Exam 3: Avicides & Rodenticides Flashcards

1
Q

MOA: 3-Chloro-P-Toluidine Hydrochloride

A

Kidney damage - renal failure
Metabolized to reactive form
Targets = blackbirds

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2
Q

Clinical Signs: 3-Chloro-P-Toluidine Hydrochloride

A

Birds: decreased activity, increased RR, mild dyspnea
Mammals: methemoglobinemia, CNS depression, flaccid paralysis, hypothermia

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3
Q

Mechanism of Exposure: 4-Aminopyridine

A

Ingestion of 4-AP containing corn or other grain used as bait
Ingestion of contaminated water

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4
Q

MOA: 4-Aminopyridine

A

Potassium channel blocker

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5
Q

Clinical Signs: 4-Aminopyridine

A

Salivation, hyperexcitability, tremors, incoordination, tonic-clonic seizures, cardiac arrythmias

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6
Q

Treatment: 4-Aminopyridine

A

Pancuronium bromide
Xylazine
Propranolol
Intubation

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7
Q

MOA: Anticoagulant Rodenticides

A

Inhibition of Vitamin K reduction

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8
Q

What is the major determining factor of Anticoagulant Rodenticides duration of toxicosis?

A

Half-life

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9
Q

Asymptomatic Treatment: Anticoagulant Rodenticides

A

Emetic, adsorbent, cathartic (if ingestion w/in a few hours)
Monitor PT or PIVKA
Vitamin K1 therapy

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10
Q

Symptomatic Treatment: Anticoagulant Rodenticides

A

Stabilize
Blood Transfusion
Serial coag and CBC performed
High dose Vitamin K
Rest

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11
Q

Which of the rodenticide agents may cause secondary poisonings via the eating of rodents that are killed?

A

Strychnine

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12
Q

MOA: Bromethalin

A

Uncouples ox phos

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13
Q

High Dose Bromethalin Clinical Signs

A

Severe mm tremor, hyperthermia, excitability, hyperesthesia, focal motor or generalized seizures

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14
Q

Low Dose Bromethalin Clinical Signs

A

Hindlimb ataxia/paresis to paralysis
Loss of deep pain response, patellar hyperreflexia, UMN bladder paralysis
Mild to severe CNS depression to coma
Focal motor or generalized seizures

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15
Q

MOA: Cholecalciferol

A

Buildup of Vit D3 causes increases in plasma calcium and phosphorus leading to soft tissue mineralization

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16
Q

Treatment: Cholecalciferol

A

GI decontamination
Monitor Ca, P, BUN, Cr
Diuresis with 0.9% saline
Furosemide = decrease Ca reabsorption
Pred = decreases Ca reabsorption, increases renal excretion

Phosphate binders, low Ca and P diets
Bisphosphonate pamidronate = inhibit bone resorption
Calcitonin = blocks osteoclastic activity

17
Q

MOA: Fluoroacetate

A

Converted to fluorocitrate = inhibition of TCA cycle
Ca depletion

18
Q

Exposure Scenario: Sodium Fluoroacetate

A

Livestock protection collars

19
Q

MOA: Strychnine

A

Blocks inhibitory action of glycine = excessive neuronal activity

20
Q

Exposure Scenarios: Strychnine

A

Grain bait
Dogs most frequent (malicious or accidental)

21
Q

Are there specific toxicities or attributes associated with strychnine poisoning?

A

Opisthotonus
Severe hyperextension and spasticity in which an animal’s head, neck, and spinal column enter into a complete “bridging” or “arching” position

22
Q

Why is there a difference in the potential toxicity of zinc phosphide in animals that can or cannot vomit?

A

Early decontamination improves prognosis
Activated charcoal in animals that cannot vomit
Some formulations of zinc phosphide contain an emetic so nontarget species frequently vomit recently ingested product thus preventing poisoning

23
Q

MOA: Zinc Phosphide

A

Formation of phosphine gas - blocks cytochrome oxidase and ox phos
Increases ROS