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Anticoagulant Rodenticide Toxicity (view source)
Revision as of 12:31, 23 August 2010
, 12:31, 23 August 2010→Description
==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==