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Mechanism of action
Sign of toxicity
Diagnosis
Treatment
Anticholinesterase insecticides
Organophosphates
Carbamates
Variable toxicity
Toxicity usually occurs from misuse of
products or improper storage
3 stages of intoxication
stage I (30 min 3 hrs) ,drunkness, ataxia
stage II (12- 24 hrs)
1. tachypnea, tachycardia (or bradycardia)
2. often not observed
stage III (12 72 hrs) oliguric renal failure
Acetaminophen
Present in many overcounter pain and odd
remedies
GI decontamination
N- acetylcysteine (Mucomyst) to replenish and
substitute for GSH
Ascorbic acid used to treat methemoglobinemia
in cats, methylene blue in other animals
Monitor EKG
- treat tachyarrhthmias with lidocaine (not in
cats) or metoprolol
Treat seizures with diazepam or barbiturates
Methylxanthines
Antagonist of adenosine
Caffeine, theobromine, theophylline
receptors; causes CNS
stimulation, vasoconstriction and
Usually a problem with dogs due to eating
tachycardia
habits
Prevent Ca++ reuptake
Found in chocolate, coffee, medications
Unsweetened baking chocolate is especially Inhibits phosphodiesterase
toxic; as little as 0.2 oz/kg may kill a dog
Anticoagulant rodenticides
First generation compounds
o Warfarine (halflife=14-15 hrs)
o Short half life(hrs) low potency
Second genarampound
o Brodifacoum, bromodialone,
diaphacinone
o Long half life (15- 20 days); high
potency
Usually a problem in small animals
Large animals can develop similar
problems from sweetclover
Vomiting, diarrhea
Hyperactivity
Tachycardia, PVC, hypertension
Ataxia
tremors, seizures
coma
Strychnine
Competitive inhibitor of glycine
Alkaloid used as pesticide to control
at post synaptic neurons
gophers, moles, rats and coyotes
Glycine is inhibitory so result is
Controlled in most states
disinhibition (simulatioin)
Still commonly used as a malicious poison
All species are sensitive but dogs are most
commonly poisoned
Toxicology
acidosis
anion and osmolal gap
crystalluria
crystals in kidney
Vit K administration
Therapy should be continued for 10 14 days
with warfarine
21 30 days for second generation comounds
Melaldehyde
Slug and snail baits
Generally 3.5% metaldehyde
Ingestion of 1-4 oz of bait will cause
toxicity in average dog
Toxicity is most common in dogs
Metaldehyde is hydrolyzed to
acetaldehyde by gastric acids
Further metabolism of
acetaldehyde to acidic products
thought to account to acidosis
Exact mechanism in unknown
Cholecalciferol
Vit D3
Used as a rodenticide and psoriasis
treatment
Usually sold as a bait preparation
Toxicity occurs at doses above 0.5 mg/kg
Metabolized to 1, 25dihydroxycholecalciferol
Increased serum Ca by increasing
GI absorption, decreasing renal
excretion, and simulating bone
resorption
Vomiting, diarrhea
PD/PU, radio-opaque kidneys
Elevated serum Cs (>11.5 mg.dl), BUN
and creatinine
Mineralized of soft tissues
Lead
Multiple actions. May based on
Affects large and small animals; waterfowl the reaction of Pb with SH
groups of key enzymes and effects
Sources include old paints, oil, grease,
on calcium regulations
batteries, lead shot
Lead inhibits delta-aminolevulinic
Toxicity usually results from acute oral
acid dehydratase and heme
exposures
synthetase, both involved in heme
synthesis
Cyanide
Acts by inhibiting cytochrome
Released from cyanogenic glycosides
oxidase which inhibits oxidative
found in some plants (wild cherry and other phosphorylation
prunus spp), sudan and johnson grass
Toxicology