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
Chromated copper arsenate (CCA) (fungicide)
Treated lumber | high toxicity in livestock that ingest ash of the burned lumber
26
Thiram (fungicide)
sulfur smell high dose needed for toxicity humans commonly have allergic hypersensitivity
27
3-CPT (Starlicide)
Mostly selective for starlings, blackbirds rapidly metabolized/cleared --> renal damage & failure Methemoglobinemia in mammals supportive care - maintain temp
28
4-AP (Avitrol)
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
Anticoagulant rodenticides
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
Bromethalin
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
Cholecalciferol (Vit D3)
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
compound 1080 (Sodium Fluoroacetate)
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
Strychnine (gopher bait)
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
Zinc Phosphide (rodenticide)
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
Ibuprofen
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
Naproxen
Same as ibuprofen but dogs more sensitive | smaller therapeutic window
37
Aspirin
Can control lameness in dogs AT CORRECT DOSE small margin of safety, more acidic (GI issues) In cats, half life 5x longer (Glucuronidation)
38
Acetominophen
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
Methemoglobinemia
Acetominophen | 3-CPT in mammals
40
Pseudoephedrine
- 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
Venlafaxine
Cats want to eat it Serotonin-NE reuptake inhibitor = increased symp Issues w/ extended release Monitor, serotonin agonists for agitation, decontaminate
42
Amphetamines
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
Xylitol
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
Methylxanthines
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
Cleaning Products - Acids
mild irritation to corrosive injury - ulcers sour taste coagulative necrosis --> thickening & stricture where direct contact occurred weeks to months later
46
Cleaning Products - Alkalis
mild irritation to corrosive injury no odor or taste (can = greater ingestion) liquefactive necrosis --> edema, inflamm, transmural necrosis, corrosive injury - ulcers, maybe stricture
47
Treat acid and alkali toxicity
``` decontaminate skin, oral membranes but NOT GI (neutralizing bad idea = thermal burns) IV drugs (not PO) gastroprotection, fluids, analgesia ```
48
essential oils, liquid potpourri
cats more sensitive (glucuronidation) absorbed through skin, mucous mems Pennyroyal oil - hepatobilliary, poor outcome liquid potpourri - good outcome
49
Lithium disk batteries or dry cell batteries are at risk of leaking if stomach acid alters casing?
dry cell batteries
50
Batteries cause what problems?
ulcers stridor hemorrhage, exsanguination liver, neuro damage w/ heavy metal toxicosis long term - stricture, esophageal malformation
51
Ethylene Glycol
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
Treat ethylene glycol or DEG poisoning
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
Propylene Glycol
"safer antifreeze" | neuro issue, heinz body anemia in cats
54
3 factors that can influences resp toxicosis
- 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
Acute responses to resp toxicosis
asphyxiation UT irritation pulmonary edema airway reactivity (bronchial smooth m. constric)
56
Chronic responses to resp toxicosis
fibrosis emphysema asthma (chronic airway reactivity) lung cancer
57
Ammonia
animal facilities where poop decomposes on solid floor | oral ingestion lead to lung damage (b/c urea formation) - goats
58
Co2
breathed out fuel burning heaters decomposing manure >40% conc = toxicity
59
Methane
product of microbial degradation (rumen flora) | concern is flammability, lg conc needed to displace oxygen
60
Hydrogen sulfide (h2s)
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
At what conc does Hydrogen sulfide cause olfactory paralysis
150-250 ppm
62
Carbon monoxide
car exhaust, fires cherry-red blood, out-competes oxygen to bind to hgb Prevention key - CO detectors
63
Nitrogen dioxide
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
Which is more toxic of nitrogen dioxide - short exposure to high conc or long exposure to low conc
short exposure to high conc more toxic either way prognosis guarded - depends on tissue ability to recover
65
PTFE (teflon) heated products
birds uniquely sensitive b/c unidirectional airflow
66
Tryptophan-3 methyl indole (3-MI)
cattle + lush pasture tryptophan --> 3-MI --> liver converts to reactive intermediates --> lung damage If low-level exposure can recover