Term
What is the most likely mechanism of exposure to non-target species?
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Definition
Placing bait in areas accessible to other species
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Term
| Are avicides selective for target bird species? If so, which ones and what is the mechanism? |
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Definition
- 3-CPT is palatable to starlings and blackbirds, but not preferred by other birds; it is metabolized different in birds than mammals (sensitive birds accumulate drug in kidneys, which leads to renal failure
- 4-Aminopyridine is not specific for birds
- Both drugs are rapidly metabolized in birds, thereby reducing the possibility of "relay toxicosis" from consumption of poisoned animals
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Term
| Are there specific treatments for 4-AP toxicosis outside of supportive and symptomatic treatments? |
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Definition
4-AP is a potassium channel blocker
Pancuronium bromide antagonizes the effects of 4-AP and can be used with respiratory support |
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Term
For rodenticides, what is the most likely mechanism for exposure to non-target species?
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Definition
| Accidental ingestion of baits by pets |
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Term
For anticoagulant rodenticides, what is the major determining factor for the duration of toxicosis?
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Definition
| half-life (warfarin = 14 days, brodifacoum = 30 days) |
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Term
1. For anticoagulant rodenticide ingestion, if the animal is asymptomatic, what is the schema of treatment?
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Definition
•Asymptomatic therapy involves decontamination and vitamin K1 treatment.
•Emetic, adsorbent and cathartic therapies are indicated if ingestion occurred within the last few hours.
•PT or PIVKA can be monitored at baseline and 48, 72 hours later to determine if decontamination was successful.
•If elevated PT or a potentially toxic dose was ingested, vitamin K1 (1.5-2.5 mg/kg bid, PO) therapy should be initiated.
–Warfarin exposure should be treated for 14 days, bromadialone for 21 days, and other 2nd generation compounds for 30 days.
•Cattle and horses can also be treated with vitamin K1, although this may be cost prohibitive.
–If not treated, animal should be stalled and fed high-quality alfalfa.
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Term
1. For anticoagulant rodenticide ingestion, if the animal is symptomatic, what is the schema of treatment?
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Definition
•Symptomatic treatment is supportive as well as higher dose vitamin K1 to control bleeding.
•Stabilize if shocky or dyspneic.
•Whole blood, plasma or a synthetic blood product should be administered if significant hemmorhage has occurred.
•Serial coagulation and complete blood counts performed.
•High dose vitamin K1 (5 mg/kg) may be indicated.
•Rest… as exercise may precipitate a bleeding crisis.
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Term
| Which of the rodenticide agents may cause secondary poisonings via the eating of rodents that are killed? |
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Definition
Bromethalin, Strychnine, anticoagulants?
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Term
How is the mechanism of action of cholecalciferol related its toxicity and treatment?
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Definition
- Increases plasma Ca and P, results in increased membrane permeability, altered ion pump function, necrosis, soft tissue mineralization, decreased organ function, renal failure, cardiac anomalies
- monitoring serum Ca, P, renal function
- Diuresis for kidneys
- Furosemide to decrease Ca reabsoprtion
- Pred to decrease Ca absorption, bone reabsorption, increase renal excretion
- Phosphate binders, low Ca/P diets
- Bisphosphonate pamidronate or calcitonin
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Term
Are there specific toxicities or attributes associated with strychnine poisoning?
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Definition
MOA: blocks glycine (inhibitory) in the anterior horn of the spinal cord = STIMULATION
Symptoms range from slight ataxia and muscle stiffness (low doses) to severe muscle spasms and convulsions (higher doses)
Opisthotonus = severe hyperextension (neck and back arched and jaw clamped shut)
Death is a result of medullary paralysis due to hypoxia from impaired respiration
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Term
1. Why is there a difference in the potential toxicity of zinc phosphide in animals that can or cannot vomit?
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Definition
- Some formulations contain an emetic and non-target species frequently vomit recently-ingested zinc phosphide, preventing poisoning
- Use activated charcoal in animals that cannot vomit
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