) as they are more
+completely bound to plasmla proteins
+and, compared to warfarin, have an
+enhanced tendency to accumulate in
+hepatic tissue. Secondary poisoning
+through ingestion ol killed target
+species is more likely to occur with
+these latter agents.
+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
+the vitamin K epoxide cycle required tf)r hepatic synthesis
+of the functional clotting factors F-II, F-VII, F-IX and
+F-X. Inhibition of the enzyme causes the accumulation of the inactive vitamin K epoxide and prevents the carboxylation
+of vitamin K-dependent coagulation proteins. The
+acarboxy precursor proteins are incapable of being activated
+during the coagulation process and thus cannot
+actively participate in fibrin formation.
==Signalment==
==Signalment==