Exam 3 Flashcards
What is the most likely mechanism of pesticide exposure to animals and what type of animal is most likely affected and why?
oral
cats - likely liking products/ingesting
organophosphate
MOA
treatment
inhibits AChE
atropine or 2-PAM
oral & dermal decontamination
carbamates
MOA
treatment
inhibits AChE
atropine
oral & dermal decontamination
organochlorine (DDT & aryl hydrocarbons/cyclodienes)
MOA
treatment
DDT- slows Na influx & K efflux causing depolarization (more pronouced at temp <30 degrees C)
aryl hydrocarbons & cyclodienes inhibit GABA
NO antidotes - oral (activated charcoal & mineral oil) & dermal decontamination & anti-seizure meds
Pyrethrins & Pyrethroids
MOA
treatment
depolarization of excitable membranes via interaction with Na+ channels
NO antidotes - dermal decontaminations, methocarabmol & diazepam
alternatives include barbiturates, isoflurane or CRI propofol
Rotenone
MOA
treatment
inhibits oxidation of NADH to NAD+, inhibiting transfer of e- = decreased ATP
NO antidotes -symptomatic/supportive treatment (diazepam & glucose)
Fipronil (frontline)
MOA
treatment
inhibits GABA regulated Cl channels “pro-seizure”
symptomatic & supportive - dermal decontamination
Imidacloprid
MOA
treatment
HIGHLY SPECIFIC FOR INSECTS (esp bees) - neonicotinoid compound - acts on postsynapatic nicotinic R in CNS of insects “biphasic response”
low toxicity in mammals (a7 R) so symptomatic - dermal & oral decontamination
Ivermectin & Selamectin
MOA
treatment
hyperpolarization via binding to glutamate gated Cl- channels in invertebrates = paralysis & death & GABA agonist (which is resp for toxicity in mammals)
Physostigmine, symptomatic, oral decontamination, IV lipid emulsion
Amitraz
MOA
treatment
alpha-2 agonist
inhibits monoamine oxidase
atipamezole/yohimbine, diazepam, saline cathartics
contraindications: atropine, emesis and activated charcoal (due to ileus)
Metaldehyde
MOA
treatment
snails/slugs - torpid & dehydration
birds/mammals - poss due to metaldehyde/acetaldehyde crossing BBB & releasing 5-HT & NE
apomorphine, methocarbamol, diazepam/phenobarbital, fluids, bicarbonate
DEET
MOA
treatment
unknown MOA
diazepam/phenobarbital, dermal or GI decontamination
How does the persistent nature of organochlorine pesticides relate to their relevance as toxins to animals?
highly persistent in the environment and in organisms and bioaccumulate
What are the clinical signs for pyrethroid poisoning (in cats) and how do you treat pyrethroid poisoning in animals improperly treated with a spot-on product?
paresthesia
cats (when treated with dog products) - hypersalivation, paw shaking, ear, skin twitching, flicking of tail
higher doses = seizures
dermal decontamination - bathing + supportive care
What is the basis of the old adage “White Feet, Don’t Treat” with regards to the use of ivermectin as an anti-parasitic agent?
Collies show toxicity at low doses due to a mutation in mdr1 (PGP, ABCB1)
What are the treatment options for amitraz poisoning? What issues arise with regards to the use of anti-cholinergic therapies?
atipamezole & yohimbine
atropine is contraindicated due to hypertension & ileus
avoid activated charcoal due to ileus
Diethyltoluamide (DEET) is widely used as an insect repellant on humans. What are the issues regarding its’ use on pets or livestock?
toxicity is low, most animals recover quickly
limit toxicosis with < 50% deet
What are the most likely mechanisms for exposure to herbicides and fungicides and how do potential exposures relate to dose and toxicity?
contact + grooming
fluid run off (highest concentration & most toxic)
discarded waste
grazing
What are the differences between paraquat and diquat with regards to mechanism of. action and organ specific toxicities?
both damage through ROS
Paraquat - accumulates in the lung via diamine-polyamine concentrator system in alveolar epithelial cells
Diquat - accumulates in GI, liver, kindey NOT the lungs
What is the toxic component of herbicide formulations?
carcinogenicity due to TCDD (dioxin) contamination in some formulations of 2,4,5-T
What are the potential acute vs. chronic toxicoses associated with Phenoxy Herbicides (2,4-D)
uncoupling of oxidative phosphorylation & direct irritant leads to…
myotonia, vomiting, opisthotonus (w/ high doses), necrotic ulcers, GI irritant, focal liver necrosis, degeneration of renal tubules, TCC in scottish terriers
What are the potential acute vs. chronic toxicoses associated with Paraquat?
acute - GI pain/vomiting, renal failure, pulmonary fibrosis
chronic - hyperplasia of type II alveolar epithelial cells & fibrosis
What are the potential acute vs. chronic toxicoses associated with Diquat?
anorexia, GI distension, renal impairment, CNS excitement, convulsions
What are the potential acute vs. chronic toxicoses associated with Phosphonomethyl Amino Acids (Glyphosate & Glufosinate)
irritating effects of anionic surfactant (polyoxyethyleneamines) = hypersalivation, vomiting, diarrhea, anorexia, lethargy
What are the potential acute vs. chronic toxicoses associated with Triazines & Triazoles (atrazine)?
grazing animals more risk(long lasting on pasture)
low toxicity, unlikely acute hazard during normal use
Pentacholorphenol
MOA
uncouples oxidative phoshorylation = irritant and CNS effects, pyrexia
Chromated Copper Arsenate (CCA)
ingested of ash of burned lumber - arsenic is liberated and bioavailable
Thiram
sulfure odor
weakness, incoordination, paralysis
What is the most likely mechanism of exposure of avicides to non-target species?
ingestion of bait
contaminated water
Are these agents (3-CPT and 4-PT) selective for target bird species? If so, which and what is the mechanism by which they are selective?
3-CPT
- starlings, red-winged blackbirds, crows, chickens, turkeys
- metabolized diff in sensitive & resistant bird species
- sensitive birds metabolize to reactive form quickly = kidney damage
- mammals get methemoglobinemia
4-PT
- inhibits K+ channels
- birds & mammals = tonic/clonic seizures and cardiac arrhythmias, horses/cattle walk backwards
Are there specific treatments for 4-AP toxicosis outside of supportive and symptomatic treatments?
no -
diazepam/barbiturates for seizures
pancuronium bromide
xylazine for tremors
propranolol for tachyarrhythmias
intubation to protect resp tract
What is the most likely mechanism for exposure of rodenticides to non-target species?
pellets, wax blocks, tracking powder
humans mix bait with foods to attract rodents
For anticoagulant rodenticides, what is the major determining factor for the duration of toxicosis?
HALF LIFE of rodenticide and plasma clotting factors
e.g. warfarin 14 days, brodifacoum 30 days
For anticoagulant rodenticide ingestion, if the animal is asymptomatic, what is the schema of treatment?
GI decontamination
PT or PIVKA monitoring
treat with low dose vitamin K1
For anticoagulant rodenticide ingestion, if the animal is symptomatic, what is the schema of treatment?
stabilize if shocky or dyspneic
whole blood, plasma or synthesis blood administered if hemorrhaging
coag & blood counts performed
high dose vitamin K1
rest - NOT exercise
Which of the rodenticide agents may cause secondary poisonings via the eating of rodents that are killed?
bromethalin
“relay toxicosis”
How is the mechanism of action of cholecalciferol (vitamin D3) related to its’ toxicity and treatment?
metabolized to calcitriol is the kidney -> increase in Ca & P -> direct effects on cells (cell necrosis) -> mineralization of kidneys, GI, cardiac, skeletal m, blood vessels and ligaments
toxicity of cholecalciferol
vomiting, diarrhea, anorexia, PUPD, renal failure, loss of MSK function, cardiac abnormalities
treatment for cholecalciferol toxicity
GI decontamination, monitor kidney values, Diuresis with 0.9% saline, furosemide, prednisone, phosphate binders with low Ca/P diet, bisphosphate pamidronate or salmon calcitonin
Are there specific toxicities or attributes associated with strychnine poisoning?
inhibition of glycine = opisthotonus
Sodium Fluoroacetate MOA and treatment
inhibits TCA cycle = no ATP & depletion of Ca2+
sodium bicarbonate
Zinc Phosphide MOA
rapidly forms phosphine gas in acidic conditions (enzyme dependent) - blocks cytochrome oxidase & oxidative phosphorylation
increases ROS
Why is there a difference in the potential toxicity of zinc phosphide in animals that can or cannot vomit?
some formulations contain an emetic
induces vomiting in animals that can vomit
non-target species freq vomit preventing poisoning
