NAVLE Feline Pharmacology and Toxicology 4

Question 1

A 4-year-old DSH cat is being treated for chronic pain with buprenorphine. The owner inadvertently administers a full tablet of acetaminophen (500 mg) intended for herself. Which mechanism is primarily responsible for acetaminophen toxicity in cats compared to dogs and humans?

Accepted Answer

Cats lack sufficient UDP-glucuronosyltransferase 1A6 (UGT1A6) activity to conjugate NAPQI, leading to accumulation

Answer

Cats are exceptionally susceptible to acetaminophen toxicity due to a genetic deficiency in UGT1A6 (and related isoforms), the glucuronidation enzyme responsible for conjugating NAPQI — the reactive intermediate produced by CYP450 metabolism of acetaminophen. Without adequate glucuronidation capacity, NAPQI accumulates, depletes glutathione, and binds covalently to hemoglobin (causing methemoglobinemia and Heinz body formation) and hepatocytes (causing hepatic necrosis). Dogs and humans can glucuronidate NAPQI efficiently; cats largely cannot. The sulfation pathway is also limited in cats and becomes quickly saturated.

Question 2

A cat on long-term phenobarbital for seizure control is started on chloramphenicol for a resistant infection. Two weeks later the owner reports markedly increased sedation and ataxia with no dose change of phenobarbital. What is the most likely pharmacokinetic explanation?

Accepted Answer

Chloramphenicol inhibits hepatic cytochrome P450 enzymes, reducing phenobarbital clearance and raising its serum concentration

Answer

Chloramphenicol is a potent inhibitor of hepatic cytochrome P450 enzymes (particularly CYP2B and CYP3A isoforms) in cats. Phenobarbital is primarily metabolized by these hepatic CYP enzymes. When chloramphenicol inhibits phenobarbital's metabolism, clearance decreases and phenobarbital plasma concentrations rise significantly — often into toxic ranges — despite no change in dose. This is a clinically important drug interaction in feline practice. Phenobarbital monitoring (serum levels) is mandatory when adding chloramphenicol, and dose reduction is frequently required.

Question 3

You are managing a cat that ingested topical permethrin flea spray (concentrated dog formulation) 90 minutes ago. The cat is tremoring severely. After decontamination with dish soap, which treatment combination is MOST appropriate for controlling permethrin-induced tremors in this cat?

Accepted Answer

Methocarbamol IV combined with diazepam; avoid pyrethroid-specific antidotes

Answer

Permethrin toxicosis in cats causes sodium channel dysfunction leading to repetitive neuronal firing, manifesting as tremors and seizures. The treatment of choice for tremor control is methocarbamol (a muscle relaxant; 44–220 mg/kg IV slowly to effect) combined with diazepam or other benzodiazepines for CNS sedation and seizure control. There is no specific antidote. Atropine + pralidoxime is the antidote regimen for organophosphate/carbamate toxicity (which acts via AChE inhibition), not pyrethroids. Cyproheptadine (a serotonin antagonist) is used for serotonin syndrome, not permethrin toxicosis. IVLipid emulsion can be a useful adjunct in severe refractory cases but is not the primary or sole treatment.

Question 4

A 7-year-old cat with hyperthyroidism is well-controlled on methimazole. The owner reports the cat has developed facial pruritus, excoriations, and a mild leukopenia on recent CBC. What is the MOST appropriate next step?

Accepted Answer

Discontinue methimazole immediately and transition to radioactive iodine (I-131) or surgical thyroidectomy after stabilization

Answer

Facial pruritus/excoriations and hematologic abnormalities (leukopenia, thrombocytopenia, agranulocytosis) are recognized adverse effects of methimazole in cats, occurring in approximately 15–20% of treated cats. Agranulocytosis is the most life-threatening hematologic complication. When these reactions occur, methimazole must be discontinued — not dose-reduced — because rechallenge carries high risk of recurrence. Carbimazole is a prodrug that is converted to methimazole in vivo, so it carries the same adverse effect risk and is NOT a safe alternative. After methimazole withdrawal and patient stabilization, definitive therapy (radioactive iodine or surgical thyroidectomy) is the recommended path forward.

Question 5

A cat presents with acute-onset ptyalism, vomiting, ataxia, and mydriasis after being seen chewing on a lily bouquet. Bloodwork 36 hours later reveals a BUN of 98 mg/dL and creatinine of 7.2 mg/dL. Which statement BEST describes the mechanism of lily nephrotoxicity in cats?

Accepted Answer

The nephrotoxic principle causes direct proximal tubular epithelial cell death via a mechanism not yet fully elucidated at the molecular level, with no known antidote

Answer

True lily nephrotoxicity (Lilium and Hemerocallis species) in cats is a well-documented but mechanistically incompletely understood toxidrome. The toxic principle causes acute, severe proximal tubular necrosis, but the exact molecular mechanism has not been definitively identified in peer-reviewed literature. There is no antidote — treatment is aggressive IV fluid diuresis initiated within hours of exposure, before renal injury is established. Calcium oxalate crystals causing obstructive nephropathy are associated with Oxalis and Araceae species (e.g., Philodendron, Dieffenbachia), not true lilies. Lycorine is found in Narcissus/Amaryllidaceae; tuliposide A is found in Tulipa. Cats are uniquely and exquisitely sensitive to Lilium/Hemerocallis; dogs are not.

NAVLE - North American Veterinary Licensing Examination Practice Test

NAVLE - North American Veterinary Licensing Examination Practice Test

NAVLE Feline Pharmacology and Toxicology 4