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Questions and Answers
What is a common clinical sign observed in patients with amitrazois toxicosis?
Which treatment is indicated for iron toxicosis?
What should be avoided in treating cases involving heavy metal ingestion?
Which of the following substances poses a risk of foreign body obstruction?
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Which is NOT a clinical sign of dyethylene glycol (DEG) toxicosis?
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What is the lethal dosage of amitrazois for dogs?
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What can occur as a consequence of ingesting batteries?
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Which treatment should NOT be pursued for insect bait station ingestion?
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What is the suggested dosage range for emetics in cats?
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In which scenario is dilution appropriate for reducing oral irritation due to toxic plant ingestion?
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What percentage of stomach contents do emetics typically empty?
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Why is emesis contraindicated after ingestion of corrosive agents?
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What condition may make emesis hazardous due to the risk of aspiration?
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What effect can feeding a small moist meal have before inducing vomiting?
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Which of the following is NOT a commonly used emetic in veterinary settings?
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When is it unnecessary to induce emesis in a patient?
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What is the minimum lethal dose of ethylene glycol (EG) in dogs?
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Which of the following is NOT a source of ethylene glycol?
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What clinical signs are observed in stage 1 of EG toxicosis?
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When do severe internal injuries occur during the stages of EG toxicosis?
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Which of the following diagnostics is critical for suspecting EG toxicosis?
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What is a significant feature of stage 3 in cats regarding EG toxicosis?
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How accurately can EG testing within the first 24 hours inform clinical decision-making?
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What common metabolite of ethylene glycol contributes to the development of calcium oxalate crystalluria?
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What is the proof value of an alcohol solution that contains 50% ethanol?
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How much IV fluid should be removed to create a 7% ethanol solution using 40% alcohol?
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What is the dose of 20% ethanol solution recommended for administration?
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What is a potential adverse reaction in animals following ethanol administration?
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What is the LD50 of propylene glycol reported for dogs?
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Which of the following is NOT a property of propylene glycol?
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What metabolic effects does propylene glycol ingestion contribute to in animals?
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Which medication is commonly combined with propylene glycol for injection?
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What is the primary reason diagnostic testing for toxins can be frustrating?
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Which of the following is NOT a common toxidrome in veterinary medicine?
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What should be the primary focus of treatment for toxin exposure?
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In the case of acute kidney injury in a cat, which specific inquiry is vital?
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Which of the following is a hallmark sign of Beta-agonist toxicity?
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What characterizes the approach to treating toxicities in veterinary medicine?
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Which group of substances can be screened for in veterinary diagnostic labs?
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What is the advantage of asking specific questions about toxin exposure?
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What is the primary treatment method recommended immediately after ingestion of corrosive household bleach?
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What potential effect can xylitol ingestion have on non-primate species?
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What is a major concern when using cathartics in animals with certain health conditions?
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In cases of detergent ingestion, what supportive care is frequently necessary?
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Which type of cathartic is primarily designed to increase water volume in the GI tract?
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What is the range of sodium hypochlorite concentration in typical household bleach?
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How does activated charcoal function in binding toxicants?
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Why is mineral oil not recommended after administering activated charcoal?
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What common symptom can result from ingestion of detergents in cats?
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Which chemical component in 'ultra' bleach increases the risk of corrosive damage?
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What is the primary risk associated with cathartics that alter water balance in the GI tract?
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Which is the most commonly used bulk cathartic in veterinary practice?
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Why might determining the xylitol content in sugarless products be challenging?
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What should be monitored to prevent complications when using cathartics?
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What is a critical step to minimize injury after ingestion of corrosive agents before veterinary attention?
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Which of the following statements about osmotic cathartics is correct?
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What is a documented clinical sign observed in cats exposed to propylene glycol toxicosis?
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Which mechanism of action is associated with imidazolinone herbicides?
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Which of the following herbicides is primarily recognized for its nontoxic profile to mammals?
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What is a common clinical effect of ingesting large amounts of glyphosate?
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What is the effect of pyridine herbicides on plant growth?
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Which organ system is primarily affected by the CNS depression observed in moths following propylene glycol exposure?
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In cat cases of chronic propylene glycol ingestion, what hematological change is expected?
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What is a crucial component of supportive treatment for propylene glycol toxicity in veterinary medicine?
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Which patient population may necessitate the induction of emesis and activated charcoal administration even for non-toxic ingestions?
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What is a significant risk associated with the one-time administration of vitamin K1 at the time of decontamination?
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Which insecticides have been removed from the market due to severe clinical signs observed in poisonings?
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Which clinical signs are primarily associated with pyrethrin or pyrethroid toxicity in cats?
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When is it considered unnecessary to test for PT after ACR ingestion?
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What concentration threshold of pyrethrins poses a risk for systemic toxicosis in cats?
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Which of the following treatments is commonly employed for managing pyrethrin intoxication?
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What rare risk is associated with the ingestion of silica gel packs?
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What is the recommended maximal daily dosing of 20% ILE?
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Which of the following describes high-dose insulin therapy's proposed therapeutic mechanism?
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What is the main purpose of plasmapheresis in the context described?
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Which of the following is a critical requirement when administering high-dose insulin therapy?
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What was the outcome for the majority of dogs that underwent gastrointestinal decontamination after anticoagulant rodenticide ingestion?
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What type of monitoring is suggested prior to initiating treatment with high-dose insulin therapy?
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What is the outcome of proper decontamination within 6 hours after anticoagulant rodenticide ingestion among dogs?
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Which component is typically discarded during the plasmapheresis process?
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What is the minimum lethal dosage of Brodifacoum for dogs?
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Which clinical sign typically develops first in cases of ACR toxicity?
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What is the primary initial action that should be taken for a patient exposed to toxicants?
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What is the primary method for determining if a toxic dose of rodenticide has been ingested?
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Which factors influence the method of decontamination in cases of toxicant exposure?
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At what point after ingestion is prothrombin time (PT) typically measured for signs of coagulopathy?
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What is the recommended dosage of atropine for dogs and cats exposed to organophosphates?
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What is a potential consequence of incorrectly administering acepromazine to dogs exposed to amphetamines?
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What treatment should be initiated if prothrombin time is prolonged following ACR toxic ingestion?
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Which decontamination method is NOT listed as an option in the treatment of patients exposed to toxicants?
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In cases of ACR toxicity, which of the following is NOT a common clinical sign?
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Which species is known to be more resistant to the effects of ACR?
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In cases of amitraz toxicosis, what effect does atipamezole have?
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What should be done for pets experiencing clinical bleeding due to ACR toxicity?
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What is the significance of administering a test dose before atropine treatment?
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What is the purpose of patient decontamination in toxicant exposure cases?
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What is a clinical sign associated with xylitol toxicosis?
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What should be avoided before inducing emesis in a hypoglycemic patient?
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What is the primary rationale for not inducing emesis after hydrocarbon ingestion?
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What can result from ingesting higher dosages of xylitol (>0.5 g/kg)?
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Which hepatoprotectant is recommended for xylitol toxicosis treatment?
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What is a potential effect of xylitol ingestion in non-primate species?
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What is the recommended bolus for a hypoglycemic patient after xylitol ingestion?
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What type of fluid therapy is suggested for hypoglycemic patients after xylitol ingestion?
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What is the mechanism of action of bromethalin as a rodenticide?
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Which factor contributed to the reduced usage of second-generation anticoagulant rodenticides in the U.S.?
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What is a common antidote used for treating anticoagulant rodenticide poisoning?
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What percentage of exposure cases reported to the ASPCA APCC involves human and veterinary medications?
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What treatment is indicated for bromethalin poisoning?
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What occurs as a result of sodium accumulation within cells due to bromethalin toxicity?
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Which of the following is NOT a primary toxicant category reported in animal poisonings?
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Which non-anticoagulant rodenticide is mentioned as increasing in use as anticoagulant rodenticides decline?
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What is a key challenge in diagnosing toxin exposures?
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Which of the following describes a common characteristic of toxidromes?
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In treating toxin exposure, what is often the primary method of management?
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Which of the following scenarios would most likely prompt inquiry about specific toxins in a cat with acute kidney injury?
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What should veterinarians focus on when treating beta-agonist toxicity?
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Which type of toxins might be screened for in veterinary diagnostics labs?
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What is often a result of asking specific questions during toxin exposure evaluations?
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Which potential symptom could indicate exposure to tremorogenic mycotoxins?
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Which aspect should be prioritized before administering antidotal medications for toxin exposure?
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Which of the following factors does NOT determine the appropriate method of patient decontamination?
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In the case of amitraz toxicosis, which medication is used for reversing CNS depression?
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Which method of patient decontamination is primarily designed to counter the absorption of toxicants by binding them?
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What is the correct dosage of atropine for countering muscarinic effects in dogs and cats?
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Which of the following is NOT considered a life-threatening disorder requiring stabilization before antidote administration?
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After stabilizing a patient exposed to toxicants, which decontamination method may require repetition until the toxicant is removed?
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What potential adverse effect must be considered when administering atipamezole for amitraz toxicosis?
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What immediate clinical sign indicates that a patient has NOT been poisoned by a carbamate or organophosphate?
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Which treatment for ethylene glycol toxicosis must be administered within 3 hours for optimal prognosis?
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What are the primary signs to monitor for in a patient presenting with tremorgenic mycotoxin exposure?
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Which of the following treatments is NOT recommended for de-icing salt toxicity in dogs?
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What dosage of Digoxin immune fab is standard for treating digoxin toxicity in dogs?
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In cases of cocoa mulch ingestion, which clinical signs should be expected due to methylxanthine toxicosis?
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What is a potential adverse reaction to the administration of ethanol in animals?
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Which treatment is indicated for severe CNS and respiratory depression caused by benzodiazepines?
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What is the primary risk associated with household cleaners that are highly concentrated?
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What is a common clinical sign observed after ingestion of by-products from the meatpacking industry?
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What initial dose of Fomepizole is recommended for cats exposed to ethylene glycol?
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What is the standard bolus dose for Intralipid emulsion when treating bupivacaine toxicity?
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What toxins are associated with exposure to moldy food and potentially affect neurotransmitter activity?
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Which of the following medications is often used to treat serotonin syndrome?
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For which of the following conditions is treatment typically aimed at decontamination, muscle relaxants, and anticonvulsants?
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What would be a likely clinical outcome of direct ingestion of de-icing salt by a dog?
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In what situations is decontamination with emesis induction potentially unnecessary?
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Why is the administration of a one-time shot of vitamin K1 during decontamination considered potentially detrimental?
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What are common clinical signs associated with pyrethrins and pyrethroids toxicosis?
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Which type of insecticides has predominantly been removed from the market due to toxicity concerns?
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How is decontamination typically approached for cats exposed to pyrethrins?
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In which of the following scenarios would you consider monitoring PT essential?
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What is a rare consequence of ingesting silica gel packs?
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What is the general concentration range of pyrethrins in household insect sprays?
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What happens when doses of xylitol exceed 0.5 g/kg?
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Which clinical sign is associated with xylitol toxicosis due to hypoglycemia?
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What should be done if a patient presents after ingesting a toxic amount of xylitol?
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Which of the following is NOT a recognized clinical sign of hepatotoxicity in xylitol toxicosis?
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Why is it contraindicated to induce emesis after hydrocarbon ingestion?
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Which supportive measure is recommended for hypoglycemic patients after xylitol ingestion?
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What is a key reason activated charcoal is not routinely recommended for xylitol toxicosis?
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What laboratory findings might indicate acute hepatic necrosis from xylitol ingestion?
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What is the expected clinical sign that suggests CNS involvement in cases of amitrazois toxicosis?
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How does activated charcoal interact with heavy metals, according to protocols for treating intoxications?
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What is a rare but significant complication when ingesting insect bait stations?
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What treatment is generally indicated for severe cases of iron toxicosis?
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Which clinical sign indicates that a patient has NOT been poisoned by a carbamate or organophosphate?
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In cases of diethylene glycol (DEG) toxicosis, which clinical sign is least likely to be observed?
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What is the primary concern when dealing with battery ingestion in animals?
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What is the expected duration for a patient to improve after administration of Digoxin immune fab?
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Which ingredient primarily contributes to the risk of hypernatremia following paintball ingestion?
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What is a critical time frame for initiating treatment in cats exposed to ethylene glycol?
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What is one of the risks associated with the use of Flumazenil in treating benzodiazepine toxicity?
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What is the most crucial initial step in managing a case of acute intoxication from amitrazois?
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Which medication should be administered with caution due to the risk of CNS depression in cats?
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In the treatment of bupivacaine toxicity, what is the recommended initial bolus dosage of Intralipid emulsion?
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Which of the following is a consequence of ethanol administration in animals?
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What symptom may signify severe respiratory depression due to poisoning?
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Which treatment is appropriate for managing symptoms associated with tremorgenic mycotoxins ingestion?
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What is a potential risk associated with ingesting cocoa mulch?
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What clinical signs might indicate the presence of salt toxicosis in dogs?
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Which of the following substances is typically considered benign when ingested by dogs?
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What is a key treatment component for addressing cocoa mulch ingestion?
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What clinical signs are most likely to be associated with high salt toxicosis in dogs?
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Which treatment modality is explicitly NOT recommended for salt toxicosis?
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Which of the following is NOT a clinical manifestation of tremorgenic mycotoxins?
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What is the primary clinical sign that indicates a patient has potentially ingested a hepatotoxic dose of xylitol?
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When treating a hypoglycemic patient after xylitol ingestion, what is the recommended bolus of dextrose?
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What risk is associated with inducing emesis following hydrocarbon ingestion?
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Which of the following symptoms is least associated with xylitol toxicosis?
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What is an appropriate duration for IV fluid therapy in hypoglycemic patients post xylitol ingestion?
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What should be monitored every 1-4 hours during the treatment of a hypoglycemic patient after xylitol ingestion?
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What treatment option is NOT routinely recommended for xylitol toxicosis?
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What effect can high doses of xylitol (>0.5 g/kg) have on the liver?
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What is the primary mechanism by which calcium channel blockers reduce blood pressure?
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Which of the following is a potential side effect of calcium channel blocker overdose in pets?
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What complication could result from severe hypotension caused by calcium channel blocker toxicity?
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Which non-cardiac sign is commonly associated with calcium channel blocker exposure in pets, particularly in cats?
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Calcium channel blockers are commonly used to treat which of the following conditions?
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What is a potential consequence of a pet unintentionally consuming calcium channel blockers?
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In the context of calcium channel blocker toxicity, what does the term 'iatrogenic intoxications' refer to?
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Why is it difficult to establish toxic dosages for calcium channel blockers in pets?
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What is the primary purpose of stabilizing patients exposed to toxicants before administering antidotal medications?
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Which of the following factors does NOT influence the method of patient decontamination in toxicant exposure cases?
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What is a key reason why a clinician may choose to use multiple decontamination methods after toxin exposure?
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Which antidotal medication is specifically indicated for reversing the effects of amitraz toxicosis?
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In the context of antidotal therapy, what is a significant action of atropine when treating organophosphate poisoning?
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What does systemic absorption of a toxicant refer to in the context of patient decontamination?
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What is a potential consequence of administering a test dose of atropine in cases of suspected organophosphate toxicity?
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Why might gastric lavage be chosen as a decontamination method in certain toxicant exposures?
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What is the appropriate treatment for a dog that ingested an anticoagulant rodenticide and shows clinical signs of bleeding?
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Which rodenticide has the lowest lethal dose (LD50) for dogs based on the information provided?
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How long after ingestion of anticoagulant rodenticides are clinical signs typically observed?
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What is the recommended dosage of vitamin K1 therapy for a patient that has ingested an anticoagulant rodenticide?
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Which of the following clinical signs is NOT typically associated with anticoagulant rodenticide poisoning?
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What critical observation period should be followed after an ingestion of anticoagulant rodenticide to measure prothrombin time?
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Which factor indicates a higher resistance of cats to anticoagulant rodenticide compared to dogs?
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What should be done in cases where client compliance with follow-up treatment is questionable?
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What is the primary therapeutic effect of calcium channel blockers in veterinary medicine?
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What type of arrhythmia is most commonly associated with calcium channel blocker overdose?
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Which of the following signs could indicate non-cardiac toxicity related to calcium channel blockers?
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In cases of calcium channel blocker intoxication, what reaction may occur as a reflex to severe hypotension?
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Which clinical sign is least likely to be associated with calcium channel blocker toxicity in animals?
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What is a key characteristic of the therapeutic use of calcium channel blockers in veterinary medicine?
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Which of the following is a common clinical effect of calcium channel blocker overdose in animals?
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What mechanism do calcium channel blockers use to exert their effects on the cardiovascular system?
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What is a key clinical sign associated with amitrazois toxicosis in dogs?
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What is the appropriate treatment for severe iron toxicosis?
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Which of the following is a possible risk associated with battery ingestion?
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What characteristic sets diethylene glycol (DEG) toxicosis apart from other similar toxicoses?
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What is a common feature of insect bait station ingredients like abamectin and fipronil?
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Which treatment is NOT indicated for decontaminating patients that have ingested amitrazois?
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What critical step should be taken if an animal ingests paintballs?
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In cases of poisoning from substances in insect bait stations, when might treatment be indicated?
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What aspect of diagnostic testing for toxins is particularly challenging?
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Which clinical sign specifically suggests potential Beta-agonist toxicity?
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Supportive care for toxin exposure primarily includes which of the following?
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Which of the following is NOT a commonly recognized toxidrome in veterinary medicine?
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Why might a veterinarian end up with a diagnosis of 'suspected' toxin exposure?
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Which of the following toxins is commonly screened by veterinary diagnostic labs?
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What is a primary concern regarding the treatment of toxin exposure in veterinary medicine?
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In assessing acute kidney injury in a cat, why is it critical to inquire about the presence of certain plants?
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What is the approximate dosage that will lead to clinical signs in a 5 kg dog after bromethalin ingestion?
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Which therapy is preferred over corticosteroids for reducing intracranial pressure in bromethalin toxicosis?
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What class of clinical signs is associated with bromethalin toxicosis?
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What is the lethal dosage (LD50) of bromethalin for a cat?
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What is an important step in treating an asymptomatic patient with recent bromethalin ingestion?
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What is the prognosis for a patient with bromethalin toxicosis if treated appropriately before clinical signs develop?
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How long after acute ingestion of bromethalin can clinical signs typically be observed?
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What effect does bromethalin undergo in the body, complicating its elimination?
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What is the primary effect of cholecalciferol ingestion in pets?
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What is a critical reason for the necessity of intensive treatment in cholecalciferol toxicosis?
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What is a common source of cholecalciferol exposure in pets?
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What clinical sign may develop as early as 12-36 hours after cholecalciferol ingestion?
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When should emesis induction be implemented after zinc phosphide ingestion?
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What is the primary component necessary for the effective management of zinc phosphide toxicosis?
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Which of the following clinical signs is NOT typically associated with cholecalciferol toxicity in pets?
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What is the primary consideration when administering activated charcoal for toxin exposure?
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Which clinical signs are most commonly observed with the ingestion of compost containing tremorgenic mycotoxins?
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In cases of cocoa mulch ingestion, which treatment is particularly focused on addressing methylxanthine toxicosis?
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What is a common gastrointestinal side effect associated with the ingestion of de-icing salts?
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Which of the following is a primary concern when treating exposure to organic meal fertilizers?
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What complication can arise from the ingestion of highly concentrated household cleaners?
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How should treatment of a patient exposed to organic meal fertilizer be approached?
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Which of the following clinical manifestations is least likely to be associated with cocoa mulch ingestion?
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What is a critical component of the treatment for an animal that consumed compost with tremorgenic mycotoxins?
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What is a common consequence of propylene glycol ingestion in dogs?
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Which of the following substances is associated with the development of calcium oxalate crystals in dogs?
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What defines the primary clinical concern following the ingestion of household bleach in pets?
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What differentiates stage 1 of ethylene glycol toxicosis in pets?
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Which treatment is generally contraindicated in cases of corrosive substance ingestion?
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What is the primary risk associated with xylitol ingestion in pets?
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What aspect of herbicide exposure poses a risk for transitional cell carcinoma in dogs?
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After the initial treatment for heavy metal ingestion, what is a significant follow-up concern?
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What is a necessary component of the treatment protocol for cholecalciferol toxicity to promote calciuresis?
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Which medication is NOT commonly used to manage hypercalcemia in patients following cholecalciferol ingestion?
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What aspect of monitoring is critical for patients treated for hypercalcemia due to cholecalciferol toxicity?
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Why are oral doses of activated charcoal indicated for cholecalciferol toxicity?
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Which of the following represents a potential long-term complication of cholecalciferol toxicity treatment?
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What was a significant factor contributing to the reduction of second-generation anticoagulant rodenticides in the market?
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What factor differentiates various anticoagulant rodenticides in terms of their safety margin?
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How often should renal parameters and electrolytes be evaluated for patients recovering from cholecalciferol toxicity?
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What severe effect can occur in cats due to ingestion of liquid potpourri?
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Which of the following treatments is indicated for metaldehyde toxicosis?
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What is a primary reason for the contraindication of activated charcoal in tea tree oil toxicosis?
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What clinical sign is commonly observed within hours after exposure to concentrated tea tree oil?
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What is the recommended treatment approach for plant food and fertilizers toxicosis?
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What is the primary treatment approach for methanol toxicosis in dogs?
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What essential oil-related risk is particularly significant for cats exposed to liquid potpourri?
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Which clinical sign is commonly associated with methanol toxicosis in dogs?
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Which compound is frequently replaced with a safer alternative in pesticide formulations for slugs and snails?
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What is the consequence of methanol metabolism in non-primate species?
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What is the expected time frame for a patient to show improvement after administration of digoxin immune fab?
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What is a potential consequence of using the concentrated form of tea tree oil in pets?
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What type of clinical sign is typically self-limiting in patients after exposure to toxic agents?
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Which substance is NOT commonly found in windshield wiper fluids designed for extreme cold weather?
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Which treatment is specifically indicated for ethylene glycol toxicity in cats, and must be initiated within 3 hours of exposure?
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What should be performed for patients showing respiratory signs after toxin ingestion?
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Which of the following medications is often administered to reverse severe CNS and respiratory depression caused by benzodiazepines?
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What is a significant risk associated with the use of fomepizole for treating ethylene glycol toxicity in dogs?
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Why is the use of activated charcoal contraindicated in cases of methanol toxicosis?
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What component found in certain windshield wiper fluids can cause serious toxicosis in dogs?
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Which clinical signs are characteristic of serotonin syndrome that may be countered by treatment with cyproheptadine?
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What is the recommended dosage of cyproheptadine for dogs when treating serotonin syndrome?
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What treatment is indicated for cardiac glycoside poisoning in dogs, particularly from plants?
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Which statement regarding treatment timing for ethylene glycol toxicity is accurate?
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Which of the following compounds can lead to false positive results in veterinary EG tests?
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What is the preferred antidote for ethylene glycol toxicosis in veterinary medicine?
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What timeframe is critical for administering antidotal therapy to cats after ethylene glycol exposure?
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What adverse effect is NOT associated with ethanol treatment for ethylene glycol toxicosis?
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Which veterinary brands are currently available for ethylene glycol testing?
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What is a potential consequence of not treating ethylene glycol toxicosis promptly in dogs?
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How should euthanol be prepared for treatment of ethylene glycol toxicosis?
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What is the loading dose of fomepizole for dogs in treating ethylene glycol toxicosis?
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What is a primary consequence of calcium channel blocker overdose in pets?
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Which of the following is NOT a common sign of toxicity from calcium channel blockers?
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What mechanism primarily contributes to decreased blood pressure when calcium channel blockers are administered?
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What non-cardiac sign might indicate an overdose of calcium channel blockers in pets?
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Which of the following best describes the therapeutic use of calcium channel blockers in veterinary medicine?
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What is a potential reflexive response that can occur as a result of severe hypotension due to calcium channel blocker overdose?
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Which of the following is a characteristic effect of calcium channel blockers that may manifest during an overdose?
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What is a significant health concern regarding the toxicity of calcium channel blockers in pets?
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What is a critical clinical sign indicating hypoglycemia after a xylitol overdose?
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What should be done if a patient is hypoglycemic after ingesting xylitol?
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Which of the following is NOT a suggested treatment for xylitol hepatotoxicity?
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What is one significant risk associated with the ingestion of 2,4-dichlorophenoxyacetic acid herbicides in dogs?
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What is the main reason for not inducing emesis after hydrocarbon ingestion?
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Which of the following clinical signs may indicate xylitol poisoning has progressed to hepatotoxicity?
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Which of the following substances is commonly recognized for causing hypoglycemia in dogs?
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What factor influences the severity of clinical signs in ethylene glycol toxicosis?
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When should blood glucose concentrations be measured in a patient suspected of xylitol poisoning?
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Which statement best describes the treatment approach for insecticide toxicosis in pets?
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What is a common effect of xylitol ingestion in non-primate species?
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What is the recommended supportive care duration for hypoglycemic patients after xylitol ingestion?
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What is the primary concern when using cathartics in veterinary medicine?
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Which of the following symptoms is associated with propylene glycol ingestion in dogs?
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What is a potential consequence of administering 5 g/kg of propylene glycol daily to dogs?
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Which findings are associated with chronic administration of propylene glycol in cats?
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What clinical sign is indicative of detergent ingestion in cats?
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What defines the major concern when administering activated charcoal after a toxin ingestion?
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What is a common effect seen in both dogs and cats following herbicide ingestion?
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Which herbicide is known to be regarded as non-toxic in mammals?
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What supportive treatment is indicated for propylene glycol toxicosis in animals?
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Which of the following herbicide classes mimics natural plant hormones to inhibit growth?
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Which of the following is NOT a clinical sign associated with propylene glycol toxicosis?
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What is the mechanism by which glyphosate affects plants?
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What is a potential effect of 2,4-D herbicide on the central nervous system?
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Which clinical signs are commonly associated with exposure to 2,4-D in animals?
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What is the primary treatment goal for animals exposed to herbicides like 2,4-D?
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At what dosage of 2,4-D were gastrointestinal signs observed in experimental studies on dogs?
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Which herbicide is related to chlorophenoxy compounds like 2,4-D?
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What should be done in cases of life-threatening emergencies due to herbicide exposure?
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Which of the following statements best describes the safety margin of chlorophenoxy compounds?
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What is a significant concern when using phenoxy herbicides like 2,4-D in animals?
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What is the preferred method of fluid management in hypercalcemic patients following cholecalciferol toxicity?
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After discharge from the hospital, how long may oral therapy for a hypercalcemic patient continue?
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Which anticoagulant involves inhibiting vitamin K epoxide reductase and affects clotting factors II, VII, IX, and X?
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Why is the prognosis poor once clinical signs and azotemia develop in patients with cholecalciferol toxicity?
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Which of the following is a treatment option specifically aimed at preventing hypercalcemia?
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What is the recommended frequency for evaluating serum calcium and electrolytes during hospitalization for a patient with cholecalciferol toxicity?
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Which factor is crucial when managing escalated rodenticide toxicity risks due to anticoagulants, especially regarding their safety?
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Which of the following best describes the timeline for the removal of second-generation anticoagulant rodenticides from the market?
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What is the maximum total dosage of methocarbamol that should be administered to a dog or cat in a day?
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Which medication is most effective when administered within 24-36 hours of exposure to cholecalciferol?
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What route of administration is preferred for Vitamin K1 in cases of anticoagulant rodenticide exposure?
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Which medication is used to reverse the respiratory and central nervous system depression caused by opioids?
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What should be avoided when administering pamidronate to treat cholecalciferol toxicity?
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Which is the correct dosage for administering naloxone in cats experiencing opioid toxicity?
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What is a potential side effect of N-acetylcysteine if not properly diluted?
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Which medication is specifically indicated for countering nicotinic effects related to organophosphate toxicity?
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What should be done if a toxic dose of anticoagulant rodenticide (ACR) is suspected to have been ingested in a pet?
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Which clinical signs are typically seen in cases of ACR ingestion?
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What is the correct approach to treat a patient with bleeding or coagulopathy due to ACR ingestion?
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After an ACR ingestion, when should the first PT measurement be taken for proper diagnostics?
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Why might cats experience less severe effects from ACR compared to dogs?
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What are the implications of prolongation in coagulation factors after ACR ingestion?
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What is the primary action of osmotic cathartics in the gastrointestinal tract?
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What is one major contraindication for using cathartics?
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Which factor remains unaffected in the early stages following ACR ingestion?
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What is the calculated LD50 of Brodifacoum for dogs?
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Which substance is commonly combined with activated charcoal in commercially prepared products?
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What potential health issue should be monitored when administering cathartics?
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Why is mineral oil not recommended following activated charcoal administration?
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What is the most commonly used bulk cathartic in veterinary medicine?
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Which of the following describes a risk associated with using cathartics in dehydrated animals?
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Which type of cathartic is primarily used to add bulk to fecal matter?
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What percentage of calls to the ASPCA Animal Poison Control Center involve exposure to human and veterinary medications?
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Which rodenticide type is becoming less frequently used due to EPA regulations mandated in 2011?
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What is the primary effect of bromethalin, a neurotoxic rodenticide, on cellular function?
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What treatment is NOT appropriate for bromethalin poisoning?
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What is a common source of animal exposure to toxicants apart from medications?
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Which of the following toxicants primarily affects the central nervous system due to lipid peroxidation?
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Which method is expected to be less frequently required due to the shift away from anticoagulant rodenticides?
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What clinical sign is often observed in cats after exposure to liquid potpourri?
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What type of rodenticide has become more commonly used, which is not classified as an anticoagulant?
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What adverse effect can be associated with methaldehyde toxicosis?
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Which treatment is appropriate for tea tree oil toxicosis?
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What is a common sign of CNS impairment due to hypernatremia?
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What clinical sign is NOT typically associated with plant food and fertilizers ingestion?
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What severe effects can result from concentrated tea tree oil use in cats?
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Which toxicant is commonly used in pesticides for snails and slugs?
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What treatment should NOT be utilized for treating hypernatremia?
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What is the primary function of bulk cathartics in the gastrointestinal (GI) tract?
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What potential issue arises from administering excessive amounts of emetics in cats?
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Under what condition are cathartics contraindicated?
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Which type of cathartic is known to draw water into the gastrointestinal tract rather than simply increasing bulk?
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In which situation is dilution with dairy products specifically indicated?
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What potential risk is associated with the use of cathartics in veterinary medicine?
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What is the time frame in which emetics are most effective after the ingestion of a toxicant?
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Why is mineral oil not recommended to be administered after activated charcoal?
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What is a contraindication for the use of emesis in veterinary practice?
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Why might the presence of pre-existing conditions impact the decision to induce emesis?
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Which substance is typically combined with activated charcoal in commercially prepared products?
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Which of the following emetics can be used in the veterinary clinical setting?
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What is the most commonly used bulk cathartic for animals?
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What is a common side effect of using cathartics in animals?
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What is a potential outcome of inducing emesis in an animal that has ingested a stimulant?
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What effect does feeding a small moist meal have before inducing vomiting?
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What is the mechanism of action by which bromethalin, a neurotoxic rodenticide, affects cellular function?
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Which of the following statements is true regarding the changes in rodenticides available in the U.S. market since 2011?
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What is a significant consequence of bromethalin poisoning in terms of cellular physiology?
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What type of antidote would be ineffective in treating bromethalin poisoning?
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What percentage of calls to the ASPCA Animal Poison Control Center involve exposures to human and veterinary medications?
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Which toxin requires a different treatment approach than anticoagulant rodenticides due to its neurotoxic effects?
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What environmental regulation, mandated by the EPA in 2011, has influenced the types of rodenticides available in the U.S. market?
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What complication arises from the ingestion of bromethalin in animals?
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What is the primary reason for measuring prothrombin time (PT) after 36-48 hours post-ingestion of ACR?
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Which of the following is a common clinical sign of generalized hemorrhage due to ACR intoxication?
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What treatment may be warranted if the prothrombin time (PT) is prolonged after ACR ingestion?
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How do the LD50 values of difethialone compare between dogs and cats?
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Which of the following reflects a major difference in the effects of ACR on canines versus felines?
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What is a key factor influencing the choice of management for ACR intoxication in pets?
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Which of the following conditions could occur as a result of ACR ingestion characterized by bleeding?
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What is the recommended duration for monitoring PT after completing vitamin K1 therapy for ACR intoxication?
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Which substance is commonly associated with causing hypoglycemia in animals?
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What is a major metabolite of ethylene glycol that contributes to renal toxicity?
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In cases of acute ethylene glycol toxicosis, which stage typically presents with neurological symptoms?
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What common symptom may occur following the ingestion of detergents in cats?
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Which treatment should be avoided when managing a case of corrosive substance ingestion?
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Which of the following substances is commonly tested for in veterinary diagnostics related to toxic exposures?
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What is a significant concern when administering cathartics to animals with certain pre-existing conditions?
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Which of the following is NOT a known effect of propylene glycol ingestion in animals?
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What is the primary concern when inducing emesis in patients with severe cardiac disease?
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Which scenario would necessitate caution against inducing emesis despite the ingestion of a toxic substance?
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What is an important factor in determining the effectiveness of emesis after ingestion of certain toxicants?
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Why is dilution with dairy products recommended in specific cases of oral irritation?
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Which of the following is a risk associated with the ingestion of petroleum distillates?
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What is the primary role of cathartics when used with activated charcoal?
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Which of the following is a contraindication for using cathartics?
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What effect does administering a small moist meal before inducing vomiting have on emesis effectiveness?
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What is a primary consideration when choosing an emetic for veterinary purposes?
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Which type of cathartic is primarily known for its water retention properties?
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Why is mineral oil generally avoided after activated charcoal administration?
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Why is it critical to weigh the risks of emesis against the benefits when treating an intoxicated animal?
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What is the most common osmotic cathartic used in veterinary practice?
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Hydration status should be monitored when using cathartics due to the risk of?
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What effect might bulk cathartics like psyllium have in animals?
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What is a primary concern when using cathartics in treating overdose cases?
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What should be done if a toxic dosage has been calculated or a rodenticide has been ingested?
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Why might cats be less likely to develop toxicosis from ACR compared to dogs?
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What is the timing for observing measurable changes in clotting factors after ACR ingestion?
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What is the appropriate duration for administration of vitamin K1 therapy for a patient that ingested a second-generation ACR?
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Which clinical signs may indicate significant internal bleeding due to ACR toxicity?
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What is the testing interval to measure prothrombin time after a toxic ingestion of ACR?
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If a pet shows clinical signs of bleeding, what treatment should be prioritized?
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What common misunderstanding may veterinary professionals have regarding ACR management?
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What is a potential consequence of cholecalciferol ingestion in pets?
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What is the critical laboratory finding that may occur within 12-36 hours after cholecalciferol ingestion?
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Which aspect of treatment is most imperative when dealing with cholecalciferol toxicosis?
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What might indicate a significant toxic dose of zinc phosphide in an asymptomatic patient?
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What is the recommended precaution before inducing emesis in cases of zinc phosphide ingestion?
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What is the LD50 for cholecalciferol in dogs based on the rodenticide concentration?
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What common clinical signs might indicate cholecalciferol toxicosis after 1-3 days?
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Which substances commonly contain cholecalciferol, posing a risk to pets?
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What type of diagnostic testing is noted to be often frustrating in the case of toxin exposure?
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Which of the following toxidromes is often associated with symptoms such as tachyarrhythmia and severe hypokalemia?
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What is typically emphasized in the treatment of toxicities due to the lack of specific antidotes?
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What common substances can veterinary diagnostic labs screen for regarding toxin exposures?
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When diagnosing a cat with acute kidney injury, which specific inquiry is critical related to potential toxins?
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Which of the following is an example of a tremorogenic toxin that can be screened in diagnostic labs?
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What should be included when taking a history to assess for a specific toxicity based on clinical signs?
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In veterinary medicine, how are most treatments for toxin exposures characterized?
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Which clinical sign is most likely to occur as a result of ingestion of organic meal fertilizers?
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What is a significant treatment approach for pets exhibiting symptoms of tremorgenic mycotoxins ingestion?
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Which of the following is a common clinical manifestation associated with cocoa mulch ingestion?
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In cases of de-icing salts toxicity in dogs, which sign is least likely to occur?
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What is the primary reason household cleaners may result in significant toxicity?
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Which of the following treatments is not recommended for managing salt toxicosis?
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Which by-product of the meatpacking industry is recognized for its palatability to dogs but can lead to severe gastrointestinal issues?
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What role do tremorgenic mycotoxins play in clinical toxicity?
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What is the minimum dose of xylitol that is considered toxic and can cause profound hypoglycemia?
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What is the primary treatment focus for Tea Tree Oil toxicosis in pets?
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Which of the following is NOT a clinical sign associated with xylitol toxicosis?
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What central nervous system sign is indicative of hypernatremia?
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What is the recommended initial treatment for a patient presenting with hypoglycemia after xylitol ingestion?
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What should be monitored regularly for patients diagnosed with hepatotoxicity due to xylitol ingestion?
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Which of the following substances is known to cause cardiac effects primarily in cats?
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Why is inducing emesis contraindicated after hydrocarbon ingestion?
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What is a symptom indicative of Metaldehyde toxicosis?
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Which of the following conditions are commonly associated with the ingestion of hepatotoxic doses of xylitol?
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Which best describes the indication for activated charcoal in cases of Metaldehyde ingestion?
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In the case of Plant Food and Fertilizers ingestion, what is the likely clinical outcome?
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What type of substances are considered hydrocarbons?
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What is the primary reason activated charcoal is not recommended for xylitol toxicosis?
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Which treatment is indicated for managing symptoms following Liquid Potpourri ingestion in cats?
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What is the primary concern when treating for Tea Tree Oil toxicosis?
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What is the purpose of administering multiple oral doses of activated charcoal in cholecalciferol treatment?
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Why is IV 0.9% saline fluid diuresis utilized in the treatment of hypercalcemia?
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What should patient monitoring entail after discharge when treating hypercalcemia?
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What is a consequence of acute rodenticide ingestion involving anticoagulants?
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What implication does the removal of second-generation anticoagulant rodenticides from the market have for veterinarians?
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What is a primary therapeutic effect of calcium channel blockers (CCBs) in veterinary medicine?
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Which anticoagulant has a very narrow margin of safety?
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What is often necessary for chronic management after acute hypercalcemia due to cholecalciferol toxicity?
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Which of the following clinical signs is commonly associated with overdose of calcium channel blockers?
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What non-cardiac sign may indicate calcium channel blocker intoxication in pets?
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What can be a secondary sequelae of acute cholecalciferol toxicity despite treatment?
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How do calcium channel blockers primarily exert their effects in the body?
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What type of arrhythmia is most commonly seen in cases of calcium channel blocker overdose?
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Which of the following is a likely consequence of severe hypotension caused by calcium channel blocker overdose?
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Why is dosing for calcium channel blockers in pets particularly complicated?
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Which of the following statements accurately describes the effects of calcium channel blockers?
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What is the expected onset of improvement in a dog treated with digoxin immune fab?
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In treatment for ethylene glycol toxicity, what is the consequence of delaying treatment in cats beyond 3 hours?
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What is the primary indication for using flumazenil in veterinary medicine?
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Which medication is typically administered to counteract serotonin syndrome in dogs?
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What is the initial dosing protocol for fomepizole in cats with ethylene glycol toxicity?
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Which is a common sign of mydriasis associated with poisoning?
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What does the use of intralipid emulsion in veterinary medicine primarily address?
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What potential adverse effect should be monitored for when administering digoxin immune fab?
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What is the primary goal of stabilization in patients exposed to toxicants?
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Which factor is NOT typically considered when determining the method of patient decontamination?
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What is a potential effect of atropine administration in cases of carbamate or organophosphate toxicity?
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What is the recommended route of administration for atipamezole in cases involving amitraz?
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Which of the following methods is commonly used for patient decontamination?
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What does the antidotal medication atropine primarily address in relation to toxic exposure?
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In the context of toxic exposure, why is it important to consider the exposure circumstances?
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Which of the following statements about antidotal therapy is accurate?
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What clinical sign is least commonly associated with metaldehyde toxicosis?
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Which treatment is primarily indicated for Tea Tree Oil toxicosis?
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In cases of liquid potpourri ingestion in cats, which clinical sign is typically observed?
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What risk is specifically noted regarding plant food and fertilizers?
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What is the expected onset time for clinical signs following Tea Tree Oil application?
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Which approach is proper for treating metaldehyde toxicosis in pets?
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Which specific reason makes cats particularly susceptible to liquid potpourri toxicosis?
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Which of the following treatments is contraindicated for metaldehyde ingestion?
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What is a clinical sign indicative of PG toxicosis in cats?
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Which of the following herbicides is identified as nonselective and post-emergent?
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What effect can ingestion of high doses of propylene glycol have on dogs?
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Which symptom is associated with glyphosate toxicity in animals?
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What is the recommended treatment approach for a case of PG toxicosis?
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What mechanism of action do pyridine herbicides primarily utilize to inhibit plant growth?
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What hematological change is most notably observed with the ingestion of high doses of propylene glycol in cats?
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Which of the following statements is true regarding the toxicity of herbicides such as glyphosate?
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What is the typical first-line treatment for bradycardia resulting from calcium channel blocker (CCB) intoxication?
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What is the mechanism proposed for the beneficial effects of intravenous lipid emulsion (ILE) therapy?
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Which of the following dosages is advised for calcium gluconate administration in cases of CCB overdose?
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What laboratory parameters should be monitored in symptomatic animals after CCB exposure?
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What should be done if no significant improvement occurs after intravenous lipid emulsion therapy?
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What is the recommended initial bolus dosage for intravenous lipid emulsion therapy?
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What effect does the use of calcium supplements in CCB intoxication primarily aim to achieve?
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Which of the following is NOT a typical aspect of monitoring for animals suspected of CCB overdose?
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What is the effectiveness percentage of hydrogen peroxide and apomorphine as emetics in dogs?
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Which dosing method is least preferred for administering apomorphine in dogs?
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Activated charcoal is primarily used for what purpose in the context of toxicant exposure?
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What is a potential drawback of using xylazine as an emetic in cats?
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Why is gastric lavage considered in cases of toxicant ingestion?
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Which of the following toxicants is known for undergoing enterohepatic recirculation?
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What is the reversal agent for xylazine if vomiting is complete?
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In symptomatic patients, how is activated charcoal typically administered?
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What is the first step in the management of patients exposed to toxicants?
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Which method is specifically used to counteract muscarinic effects in organophosphate toxicity?
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What factors determine the method of patient decontamination after toxicant exposure?
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Which of the following antidotal therapies is used specifically for amitraz toxicosis in dogs?
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What is a potential effect of administering Acepromazine to dogs treated for amphetamine toxicity?
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Which decontamination method involves inducing vomiting in patients after toxic exposure?
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What type of toxicity might necessitate a test dose of atropine before treatment?
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Which of the following components is included in a comprehensive treatment plan for toxin exposure?
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What is the recommended frequency for administering multiple oral doses of activated charcoal in the treatment of cholecalciferol toxicity?
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Which medication is NOT typically used to promote calciuresis in hypercalcemic patients?
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How often should serum calcium and other renal parameters be monitored during hospitalization for hypercalcemic patients?
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What is a significant concern regarding the prognosis of cholecalciferol toxicity once clinical signs develop?
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Which anticoagulant is characterized by a very narrow margin of safety?
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What is the preferred antidote for treating ethylene glycol (EG) toxicosis in animals?
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What treatment should be emphasized after hospitalization for a patient who has been treated for hypercalcemia?
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Which adverse effect is commonly associated with the administration of ethanol in cases of EG toxicosis?
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Which agent is used to prevent hypercalcemia in cholecalciferol toxicity treatment?
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What is the potential regulatory impact of the U.S. EPA's mandate regarding second-generation rodenticides?
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What is the time frame within which antidotal therapy should be administered for cats after exposure to ethylene glycol?
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Which of the following compounds can lead to false positive results in veterinary EG tests?
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Which patient condition generally results in a poor prognosis for those with ethylene glycol (EG) toxicosis without hemodialysis?
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What is the initial loading dose of fomepizole for dogs experiencing EG toxicosis?
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Which of these substances is recommended to compete with alcohol dehydrogenase in cases of ethylene glycol ingestion?
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Study Notes
Emetics
- Dosage for cats: 2-6 mL/kg (approx. 1-2 teaspoons)
- Important to use small amount to avoid vomiting and re-exposure to the damaging material
- Dilution not appropriate in patients at risk for aspiration (e.g., actively seizing or obtunded)
- Dilution with dairy products (milk, yogurt, cottage cheese) useful for oral irritation from insoluble calcium oxalate crystals (e.g., Philodendron species)
- Emetics empty 40-60% stomach contents, most effective within 2-3 hours after ingestion
- Emesis can be effective later than 3 hours if substance ingested forms a bezoar (e.g., chocolate, chewable medications)
- Feeding a small moist meal before inducing vomiting can increase likelihood of adequate emesis
- Contraindicated with ingestion of corrosive agents (e.g., alkalis, acids), petroleum distillate, or in patients with severe cardiac disease or seizure disorder
- Emesis may not be needed if animal has already vomited, or if exhibiting clinical signs (e.g., coma, seizures, recumbency) that make emesis hazardous
- Additional stimulation from vomiting can lead to seizures in patients who have ingested a stimulant
Common Emetics
- Hydrogen peroxide (3% concentration), apomorphine hydrochloride, xylazine hydrochloride
Iron Toxicosis
- Rare risk if ingested by small-size patients
- Treatment includes antacid therapy (e.g., milk of magnesia), supportive care, monitoring blood iron levels, and potentially chelation (severe cases)
- Activated charcoal not warranted (does not bind reliably to heavy metals)
Amitraz
- Formamidine pesticide found in tick collars
- Monoamine oxidase inhibitor and an alpha-adrenergic agonist
- Toxicosis occurs when collar is accidentally ingested (GI absorption)
- Lethal dosage: 100 mg/kg (dogs, PO)
- Toxic doses as low as 10-20 mg/kg reported
- Clinical signs: CNS (ataxia, sedation, mydriasis, hypothermia, coma), cardiac (bradycardia, tachycardia), GI (vomiting, diarrhea)
- Treatment: Decontamination, collar removal (e.g., via endoscopy), alpha-2-antagonists (e.g., yohimbine or atipamezole), supportive care
Insect Bait Stations
- Typically contain abamectin, hydramethylnon, or fipronil
- Rarely toxic due to low-concentration of active ingredients
- Plastic container can result in foreign body obstruction
- Treatment rarely indicated unless dog has the ABCB1 gene mutation (MDR-1 polymorphism)
Batteries
- Several types: acid dry cell, alkaline dry cell, disk-shaped, lithium
- Corrosive injury or current-induced injury can result in GI perforation
- Clinical signs: dysphagia, anorexia, tachypnea, abdominal pain, fever
- Treatment: Radiographic confirmation of ingestion, removal (e.g., endoscopy, surgery), antacids, supportive care
Diethylene Glycol (DEG)
- Industrial solvent used in canned cooking fuels, hydraulic fluid, lubrication, and brake fluid
- Does not cause calcium oxalate crystalluria
- Can result in severe kidney injury
- Clinical signs: CNS (depression, coma), GI (vomiting), renal (azotemia) dysfunction
- Treatment and prognosis similar to ethylene glycol
Paintballs
- Contain polyethylene glycol, sorbitol, glycerin, gelatin, and other ingredients that can result in free water loss and secondary, severe hypernatremia
- Minimum lethal dose: 6.6 mL/kg (dogs), 1.4 mL/kg (cats)
Ethylene Glycol (EG)
- Sources: automotive antifreeze, windshield deicing agents, motor oils, hydraulic brake fluid, paints, solvents
- As little as 1 tablespoon (15 mL) can cause severe AKI in a dog, 1 teaspoon (5 mL) can cause AKI in a cat
- Metabolized by the body to toxic metabolites (glycoaldehyde, glycolic acid, oxalic acid) which lead to severe AKI
- Three clinical stages:
- Stage 1 (within 30 minutes to 12 hours): Ataxia, hypersalivation, vomiting, seizures, polyuria/polydipsia
- Stage 2 (within 12-24 hours): Clinical signs seem to resolve, but severe internal injury is occurring; ataxia might improve, but signs of dehydration, tachycardia, and tachypnea can be seen
- Stage 3 (cats: 12-24 hours, dogs: 36-72 hours): Severe AKI occurs secondary to calcium oxalate crystalluria; anorexia, lethargy, hypersalivation, uremic halitosis, coma, depression, vomiting, seizures
- Diagnosis: Clinical suspicion, accurate interpretation of diagnostic testing (EG blood test, venous blood gas, urinalysis), clinical signs, patient history
- Positive EG test with known or suspected exposure warrants immediate treatment
- Metabolic acidosis, elevated anion gap, and calcium oxalate crystalluria support the diagnosis but confer a worse prognosis
- EG testing accurate within the first 24 hours after ingestion, false negatives possible after due to complete transformation of EG to its more toxic metabolites
Ethanol Administration
- Alcoholic proof is twice the percentage of alcohol (e.g., 100 proof = 50% ethanol = 500 mg/mL)
- Formula to calculate percentage alcohol solution: C1 × V1 = C2 × V2
- Two IV treatment recommendations:
- CRI method: 7% ethanol (70 mg/mL), give 8.6 mL/kg (600 mg/kg) IV once slowly, followed by 1.43 mL/kg/h (100 mg/kg/h) IV CRI for 24-36 h
- Alternative method: 20% ethanol solution (200 mg/mL), give 5.5 mL/kg q 4 h × 5 doses, followed by 5.5 mL/kg q 6 h × 4 more doses
- Potential adverse reactions: severe CNS depression, sedation, bradycardia, hypoventilation, metabolic acidosis, hypothermia, hypoglycemia
Propylene Glycol (PG)
- Odorless, tasteless, colorless dihydroxy alcohol
- Found in many household products (pet-friendly antifreeze fluids, moist pet foods, disinfectants, medications, room deodorants, suntan lotions, etc.)
- Metabolized to D- and L-lactic acid, contributing to metabolic acidosis
- Absorbed rapidly from the GI tract
- LD50 for dogs reported as low as 9 mL/kg, but severe clinical signs rarely seen clinically
- Important to ask specific questions about potential toxin exposure (e.g., lilies, renal/hepatotoxins)
- Diagnostic testing can be frustrating, as there is no one test for all toxicants, and multiple tests for specific agents may be expensive
- Most treatment for toxicities is supportive and not specific
- Many veterinary diagnostic labs offer basic screening tests for suspected rodenticide, insecticide, or heavy metal exposure, and some may also offer specialty screenings (e.g., "convulsant" screens)
Toxidromes
- Recognizable syndromes resulting from toxicants or classes of toxicants
- Common in veterinary medicine: ethylene glycol toxicity, xylitol toxicity, serotonin syndrome, sympathomimetic syndrome, cholinergic syndrome, anticholinergic syndrome
- Example: Beta-agonist toxicity (e.g., albuterol) - typically see tachyarrhythmia combined with severe hypokalemia and hypophosphatemia
Symptomatic Treatment
- Focus on monitoring and supportive care: fluid therapy, cardiovascular, gastrointestinal and neurologic support as needed, appropriate analgesia and sedation
Activated Charcoal and Cathartics
- Activated charcoal binds to toxicants with weak chemical forces.
- Cathartics help remove the bound toxicant from the body before it can be reabsorbed.
- Common cathartics include psyllium hydrophilic mucilloid (e.g., Metamucil), unspiced canned pumpkin, sorbitol, and mineral oil.
- Mineral oil should not be used after activated charcoal administration.
- Cathartics can lead to electrolyte imbalances, particularly hypernatremia.
Xylitol Toxicity
- Xylitol is a sugar-free sweetener found in various products, including gum, candy, and toothpaste.
- Xylitol ingestion causes a rapid insulin spike in dogs and cats, leading to severe hypoglycemia.
- Toxic doses of xylitol can cause hemolytic anemia, reticulocytosis, and hyperbilirubinemia.
- Treatment includes supportive care, including fluid therapy.
Herbicides
- Most herbicides are mildly toxic to dogs and cats.
- Glyphosate, an aminophosphonate, has a wide margin of safety in mammals.
- Pyridine herbicides, commonly ending in “pyr,” mimic auxin, a growth hormone in plants.
- Imidazolinone herbicides inhibit acetohydroxy acid synthase, disrupting amino acid formation in plants.
Calcium Channel Blocker (CCB) Toxicity
- ILE (Isoproterenol) can be used to treat CCB intoxication in both humans and animals.
- High-dose insulin therapy (HDI) is also effective in treating CCB intoxication.
- HDI requires a central line and concurrent dextrose administration to maintain euglycemia.
Plasmapheresis
- Plasmapheresis separates blood into red blood cell fractions and plasma.
- The plasma component containing toxins, antibodies, and other harmful substances is discarded and replaced with fluids.
Anticoagulant Rodenticide Toxicity
- Gastrointestinal decontamination performed within 6 hours is highly effective in preventing anticoagulant rodenticide toxicity.
- Only 8.3% of dogs treated within 6 hours developed prolonged PT requiring vitamin K treatment.
Diagnostic Testing
- When an animal suspected to be poisoned, consider other possible causes such as metabolic, neurologic, or cardiovascular disease.
Toxin Exposure Therapy/Decontamination
- All patients exposed to toxicants should be stabilized prior to attempts at administration of antidotal medications or patient decontamination
- Decontamination of the patient should be considered to prevent systemic absorption of the toxicant
- Multiple options for patient decontamination include dilution, induction of emesis, gastric lavage, and the use of adsorbents and cathartics
Chemical Toxicoses
- Approximately 150,000 animals are exposed to toxins each year in the U.S.
- 40% of calls to the ASPCA APCC are related to human and veterinary medication exposures
- Bromethalin is a neurotoxic rodenticide that works by uncoupling oxidative phosphorylation in the brain and liver mitochondria
- Bromethalin is not an anticoagulant rodenticide and should not be treated with vitamin K1 as an antidote
- Cats are much more resistant to the effects of ACR compared to dogs, and rarely develop toxicosis from ACR
- Clinical signs of ACR toxicosis do not develop for 3-5 days and are due to clotting factor depletion, resulting in generalized hemorrhage secondary to hypocoaguability
- Optimal management for ACR toxicosis depends on clinician preference and client commitment to follow up
- Xylitol is a sugar alcohol that is commonly found in sugar-free products
- Doses >0.1 g/kg of xylitol are considered toxic and result in profound, sudden hypoglycemia from stimulation of insulin secretion
- Higher dosages (>0.5 g/kg) of xylitol have been associated with acute hepatic necrosis
- Clinical signs of xylitol toxicosis include lethargy, weakness, vomiting, collapse, anorexia, generalized malaise, tremors, and seizures (from hypoglycemia)
- When a patient is presented after ingesting a toxic amount of xylitol, the clinician should measure a blood glucose concentration immediately upon presentation; if the patient is hypoglycemic, a bolus of 1 mL/kg of 50% dextrose, diluted with 0.9% NaCl (in a 1 : 3 ratio of dextrose : NaCl) should be given IV over 1-2 minutes.
- Emesis induction should not be performed until the patient is euglycemic
- Activated charcoal does not reliably bind well to xylitol, and its administration is not routinely recommended for xylitol toxicosis
- Hypoglycemic patients should be hospitalized for IV fluid therapy [supplemented with dextrose (2.5-5%, CRI, IV)] for approximately 12-24 hours, and blood glucose concentrations should be measured every 1-4 hours
- For patients ingesting a hepatotoxic amount of xylitol, the use of hepatoprotectants (e.g., SAMe, n-acetylcysteine), antiemetics, and supportive care (including frequent liver enzyme monitoring) are warranted
- Hydrocarbons consist of chemicals containing a hydrogen and carbon group as their main constituents
- Examples of hydrocarbons include liquid fuels such as kerosene, engine oil, tiki-torch fuels, gasoline, diesel fuels, paint solvents, wood stains, wood strippers, liquid lighter fluids, and asphalt/roofing tar
- It is contraindicated to induce emesis after hydrocarbon ingestion due to the risks of aspiration pneumonia
- In general, hydrocarbons are GI tract irritants, but also can be irritants to the respiratory system (if inhaled), eyes, and skin
- It is important to ask specific questions in regards to any possible toxin exposure
- Diagnostic testing for toxins can be frustrating, as there is no one test for all toxicants, and multiple tests for specific agents may be expensive
- Many veterinary diagnostic labs offer basic screening tests for suspected rodenticide, insecticide, or heavy metal exposure, and some may also offer specialty screenings such as “convulsant” screens including toxins such as bromethalin, tremorogenic mycotoxins and strychnine etc.
- Toxidromes are recognizable syndromes resulting from toxicants or classes of toxicants
- Common toxidromes in veterinary medicine include: Ethylene glycol toxicity, xylitol toxicity, serotonin syndrome, sympathomimetic syndrome, cholinergic syndrome, and Anticholinergic syndrome.
- Symptomatic treatment should focus on monitoring and supportive care, including fluid therapy, cardiovascular, gastrointestinal, and neurologic support as needed, as well as appropriate analgesia and sedation
Patient Stabilization
- Before administering antidotal medications or decontamination procedures, patients exposed to toxicants should be stabilized.
- Stabilization involves addressing life-threatening conditions such as hemodynamic instability, respiratory distress, neurological dysfunction, and immunologic reactions like anaphylaxis.
Decontamination Methods
- Decontamination aims to prevent systemic absorption of ingested toxicants.
- Decontamination methods include dilution, inducing emesis, gastric lavage, and using adsorbents and cathartics.
Antidotal Therapies
- Antidotal medications target specific toxicants.
- Acepromazine can be used for amphetamine toxicosis, but it can cause hypotension.
- Atipamezole (Antisedan) reverses the effects of amitraz toxicity.
- Atropine is effective for carbamate and organophosphate poisonings by counteracting muscarinic effects.
- Cyproheptadine (Periactin) can be used for serotonin syndrome caused by selective serotonin reuptake inhibitors (SSRIs).
- Digoxin immune fab (Digibind) is effective for digoxin poisoning, leading to rapid improvement.
- Ethanol is an antidote for ethylene glycol poisoning, but treatment must start within three hours in cats.
- Flumazenil (Romazicon) is a short-acting antidote for benzodiazepine poisoning.
- Fomepizole (4MP) is an antidote for ethylene glycol toxicity, with a higher dose for cats.
- Intralipid emulsion (ILE) can be used for bupivacaine and verapamil toxicities.
Anticoagulant Rodenticides (ACRs)
- While emesis induction and administering activated charcoal may be appropriate for non-toxic ingestions, they are often unnecessary for ACRs.
- A single dose of vitamin K1 is unnecessary and potentially detrimental, as it can mask the patient's coagulopathy and lead to delayed clinical bleeding.
- Prothrombin Time (PT) is the first blood test to show prolongation after ACR ingestion, typically 36-48 hours post-ingestion.
Insecticides
- Pyrethrins and pyrethroids are found in common household insect sprays and insecticides.
- Cats are highly sensitive to pyrethrins due to their altered liver metabolism.
- Clinical signs of pyrethrin toxicity include hypersalivation, vomiting, ataxia, tremors, seizures, AKI, and hepatotoxicosis.
Silica Gel Packs
- Silica gel packs have a wide margin of safety and rarely cause toxicosis.
- Massive ingestions in small pets could lead to constipation or foreign body obstruction.
Food Oxidizer Packs
- Food oxidizer packs, found in food containers, are often non-toxic.
Organic Meal Fertilizers
- They are palatable for dogs and can cause GI upset, pancreatitis, and a risk of foreign body obstruction.
Compost
- Moldy compost can contain tremorgenic mycotoxins, leading to GI and CNS signs.
- Clinical signs include hypersalivation, vomiting, diarrhea, agitation, hyperesthesia, ataxia, tremors, seizures, and hyperthermia.
Cocoa Mulch
- Can lead to secondary theobromine poisoning, causing GI, cardiac, and CNS signs.
De-Icing Salts
- High salt concentrations can be mildly toxic to dogs, especially with dermal exposure.
- Large ingestions can lead to electrolyte abnormalities.
- Activated charcoal is not recommended for salt toxicosis.
Household Cleaners
- Household cleaners can cause minor GI signs, but concentrated cleaners are highly toxic or corrosive.
- Xylitol is highly toxic, causing profound hypoglycemia and hepatic necrosis at higher doses.
- Clinical signs of xylitol toxicosis include lethargy, weakness, vomiting, collapse, anorexia, tremors, and seizures.
- Emesis induction should only be performed after the patient is euglycemic.
- Activated charcoal is not routinely recommended for xylitol toxicosis.
- Hypoglycemic patients should be hospitalized for IV fluid therapy with dextrose supplementation.
Garage Toxicants: Hydrocarbons
- Hydrocarbons are liquid fuels like kerosene, gasoline, motor oil, and paint solvents.
- Emesis induction is contraindicated due to the risk of aspiration pneumonia.
- Hydrocarbons cause GI irritation and can be irritants to the respiratory system, eyes, and skin.
Carbamate and OP Poisoning
- Mydriasis and tachycardia can indicate that a patient has NOT been poisoned by a carbamate or organophosphate
Serotonin Syndrome
- Cyproheptadine (Periactin) is used to counter serotonin syndrome
- Dog dosage: 1.1 mg/kg PO or per rectum up to every 8 hours if effective.
Digoxin Poisoning
- Digoxin immune fab (Digibind) is used to treat digoxin poisoning
- Dog dosage: 1-2 vials slow IV administration (over 30 minutes)
- Patients are expected to improve rapidly within 20-90 minutes.
Ethanol and Ethylene Glycol (EG) Poisoning
- Ethanol and EG cause severe respiratory and CNS depression, and metabolic acidosis
- Cat treatment for EG poisoning must be started within 3 hours of exposure or the prognosis is grave.
Benzodiazepine Poisoning
- Flumazenil (Romazicon) is used to treat benzodiazepine poisoning
- Dosage: 0.01-0.02 mg/kg IV
- Flumazenil has a short half-life and may need to be repeated
- Reserved for cases of severe CNS and respiratory depression
Ethylene Glycol Poisoning
- Fomepizole (4MP, 4-methylpyrrazole) is used to treat ethylene glycol poisoning
- Dog dosage: Initial dose of 20 mg/kg IV, then subsequent doses at 12 and 24 hours with 15 mg/kg and 36 hours with 5 mg/kg
- Cat dosage: Initial dose of 125 mg/kg IV, then subsequent doses at 12, 24, and 36 hours with 31.25 mg/kg
- Fomepizole can cause CNS depression
- Cat treatment must be started within 3 hours of exposure or the prognosis is grave
Bupivacaine and Verapamil Poisoning
- Intralipid emulsion (ILE) is used to treat bupivacaine and verapamil poisoning
- Dosage: Using a 20% solution, initial bolus of 1.5 mL/kg slowly IV, then CRI of 0.25 mL/kg/min IV for 30-60 minutes.
Iron Toxicosis
- These packages contain iron, where the powder is often black or brown in color and magnetized.
- Rare risks of iron toxicosis if ingestion by small-size patients.
- Treatment for iron toxicosis includes antacid therapy, supportive care, monitoring blood iron levels, and potentially chelation (in severe cases).
- Activated charcoal is not warranted (does not bind reliably to heavy metals).
Amitraz Poisoning
- Amitraz is found in tick collars
- It is a monoamine oxidase inhibitor and an alpha-adrenergic agonist.
- Toxicosis occurs when the collar is accidentally ingested.
- Lethal dosage: 100 mg/kg (dogs, PO)
- Clinical signs: CNS (e.g., ataxia, sedation, mydriasis, hypothermia, coma), cardiac (e.g., bradycardia, tachycardia), and GI (e.g., vomiting, diarrhea)
- Treatment: Decontamination, removal of the collar from the GI tract (e.g., via endoscopy), alpha-2-antagonists (e.g., yohimbine or atipamezole), and supportive care
Insect Bait Stations
- Typically contain abamectin, hydramethylnon, or fipronil.
- Rarely toxic due to low-concentration of active ingredients
- Rarely, plastic container can result in foreign body obstruction
- Treatment is rarely indicated unless the dog has the ABCB1 gene mutation (MDR-1 polymorphism).
Batteries
- Several types of batteries: acid dry cell, alkaline dry cell, disk-shaped, lithium.
- Corrosive injury or current-induced injury potentially can result in GI perforation.
- Clinical signs: dysphagia, anorexia, tachypnea, abdominal pain, and fever
- Treatment: Radiographic confirmation of ingestion, removal (e.g., endoscopy, surgery), antacids, and supportive care.
Diethylene Glycol (DEG) Poisoning
- Used as an industrial solvent
- Clinical signs: CNS (e.g., depression, coma), GI (e.g., vomiting), renal (e.g., azotemia) dysfunction
- Treatment and prognosis are similar to those of ethylene glycol
Paintballs
- Contain polyethylene glycol, sorbitol, glycerin, gelatin, and other ingredients
- Can result in free water loss and secondary, severe hypernatremia
Organic Meal Fertilizers
- By-products from the meatpacking industry used as a soil amendment, typically made of bone, blood, feather, fish, etc.
- Very palatable to dogs.
- Clinical manifestations: GI signs (e.g., hypersalivation, abdominal distension, vomiting, bloody diarrhea), metabolic (e.g., pancreatitis), and rare risk of foreign body obstruction
- Treatment: Emesis induction, fluid therapy, antiemetics, bland diet, and supportive care.
Compost (e.g., moldy food)
- Presence of tremorgenic mycotoxins (e.g., penitrem A and roquefortine), which interfere with the release of neurotransmitter amino acids.
- Clinical signs: GI (e.g., hypersalivation, vomiting, diarrhea, distended abdomen) and CNS signs (e.g., agitation, hyperesthesia, ataxia, muscle tremors, seizures, and secondary hyperthermia)
- Treatment: Decontamination, muscle relaxants, antiemetics, anticonvulsants, fluid therapy, thermoregulation, and supportive care.
Cocoa Mulch
- Rarely seen as a toxicant
- Can result in secondary theobromine toxicosis
- Clinical signs: GI, cardiac, CNS
- Treatment: Decontamination (e.g., emesis induction, charcoal administration), fluid therapy, anti-emetics, sedation, anxiolytics, beta-blocker therapy, anticonvulsants, and supportive care.
De-Icing Salts
- High concentrations of salt mixtures (e.g., sodium chloride, calcium chloride, potassium chloride, magnesium chloride hexahydrate, etc.)
- Mildly toxic to dogs when exposed
- Typical toxicosis: Dermal exposure (e.g., licking fur off snow-covered sidewalk)
- Rarely: More severe clinical signs can be seen if directly ingested
- Clinical signs: GI (e.g., vomiting, diarrhea); rarely, electrolyte abnormalities can be seen (e.g., hypernatremia), typically associated with large ingestions
- Treatment: IV fluid therapy, electrolyte monitoring, antiemetics, and supportive care.
- Charcoal is not recommended with salt toxicosis.
Household Cleaners
- Most household surface cleaners are generally benign
- When ingested directly from the bottle, may result in minor GI signs
- Certain concentrated cleaners can be highly toxic or corrosive
Xylitol
- Doses > 0.1 g/kg are considered toxic and result in profound, sudden hypoglycemia from stimulation of insulin secretion.
- Higher dosages (> 0.5 g/kg) of xylitol have been associated with acute hepatic necrosis.
- Clinical signs of xylitol toxicosis: lethargy, weakness, vomiting, collapse, anorexia, generalized malaise, tremors, and seizures (from hypoglycemia)
- When hepatotoxic doses are ingested, clinical signs and clinicopathologic findings can include icterus, diarrhea, melena, hypoglycemia, increased liver enzymes, hypoalbuminemia, hypocholesterolemia, and decreased blood urea nitrogen.
-
Treatment:
- Measure blood glucose concentration immediately upon presentation
- If hypoglycemic, give a bolus of 1 mL/kg of 50% dextrose, diluted with 0.9% NaCl (in a 1 : 3 ratio of dextrose : NaCl) IV over 1-2 minutes
- Do not perform emesis induction until the patient is euglycemic.
- Activated charcoal does not reliably bind well to xylitol, and its administration is not routinely recommended for xylitol toxicosis.
- Hospitalize for IV fluid therapy [supplemented with dextrose (2.5-5%, CRI, IV)] for approximately 12-24 hours, and blood glucose concentrations should be measured every 1-4 hours.
- For patients ingesting a hepatotoxic amount of xylitol, the use of hepatoprotectants (e.g., SAMe, n-acetylcysteine), antiemetics, and supportive care (including frequent liver enzyme monitoring) are warranted.
Garage Toxicants
Hydrocarbons
- Hydrocarbons consist of chemicals containing a hydrogen and carbon group as their main constituents.
- Examples: liquid fuels such as kerosene, engine oil, tiki-torch fuels, gasoline, diesel fuels, paint solvents, wood stains, wood strippers, liquid lighter fluids, and asphalt/roofing tar.
- Contraindicated to induce emesis after hydrocarbon ingestion due to the risks of aspiration pneumonia.
- Hydrocarbons are GI tract irritants
- Can be irritants to the respiratory system (if inhaled), eyes, and skin.
Prescription and Over-the-Counter Drug Poisonings
- Account for approximately 40% of all cases reported to Pet Poison Helpline.
- Most often involve unintentional overdoses.
- Intentional administration of medication by the pet owner and iatrogenic intoxications also occur.
Calcium Channel Blockers (CCBs)
- Commonly used in both human and veterinary medicine for the treatment of systemic hypertension, cardiac disease, and other cardiac issues.
- In general, CCBs inhibit the transmembrane influx of extracellular calcium through slow or long-lasting (L-type) ion channels primarily located in myocardial and arterial smooth muscle cells.
- Mechanism: Decreased myocardial contractility, and arterial dilation, with a subsequent decrease in peripheral resistance, blood pressure, and afterload.
- Overdose or intoxication results in an exaggeration of therapeutic effects.
- Predominant signs: Sinus bradycardia, bradyarrhythmias (e.g., all degrees of heart block), and hypotension secondary to vasodilation.
- Non-cardiac signs: Vomiting (especially in cats), hypothermia, central nervous system (CNS) depression, non-cardiogenic pulmonary edema, hypokalemia, hyperglycemia, metabolic acidosis (secondary to hypoperfusion), and increased lactate production.
- Rarely: Signs of CNS stimulation such as tremors or seizures occur.
- Toxic dosages for CCBs in dogs and cats have not been determined.
Toxin Exposure Therapy/Decontamination
-
Stabilization is crucial for patients exposed to toxicants before administering antidotal medications or decontamination.
- This involves addressing life-threatening issues like hemodynamic instability, respiratory distress, neurological complications, and immunologic reactions.
-
Decontamination should be considered after stabilization to prevent further systemic absorption of the toxicant.
- Exposure circumstances like species involved, time elapsed, toxicant nature, and amount ingested determine the appropriate method.
-
Methods of decontamination include:
- Dilution
- Induction of emesis
- Gastric lavage
- Adsorbents
- Cathartics
Antidotal Therapies
-
Acepromazine is an anti-anxiety medication used to treat amphetamine overdoses in dogs.
- Caution: It can lower blood pressure.
-
Atipamezole (Antisedan) is an antidote for amitraz toxicosis in dogs.
- It reverses the CNS depression, bradycardia, GI stasis, and hyperglycemia associated with amitraz poisoning.
-
Atropine is a medication used to counteract the effects of carbamates and organophosphates (OPs).
- It addresses muscarinic effects like salivation, lacrimation, urinary incontinence, diarrhea, dyspnea, and emesis (SLUDDE).
-
Vitamin K1 is used for the treatment of anticoagulant rodenticide (ACR) ingestion.
- It takes 36-48 hours for coagulation factors to be affected, and clinical signs often don't appear for 3-5 days due to clotting factor depletion.
- Signs include lethargy, exercise intolerance, inappetence, pallor, dyspnea, coughing, and hemoptysis.
- Treatment may involve vitamin K1 administration, plasma transfusions, intensive care, oxygen therapy, and monitoring of coagulation parameters.
-
Iron Toxicity: Ingestion of iron-containing products can lead to toxicity.
- Treatment may include antacid therapy, supportive care, monitoring blood iron levels, and potentially chelation in severe cases.
-
Amitraz is a toxicant found in tick collars and can cause CNS, cardiac, and GI issues.
- Removal of the collar from the GI tract, alpha-2-antagonists, and supportive care are essential.
- Insect Bait Stations: Typically contain low concentrations of toxicants and pose minimal risk unless ingested by dogs with the ABCB1 gene mutation.
-
Batteries: Can cause corrosive injury or current-induced injury, potentially leading to GI perforation.
- Treatment involves radiographic confirmation of ingestion, removal, antacids, and supportive care.
-
Diethylene Glycol (DEG): Industrial solvent that can cause severe kidney injury.
- Signs include CNS depression, vomiting, and renal dysfunction.
- Treatment and prognosis are similar to ethylene glycol toxicosis.
- Paintballs: Contain ingredients that can lead to free water loss and hypernatremia.
Client Information Sheet: Prescription and Over-the-Counter Drug Poisonings in Dogs and Cats
- Prescription and over-the-counter drug exposures account for approximately 40% of all cases reported to Pet Poison Helpline.
- Common causes include unintentional overdoses, intentional administration by pet owners, and iatrogenic intoxications.
Calcium Channel Blockers (CCBs)
- CCBs such as amlodipine, diltiazem, and verapamil are used to treat hypertension, cardiac disease, and other cardiac issues.
- They inhibit calcium influx, resulting in decreased myocardial contractility and arterial dilation.
- Overdose can lead to exaggerated therapeutic effects, chiefly sinus bradycardia, bradyarrhythmias, and hypotension.
- Other possible signs include vomiting, hypothermia, CNS depression, pulmonary edema, hypokalemia, hyperglycemia, and metabolic acidosis.
Considerations for Toxicity Diagnosis
- Ask specific questions about potential toxin exposure, including lilies and specific toxicants that can cause organ damage or specific clinical signs.
- Diagnostic testing may be expensive and results can take days.
- Treatment is often supportive and not specific in nature.
- Many veterinary labs offer basic screening tests for suspected rodenticide, insecticide, or heavy metal exposures.
Toxidromes
- Recognizable syndromes caused by toxicants or classes of toxicants.
- Common examples: ethylene glycol toxicity, xylitol toxicity, serotonin syndrome, sympathomimetic syndrome, cholinergic syndrome, and anticholinergic syndrome.
Symptomatic Treatment
- Focus on monitoring and supportive care, including fluid therapy, cardiovascular, gastrointestinal, and neurological support.
- Analgesia and sedation may also be necessary.
Bromethalin
- Bromethalin is a rodenticide sold under various brand names like Assault, Tomcat Mole Killer, Talpirid, Real Kill, Clout, Fastrac, Vengeance, etc.
- It has a narrow margin of safety, meaning small amounts can be lethal.
- The LD50 (lethal dose for 50% of subjects) in dogs is 2.38-3.65 mg/kg, with a minimum lethal dosage of 2.5 mg/kg.
- This translates to a 5 kg dog ingesting 120 grams (4 ounces) of typical 0.01% bait.
- A typical 5 kg dog needs to ingest only 12 grams (0.4 ounces) to develop clinical signs.
- Cats are more sensitive to bromethalin, with an LD50 of 0.54 mg/kg.
- Clinical signs appear within 2-24 hours of ingestion and vary with the amount ingested.
- Common signs include CNS stimulation or depression, abnormal behavior, ataxia, hyperesthesia, seizures, coma, paresis, hindlimb paralysis, anisocoria, nystagmus, changes in pupillary light reflex, and tremors.
- Treatment involves early decontamination, preventing cerebral edema, and supportive care.
- Decontamination methods include emesis induction, gastric lavage, and activated charcoal administration.
- Multiple oral doses of activated charcoal are recommended due to enterohepatic recirculation.
- Additional treatment options include intravenous fluid therapy, oxygen support, head elevation, mannitol for cerebral edema, anticonvulsants, and thermoregulation.
- Corticosteroids are no longer recommended for intracranial pressure; mannitol is preferred.
- Prognosis depends on the amount ingested and the severity of clinical signs.
- Prognosis is generally fair to excellent with early decontamination and treatment.
- Persistent seizures or paralytic syndrome have a poorer prognosis.
Phosphide Rodenticides
- Phosphide rodenticides produce phosphine gas upon contact with water or stomach acids.
- Pet owners should be educated about the risks of toxic gas exposure to themselves.
- Owners should be instructed not to feed their pets to prevent further phosphine gas production.
- Antacids like aluminum hydroxide or milk of magnesia should be administered before emesis induction or veterinary attention to decrease phosphine gas production.
- Emesis induction following antacid administration and a single dose of activated charcoal with a cathartic are recommended for recent ingestion in asymptomatic patients.
- Supportive care including antiemetics, IV fluid therapy, and gastric protectants is warranted.
- Prognosis is excellent with supportive care.
Cholecalciferol (Vitamin D3)
- Cholecalciferol is one of the most deadly rodenticides to pets.
- Ingestion of toxic levels results in severe hypercalcemia and hyperphosphatemia, leading to acute kidney injury (AKI).
- Other sources of vitamin D3 include over-the-counter or prescription vitamins and psoriasis creams.
- Cholecalciferol-containing rodenticides have a narrow safety margin, requiring only small amounts for toxicity.
- Canine LD50 is 85 mg/kg, but doses as low as 0.1-0.5 mg/kg can lead to clinical signs and hypercalcemia.
- A 30 kg dog needs to ingest about 30 grams (1 ounce) for toxicosis.
- Clinical signs typically don't appear for 1-3 days after ingestion, with azotemia developing as early as 12-36 hours.
- Common signs include polyuria/polydipsia, weakness, lethargy, anorexia, vomiting, malaise, uremic halitosis, dehydration, hypercalcemia, hyperphosphatemia, azotemia, melena, hemorrhagic diarrhea, weight loss, and death.
- Intensive treatment is essential due to the narrow safety margin.
- Treatment includes thorough decontamination using emesis induction, gastric lavage, and charcoal administration.
- Multiple doses of activated charcoal are warranted due to enterohepatic recirculation.
- Further treatment includes aggressive IV saline fluid diuresis, serum calcium monitoring, GI support, medications for increasing calciuresis and preventing hypercalcemia.
- Treatment is expensive and often requires hospitalization for 2-7 days.
- Oral therapy may need to continue for weeks after discharge.
- Frequent monitoring of renal parameters and electrolytes is crucial.
- Even with intensive treatment, chronic kidney disease (CKD) can occur.
- Prognosis is poor once clinical signs and azotemia develop due to the risk of CKD.
Anticoagulant Rodenticides (ACR)
- First- and second-generation ACRs inhibit vitamin K epoxide reductase, inactivating clotting factors II, VII, IX, and X.
- First-generation rodenticides (warfarin, pindone) were replaced with more potent, longer-lasting second-generation ACRs (brodifacoum, bromadiolone, diphacinone, chlorophacinone).
- The U.S.EPA mandated the removal of second-generation ACRs from the U.S. market in 2011, impacting veterinary cases.
- The margin of safety and LD50 vary between ACRs.
- Brodifacoum has a very narrow margin of safety, while bromadiolone has a wide margin of safety.
Organic Meal Fertilizers
- By-products from meatpacking industry used as soil amendments, containing bone, blood, feather, fish, etc.
- Highly palatable to dogs.
- Clinical manifestations include gastrointestinal signs (hypersalivation, abdominal distension, vomiting, bloody diarrhea), metabolic signs (pancreatitis), and rare risk of foreign body obstruction.
- Treatment focuses on emesis induction, fluid therapy, antiemetics, bland diet, and supportive care.
Compost (Moldy Food)
- Presence of tremorgenic mycotoxins (penitrem A and roquefortine) that interfere with neurotransmitter amino acid release.
- Clinical signs appear within 2-4 hours of ingestion and include gastrointestinal signs (hypersalivation, vomiting, diarrhea, distended abdomen) and central nervous system signs (agitation, hyperesthesia, ataxia, muscle tremors, seizures, secondary hyperthermia).
- Treatment aims at decontamination, muscle relaxants, antiemetics, anticonvulsants, fluid therapy, thermoregulation, and supportive care.
Cocoa Mulch
- Rarely seen as a toxicant but can result in secondary theobromine toxicosis.
- Clinical signs of methylxanthine toxicosis (gastrointestinal, cardiac, central nervous system) can be observed.
- Treatment focuses on decontamination (emesis induction, charcoal administration), fluid therapy, anti-emetics, sedation, anxiolytics, beta-blocker therapy, anticonvulsants, and supportive care.
De-Icing Salts
- Contains high concentrations of salt mixtures like sodium chloride, calcium chloride, potassium chloride, and magnesium chloride hexahydrate.
- Mildly toxic to dogs upon exposure.
- Toxicity primarily arises from dermal exposure through licking fur after contact with snow-covered sidewalks.
- Rare severe clinical signs can occur if directly ingested from the bag.
- Clinical signs include gastrointestinal signs (vomiting, diarrhea), and rarely, electrolyte abnormalities (hypernatremia) associated with large ingestions.
- Treatment consists of intravenous fluid therapy, electrolyte monitoring, antiemetics, and supportive care.
- Charcoal is not recommended for salt toxicosis.
Household Cleaners
- Most surface cleaners are generally benign but can cause minor GI signs if ingested directly.
- Concentrated cleaners can be highly toxic or corrosive.
Serotonin Syndrome
- Cyproheptadine (Periactin) is a selective serotonin reuptake inhibitor (SSRI) used to counter serotonin syndrome.
- Serotonin syndrome symptoms include hyperthermia, tremors, seizures, ataxia, excitation, depression, hyperesthesia, and GI distress.
Cardiac Glycosides
- Digoxin immune fab (Digibind) is an antidote for digoxin poisoning.
- Digoxin poisoning can cause cardiac arrhythmias, bradycardia, and other cardiac issues.
- Digoxin is a cardiac glycoside found in plants.
Ethanol
- Causes severe respiratory and CNS depression, and metabolic acidosis.
- Cats need treatment within 3 hours of exposure or prognosis is grave.
Flumazenil
- Flumazenil (Romazicon) is an antidote for benzodiazepine poisoning.
- Flumazenil has a short half-life and may need to be repeated.
- It's reserved for cases of severe CNS and respiratory depression.
Fomepizole
- Fomepizole (4-MP, 4-methylpyrrazole) is an antidote for ethylene glycol poisoning.
- It may cause CNS depression
- Cats need treatment within 3 hours of exposure or prognosis is grave.
Intralipid Emulsion (ILE)
- Intralipid emulsion (ILE) is used to treat bupivacaine and verapamil poisoning.
- It works by reducing the effects of the toxic substance in the body.
Tea Tree Oil
- Concentrated tea tree oil (100%) can be toxic to dogs and cats.
- Clinical signs include CNS depression, weakness, ataxia, hypothermia, and muscle tremors.
- Treatment focuses on dermal and oral decontamination, fluid support, thermoregulation, clinicopathologic monitoring, and supportive care.
Liquid Potpourri
- Liquid potpourri can be toxic to cats, but not dogs.
- Contains essential oils and cationic detergents, which can cause chemical burns in the mouth, dermal and ocular irritation.
- Treatment includes oral and dermal decontamination, analgesics, antacids, fluid therapy, clinicopathologic monitoring, and supportive care.
Metaldehyde
- Metaldehyde is a pesticide used to control snails and slugs.
- Can cause GI, CNS, and miscellaneous signs like DIC and hepatopathy.
- Treatment aims to decontaminate the patient, provide antiemetic and muscle relaxant therapy, thermoregulate, and provide supportive care.
Plant Food and Fertilizers
- Plant food and fertilizers typically have a wide margin of safety.
- Contain natural elements like nitrogen, phosphorus, and potassium.
- Can cause GI disturbance with direct ingestion.
- Treatment includes antiemetic therapy, fluid therapy, and supportive care.
Windshield Wiper Fluid (Methanol)
- Most windshield wiper fluids contain methanol.
- Methanol can cause toxicosis in dogs, but not retinal toxicosis as seen in humans.
- Clinical signs include CNS, GI, and respiratory signs.
- Treatment includes IV fluid therapy, antiemetic therapy, and supportive care.
- Fomepizole is not necessary for methanol toxicosis.
Ethylene Glycol
- Ethylene glycol (EG) is a common ingredient in antifreeze and can be toxic to pets.
- EG toxicosis can cause kidney failure and death.
- Treatment includes antidotal therapy (fomepizole or ethanol), intensive IV fluid therapy, monitoring urine output and clinicopathologic parameters, antiemetic therapy, and supportive care.
- Fomepizole is the preferred antidote over ethanol.
- Cats need treatment within 3 hours of exposure or prognosis is grave.
Calcium Channel Blockers (CCBs)
- CCBs are commonly used to treat systemic hypertension, cardiac disease, and other cardiac issues.
- Overdose or intoxication from CCBs can cause sinus bradycardia, bradyarrhythmias, hypotension, and other non-cardiac signs.
- Treatment typically involves supportive care, such as IV fluids and monitoring.
- No toxic dosage for CCBs in dogs and cats has been determined.
Cholecalciferol
- Multiple oral doses of activated charcoal (without a cathartic) are warranted to treat cholecalciferol poisoning due to enterohepatic recirculation of the toxin.
- Treatment also includes aggressive IV fluid diuresis to promote calciuresis (urinary excretion of calcium), serum calcium monitoring, GI support (antiemetics, H2 blockers, sucralfate, phosphate binders), and medications to increase calciuresis (prednisone, furosemide) and prevent hypercalcemia (pamidronate, calcitonin).
- Hospitalization typically lasts 2-7 days, with oral therapy often continued for several weeks after discharge.
- Frequent monitoring of renal parameters (blood urea nitrogen, creatinine) and electrolytes (serum calcium, phosphorus, ionized calcium) is essential, with evaluations every 12-24 hours during hospitalization and then every 2-3 days for the next 2-4 weeks.
- CKD may develop as a late complication despite intensive treatment.
- Prognosis is poor once clinical signs and azotemia (elevated blood urea nitrogen) develop due to the risk of CKD.
Anticoagulants
- First- and second-generation anticoagulants (ACRs) work by inhibiting vitamin K epoxide reductase, leading to inactivation of clotting factors II, VII, IX, and X.
- Second-generation ACRs (e.g., brodifacoum, bromadiolone, diphacinone, chlorophacinone) were initially favoured over first-generation rodenticides (e.g., warfarin, pindone) due to their increased potency and longer duration of action.
- Second-generation ACRs are now being phased out in the U.S. market.
- The margin of safety and LD50 (lethal dose for 50% of subjects) vary between ACRs, with some having very narrow margins (e.g., brodifacoum) and others having wider margins (e.g., bromadiolone).
Xylitol
- Xylitol doses exceeding 0.1 g/kg are considered toxic and can result in profound, sudden hypoglycemia from stimulation of insulin secretion.
- Higher dosages (>0.5 g/kg) are associated with acute hepatic necrosis.
- Clinical signs of xylitol toxicosis include lethargy, weakness, vomiting, collapse, anorexia, generalised malaise, tremors, and seizures (caused by hypoglycemia).
- Hepatotoxic doses can lead to clinical signs and clinicopathologic findings like icterus (jaundice), diarrhoea, melena (black, tarry stools), hypoglycemia, increased liver enzymes, hypoalbuminemia, hypocholesterolemia, and decreased blood urea nitrogen.
- Immediate blood glucose measurement is crucial upon presentation.
- For hypoglycemic patients, a bolus of 1 mL/kg of 50% dextrose diluted with 0.9% NaCl (1:3 ratio) should be administered IV over 1-2 minutes.
- Emesis induction should not be performed until the patient is euglycemic (normal blood glucose).
- Activated charcoal is not routinely recommended for xylitol toxicosis due to its limited binding capacity.
- Hospitalization may be required for IV fluid therapy (supplemented with dextrose) for 12-24 hours, with blood glucose monitoring every 1-4 hours.
- Hepatotoxic doses warrant the use of hepatoprotectants (e.g., SAMe, n-acetylcysteine), antiemetics, and supportive care, including frequent liver enzyme monitoring.
Hydrocarbons
- Hydrocarbons are chemicals containing a hydrogen and carbon group as their main constituents.
- Common examples include liquid fuels (kerosene, engine oil, tiki-torch fuels, gasoline, diesel fuels), solvents (paint thinners, wood stains, wood strippers), lighter fluids, and asphalt/roofing tar.
- Emesis is contraindicated following hydrocarbon ingestion due to the risk of aspiration pneumonia.
- Hydrocarbons are GI irritants and can also irritate the respiratory system, eyes, and skin.
- Doses of 5 g/kg daily can result in hemolytic anemia, reticulocytosis, and hyperbilirubinemia in dogs.
- Clinical signs of hydrocarbon toxicosis include CNS depression, narcosis, tachypnea (due to metabolic acidosis), muscle twitching (cats), hypotension (cats), cardiovascular collapse, polyuria/polydipsia (due to an osmotic diuretic effect), and hematological changes (hemolytic anemia, Heinz body anemia).
- Treatment is supportive, including fluid therapy to correct metabolic acidosis, red blood cell morphology monitoring, and rarely, red blood cell transfusions.
- Antidotal therapy is not necessary.
Herbicides
- Most herbicides are considered mildly toxic to dogs and cats.
- Common types of herbicides include glyphosate (e.g., Roundup), pyridine herbicides, imidazolinone compounds, chlorophenoxy compounds (e.g., 2,4-D), and dicamba.
- Clinical signs usually involve GI abnormalities (hypersalivation, vomiting, diarrhoea) or dermal irritation.
- Glyphosate, an aminophosphonate, is a nonselective post-emergent herbicide with a wide margin of safety in mammals.
- Pyridine herbicides work by mimicking auxin, a plant hormone that inhibits growth.
- Imidazolinone herbicides inhibit acetohydroxy acid synthase, preventing amino acid formation in plants.
- 2,4-D, a chlorophenoxy compound, can uncouple oxidative phosphorylation and affect ribonuclease synthesis, leading to potential CNS effects (demyelination).
- Clinical signs reported after exposure include GI (vomiting, diarrhoea, abdominal pain) and CNS signs (myotonia, muscle stiffness, extensor rigidity).
- Dicamba, a benzoic acid herbicide, also has a wide margin of safety.
- Treatment for herbicide exposures is supportive. Decontamination is usually sufficient for large ingestions.
General Prognosis
- Prognosis is generally fair to excellent with immediate recognition and treatment, except for toxicants with narrow margins of safety (e.g., organophosphates, carbamates, ethylene glycol).
- Consult the ASPCA Animal Poison Control Center for life-threatening emergencies or when the mechanism of action, clinical signs, and treatment are uncertain.
Rodenticides
- Rodenticides are one of the top 10 toxicants affecting dogs
- Second-generation anticoagulant rodenticides (ACR), such as brodifacoum and bromadiolone, are being removed from the U.S. market
- Bromethalin is a neurotoxic rodenticide not an anticoagulant rodenticide
- Bromethalin works by uncoupling oxidative phosphorylation in the brain and liver mitochondria
- Cats are much more resistant to the effects of ACR compared to dogs and rarely develop toxicosis from ACR
- Clinical signs of ACR toxicosis typically don't develop for 3-5 days
- Clinical signs of ACR toxicosis include lethargy, exercise intolerance, inappetence, pallor, dyspnea, coughing, hemoptysis, hemoabdomen, hemothorax, pericardial effusion, gingival bleeding, epistaxis, ecchymoses, petechiae, hematuria, bleeding into the subcutaneous space or joint space, melena
- Treatment for ACR toxicosis can include decontamination, vitamin K1 therapy, plasma transfusions, intensive care, oxygen therapy
Bromethalin Toxicosis
- Bromethalin is not an anticoagulant rodenticide and should not be treated with vitamin K1
- Bromethalin toxicosis results in decreased ATP production, which affects cellular sodium and potassium pumps
- Bromethalin toxicosis can result in edema of the central nervous system (CNS)
- Treatment includes IV fluids, antiemetics, electrolyte monitoring and anticonvulsants
Tea Tree (Melaleuca) Oil
- Toxicosis has been reported in dogs and cats when concentrated (100%) oil is used
- Clinical signs of Tea Tree oil toxicosis can be seen within 1-2 hours after application
- Clinical signs include CNS depression, weakness, ataxia, hypothermia, and muscle tremors
- Rare signs include coma, increased serum liver enzyme activities, dermal or oral irritation, or cardiorespiratory effects
- Treatment includes decontamination, fluid support, thermoregulation, clinicopathologic monitoring, and supportive care
Liquid Potpourri
- Liquid potpourri contains essential oils and only results in toxicosis in cats
- Cats are sensitive to cationic detergents and essential oils
- Clinical signs include severe chemical burns in the mouth, along with dermal and ocular irritation
- Rare signs include CNS depression, pulmonary edema, seizures, and hepatopathy
- Treatment includes oral and dermal decontamination, analgesics, antacids, fluid therapy, clinicopathologic monitoring, and supportive care
Metaldehyde
- Metaldehyde is a commonly-used pesticide for controlling snails and slugs
- Metaldehyde toxicosis can result in GI signs including vomiting and diarrhea, CNS signs including tremors, seizures, and secondary hyperthermia, and miscellaneous signs including DIC, hepatopathy
- Treatment includes decontamination, antiemetic therapy, muscle relaxants, anticonvulsants, muscle relaxants, thermoregulation and supportive care
Plant Food and Fertilizers
- Plant food and fertilizers contain natural elements (e.g., nitrogen, phosphorus, potassium)
- Clinical signs include GI disturbance with direct ingestions from the bag
- Treatment includes antiemetic therapy, fluid therapy, and supportive care
Rodenticides
- Rodenticides are a common poison for dogs.
- Second-generation anticoagulant rodenticides (ACRs) are being removed from the market, and less common rodenticides are becoming more prevalent.
- Bromethalin is a neurotoxic rodenticide and should not be treated with vitamin K1.
- Bromethalin can cause CNS edema.
- Different species have different sensitivities to rodenticides, with cats being resistant.
Anticoagulant Rodenticides
- ACRs, like brodifacoum, bromadiolone, and diphacinone, are toxic to dogs.
- ACRs cause prolonged coagulation factors, evidenced by an extended prothrombin time (PT) or activated partial thromboplastin time (aPTT).
- Clinical signs may not appear for 3-5 days.
- Clinical signs include lethargy, exercise intolerance, pallor, bleeding, and respiratory distress.
Anticoagulant Rodenticide Treatment
- Decontamination is important if ingested recently.
- Baseline PT should be measured 36-48 hours post-ingestion.
- If PT is prolonged, vitamin K1 therapy is warranted for 7-30 days, depending on the type of rodenticide.
- For patients with clinical bleeding, treatment includes vitamin K1 therapy, plasma transfusions, intensive care, and oxygen therapy.
- In severe cases, ongoing monitoring of PT is crucial.
- Vitamin K1 therapy should be continued for at least 30 days in cases with unreliable client compliance.
Emetics
- Dosage for emetics in cats is 2-6 mL/kg, approximately 1-2 teaspoons.
- Excessive amounts can lead to vomiting and re-exposure of the esophagus to the damaging material.
- Dilution is not appropriate in patients at risk for aspiration, including those experiencing seizures or obtundation.
- Dilution with dairy products like milk, yogurt, and cottage cheese can be beneficial for oral irritation caused by insoluble calcium oxalate crystals.
- Emetics are most effective within 2-3 hours after ingestion, emptying 40-60% of the stomach contents.
- Emesis is not recommended with ingestion of corrosive agents like alkalis and acids, or petroleum distillates due to the risk of aspiration.
- Consider pre-existing conditions like heart disease or seizures that could make emesis hazardous.
- Emesis might not be necessary if the animal has already vomited, and is not recommended if the animal is experiencing coma, seizures, or recumbency.
Activated Charcoal and Cathartics
- Activated charcoal binds to toxicants but can be reabsorbed without a cathartic.
- Cathartics are given immediately after or mixed with activated charcoal.
- Cathartics are contraindicated in cases of dehydration, diarrhea, ileus, intestinal obstruction, or perforation.
Types of Cathartics
- Bulk cathartics: Include psyllium hydrophilic mucilloid (e.g., Metamucil) and unspiced canned pumpkin.
- Osmotic cathartics: Draw water into the GI lumen, stimulating motility and expulsion. Sorbitol is the most common osmotic cathartic.
- Lubricant cathartics: Mineral oil is the most common. Not recommended after activated charcoal administration as it can decrease the effectiveness.
Concerns with Cathartics
- Can alter water balance and lead to electrolyte abnormalities, especially hypernatremia.
- Monitor hydration status closely and administer fluids intravenously or via enemas as needed.
Cholecalciferol (Vitamin D3) Toxicity
- A highly deadly rodenticide to pets.
- Causes severe hypercalcemia and hyperphosphatemia, leading to acute kidney injury.
- Common sources include OTC or prescription vitamins (calcium/vitamin D3 combinations) and psoriasis creams.
- Narrow margin of safety, with clinical toxicosis occurring after ingesting small amounts.
- LD50 for dogs is 85 mg/kg, but clinical signs can develop with dosages as low as 0.1-0.5 mg/kg.
- Clinical signs typically develop 1-3 days after ingestion, by which time overt manifestations of AKI are present.
- Azotemia can develop as early as 12-36 hours after ingestion.
- Clinical signs include polyuria, polydipsia, weakness, lethargy, anorexia, vomiting, malaise, uremic halitosis, dehydration, hypercalcemia, hyperphosphatemia, azotemia, melena, hemorrhagic diarrhea, weight loss, and death.
Management of Cholecalciferol Toxicity
- Intensive treatment is crucial due to the narrow margin of safety.
- If uncertain about toxic dose, contact rodenticide company or ASPCA APCC for guidance.
- Cats are more resistant to cholecalciferol compared to dogs.
Anticoagulant Rodenticides (ACR)
- Examples of ACRs include difethialone, brodifacoum, bromadiolone, and diphacinone.
- LD50s vary between species with cats being more resistant than dogs.
- Prolongation in coagulation factors (PT or aPTT) is not observed until 36-48 hours after ingestion.
- Clinical signs develop 3-5 days after ingestion due to clotting factor depletion, resulting in generalized hemorrhage.
- Common clinical signs include lethargy, exercise intolerance, inappetence, pallor, dyspnea, coughing, hemoptysis, hemoabdomen, hemothorax, pericardial effusion, gingival bleeding, epistaxis, ecchymoses, petechiae, hematuria, bleeding into subcutaneous or joint spaces, or melena.
Management of ACR Toxicity
- For recent ingestion, decontamination and baseline PT measurement at 36-48 hours post-ingestion is recommended.
- If PT is prolonged, administer vitamin K1 2.5-5 mg/kg PO q 24h for 7-30 days depending on the generation of ACR ingested.
- Recheck PT 2-3 days after discontinuing vitamin K1.
- For patients with clinical bleeding or coagulopathy, treatment includes vitamin K1 therapy, plasma transfusions, intensive care, oxygen therapy, and monitoring of PT 2-3 days after discontinuing vitamin K1.
Importance of Specific Toxin History
- Ask specific questions about potential toxin exposures instead of simply inquiring about "suspected toxin exposure."
- Understanding the toxins that cause specific organ damage or clinical signs can lead to better diagnosis and treatment.
Diagnostic Challenges with Toxin Exposure
- No single test for all toxicants.
- Tests for specific agents can be expensive and time consuming, with results taking several days.
- Many times, diagnosis of toxic exposure will be "suspected" or "possible" based on clinical signs and history.
Supportive Care for Toxicity
- Most treatments for toxicities are supportive and not specific.
- Focus on monitoring and supportive care, including fluid therapy, cardiovascular, gastrointestinal, and neurologic support as needed.
- Provide appropriate analgesia and sedation.
Toxidromes
- Recognizable syndromes resulting from specific toxins or classes of toxins.
- Common examples in veterinary medicine include ethylene glycol toxicity, xylitol toxicity, serotonin syndrome, sympathomimetic syndrome, cholinergic syndrome, and anticholinergic syndrome.
- Beta-agonist toxicity can cause tachyarrhythmia, hypokalemia, and hypophosphatemia. These signs should raise concern for this specific toxicity.
Rodenticides
- Cholecalciferol (Vitamin D) is a rodenticide that causes hypercalcemia.
- Treatment includes decontamination with activated charcoal, aggressive IV saline fluid diuresis, GI support, and medications to increase calciuriesis and prevent hypercalcemia.
- Chronic kidney disease (CKD) can be a secondary complication.
- Prognosis is poor once clinical signs and azotemia develop.
Anticoagulants
- First- and second-generation Anticoagulant Rodenticides (ACR) inhibit vitamin K epoxide reductase, leading to inactivation of clotting factors II, VII, IX, and X.
- First-generation rodenticides are less potent and have a longer duration of action than second-generation rodenticides.
- Second-generation rodenticides were removed from the U.S. market in 2011 by the U.S. EPA.
Tea Tree (Melaleuca) Oil
- Toxicosis occurs in dogs and cats when concentrated (100%) oil is used.
- Clinical signs include CNS depression, weakness, ataxia, hypothermia, and muscle tremors.
- Treatment includes dermal and oral decontamination, fluid support, thermoregulation, clinicopathologic monitoring, and supportive care.
Liquid Potpourri
- Toxicosis is only reported in cats, not dogs.
- Cats are highly sensitive to essential oils and cationic detergents.
- Clinical signs can include severe chemical burns in the mouth, dermal and ocular irritation, CNS depression, pulmonary edema, seizures, and hepatopathy.
- Treatment includes oral and dermal decontamination, analgesics, antacids, fluid therapy, clinicopathologic monitoring, and supportive care.
Metaldehyde
- A pesticide used to control snails and slugs.
- Toxicosis can result in GI signs, CNS signs, such as tremors, seizures, and secondary hyperthermia.
- Treatment includes decontamination, antiemetic therapy, muscle relaxants, anticonvulsants, thermoregulation, and supportive care.
Plant Food and Fertilizers
- Wide margin of safety with clinical signs only seen in moderate to large amounts.
- Clinical signs include GI disturbance with direct ingestions from the bag.
- Treatment includes antiemetic therapy, fluid therapy, and supportive care.
Organic Meal Fertilizers
- By-products from the meatpacking industry.
- Very palatable to dogs with possible foreign body obstruction.
- Treatment includes emesis induction, fluid therapy, antiemetics, bland diet, and supportive care.
Compost
- Contains tremorgenic mycotoxins, which interfere with neurotransmitter amino acids.
- Clinical signs include GI signs and CNS signs such as agitation, hyperesthesia, ataxia, muscle tremors, seizures, and secondary hyperthermia.
- Treatment includes decontamination, muscle relaxants, antiemetics, anticonvulsants, fluid therapy, thermoregulation, and supportive care.
Cocoa Mulch
- Can result in secondary theobromine toxicosis.
- Clinical signs of methylxanthine toxicosis can be seen.
- Treatment includes decontamination, fluid therapy, anti-emetics, sedation, anxiolytics, beta-blocker therapy, anticonvulsants, and supportive care.
De-Icing Salts
- High concentrations of salt mixtures, mildly toxic to dogs.
- Clinical signs include GI signs, rarely electrolyte abnormalities, typically associated with large ingestions.
- Treatment includes IV fluid therapy, electrolyte monitoring, antiemetics, and supportive care.
Household Cleaners
- Most household surface cleaners are benign.
- Concentrated cleaners can be highly toxic or corrosive.
Xylitol
- Doses exceeding 0.1 g/kg are considered toxic and result in hypoglycemia.
- Clinical signs are lethargy, weakness, vomiting, collapse, anorexia, generalized malaise, tremors, and seizures.
- Treatment includes immediate blood glucose measurement with IV bolus of 50% dextrose, diluted with 0.9% NaCl. Emesis induction should only be performed once euglycemic.
- For patients ingesting a hepatotoxic amount of xylitol, hepatoprotectants, antiemetics, and supportive care are warranted.
Garage Toxicants
- Hydrocarbons include kerosene, engine oil, gasoline, diesel fuels, paint solvents, and roofing tar.
- Emesis induction is contraindicated due to the risk of aspiration pneumonia.
- Hydrocarbons are GI tract irritants, but can also irritate the respiratory system, eyes, and skin.
Drugs
- Calcium Channel Blockers (CCBs) are commonly used to treat systemic hypertension and cardiac disease.
- CCBs inhibit transmembrane influx of calcium, resulting in decreased myocardial contractility and arterial dilation.
- Overdose results in an exaggeration of therapeutic effects, predominantly sinus bradycardia, bradyarrhythmias, and hypotension.
- Non-cardiac signs include vomiting, hypothermia, CNS depression, non-cardiogenic pulmonary edema, hypokalemia, hyperglycemia, metabolic acidosis, and increased lactate production.
- Toxic dosages for CCBs in dogs and cats have not been determined.
Toxin Exposure Therapy/Decontamination
- Prioritize patient stabilization before antidotal medications or decontamination
- Stabilization includes addressing:
- Hemodynamic issues: hypotension, cardiac arrhythmias
- Respiratory issues: respiratory distress
- Neurologic issues: seizures
- Immunologic issues: anaphylaxis
- Decontamination methods:
- Dilution
- Induction of emesis
- Gastric lavage
- Adsorbents and cathartics
Antidotal Therapies
- Acepromazine: used for amphetamines, can cause hypotension
- Atipamezole: used for amitraz toxicosis, reverses CNS depression, bradycardia, GI stasis, and hyperglycemia
- Atropine: used for carbamates and organophosphates (OPs), countering muscarinic effects (SLUDDE: salivation, lacrimation, urinary incontinence, diarrhea, dyspnea, emesis)
- Cyproheptadine: used for selective serotonin reuptake inhibitors (SSRIs) and 5-hydroxytryptophan (5-HTP), countering serotonin syndrome
- Digoxin immune fab (Digibind): used for digoxin intoxication, rapid improvement within 20-90 minutes
- Ethanol: used for ethylene glycol poisoning, details in chapter 152
- Flumazenil: used for benzodiazepine overdose, short half-life, repeated doses may be needed
- Fomepizole: used for ethylene glycol poisoning, initial dose followed by subsequent doses at 12, 24, and 36 hours
- Intralipid emulsion (ILE): used for bupivacaine and verapamil poisoning, initial bolus followed by CRI
- Tea Tree (Melaleuca) Oil: can cause CNS depression, hypothermia, muscle tremors, rarely coma and liver enzyme abnormalities, treatment includes activated charcoal, fluid support, thermoregulation
- Liquid Potpourri: toxic to cats, not dogs, due to their altered glucuronidation, causes oral burns, dermal and ocular irritation, rarely CNS depression, seizures, and hepatopathy, treatment includes decontamination, analgesics, antacids, fluid therapy
- Metaldehyde: pesticide toxicosis, results in GI, CNS, and miscellaneous signs, treatment includes decontamination, antiemetics, muscle relaxants, anticonvulsants, thermoregulation
- Plant Food and Fertilizers: wide margin of safety, clinical signs of GI disturbance with direct ingestion, large doses can cause hemolytic anemia, treatment includes antiemetics, fluid therapy
- Herbicides: majority are mildly toxic, types include glyphosate, pyridine herbicides, imidazolinone compounds, chlorophenoxy compounds, and dicamba
- Glyphosate: nonselective post-emergent herbicide, wide margin of safety, clinical signs include hypersalivation, vomiting, diarrhea
- Pyridine herbicides: used to control broad-leafed weeds, mimic auxin, inhibiting plant growth
- Imidazolinone herbicides: also used for controlling broad-leafed weeds, inhibits acetohydroxy acid synthase, inhibiting amino acid formation in plants
Calcium Channel Blocker (CCB) Toxicity
- Treatment:
- Gastrointestinal decontamination
- Close monitoring of heart rate, rhythm, and blood pressure
- Laboratory monitoring of electrolytes, blood glucose, acid/base status and lactate
- IV crystalloids for hypotension
- Atropine for bradycardia
- Calcium gluconate or calcium chloride to increase transmembrane calcium flow
- Intravenous lipid emulsion (ILE) and high-dose insulin (HDI) therapy may be considered
Intravenous lipid emulsion (ILE) Therapy
- Mechanism not fully elucidated, multifactorial
- "Lipid sink" theory: lipophilic agents sequestered in the lipid compartment of the blood
- Direct benefit to the myocardium: utilizes free fatty acids, increases intracellular calcium, alpha-adrenergic receptor mediated vasopressor effect, reduces vasodilatation
- Dosage: 1.5 mL/kg IV bolus followed by CRI of 0.25 mL/kg/min
- Improvement expected within minutes, additional boluses may be administered if needed
Stabilizing Patients
- Before administering antidotal medications or decontamination, ensure patient stabilization.
- Stabilize life-threatening issues including hemodynamic, respiratory, neurologic, and immunologic problems.
Decontamination
- Once stabilized, consider decontamination to prevent systemic absorption of the toxicant.
- The appropriate decontamination method depends on the exposure circumstances (species, time elapsed, chemical nature, amount ingested).
- Decontamination methods include dilution, induction of emesis, gastric lavage, adsorbents, and cathartics.
- Often, a combination of these methods is most effective.
Antidotal Therapies
- Antidotal therapies target specific toxicants and their effects.
- Acepromazine can be used for amphetamine toxicity, but may cause hypotension.
- Atipamezole reverses the effects of amitraz toxicosis.
- Atropine counteracts the muscarinic effects of carbamates and organophosphates.
Emesis for Toxicant Removal
- Hydrogen peroxide is effective for inducing emesis in dogs.
- Administer 2.2 mL/kg orally once, and repeat once if necessary.
- Vomiting should occur within 20 minutes.
- Apomorphine is effective in dogs but controversial for use in cats.
- Xylazine is only effective in 42% of cats.
- Dexmedetomidine may be used as an emetic in cats.
Gastric Lavage
- If emesis is contraindicated, impossible, or unsuccessful, consider gastric lavage.
Adsorbents
- Adsorbents bind to toxicants in the GI tract to facilitate excretion.
- Activated charcoal is the most common adsorbent.
- Administer orally in asymptomatic patients, or via an orogastric tube in symptomatic patients under anesthesia.
- Repeat doses are recommended for toxicants undergoing enterohepatic recirculation.
Ethylene Glycol (EG) Toxicity
- EG is toxic due to its metabolites.
- Symptoms can include CNS depression, metabolic acidosis, and renal failure.
- Treat with antidotes (fomepizole, ethanol) and supportive care within a specific time frame.
- Fomepizole is preferred, but it is often expensive.
- Ethanol can be used as an alternative.
- Hemodialysis is often necessary if azotemia develops.
Antidotals for EG Toxicity
- Fomepizole is used for EG toxicity.
- The dosage varies by species and time of administration.
- Fomepizole can cause anaphylaxis, CNS depression, tachypnea, hypersalivation, trembling, and osmotic diuresis.
- Ethanol is an alternative for EG toxicity.
2,4-D Herbicide
- 2,4-D is a commonly used herbicide, known as Agent Orange.
- It has a relatively wide margin of safety in animals.
- Large ingestions can affect ribonuclease synthesis and may cause CNS effects.
- Treatment for 2,4-D exposure is primarily supportive care and decontamination.
Prognosis for Poisoning
- The prognosis for poisoned animals is generally fair to excellent if recognized and treated promptly.
- However, some toxicants have a narrow margin of safety (OPs, carbamates, EG) and require intensive therapy.
- Consult the ASPCA Animal Poison Control Center for life-threatening emergencies or when information on the toxicant, symptoms, and treatment is unclear.
Chemical Toxicoses
- Approximately 150,000 animals are exposed to toxicants in the US each year.
- 40% of calls to animal poison control are due to human and veterinary medications.
- Rodenticides are among the top 10 toxicants affecting dogs.
Rodenticides
- Second-generation anticoagulant rodenticides (ACR) are being removed from the US market.
- Bromethalin and cholecalciferol are becoming more prominent as active ingredients.
- Bromethalin is a neurotoxic rodenticide that uncouples oxidative phosphorylation in the brain and liver mitochondria.
- This results in decreased ATP production, affecting cellular sodium and potassium pumps, leading to lipid peroxidation and sodium accumulation within the cell.
- Edema of the central nervous system (CNS) can occur.
- Bromethalin is not an anticoagulant rodenticide and should not be treated with vitamin K1.
- The minimum lethal dose in dogs is approximately 6.6 mL/kg, while in cats it is 1.4 mL/kg.
Ethylene Glycol (EG)
- Sources of EG include automotive antifreeze, windshield deicing agents, motor oils, hydraulic brake fluid, paints, and solvents.
- As little as one tablespoon (15 mL) can result in severe acute kidney injury (AKI) in a dog, while as little as 1 teaspoon (5 mL) can result in AKI in feline patients.
- EG is metabolized by the body to highly poisonous metabolites, including glycoaldehyde, glycolic acid, and oxalic acid, leading to severe AKI secondary to the development of calcium oxalate crystalluria.
Ethylene Glycol (EG) Toxicosis Stages
- Stage 1: Occurs within 30 minutes to 12 hours and resembles alcohol poisoning. Signs include ataxia, hypersalivation, vomiting, seizures, and polyuria/polydipsia.
- Stage 2: Occurs within 12-24 hours post-exposure. Clinical signs may seem to resolve, but severe internal injury is still occurring. Ataxia may improve, but signs of dehydration, tachycardia, and tachypnea can be seen.
- Stage 3: Occurs 12-24 hours after EG exposure in cats and 36-72 hours post-ingestion in dogs. Severe AKI occurs secondary to calcium oxalate crystalluria. Signs include severe anorexia, lethargy, hypersalivation, uremic halitosis, coma, depression, vomiting, and seizures.
Propylene Glycol (PG)
- Doses of 5 g/kg daily can result in hemolytic anemia, reticulocytosis, and hyperbilirubinemia in dogs.
- In cats, 1.6 g/kg and 8 g/kg of oral PG chronically for 2-4 weeks resulted in dose-related increases in Heinz bodies of 28% and 92%, respectively.
- Clinical signs of PG toxicosis include CNS depression, narcosis, tachypnea, muscle twitching, hypotension, cardiovascular collapse, polyuria/polydipsia, and hematological changes.
Herbicides
- The majority of herbicides are considered mildly toxic to dogs and cats.
- Common types include glyphosate, pyridine herbicides, imidazolinone compounds, chlorophenoxy compounds, and dicamba.
- Clinical signs are typically limited to GI abnormalities (e.g., hypersalivation, vomiting, diarrhea) or dermal irritation.
Prescription and Over-the-Counter Drug Poisonings
- Exposures to human and veterinary prescription and over-the-counter drugs account for approximately 40% of all cases reported to Pet Poison Helpline.
- Such exposures most often involve unintentional overdoses, but intentional administration by the pet owner and iatrogenic intoxications also occur.
Calcium Channel Blockers (CCBs)
- CCBs, such as amlodipine, diltiazem, and verapamil, are commonly used for the treatment of systemic hypertension, cardiac disease, and other cardiac issues.
- CCBs inhibit the transmembrane influx of extracellular calcium through slow or long-lasting (L-type) ion channels, resulting in decreased myocardial contractility and arterial dilation.
- Overdose or intoxication from CCBs results in exaggerated therapeutic effects, predominantly sinus bradycardia, bradyarrhythmias, and hypotension.
- Non-cardiac signs include vomiting, hypothermia, CNS depression, non-cardiogenic pulmonary edema, hypokalemia, hyperglycemia, metabolic acidosis, and increased lactate production.
- Rarely, tremors or seizures occur.
Gastrointestinal Decontamination
- Activated charcoal is a highly effective adsorbent of many toxins.
- It should be administered as soon as possible after ingestion of the toxic substance.
- Activated charcoal can bind to and prevent the absorption of many substances, but it is not effective for all poisons.
Emetics
- Apomorphine is the most commonly used emetic in dogs and cats.
- It is often administered subcutaneously, but can also be given intravenously.
- Xylazine is another emetic that can be used in dogs and cats, but it is less effective than apomorphine.
- Emetics should be administered with caution, as they can cause vomiting and aspiration pneumonia.
- Emetics should only be used in the first 2-4 hours after a toxin is ingested.
Gastric Lavage
- Gastric lavage involves flushing the stomach with water or saline to remove the ingested toxin.
- Gastric lavage is not as effective as activated charcoal at absorbing toxins.
- It is sometimes used in conjunction with activated charcoal.
Whole-Bowel Irrigation
- Whole-bowel irrigation involves giving large amounts of polyethylene glycol (PEG) orally or rectally to flush the intestines.
- It is sometimes used in conjunction with activated charcoal to remove toxins that have already been absorbed.
Plasmapheresis
- Plasmapheresis involves removing plasma from the blood and replacing it with fresh plasma or other replacement fluids.
- It can be used to remove toxins, antibodies, and other substances from the blood.
- Plasmapheresis is most effective in removing toxins that are bound to proteins in the blood.
Hemodialysis
- Hemodialysis involves filtering the blood to remove waste products and toxins.
- It is particularly effective in removing toxins that are not bound to proteins in the blood.
Diagnostic Testing
- Testing should be done to confirm suspected exposure to a toxin and assess patient condition.
- Diagnostic tests include blood work, urinalysis, ECG, radiographs, and toxicology screens.
Treatment Considerations
- Treatment goals include preventing further absorption of the toxin, removing the toxin from the body, and treating clinical signs.
- Treatment choices depend on the type of toxin involved, the severity of clinical signs, and the patient’s health status.
- Early treatment is critical for a better prognosis.
Activated Charcoal Administration
- Activated charcoal is often used as a treatment after animal ingests a toxic substance, but it does not bind all compounds equally.
- Caustic materials are not bound by activated charcoal, and its administration to animals that have ingested these substances can be irritative and make visualization of oral and esophageal burns difficult.
- Activated charcoal administration carries a risk of aspiration, which can have a poor prognosis.
- Activated charcoal can cause constipation and black bowel movements, making it difficult to determine if melena is present.
- If activated charcoal stays in the GI tract for an extended period, it can release the toxicant.
- To minimize the risk of toxicant release, activated charcoal is often administered with a cathartic.
- The osmotic pull of activated charcoal can lead to a water shift from the intracellular and extracellular spaces into the GI tract, resulting in hypernatremia.
- Hypernatremia appears to be reported more often in small dogs receiving multiple doses of activated charcoal, however, it has also been reported in large dogs and even in cases receiving only a single dose.
Cholecalciferol
- Cholecalciferol, or vitamin D3, is one of the most deadly rodenticides to pets.
- It can cause severe hypercalcemia and hyperphosphatemia, leading to acute kidney injury.
- Cholecalciferol can also be found in over-the-counter and prescription vitamins, and psoriasis creams.
- Cholecalciferol has a narrow margin of safety and only a small amount needs to be ingested for clinical toxicosis to occur.
- Clinical signs of poisoning can develop within 1-3 days, often after the patient has developed overt manifestations of AKI.
- Azotemia can develop as early as 12-36 hours following toxic ingestion.
Insecticides
- Some insecticides carry a wide margin of safety (e.g., pyrethrins, and pyrethroids), while others have a narrower margin and have been removed from the market due to the severity of clinical signs seen with accidental or intentional poisonings.
- Cats are more sensitive to pyrethrins than dogs due to altered liver glucuronidation metabolism.
- Products containing 5-10% concentrations of pyrethrins can lead to systemic toxicosis in cats.
- Clinical signs of poisoning may include GI issues (e.g., hypersalivation, vomiting), CNS issues (e.g., ataxia, tremors, seizures), AKI, and hepatotoxicosis.
Silica Gel Packs and Food Oxidizer Packs
- Silica gel packs and food oxidizer packs rarely result in toxicosis due to their wide margin of safety.
- In rare cases, large ingestions in small patients may cause constipation or foreign body obstruction.
ILE
- ILE is a useful treatment agent for many types of toxic ingestions, including CCB overdoses.
- There is no established maximum safe dosage, however, a daily dosage of up to 8 mL/kg of 20% ILE has been shown to be safe.
- ILE has been shown to be beneficial in canine verapamil intoxications.
- ILE works by increasing plasma volume and reducing the plasma concentration of the ingested toxin.
High-Dose Insulin Therapy (HDI)
- HDI has also been shown to be successful in treating CCB intoxication in dogs.
- It has been shown to be effective in cases of human CCB overdose.
- The mechanism of HDI is multifactorial and includes enhanced myocardial uptake of glucose, suppression of phosphodiesterase III, and induction of mild hypokalemia.
- Administration of HDI requires a central line and concurrent administration of dextrose to support euglycemia.
Plasmapheresis (TPE)
- TPE is a procedure that removes blood plasma and replaces it with other fluids, effectively removing toxins or antibodies from the bloodstream.
- TPE is effective in treating toxic ingestions when the toxicant is bound to plasma proteins or when the toxicant is a large molecule (e.g., heavy metals).
Anticoagulant Rodenticides
- Gastrointestinal decontamination performed within 6 hours after ingestion of an anticoagulant rodenticide significantly reduces the risk of prolonged PT and the need for vitamin K treatment.
Diagnostic Testing
- In many cases, if the owner suspects animal poisoning without suspicion of a specific toxin, the issue may be something else such as metabolic, neurologic, or cardiovascular disease.
Serotonin Syndrome
- Cyproheptadine (Periactin) is an effective countermeasure for serotonin syndrome
- Administered orally or rectally at 1.1 mg/kg every 8 hours as needed
Digoxin Toxicity
- Digoxin immune Fab (Digibind) is the treatment for digoxin toxicity
- Dosage is 1-2 vials given slowly intravenously over 30 minutes
- Expect the patient to improve within 20-90 minutes
- Monitor for hypokalemia and hypersensitivity reactions
Ethanol and Ethylene Glycol Toxicity
- Causes severe respiratory and CNS depression, and metabolic acidosis
- In cats, treatment must be started within 3 hours of exposure or prognosis is grave
- Consult information in chapter 152, Box 152-2 for detailed information
Benzodiazepine Toxicity
- Flumazenil (Romazicon) is the antidote
- Administered intravenously at 0.01-0.02 mg/kg
- Has a short half-life so may need to be repeated
- Reserved for severe CNS and respiratory depression
Ethylene Glycol Toxicity
- Fomepizole (4-methylpyrrazole, 4-MP) is the antidote
- Initial dose is 20 mg/kg intravenously, followed by subsequent doses at 12 and 24 hours with 15 mg/kg and 36 hours with 5 mg/kg
- In cats, the initial dose is 125 mg/kg intravenously, followed by subsequent doses at 12, 24 and 36 hours with 31.25 mg/kg
- May cause CNS depression
- Treatment must be started within 3 hours of exposure or prognosis is grave
Iron Toxicosis
- Treatment includes antacids (e.g., milk of magnesia), supportive care, blood iron level monitoring, and chelation (in severe cases)
- Activated charcoal is not effective
Amitraz Toxicosis
- Found in tick collars
- Clinical signs include CNS, cardiac, and GI issues
- Treatment includes decontamination, collar removal, alpha-2-antagonists (e.g., yohimbine or atipamezole), and supportive care
Insect Bait Stations
- Often contain abamectin, hydramethylnon, or fipronil
- Rarely toxic due to low concentrations
- Plastic container can result in foreign body obstruction
- Treatment rarely indicated unless the dog has the ABCB1 gene mutation
Batteries
- Can cause corrosive or current-induced injury leading to GI perforation
- Clinical signs include dysphagia, anorexia, tachypnea, abdominal pain, and fever
- Treatment includes radiographic confirmation of ingestion, removal (e.g., endoscopy, surgery), antacids, and supportive care
Diethylene Glycol (DEG) Toxicity
- Used as an industrial solvent
- Does not cause calcium oxalate crystalluria
- Can cause severe kidney injury
- Clinical signs include CNS, GI, and renal dysfunction
- Treatment and prognosis are similar to ethylene glycol
Paintballs
- Can cause severe hypernatremia
- Clinical signs include GI and CNS problems
- Treatment includes rapid reduction of blood sodium levels via IV fluids, antiemetics, electrolyte monitoring, anticonvulsants, and supportive care
- Activated charcoal is contraindicated
Tea Tree (Melaleuca) Oil
- Toxic in dogs and cats when used as a holistic remedy
- Clinical signs of CNS depression, weakness, ataxia, hypothermia, and muscle tremors
- Rare complications include coma, increased liver enzymes, dermal or oral irritation, or cardiorespiratory effects (more often in cats)
- Treatment includes dermal and oral decontamination, fluid support, thermoregulation, clinicopathologic monitoring, and supportive care
Liquid Potpourri
- Toxic only in cats
- Causes chemical burns in the mouth, dermal and ocular irritation
- Rare complications include CNS depression, pulmonary edema, seizures, and hepatopathy
- Treatment includes oral and dermal decontamination, analgesics, antacids, fluid therapy, clinicopathologic monitoring, and supportive care
Metaldehyde Toxicity
- A common snail and slug pesticide
- Clinical signs include GI, CNS, and miscellaneous signs
- Treatment includes decontamination, antiemetic therapy, muscle relaxants, anticonvulsants, thermoregulation, and supportive care
Plant Food and Fertilizers
- Wide margin of safety
- Clinical signs of direct ingestion include GI disturbance
- Treatment includes antiemetic therapy, fluid therapy, and supportive care
Windshield Wiper Fluid (Methanol)
- Most contain water and methanol
- Can cause toxicosis in dogs, but not blindness as seen in humans
- Clinical signs include CNS, GI, and respiratory signs
- Decontamination is not usually indicated
- Activated charcoal is contraindicated
- Treatment includes IV fluids, antiemetics, and supportive care
- Fomepizole is not necessary
Calcium Channel Blocker (CCB) Toxicity
- CCB toxicosis is rare
- Treatment begins with gastrointestinal decontamination (if appropriate)
- Monitor heart rate, rhythm, and blood pressure for 12-24 hours after exposure
- Symptomatic animals also require laboratory monitoring
- Typical treatment includes IV crystalloids for hypotension, atropine for bradycardia, and calcium gluconate or calcium chloride
- If the patient is unresponsive to these treatments, consider intravenous lipid emulsion (ILE) and high-dose insulin (HDI) therapy
- Intravenous lipid emulsion therapy is likely multifactorial: removal of lipophilic agents, increased myocardial energy, increased intracellular calcium, increased vasopressor effects, and reduced vasodilation
- Current dosage for ILE is 1.5 mL/kg IV bolus followed by CRI of 0.25 mL/kg/min until clinical signs resolve or for 30-60 minutes, whichever is shorter
- Expect improvement within minutes of ILE administration
- Repeat doses may be administered if necessary
Emetics
- A dosage of 2-6 mL/kg is suggested for an average-sized cat, which would be approximately only 1-2 teaspoons
- Using excessive amounts could lead to vomiting and re-exposure of the esophagus to the damaging material
- Dilution is not appropriate in patients who are at an increased risk for aspiration, including those actively seizing or obtunded
- Dilution with dairy products, such as milk, yogurt, and cottage cheese, has been useful in cases of oral irritation following ingestion of plants containing insoluble calcium oxalate crystals
- Emetics generally empty 40-60% of the stomach contents and are usually most effective if used within 2-3 hours after ingestion of a toxicant
- If the substance ingested could coalesce to form a bezoar in the stomach, emesis can be effective later than 3 hours after the ingestion
- Chocolate and chewable medications are examples of products which may form bezoars
- Feeding a small moist meal before inducing vomiting can increase the likelihood of adequate emesis
- Induction of emesis is contraindicated with ingestion of corrosive agents including alkalis and acids, due to the risk of caustic effects on the esophageal and oral mucosa
- Emesis is also not recommended after petroleum distillate ingestion due to the risk of aspiration
- The clinician must take into account, when deciding whether to induce emesis, any pre-existing conditions of the patient that can cause vomiting to be hazardous
- Emesis may not be needed if the animal has already vomited, and it is not appropriate if the animal is already exhibiting clinical signs such as coma, seizures, or recumbency, which make emesis hazardous
- Additionally, if the patient has ingested a stimulant and is already agitated, the additional stimulation of vomiting could lead to seizures
Zinc Phosphide
- Zinc phosphide is a rodenticide that has been used since the 1930s and is still available on the market
- Zinc phosphide is readily used and is labeled to kill mice, rats, squirrels, voles, nutria, muskrats, gophers, and other vermin
- Zinc phosphide is available as a 2-10% concentration, and comes as powder, paste, pellet, or tablet formulations
- Formulations of phosphides have a malodorous, unique odor similar to rotten garlic, fish, or acetylene
- The toxic dosage of zinc phosphide in dogs is approximately 20-40 mg/kg, but up to 300 mg/kg on empty stomachs
- Administration of food (e.g., bread, milk, etc.) is contraindicated with zinc phosphide toxicosis, as it triggers gastric acid secretion, promoting hydrolysis and further production of phosphine gas
- Clinical signs of Zinc phosphide toxicosis can be seen within 15 minutes to 4 hours of ingestion and can include: severe GI signs (e.g., vomiting, bloat, abdominal pain, hematemesis, melena), CNS signs (e.g., tremor, seizures, death), and rarely, cardiopulmonary signs (e.g., pulmonary edema, tachypnea, pleural effusion) or other organ dysfunction
- Zinc phosphide carries a public health risk, emesis—whether intentionally induced or occurring due to clinical signs—can result in secondary exposure of phosphine gas to the pet owner or the veterinary professional
- In humans, clinical signs of nausea and difficulty breathing have been reported
- To minimize these risks, emesis induction should always be performed in a well-ventilated area (e.g., opening the car window if the patient vomits or inducing emesis outside)
Organic Meal Fertilizers
- By-products from the meatpacking industry used as a soil amendment, typically made of bone, blood, feather, fish, etc
- Organic meal fertilizers are very palatable to dogs
- Clinical manifestations include GI signs (e.g., hypersalivation, abdominal distension, vomiting, bloody diarrhea), metabolic (e.g., pancreatitis), and rare risk of foreign body obstruction
- Treatment is aimed at emesis induction, fluid therapy, antiemetics, bland diet, and supportive care
Compost
- The presence of tremorgenic mycotoxins (e.g., penitrem A and roquefortine) in compost can interfere with the release of neurotransmitter amino acids
- Clinical signs can be seen within 2-4 hours of ingestion and include GI (e.g., hypersalivation, vomiting, diarrhea, distended abdomen) and CNS signs (e.g., agitation, hyperesthesia, ataxia, muscle tremors, seizures, and secondary hyperthermia)
- Treatment should be aimed at decontamination of the patient, muscle relaxants, antiemetics, anticonvulsants, fluid therapy, thermoregulation, and supportive care
Cocoa Mulch
- Can result in secondary theobromine toxicosis
- Clinical signs of methylxanthine toxicosis can be seen (e.g., GI, cardiac, CNS)
- Treatment is aimed at decontamination (e.g., emesis induction, charcoal administration), fluid therapy, anti-emetics, sedation, anxiolytics, beta-blocker therapy, anticonvulsants, and supportive care
De-Icing Salts
- High concentrations of salt mixtures (e.g., sodium chloride, calcium chloride, potassium chloride, magnesium chloride hexahydrate, etc.), which is mildly toxic to dogs when exposed
- Typical toxicosis due to dermal exposure (e.g., licking fur off snow-covered sidewalk)
- Rarely, more severe clinical signs can be seen if directly ingested from the bag
- Clinical signs include GI (e.g., vomiting, diarrhea) signs; rarely, electrolyte abnormalities can be seen (e.g., hypernatremia), typically associated with large ingestions
- Treatment includes IV fluid therapy, electrolyte monitoring, antiemetics, and supportive care
- The use of charcoal is not recommended with salt toxicosis
Toxidromes
- Recognizable syndromes resulting from toxicants or classes of toxicants
- These are common ones in veterinary medicine: Ethylene glycol toxicity, xylitol toxicity, serotonin syndrome, sympathomimetic syndrome, cholinergic syndrome, and Anticholinergic syndrome
- One example is the toxidrome seen with Beta-agonist toxicity (such as albuterol) where you will typically see a tachyarrhythmia, combined with severe hypokalemia, and hypophosphatemia
- The signs combined with Beta-agonist toxicity should raise concern for this specific toxicity, and owner history should be reviewed
Symptomatic Treatment
- Treatment for toxins should focus on monitoring and supportive care, including fluid therapy, cardiovascular, gastrointestinal, and neurologic support as needed, as well as appropriate analgesia and sedation
Propranolol (Inderal)
- Can be used to treat intoxications with lipid-soluble toxicants
- Examples of toxicants include: ivermectin, cholecalciferol, amlodipine, baclofen, diltiazem, marijuana, permethrin, bupropion, trazodone, barbiturates, and tricyclic antidepressants
Methocarbamol (Robaxin)
- Can be used for tremorgenic mycotoxins and other intoxications causing severe tremors
- Dog/cat dosing: 55-220 mg/kg slow IV or PO. Total dosage should not exceed 330 mg/kg/day
Naloxone (Narcan)
- Used to reverse respiratory and CNS (central nervous system) depression from opioid intoxications
- Dog dosing: 0.04 mg/kg IV, IM, SC
- Cat dosing: 0.02-0.04 mg/kg IV
- Naloxone does not reverse GI (gastrointestinal) effects of opioids
N-acetylcysteine (NAC)
- Used to treat acetaminophen toxicity
- Dog/cat dosing: 5% solution, loading dose of 140 mg/kg PO or IV, then 70 mg/kg PO or IV every 6 hours for 7 treatments
- Can cause oral mucosal ulceration if not diluted to a 5% solution
Pamidronate (Aredia)
- Used to treat cholecalciferol (Vitamin D3) toxicity
- Dog dosing: 1.3-2 mg/kg slow IV
- Must be given as a slow IV infusion
- Do not mix with calcium-containing IV fluids
Pralidoxime (2-PAM)
- Used to counter nicotinic effects (tremors, muscle weakness) of organophosphate (OPs) intoxications
- Dog/cat dosing: 20 mg/kg q 8-12 h
- Initial dose IM or slow IV, subsequent doses IM or SC
- Works best when used in conjunction with atropine
Vitamin K1
- Used to treat anticoagulant rodenticides
- Dog/cat dosing: 1.5-2.5 mg/kg PO q 12 h
- Oral route preferred for better absorption
- Warfarin should be given with a fatty meal to enhance absorption
Yohimbine (Yobine)
- Used to treat Amitraz toxicity
- Dog dosing: 0.1 mg/kg IV
- Short half-life, may need repeated dosing
Hydrogen Peroxide
- Used to induce emesis in dogs
- Dosing: 2.2 mL/kg PO once; can repeat once
- Effective in 92% of dogs
- No significant adverse effects observed after use
- Not effective in cats
Apomorphine
- Used to induce emesis in dogs
- Dosing: 0.03 mg/kg IV; or 0.04 mg/kg IM
- Can be crushed and dissolved in saline, administered in the conjunctival sac, followed by saline eye rinse
- Effective in 92% of dogs
- Not effective in cats
Xylazine
- Used to induce emesis in cats, but not very effective
- Dosing: 0.44 mg/kg IM
- Effective in only 42% of cats
- Can be reversed with yohimbine (0.1 mg/kg slow IV) after vomiting is complete
Dexmedetomidine
- Used to induce emesis in cats
- Dosing: 40 mcg/kg IM
- Can be reversed with atipamezole (0.4 mg/kg IM) after vomiting is complete
Activated Charcoal
- Most commonly used adsorbent to prevent systemic absorption of toxicants
- Asymptomstic patients can receive activated charcoal orally via syringe or mixed with food
- Symptomatic patients require orogastric tube administration under general anesthesia
- Repeated doses should be considered if the ingested toxicant undergoes enterohepatic recirculation
Calcium Channel Blockers
- Common examples in both human and veterinary medicine: amlodipine, diltiazem, and verapamil
- Treat systemic hypertension, cardiac disease, and other cardiac issues
- Inhibit calcium influx through L-type ion channels
- Result in decreased myocardial contractility, arterial dilation, and decreased peripheral resistance, blood pressure, and afterload
Calcium Channel Blocker Toxicity
- Exaggerates therapeutic effects: sinus bradycardia, bradyarrhythmias, and hypotension
- Non-cardiac signs: vomiting, hypothermia, CNS depression, non-cardiogenic pulmonary edema, hypokalemia, hyperglycemia, metabolic acidosis, and increased lactate production
- Toxic dosages not known, but considered potentially toxic due to narrow safety margin
Toxidromes
- Recognizable syndromes resulting from toxicants or classes of toxicants: Ethylene glycol toxicity, xylitol toxicity, serotonin syndrome, sympathomimetic syndrome, cholinergic syndrome, and Anticholinergic syndrome
Treatment for Toxicities
- Primarily focused on supportive care and monitoring, including fluid therapy, cardiovascular, gastrointestinal, and neurologic support
- Appropriate analgesia and sedation may also be necessary
Antidotes for Toxicants in Pets
- Propranolol can be used for intoxications with lipid-soluble toxicants like ivermectin, cholecalciferol, amlodipine, baclofen, diltiazem, marijuana, permethrin, bupropion, trazodone, barbiturates, and tricyclic antidepressants.
- Methocarbamol (Robaxin) can be used for intoxications with permethrin, metaldehyde, and strychnine, especially those causing tremors. Dosage for dogs and cats is 55-220 mg/kg slow IV or PO, not exceeding 330 mg/kg/day.
- Naloxone (Narcan) reverses respiratory and CNS depression caused by opioids. Dosage: Dog: 0.04 mg/kg IV, IM, SC. Cat: 0.02-0.04 mg/kg IV.
- N-acetylcysteine (NAC) is an antidote for acetaminophen poisoning. Dosage: Dog/cat: 5% solution, loading dose 140 mg/kg PO or IV, then 70 mg/kg PO or IV every 6 hours for 7 treatments.
- Pamidronate (Aredia) is used for cholecalciferol (vitamin D3) poisoning. Dosage: Dog: 1.3-2 mg/kg slow IV. Do not mix with calcium-containing IV fluids.
- Pralidoxime (2-PAM) is used to counteract nicotinic effects (tremors, muscle weakness) of organophosphates (OPs). Dosage: Dog/cat: 20 mg/kg q 8-12 h, initial dose IM or slow IV, subsequent doses IM or SC. Works best in combination with atropine.
- Vitamin K1 is used for anticoagulant rodenticides like warfarin. Dosage: Dog/cat: 1.5-2.5 mg/kg PO q 12 h. Administer with a fatty meal for enhanced absorption.
- Yohimbine (Yobine) is used for amitraz poisoning. Dosage: Dog: 0.1 mg/kg IV. Short half-life may require repeated doses.
- Activated Charcoal is a commonly used adsorbent to prevent systemic absorption of toxicants. Administer via an orogastric tube under general anesthesia for symptomatic patients. Repeat doses are recommended for toxicants undergoing enterohepatic recirculation.
-
Ethylene Glycol poisoning can be lethal, even in small amounts. It causes severe AKI due to calcium oxalate crystalluria. Three clinical stages:
- Stage 1 (within 30 minutes to 12 hours): Ataxia, hypersalivation, vomiting, seizures, polyuria/polydipsia.
- Stage 2 (within 12-24 hours): Clinical signs may seem to resolve, but internal injury is ongoing. Dehydration, tachycardia, tachypnea.
- Stage 3 (cats 12-24 hours, dogs 36-72 hours): Severe AKI, anorexia, lethargy, hypersalivation, uremic halitosis, coma, depression, vomiting, seizures.
- Calcium Channel Blockers (CCBs) overdose can occur in both dogs and cats. Signs of intoxication include bradycardia, hypotension, and arrhythmias. Treatment includes IV crystalloids, atropine, calcium gluconate, and calcium chloride. Intravenous lipid emulsion (ILE) and high-dose insulin (HDI) therapy may be considered if refractory to treatment.
- Methanol poisoning does not cause retinal damage in dogs as it does in humans. Treatment focuses on IV fluids, antiemetics, and supportive care. Fomepizole, the antidote for ethylene glycol, is not necessary for methanol poisoning.
- Hydrogen Peroxide (2.2 mL/kg PO) and Apomorphine (0.03 mg/kg IV) are effective emetics to induce vomiting in dogs. Hydrogen peroxide can be repeated if vomiting does not occur within 20 minutes. Apomorphine is controversial for use in cats.
- Xylazine (0.44 mg/kg IM) is an effective emetic in cats, but can be reversed with yohimbine (0.1 mg/kg slow IV) after vomiting. Dexmedetomidine (40 mcg/kg IM) is also used as an emetic in cats, reversed with atipamezole (0.4 mg/kg IM) after vomiting.
- Gastric Lavage can be considered if emesis is contraindicated, not possible, or unsuccessful.
General Considerations
- Dilution with water or milk is recommended for ingested irritants or corrosive materials.
- The ASPCA Animal Poison Control Center (APCC) toxicology database provides extensive information on toxicants.
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This quiz covers important guidelines on the use of emetics in veterinary medicine, particularly for cats. It includes dosages, contraindications, and tips for inducing vomiting safely to prevent further complications. Test your knowledge about handling cases of poisoning in felines.