Amitraz/Ivermectin Flashcards

1
Q

what are the main reasons we use amitraz?

A
  • rapid action against ectoparasites such as ticks and mites
  • can control all life stages
  • used in beekeeping to control Varroa mite
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2
Q

what is the MOA of amitraz?

A
  • kills by interfering with nervous system
  • octopamine receptor antagonist
  • works as repellent (detachment effect)
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3
Q

what are the main CS with amitraz toxicity?

A
  • hyperexcitability, paralysis, death
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4
Q

in what species is amitraz contraindicated in?

A

cats and horse

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5
Q

what are some uses of amitraz?

A
  • used in flea and tick collars
  • topical liquid
  • generalized demodicosis in dogs
  • ascaricide/tickicide for swine and cattle
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6
Q

does amitraz bioaccumulate in the fat?

A

no

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7
Q

what are the toxicokinetics of amitraz?

A
  • dermal absorption is low (less than 10% in dogs and pigs)
  • not readily absorbed into tissues, but quickly distributed throughout the body including the brain
  • GIT absorption is moderate - most is quickly excreted unchanged
  • rapidly metabolized in liver and excreted in urine
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8
Q

what are the 3 MOAs for amitraz in mammals/vertebrates?

A
  1. alpha adrenergic receptor agonist
    - alpha 2 agonist in CNS
    - alpha 1 and alpha 2 agonist in PNS
    - increase in epinephrine, NE, and dopamine
    - neurotoxic and preconvulsant effects
  2. inhibition of monoamine oxidases
    - can lead to suppression of insulin in dogs
    - also increases NTs
  3. inhibits synthesis of PGs
    - inhibits synthesis from arachidonic acid
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9
Q

what is the MOA of amitraz with arthropods?

A

interaction with octopamine receptors

  • toxic effects on arthropods, less so on vertebrates
  • this receptor is less sensitive in vertebrates
  • kills by interfering with nervous system
  • tick’s sharp barbed mouth becomes paralyzed and cannot pierce skins so it falls off
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10
Q

what are the main CS seen with amitraz toxicity?

A
  • hyperglycemia
  • hypothermia
  • PU
  • anorexia
  • vomiting
  • diarrhea
  • depression
  • tremors
  • bradycardia

ultimately can lead to CV collapse and rep failure

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11
Q

how do we treat amitraz toxicity?

A
  • decontaminate
  • if collar ingested: induce emesis and/or remove, activated charcoal, cathartics, gastric lavage
  • supportive care
  • ANTIDOTE: alpha2 antagonists = yohimbine or atipamezole
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12
Q

what is the MOA of ivermectin?

A

gaba agonist
- induces neurological damage by binding to glutamate gates chloride ion channels in nerve and muscle cells of invertebrates that results in paralysi and death

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13
Q

what is the main use of ivermectin?

A

broad spectrum antiparasitic agent

  • kills a wide range of internal and external parasites in commercial livestock and companion animals
  • GI roundworms, lungworms, heartworms, mites, lice, and horn flies
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14
Q

how are animals exposed to ivermectin?

A
  • extra label use for parasites in dogs/cats
  • formulation errors are most common
  • excessive licking after a pour on
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15
Q

what is the gene mutation resulting in multi-drug resistance?

A
  • ABCB1/MDR1 gene codes for P-glycoprotein
  • dogs will have a dysfunctional BBB
  • don’t treat
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16
Q

true/false: cats have a higher bioavailability to ivermectin

A

false - lower

give them a higher dose

17
Q

what is the MOA of selamectin?

A
  • binds to glutamate gated Cl channels in parasite NS –> blocks berve transmission
  • no effect in mammal NS

selamectin is revolution

18
Q

what are the main CS with ivermectin toxicity?

A
  • CNS DEPRESSION!!

- mydriasis, blindness, vomiting, drooling, weakness, ataxia, coma

19
Q

how do we diagnose ivermectin toxicity?

A
  • history, clinical presentation
  • no specific lesions
  • chemical analysis possible but not usually necessary
20
Q

how do we treat ivermectin toxicity?

A
  • no specific antidote
  • decontaminate
  • activated charcoal is more useful than emesis
  • supportive care