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Toxicology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is the most likely mechanism of pesticide exposure to animals and what type of animal is most likely affected and why?

A

oral
cats - likely liking products/ingesting

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2
Q

organophosphate
MOA
treatment

A

inhibits AChE
atropine or 2-PAM
oral & dermal decontamination

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3
Q

carbamates
MOA
treatment

A

inhibits AChE
atropine
oral & dermal decontamination

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4
Q

organochlorine (DDT & aryl hydrocarbons/cyclodienes)
MOA
treatment

A

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

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5
Q

Pyrethrins & Pyrethroids
MOA
treatment

A

depolarization of excitable membranes via interaction with Na+ channels
NO antidotes - dermal decontaminations, methocarabmol & diazepam
alternatives include barbiturates, isoflurane or CRI propofol

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6
Q

Rotenone
MOA
treatment

A

inhibits oxidation of NADH to NAD+, inhibiting transfer of e- = decreased ATP
NO antidotes -symptomatic/supportive treatment (diazepam & glucose)

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7
Q

Fipronil (frontline)
MOA
treatment

A

inhibits GABA regulated Cl channels “pro-seizure”
symptomatic & supportive - dermal decontamination

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8
Q

Imidacloprid
MOA
treatment

A

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

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9
Q

Ivermectin & Selamectin
MOA
treatment

A

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

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10
Q

Amitraz
MOA
treatment

A

alpha-2 agonist
inhibits monoamine oxidase
atipamezole/yohimbine, diazepam, saline cathartics

contraindications: atropine, emesis and activated charcoal (due to ileus)

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11
Q

Metaldehyde
MOA
treatment

A

snails/slugs - torpid & dehydration
birds/mammals - poss due to metaldehyde/acetaldehyde crossing BBB & releasing 5-HT & NE
apomorphine, methocarbamol, diazepam/phenobarbital, fluids, bicarbonate

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12
Q

DEET
MOA
treatment

A

unknown MOA
diazepam/phenobarbital, dermal or GI decontamination

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13
Q

How does the persistent nature of organochlorine pesticides relate to their relevance as toxins to animals?

A

highly persistent in the environment and in organisms and bioaccumulate

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14
Q

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?

A

paresthesia
cats (when treated with dog products) - hypersalivation, paw shaking, ear, skin twitching, flicking of tail
higher doses = seizures
dermal decontamination - bathing + supportive care

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15
Q

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?

A

Collies show toxicity at low doses due to a mutation in mdr1 (PGP, ABCB1)

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16
Q

What are the treatment options for amitraz poisoning? What issues arise with regards to the use of anti-cholinergic therapies?

A

atipamezole & yohimbine

atropine is contraindicated due to hypertension & ileus
avoid activated charcoal due to ileus

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17
Q

Diethyltoluamide (DEET) is widely used as an insect repellant on humans. What are the issues regarding its’ use on pets or livestock?

A

toxicity is low, most animals recover quickly
limit toxicosis with < 50% deet

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18
Q

What are the most likely mechanisms for exposure to herbicides and fungicides and how do potential exposures relate to dose and toxicity?

A

contact + grooming
fluid run off (highest concentration & most toxic)
discarded waste
grazing

19
Q

What are the differences between paraquat and diquat with regards to mechanism of. action and organ specific toxicities?

A

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

20
Q

What is the toxic component of herbicide formulations?

A

carcinogenicity due to TCDD (dioxin) contamination in some formulations of 2,4,5-T

21
Q

What are the potential acute vs. chronic toxicoses associated with Phenoxy Herbicides (2,4-D)

A

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

22
Q

What are the potential acute vs. chronic toxicoses associated with Paraquat?

A

acute - GI pain/vomiting, renal failure, pulmonary fibrosis
chronic - hyperplasia of type II alveolar epithelial cells & fibrosis

23
Q

What are the potential acute vs. chronic toxicoses associated with Diquat?

A

anorexia, GI distension, renal impairment, CNS excitement, convulsions

24
Q

What are the potential acute vs. chronic toxicoses associated with Phosphonomethyl Amino Acids (Glyphosate & Glufosinate)

A

irritating effects of anionic surfactant (polyoxyethyleneamines) = hypersalivation, vomiting, diarrhea, anorexia, lethargy

25
Q

What are the potential acute vs. chronic toxicoses associated with Triazines & Triazoles (atrazine)?

A

grazing animals more risk(long lasting on pasture)
low toxicity, unlikely acute hazard during normal use

26
Q

Pentacholorphenol
MOA

A

uncouples oxidative phoshorylation = irritant and CNS effects, pyrexia

27
Q

Chromated Copper Arsenate (CCA)

A

ingested of ash of burned lumber - arsenic is liberated and bioavailable

28
Q

Thiram

A

sulfure odor
weakness, incoordination, paralysis

29
Q

What is the most likely mechanism of exposure of avicides to non-target species?

A

ingestion of bait
contaminated water

30
Q

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?

A

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

31
Q

Are there specific treatments for 4-AP toxicosis outside of supportive and symptomatic treatments?

A

no -
diazepam/barbiturates for seizures
pancuronium bromide
xylazine for tremors
propranolol for tachyarrhythmias
intubation to protect resp tract

32
Q

What is the most likely mechanism for exposure of rodenticides to non-target species?

A

pellets, wax blocks, tracking powder
humans mix bait with foods to attract rodents

33
Q

For anticoagulant rodenticides, what is the major determining factor for the duration of toxicosis?

A

HALF LIFE of rodenticide and plasma clotting factors
e.g. warfarin 14 days, brodifacoum 30 days

34
Q

For anticoagulant rodenticide ingestion, if the animal is asymptomatic, what is the schema of treatment?

A

GI decontamination
PT or PIVKA monitoring
treat with low dose vitamin K1

35
Q

For anticoagulant rodenticide ingestion, if the animal is symptomatic, what is the schema of treatment?

A

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

36
Q

Which of the rodenticide agents may cause secondary poisonings via the eating of rodents that are killed?

A

bromethalin
“relay toxicosis”

37
Q

How is the mechanism of action of cholecalciferol (vitamin D3) related to its’ toxicity and treatment?

A

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

38
Q

toxicity of cholecalciferol

A

vomiting, diarrhea, anorexia, PUPD, renal failure, loss of MSK function, cardiac abnormalities

39
Q

treatment for cholecalciferol toxicity

A

GI decontamination, monitor kidney values, Diuresis with 0.9% saline, furosemide, prednisone, phosphate binders with low Ca/P diet, bisphosphate pamidronate or salmon calcitonin

40
Q

Are there specific toxicities or attributes associated with strychnine poisoning?

A

inhibition of glycine = opisthotonus

41
Q

Sodium Fluoroacetate MOA and treatment

A

inhibits TCA cycle = no ATP & depletion of Ca2+
sodium bicarbonate

42
Q

Zinc Phosphide MOA

A

rapidly forms phosphine gas in acidic conditions (enzyme dependent) - blocks cytochrome oxidase & oxidative phosphorylation
increases ROS

43
Q

Why is there a difference in the potential toxicity of zinc phosphide in animals that can or cannot vomit?

A

some formulations contain an emetic
induces vomiting in animals that can vomit
non-target species freq vomit preventing poisoning

Toxicology (15 decks)

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