Insecticides Flashcards

1
Q

Describe the toxicity of Pyrethins and Pyrethroids

who is susceptible

A
  • low toxicity in mammals
  • cats more sensitive than dogs
  • very toxic to fish and birds
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2
Q

Describe the toxicokinetic features of Pyrethins and Pyrethroids

A
  • unstable in air and light
  • lipid soluble
  • rapidly metabolized in GIT, plasma, and liver
  • do not accumulate in tissues
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3
Q

How can animals get exposed to Pyrethins and Pyrethroids?

A
  • dermal exposure most common

- ingestion and inhalation possible

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4
Q

What is the mechanism of action of Pyrethins and Pyrethroids?

A
  • delay closure of Na channels in axonal membrane of insect
  • “knock down” effect: rapid paralysis
  • may inhibit ATPase leading to repetitive firing
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5
Q

What are the clinical signs of Pyrethin and Pyrethroid toxicosis?

A
  • generalized muscle tremors, depression, blindness, ataxia
  • salivation, vomiting, diarrhea, hyperexcitability
  • may progress to seizures, dyspnea, and death
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6
Q

What is the treatment of Pyrethin and Pyrethroid toxicosis?

A
  • wash skin with soap/water
  • monitor and control temp
  • symptomatic treatment (treat seizures)
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7
Q

What are the toxicokinetic features of DEET?

A
  • absorbed from skin and GI tract
  • metabolized in liver
  • excreted in urine
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8
Q

What are the clinical signs of DEET toxicosis?

A
  • rabbits/rats: depression, excitation, ataxia, tremors, seizures, coma
  • dogs/cats: salivation, vomiting, hyperexcitability, tremors, ataxia, seizures
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9
Q

What is the treatment for DEET toxicosis?

A
  • if dermal, wash with soap/water
  • emesis, activated charcoal with cathartic
  • symptomatic treatment
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10
Q

What is Amitraz, and what is it used for?

A
  • foramidine insecticide/acaracide

- paralyzes mouth parts of mites and ticks

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11
Q

What is the mechanism of action of Amitraz?

A
  • alpha-2 adrenergic agonist in CNS

- weak alpha-1 agonist and MAO inhibitor

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12
Q

What are the toxicokinetic features of Amitraz?

A
  • absorbed orally, or inhalation and dermal
  • well distributed throughout body and CNS
  • metabolized by liver
  • excreted in urine
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13
Q

What are the clinical signs of Amitraz toxicosis?

A
  • transient sedation most common
  • lethargy, bradycardia, ataxia, depression, vomiting, dyspnea, hypothermia, tremors
  • can cause CV collapse and resp failure
  • hyperglycemia
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14
Q

How is Amitraz toxicosis treated?

A
  • antidote: alpha-2 antagonists (Yohimbine, Atipamezole)
  • wash skin with soap/water
  • if collar ingested, emesis or activated charcoal
  • supportive care
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15
Q

Who is most susceptible to ivermectin toxicosis?

A
  • dogs and small birds

- collie breeds

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16
Q

What are the toxicokinetic features of Ivermectin?

A
  • absorbed orally
  • well distributed but does not cross BBB
  • some metabolism in liver
  • excreted mostly unchanged in feces
17
Q

What is the mechanism of action of Ivermectin?

A
  • GABAa agonist

- influx of Cl ions hyperpolarize cell, decreasing firing of neurons

18
Q

What are the clinical signs of Ivermectin toxicosis?

A
  • CNS depression: ataxia, salivation, weakness

- muscle fasciculations, tremors

19
Q

How is Ivermectin toxicosis treated?

A
  • emesis, activated charcoal
  • GABA antagonists (Flumazenil, Picrotoxin)
  • Physostigmine
  • supportive care