ABVT flashcards

32 cards. Read the term and the definition here. The deck at the top of this page is optional.

Theobromine toxic dose

Doses around 20 mg/kg cause GI upset; 40-50 mg/kg cause cardiac effects; 60 mg/kg and above can cause seizures in dogs.

Vitamin K1 therapy

Anticoagulant rodenticides inhibit vitamin K epoxide reductase; vitamin K1 restores clotting factor synthesis over days to weeks depending on rodenticide half-life.

Xylitol toxicosis

Xylitol causes insulin release and hypoglycemia in dogs, and at higher doses acute hepatic necrosis; it is not toxic to cats.

Grapes and raisins

Ingestion in dogs is associated with acute renal failure; the toxic principle is unknown, so all exposures are treated as potentially toxic.

Permethrin in cats

Concentrated canine flea products containing permethrin cause tremors, hypersalivation, and seizures in cats due to impaired metabolism.

Acetaminophen in cats

Cats lack glucuronidation, so acetaminophen causes Heinz body formation, methemoglobinemia, and hepatic necrosis; treat with N-acetylcysteine.

Metaldehyde snail bait

Metaldehyde ingestion causes tremors, hyperthermia, and seizures in dogs; treatment includes muscle relaxants, anticonvulsants, and supportive care.

Ethylene glycol antidote

Ethylene glycol causes acute renal failure via oxalate crystals; fomepizole or ethanol blocks alcohol dehydrogenase, and treatment must begin early.

ABCB1 (MDR1) mutation

Collies and related breeds carry a mutation reducing P-glycoprotein efflux, increasing brain exposure to ivermectin and other drugs.

Lead toxicosis signs

Lead poisoning in dogs and cats causes GI signs, anemia with basophilic stippling, and neurologic signs; chelation uses calcium EDTA or penicillamine.

Organophosphate toxidrome

SLUDGE signs (salivation, lacrimation, urination, defecation, GI distress, emesis) reflect acetylcholinesterase inhibition; treat with atropine and pralidoxime.

Zinc phosphide hazard

Zinc phosphide reacts with gastric acid to release phosphine gas; do not induce emesis, and ensure ventilation to protect personnel.

Chocolate methylxanthines

Theobromine and caffeine are methylxanthines; baking chocolate contains far more per gram than milk chocolate and causes cardiac and CNS signs.

Sago palm toxicosis

Sago palm seeds contain cycasin, causing hepatic necrosis with vomiting, icterus, and coagulopathy in dogs; treatment is supportive.

Tremorgenic mycotoxins

Penitrem A and roquefortine from moldy food cause tremors and seizures in dogs; treat with decontamination and muscle relaxants.

Rodenticide classes

Anticoagulants, cholecalciferol, bromethalin, and zinc phosphide each require distinct antidotes; identifying the class drives treatment.

LD50 definition

LD50 is the dose producing death in 50% of a test population; it is a comparative index of acute toxicity, not a measure of chronic risk.

Therapeutic index

Therapeutic index equals LD50 divided by ED50; a low ratio indicates that effective and toxic doses are close together.

Phase I biotransformation

Phase I reactions (oxidation, reduction, hydrolysis) often use cytochrome P450 enzymes and can create reactive, more toxic intermediates.

Phase II conjugation

Phase II reactions (glucuronidation, sulfation, acetylation, glutathione conjugation) increase water solubility and facilitate renal or biliary excretion.

First-pass effect

Orally absorbed compounds pass through the liver before reaching systemic circulation, reducing bioavailability and sometimes producing toxic metabolites.

Volume of distribution

Vd relates total body burden to plasma concentration; low-Vd drugs are more amenable to hemodialysis and hemoperfusion removal.

Henderson-Hasselbalch

The equation relates pH and pKa to ionized versus un-ionized fraction; un-ionized weak acids are better absorbed at acidic gastric pH.

Emesis window

Induction of emesis is most useful within 1-2 hours of ingestion and is contraindicated for caustics, hydrocarbons, and obtunded patients.

Activated charcoal

Activated charcoal adsorbs many organic toxins; it is contraindicated for caustics, hydrocarbons, and patients at risk of aspiration.

Bioavailability

Bioavailability is the fraction of an administered dose reaching systemic circulation; route, formulation, and first-pass metabolism affect it.

Chronic toxicity

Chronic toxicity results from repeated or prolonged exposure, often producing cumulative organ damage at doses below acute toxic thresholds.

Dose-response curve

A dose-response curve plots effect against dose; its slope and threshold indicate how steeply toxicity increases with dose.

Cholinergic toxidrome

SLUDGE signs plus miosis and bradycardia indicate acetylcholinesterase inhibition from organophosphates or carbamates.

Antidote versus decontamination

Decontamination reduces absorption; antidotes counteract toxicity after absorption, such as N-acetylcysteine or fomepizole.

Half-life

Half-life is the time for plasma concentration to halve; it determines dosing intervals and duration of monitoring after exposure.

Target organ toxicity

Many toxicants damage specific organs (liver, kidney, nervous system) reflecting concentration and metabolic activation at that site.