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Toxicology Flashcards

1
Q

What is the toxic dose for acetaminophen in cats and dogs

A

Cats: 10 mg/kg (but most commonly 50-100 mg/kg)

Dogs: 100-200 mg/kg

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2
Q

What is the recommended treatment in case of severe cardiovascular collapse due to a local anesthetic overdose

A
  • Positive inotrope if decreased isotropy
  • Amiodarone in case of arrhythmias (no lidocaine lol)
  • Small doses of epinephrine in case of hypotension or cardiac arrest
  • Intravenous lipid emulsion
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3
Q

Name toxins for which the use of intralipid emulsion would be recommended

A
  • Marijuana
  • Macrolytic lactones (ivermectin, moxidectin)
  • Local anesthetics
  • Calcium channel blockers
  • Permethrin
  • Cyclic antidepressants (amitriptyline)
  • Muscle relaxants
  • Psychotropic drugs
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3
Q

What chemical properties of toxins allows prediction of potential benefit of intralipid emulsion

A

Lipophilicity -> quantified by partition coefficient (log P)

If logP > 1, toxin is lipophilic and ILE could be beneficial
Benefit of ILE most likely if logP > 5

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4
Q

What is the mechanism of action of intralipids

A
  • “Lipid sink”: causes an expanded lipid phase in the plasma leading to sequestration of lipid compounds and decreasing their concentration in target tissues
  • Increased circulating free fatty acids -> energy substrate for myocardial cells -> improved myocardial function (likely to be useful especially for bupivacaine toxicosis which blocks mitochondrial use of free fatty acids)
  • Activation of voltage-gated calcium channel -> increased intracellular calcium (likely to be useful especially for calcium channel blockers)
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5
Q

What is the recommended dose and maximum dose for intralipids

A

1.5 mL/kg bolus followed by 0.25-0.5 mL/kg/min for 30-60 min

Do not exceed 10 mL/kg/day ; typically do not administer over more than 24h

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6
Q

How should the modality of treatment be decided for extra-corporeal toxin removal

A

Based on volume of distribution, protein binding, molecular weight, charcoal affinity

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7
Q

Name examples of toxins that can be removed by hemoperfusion

A
  • NSAIDs (but TPE better)
  • Caffeine
  • Theobromine
  • Barbiturates
  • Vincristine
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8
Q

Mechanism of action of anticoagulant rodenticides

A

Inhibition of vitamin K epoxide reductase in liver -> no activation of vitamin K -> no gamma-carboxylation of factors II, VII, IX, X and proteins C and S

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9
Q

Indicate if the following anticoagulant rodenticides are first or second generation:
- brodifacoum
- warfarin
- diphacinone
- bromadiolone

What is the difference?

A
  • First generation: warfarin, diphacinone
  • Second generation: brodifacoum, bromadiolone

Second generation rodenticides have a longer half-life

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10
Q

Mechanism of action of bromethalin and delay of onset of clinical signs

A
  • Neurotoxic: uncouples oxidative phosphorylation -> decreased ATP production
  • Delay of 2h to 5 days depending on ingested dose (poor prognosis once clinical signs have developed)
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11
Q

Name the 3 non-anticoagulant rodenticides and their effects

A
  • Bromethalin -> neurotoxic
  • Cholecalciferol (vitamin D3) -> hypercalcemia, hyperphosphatemia
  • Zinc and aluminum phosphides -> direct toxicity to heart, kidneys, adrenal glands, and corrosive agent
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12
Q

What can be used to decrease GI absorption of cholecalciferol

A
  • Activated charcoal q6h for 24h (entero-hepatic recirculation)
  • Cholestyramine resin for 4 days
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13
Q

What is the mechanism of action of phosphide rodenticides? What precaution should be taken with decontamination?

A
  • Direct corrosive effect
  • Inhibition of cytochrome C oxidase, disruption of mitochondrial membrane -> free radicals -> lipid peroxidation

The active compound (phosphine) is a gas ->gas exposure can happen after induction of emesis, do it outside

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14
Q

What are the ethylene glycol metabolites and their toxic effects

A
  • Glycoaldehyde -> CNS signs
  • Glycolid acid -> metabolic acidosis, high anion gap
  • Oxalic acid -> binds calcium -> calcium oxalate crystals -> AKI, hypocalcemia
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15
Q

What are the 3 phases of ethylene glycol toxicosis (with timing for cats and dogs)

A
  1. Within a few hours: CNS and GI signs ->vomiting, ataxia, depression, muscle fasciculations, possible seizures
    + PUPD from osmotic diuresis
  • Neuro signs can resolve in dogs after 12h
  1. 12-24h after ingestion: Cardiopulmonary signs -> tachypnea, arrhythmias (from hypocalcemia and acidosis)
  2. 12-24h after ingestion in cats, 24-72h in dogs: AKI
16
Q

What is the timing for increased osmolal gap in dogs with ethylene glycol toxicity

A

Increased as soon as 1h post-ingestion, peaks at 6h, stays elevated for ~48h

17
Q

What is the goal of ethylene glycol antidote therapy

A

Competitive inhibition of alcohol dehydrogenase by administration of ethanol or fomepizole (4-MP)

18
Q

What is the dose for fomepizole / ethanol as an antidote for ethylene glycol toxicity

A
  • Fomepizole:
    Dogs: 20 mg/kg IV then 15 mg/kg IV at 12 and 24h then 5 mg/kg IV at 36h
    Cats: 125 mg/kg IV initially, then 31.25 mg/kg IV at 12, 24, and 36 hours
  • Ethanol:
    Dogs: 1.3 mL/kg IV bolus of 30% ethanol followed by CRI 0.42mL/kg/h for 48 hours OR 5.5mL/kg of 20% ethanol IV q4 for 5 treatments then q6 for 4 treatments
    Cats: 5mL/kg of 20% ethanol IV q6 for 5 treatments and then q8 for 4 treatments
19
Q

What is the metabolism of acetaminophen

A
  • Glucuronidation and sulphuric acid conjugation (dogs)
  • Sulfation (cats)
  • If saturated, oxidation by cytochrome P450 enzymes (CYP2E1 and CYP1A2) to toxic metabolite NAPQI (N-acetyl-P-benzoquinone imine) -> converted to non-toxic metabolites by glutathione
20
Q

Mechanism of toxicity of acetaminophen

A
  • NAPQI binds to hepatic cell membranes -> hepatic necrosis
  • Glutathione depletion -> MetHb in dogs and cats + Heinz body anemia in cats
  • Hypoxia and increased capillary permeability -> facial edema
  • NAPQI damages renal proteins -> cell death
21
Q

What are the toxic doses for aspirin, ibuprofen and naproxen in dogs and cats

A
  • Aspirin: GI ulcerations at 25-100 mg/kg. Lethal at > 450 mg/kg in dogs and > 100 mg/kg in cats
  • Ibuprofen:
    Dogs: GI signs at 100-125 mg/kg, AKI at 175-300 mg/kg, CNS at > 400 mg/kg, lethal at > 600 mg/kg
    Cats: twice as sensitive
  • Naproxen: GI signs at > 5 mg/kg, AKI at 10-25 mg/kg, CNS at > 50 mg/kg (not established for cats)
  • Very long half life (74h)
22
Q

What is the toxic agent in grapes / raisins

A

Tartaric acid

23
Q

Name 4 examples of nephrotoxic lilies

A

Easter lily, Asiatic lily, Trumpet lily, White lily, Yellow lily, Tiger lily, Leopard lily, Panther lily, Japanese show lily, etc.

24
Q

What is the mortality for cats developing AKI from lily toxicity

A

50-100% mortality

25
Q

What it the mortality for dogs developing AKI from grape toxicity

A

Up to 50% mortality
(18% of survivors never had a return to normal of their creatinine)

26
Q

What is the mechanism of action / toxicity of cocaine

A
  • Inhibition of reuptake of norepinephrine, serotonin, dopamine
  • Stimulation of endogenous catecholamine release
  • Neuroendocrine system dysregulation -> altered sleep, appetite, temperature
27
Q

Mechanism of action / toxicity of amphetamines

A
  • Inhibition of monoamine oxidase
  • Increased catecholamine release
  • Direct serotonin and dopamine receptor agonism
28
Q

What is the toxic dose of xylitol? What is the timing of onset of toxicity?

A
  • Hypoglycemia: 0.1 g/kg, happens very quickly for 12-48h
  • Hepatotoxicity: > 0.5 g/kg, happens 9-72h after ingestion
29
Q

What is the toxic dose of methylxanthines (caffeine, theobromine) in dogs

A
  • 20 mg/kg ->GI, PUPD
  • 40-50 mg/kg ->arrhythmias
  • > 60 mg/kg -> CNS (seizures)
30
Q

What is the mechanism of toxicity of iron? Clinical signs? Treatment?

A

Very reactive ion causing oxidative damage (mostly to GI, liver, cardiovascular system) ->vomiting, diarrhea, GI ulceration (and possible secondary stricture), vasodilation, hypotension

Treatment with chelation by deferoxamine until iron < TIBC

31
Q

What are the primary systems affected in lead toxicosis? What is the treatment?

A

Mostly GI and nervous systems (vomiting, diarrhea, seizures, blindness, confusion, megaesophagus) + anemia due to increased RBC fragility and decreased Hb synthesis

Chelation with CaNa2EDTA or succimer (DMSA)

32
Q

What treatments can be used for calcium channel blockers toxicosis

A
  • Intralipids (can increase entry of Ca into cells)
  • Calcium gluconate or calcium chloride - target iCa 1.5-2 times upper range (might improve contractility)
  • Glucagon (has Gs receptors in cardiomyocytes -> cAMP -> increased contractility and chronotropy)
  • High-dose insulin with dextrose infusion (improves inotropy and cardiac output, unclear mechanism but possible increase in carbohydrate intake as energy source and improved Ca entry into cells): insulin up to 2 U/kg/h and dextrose up to 30%!
33
Q

How does xylitol cause hypoglycemia?

A

Stimulation of insulin release from beta cells + hepatic necrosis and failure

34
Q

What component of marijuana causes the toxicity?

A

Delta-9 THC

35
Q

What medication can be used in case of severe beta-blocker overdose with cardiac depression

A

Glucagon (has Gs receptors in cardiomyocytes -> increases inotropy and chronotropy independently of beta receptors)

36
Q

What is the mechanism of action of N-Acetylcysteine for treatment of acetaminophen toxicity?

A
  • NAC is a glutathione precursor –> binds with APAP metabolites making them inactive
  • Sulfur donor –> increases sulfate conjugation
  • Decreases methemoblobinemia and Heinz body formation
37
Q

What is a common biochemical finding in cats with lily toxicity?

A

More markedly elevated serum creatinine compared to a more moderate BUN

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