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VM 751 Toxicology > Tox exam 2 > Flashcards

Tox exam 2 Flashcards

1
Q

Organophosphates (nerve gas) and Carbamates (CNS reversal)

A
  • Inhibit AChE (enhance parasymp)
  • Physostigmine - carbamate that reverses ivermectin toxicosis, larkspur
  • exposure is oral (grooming) or dermal b/c ectoparasiticide
  • see SLUDGE, muscle/neuro stim
  • death by resp/cardiac arrest
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2
Q

Which has a shorter half-life - carbamates or organophospates

A

carbamates 15-30 mins

OP’s days - AChE inhibition is irreversible

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3
Q

Test for OP/CM toxicity

A

measure AChE activity

>70% activity inhibited = toxicity

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4
Q

Treat OP/CM toxicity

A

limit exposure first (oral or dermal)
Atropine to block ACh (CM & OP) - to reduce parasymp
2-PAM for OP - reactivates AChE

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5
Q

What’s the major concern about organochlorines

A
  • Persistent in environment - why no longer used (half-life days to weeks)
  • accum in liver, brain, kidneys, fat
  • neural toxicity by chronic exposure
  • Causes excess NT release by inhibiting GABA binding
  • Cats more sensitive
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6
Q

Pyrethrins & Pyrethroids (mosquito repellents, insecticides)

A
  • oral/dermal/inhaled exposure, lipophilic (wide distribution)
  • rapid metabolism (12-48 hrs)
  • CATS when inappropriately treated or licks product off dog = hypersalivation, agitated –> tremors –> seizures in 18-20 hrs
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7
Q

Rotenone (insecticide)

A
  • Inhaled, oral
  • Inhibits ox phos –> cells have E defecit
  • selective toxicity for fish, insects b/c of metabolism so mammal toxicity rare
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8
Q

Fipronil (insecticide)

A
  • active ingredient for Frontline
  • exposure by ingestion/licking product
  • inhibits GABA –> hyperexcitation, pro-seizure
  • fish, rabbits highly susceptible
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9
Q

Imidacloprid (insecticide mostly for crops)

A
  • highly specific for insect nicotinic receptor subtypes - high margin of safety for mammals
  • first increases sponaneous nerve discharge –> full nerve block
  • if potency in mammals it’s the alpha 7 subtype
  • absorption & elimination rapid - immediate supportive care needed for recovery
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10
Q

Ivermectin & Selamectin (external and external parasites)

A
  • 5x longer half life in cats, don’t give to collies
  • rapidly absorbed, large vol of distribution, slow elimiantion (5-7 days)
  • high affinity binding for glutamate-gated Cl channels of microfilaria (GABA receptor agonist)
  • doens’t act in nervous sys of mammals, does in parasite (hyperpolarizes cells)
  • Physostigmine can only reverse effects to prove diagnosis, not treat
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11
Q

Why “white feet don’t treat”

A

Some breeds (collies) have ABCB1 gene mutation - transporter can’t pump ivermectin out of brain = toxicity

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12
Q

Amitraz

A
  • exposure often by tick collar ingestion
  • alpha 2 agonist –> CNS depression, profound bradycardia, hypoglycemia
  • In EQ, GI stasis –> fatal ileus is concern
  • reversible by Yohimbine, Atipamezole (alpha 2 antagonists) NOT atropine (can worsen ileus, hypertension)
  • also give saline cathartics once stable
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13
Q

Metaldehyde (molluscicide)

A
  • death to snails and slugs by dehydration, torpidity
  • CNS, metabolic acidosis, resp alkilosos in mammals
  • dogs in coastal areas = acute exposure
  • aggressive decontamination, good supportive care up to 5 days but usually within 12-72 hrs w/ treatment
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14
Q

DEET (insect repellent)

A
  • Mosquitos don’t like the smell

- toxicity avoided by using products <50% deet

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15
Q

Methods of exposure for herbicides

A

walking on treated grass then grooming
runoff
ingestion of undilute product

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16
Q

What toxins mess with ox-phos

A 
Rotenone
Phenoxy herbicides (2,4-D)
Pentachlorophenol
Bromethalin
Zinc phosphide
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17
Q

2,4-D (phenoxy herbicide)

A
  • ingestion of undilute product
  • uncouples ox-phos
  • dogs more sensitive - saturable route of elimination (renal) = longer half life, more toxicity
  • opisthotonos
  • caustic damage to GI, kidney, liver
  • recovery good w/ supportive care, forced alkaline diuresis (traps it, forces elimination)
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18
Q

What thing does 2,4-D exposure ABSOLUTELY increase the risk of

A

TCC of the bladder in scottish terriers

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19
Q

Paraquat (Dipyridyl herbicide)

A
  • ingested before binds to soil
  • accumulates in lungs preferentially
  • prognosis really guarded especially w/ delayed treatment b/c fibrosis (decontaminate, eliminate, support)
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20
Q

Diquat (Dipyridyl herbicide)

A
  • no preferential accumulation
  • must be directly consumed to get toxicity
  • CNS signs, anorexia, GI distention, renal issues
  • prognosis good (adsorbants, support, antioxidants, forced diuresis)
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21
Q

Phophonomethly Amino Acids (Glyphosphate, Glufosinate)

A
  • water soluble

- wide margin of safety - issue is it’s usually in a soapy product (anionic surfactants)

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22
Q

Phophonomethly Amino Acids (Glyphosphate, Glufosinate)

A
  • water soluble
  • wide margin of safety - issue is it’s usually in a soapy product (anionic surfactants)
  • If ingested, small amounts of water + NPO
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23
Q

Triazines & Triazoles (herbicides)

Atrazine most common type

A

sheep and cattle have high sensitivity
avoid grazing on treated pasture
SA little risk

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24
Q

Pentachlorophenol (fungicide)

A

treated wood chips for bedding
Inhaled or dermal absorption
uncouples ox-phos
CNS effects

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25
Q

Chromated copper arsenate (CCA) (fungicide)

A

Treated lumber

high toxicity in livestock that ingest ash of the burned lumber

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26
Q

Thiram (fungicide)

A

sulfur smell
high dose needed for toxicity
humans commonly have allergic hypersensitivity

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27
Q

3-CPT (Starlicide)

A

Mostly selective for starlings, blackbirds
rapidly metabolized/cleared –> renal damage & failure
Methemoglobinemia in mammals
supportive care - maintain temp

28
Q

4-AP (Avitrol)

A

toxic for all birds
Dogs cats get exposed at production sites
Rapidly absorbed, rapid toxicity (15 min), death in 4 hrs
Blocks K channels —> enhance nerve impulses
If survives past 4 hrs will probably be ok

29
Q

Anticoagulant rodenticides

A

half-life varies depending on compound (15 days, 30 days)
Inhibits vit K reduction –> no active clotting factors
Relat toxicosis possible
Vague clinical signs - dyspnea, joint swelling, neuro, sudden death
Vit K + blood transfusions
only decontaminate if asymptomatic (3-5 days for signs to occur)

30
Q

Bromethalin

A

For Warfarin-resistant rodents
Relay toxicosis can occur (half life 5-6 days)
uncouples ox-phos
High dose exposure - neuro stuff 4-18 hrs after
low dose exposure = progressive paresis/paralysis mild CNS depression 2-7 days

31
Q

Cholecalciferol (Vit D3)

A

buildup of vit D metabolites –> increased Ca, P –> soft tissue mineralization, altered fx
SA - acute toxicosis 12-36 hrs
Monitor blood values 96 hrs, furosemide & prednisone to diurese, increase Ca loss

32
Q

compound 1080 (Sodium Fluoroacetate)

A

sheep protection collars
Rapid absorption (2-3 hrs), blocks Kreb’s cycle = decreased ATP
2-3 hrs toxic to mammals - cardiac, neuro
Prognosis poor b/c rapid onset

33
Q

Strychnine (gopher bait)

A

Blocks glycine –> excessive neuronal activity
rapid exposure 10-120 min, wide distribution
Opisthotonos
Dogs - accidental or malicious poisoning, can see relay toxicosis
ACTIVATED CHARCOAL w/ sorbitol + extensive support 1-3 days

34
Q

Zinc Phosphide (rodenticide)

A

Rapidly forms phospine gas in acidic conditions
Dogs w/ empty stomach may survive
blocks ox-phos
Vomiting in animals that can (aka SA do ok, rodents die)

35
Q

Ibuprofen

A

can be used but other ones work better in dog
Carprofen more specific for dog cox 2 - less GI effects
GI damage, renal
Cats 2x as sensitive (limited glucoronidation)

36
Q

Naproxen

A

Same as ibuprofen but dogs more sensitive

smaller therapeutic window

37
Q

Aspirin

A

Can control lameness in dogs AT CORRECT DOSE
small margin of safety, more acidic (GI issues)
In cats, half life 5x longer (Glucuronidation)

38
Q

Acetominophen

A

Accidental exposure
Accum of Nab metabolite = tissue damage, GSH depletion
Hepatocellular injury, necrosis
Mehemoglobinemia w/ high doses (esp. cats)
Treatment most effective if w/in 8 hrs
NAC or SANe to counteract toxicity - increase GSH

39
Q

Methemoglobinemia

A

Acetominophen

3-CPT in mammals

40
Q

Pseudoephedrine

A
  • alpha and beta adrenergic agonist (NE release)
  • worse toxicity if combined w/ caffine, ephedrine, or if pre-existing dz
  • hallucinating dogs, cardiovascular collapse, everything overstimmed
  • Acepromazine or phenobarbital NOT diazepam for seizures, agitation
41
Q

Venlafaxine

A

Cats want to eat it
Serotonin-NE reuptake inhibitor = increased symp
Issues w/ extended release
Monitor, serotonin agonists for agitation, decontaminate

42
Q

Amphetamines

A

CNS stim by NE, Epi
Any level of exposure = clin signs in cats (major overstim)
Supportive care, limit absorption, acidify urine to trap & eliminate it

43
Q

Xylitol

A

gum, candies
Causes insulin release –> hypoglycemia
Also GI issues, Hepatic probs, neuro probs
Monitor blood glu, protect liver, decontaminate & supportive care, emesis if asymp

44
Q

Methylxanthines

A

chocolate, teas, coffee, etc.
Think it blocks adenosine –> increased intracellular CA, increased cAMP
cardio, neuro signs 1-4 hrs post exposure
Cats more sensitive but rare (picky eaters)
Good supportive care = good prognosis unless seizures or arrhythmias

45
Q

Cleaning Products - Acids

A

mild irritation to corrosive injury - ulcers
sour taste
coagulative necrosis –> thickening & stricture where direct contact occurred weeks to months later

46
Q

Cleaning Products - Alkalis

A

mild irritation to corrosive injury
no odor or taste (can = greater ingestion)
liquefactive necrosis –> edema, inflamm, transmural necrosis, corrosive injury - ulcers, maybe stricture

47
Q

Treat acid and alkali toxicity

A 
decontaminate skin, oral membranes but NOT GI (neutralizing bad idea = thermal burns)
IV drugs (not PO)
gastroprotection, fluids, analgesia
48
Q

essential oils, liquid potpourri

A

cats more sensitive (glucuronidation)
absorbed through skin, mucous mems
Pennyroyal oil - hepatobilliary, poor outcome
liquid potpourri - good outcome

49
Q

Lithium disk batteries or dry cell batteries are at risk of leaking if stomach acid alters casing?

A

dry cell batteries

50
Q

Batteries cause what problems?

A

ulcers
stridor
hemorrhage, exsanguination
liver, neuro damage w/ heavy metal toxicosis
long term - stricture, esophageal malformation

51
Q

Ethylene Glycol

A

Antifreeze
Cats sensitive - high baseline production of oxalic acid (form calcium oxalate crystals)
GI, neuro, metabolic acidosis, acute oliguric renal failure due to oxalate crystalluria
DEG - diglycolic acid does cause kidney dysfunc but doesn’t make crystals

52
Q

Treat ethylene glycol or DEG poisoning

A

Inhibit metabolism - fomepizole or ethanol (outcompetes)
supportive care, correct acid/base, fluids, get parent compound out
Animal may survive, but renal dysfunc often permanent

53
Q

Propylene Glycol

A

“safer antifreeze”

neuro issue, heinz body anemia in cats

54
Q

3 factors that can influences resp toxicosis

A
  • tissue architecture - certain cell types or tissue pops damaged selectively
  • selective damage depending on cell type or tissue & their metabolic abilities
  • anatomic configuration (nose length_
55
Q

Acute responses to resp toxicosis

A

asphyxiation
UT irritation
pulmonary edema
airway reactivity (bronchial smooth m. constric)

56
Q

Chronic responses to resp toxicosis

A

fibrosis
emphysema
asthma (chronic airway reactivity)
lung cancer

57
Q

Ammonia

A

animal facilities where poop decomposes on solid floor

oral ingestion lead to lung damage (b/c urea formation) - goats

58
Q

Co2

A

breathed out
fuel burning heaters
decomposing manure
>40% conc = toxicity

59
Q

Methane

A

product of microbial degradation (rumen flora)

concern is flammability, lg conc needed to displace oxygen

60
Q

Hydrogen sulfide (h2s)

A

Top COD in closed animal facilites
bacterial processing of materials in liquid manure pits
concern is agitated slurry = sudden, fast high con
mechanical breathing needed to restim resp (besides moving to fresh air)

61
Q

At what conc does Hydrogen sulfide cause olfactory paralysis

A

150-250 ppm

62
Q

Carbon monoxide

A

car exhaust, fires
cherry-red blood, out-competes oxygen to bind to hgb
Prevention key - CO detectors

63
Q

Nitrogen dioxide

A

fermentation of silage - conc’s on top of silage
yellow brown color
Forms corrosive nitric acid - damages LRT lungs where direct contact, moisture conten greater (water insoluble)
>200ppm = death

64
Q

Which is more toxic of nitrogen dioxide - short exposure to high conc or long exposure to low conc

A

short exposure to high conc more toxic

either way prognosis guarded - depends on tissue ability to recover

65
Q

PTFE (teflon) heated products

A

birds uniquely sensitive b/c unidirectional airflow

66
Q

Tryptophan-3 methyl indole (3-MI)

A

cattle + lush pasture
tryptophan –> 3-MI –> liver converts to reactive intermediates –> lung damage
If low-level exposure can recover

VM 751 Toxicology (2 decks)

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