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Toxicology > Exam 1 - Insecticides > Flashcards

Exam 1 - Insecticides Flashcards

1
Q

What are the insecticides?

A

Pyrethrins and Pyrethroids
DEET
Amitraz
Ivermectin

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2
Q

What are pyrethrins and pyrethroids?

A

Pyrethrins are extracts of pyrethrum flowers

Pyrethroids are synthetic analogs of pyrethrins

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3
Q

T/F Pyrethrins and pyrethroids are very unstable in air and light, break down quickly

A

True

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4
Q

T/F the overall toxicity to mammals and fish is high with pyrethrins and pyrethroids,

A

False - overall low toxicity to mammals (no subacute or chronic form, generally acute, mild toxicity)
Very toxic to fish and some birds

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5
Q

How could a fish pond get exposed to pyrethrins and pyrethroids?

A

If your canine has a topical product and goes swimming in the pond

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6
Q

T/F - dogs are more sensitive to pyrethrins/pyrethroids than cats

A

False - cats are more sensitive than dogs. Use of canine “spot on” products on felines is a common presenting issue

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7
Q

Are pyrethrins lipid or water soluble?

A

lipid

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8
Q

What is the route of exposure with pyrethrins/pyrethroids?

A

dermal most common

Ingestion and inhalation possible

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9
Q

Do pyrethrins and pyrethroids accumulate in tissue and have residual effects?

A

no

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10
Q

What does piperonyl buttoned or MGK-264 do when added with pyrethrins/pyrethroids?

A

Have a synergist effect. Inhibit pyrethrin metabolism by insects
Not supposed to have a significant effect in mammals

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11
Q

What is the MOA of pyrethrins/pyrethroids?

A

Delay closure of sodium ion channels in the axonal membrane of the insect
“knockdown effect” rapid paralysis caused by inhibition of neurons

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12
Q

What type of pyrethroids have a greater effect on sodium channels?

A

Type y pyrethroids (alpha-cyans group)

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13
Q

Pyrethrins and pyrethroids may stimulate the adrenals which may result in

A

hyperglycemia

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14
Q

What is the difference between insects and mammals that pyrethrins and pyrethroids affects them most?

A

Pyrethrins bind more strongly at lower temps
Insect Na channels are 1000x more sensitive
Insect Na channels dont recover from depolarization as quickly
Insect metabolism of pyrethrins is slower

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15
Q

What clinical signs will you see with pyrethrin and pyrethroid toxicity?

A

Muscle tremors, depression, blindness (reversible), ataxia, salivation, vomiting, diarrhea, hyperexcitability, seizures, dyspnea, death

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16
Q

it is difficult to diagnose an animal with pyrethrins/pyrethroid toxicity, however, postmortem the best tissues are

A

Liver and brain

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17
Q

How could you treat pyrethrin/pyrethroid toxicity?

A

no specific antidote

Wash skin with soap/water (careful because hypothermia may lead to prolong clinical signs -slow Na channel kinetics)

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18
Q

T/F Activated charcoal could be used in pyrethrin/pyrethroid toxicity

A

False - its generally not used - causes too much stress

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19
Q

What drug could you use to treat severe muscle tremors in an animal with pyrethrin/pyrethroids toxicity?

A

Methocarbamol

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20
Q

What drugs could you use to treat seizures in an animal with pyrethrin/pyrethroid toxicity?

A

Diazepam, barbiturates, propofol CRI

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21
Q

What is the prognosis for an animal with pyrethrin/pyrethroid toxicity?

A

Generally very good

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22
Q

What is a common insect repellant used for control of mosquitoes, flies and ticks?

A

DEET

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23
Q

What may deet damage?

A

Synthetic fibers or plastics

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24
Q

Dogs and cats are susceptible to deet, but which one is more sensitive?

A

Cats and young animals

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25
Q

What may increase the toxicity of Deet?

A

CNS depressants

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26
Q

Does Deet have cumulative effects?

A

Yes, can accumulate and persist in the skin

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27
Q

What could Deet do to the absorption rate of other drugs, such as fenvalerate and pyrethroid?

A

Increase dermal absorption

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28
Q

What is the MOA of Deet?

A

Unknown, can cause surface irritation

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29
Q

what clinical signs would you see with Deet toxicity?

A

Hypersalivation, vomiting, hyperexcitability, tremors, ataxia, seizures

30
Q

How could you diagnose Deet toxicity?

A

no specific pathologic lesions

Chemical analysis - stomach, urine, blood, skin, vitreous, bile, kidney

31
Q

How many ppm are considered diagnostic for Deet toxicity?

A

20ppm

Urine concentration of greater than 1 ppm and tissue greater than 10 ppm considered supportive

32
Q

What are your ddx for deet toxicity?

A 
other CNS excitatory toxins
Strychnine
Metaldehyde
Organochlorine
OP/carbamate
33
Q

How could you treat Deet toxicity?

A

No specific antidote

Decontamination - wash/soap, emesis if not contraindicated, activated charcoal +/- cathartic

34
Q

What should you avoid giving an animal with Deet toxicity?

A

Magnesium cathartics - may cause CNS depression

35
Q

What is the prognosis for an animal with Deet toxicity?

A

If sublethal exposure, usually response in 24-72 hrs.

36
Q

What is a foramidine insecticide/acaracide?

A

Amitraz

37
Q

Amitraz is particularly useful for certain mites and ticks, what does it do to them?

A

Paralyzes the mouth parts

38
Q

Where might you find amitraz in ?

A

Flea and tick collars (preventic)
Mitaban
As a miticide/insecticide for swine and cattle
Plant insecticide

39
Q

What animals should you not use amitraz on?

A

Cats and horses

40
Q

What is the MOA for amitraz?

A

Alpha 2 adrenergic agonist in the CNS
Weak alpha 1 agonist activity
Weak monoamine oxidase (MAO) inhibitor

41
Q

Amitraz toxicity may be acute or subacute, what is the acute oral LD50 for dogs?

A

250mg/kg

42
Q

What increases the toxicity of amitraz?

A

Meperidine (Demerol)
Sympathomimetic amines
Stress, debilitated, old age, toy breeds

43
Q

How is amitraz absorbed?

A

Orally, inhalation or skin

44
Q

What is the peak plasma concentration time of amitraz and elimination half life?

A

5 hours

1/2 life of 24 hrs

45
Q

What clinical signs will you see with amitraz toxicity?

A

Transient sedation in seen and may last for 24-72 hrs
Lethargy, ataxia, bradycardia, depression, vomiting, dyspnea, hypothermia, tremors, seizures
Cardiovascular collapse and Resp. failure

46
Q

What can the alpha 2 inhibition of amitraz cause?

A

Hyperglycemia - alpha 2 inhibition of insulin

47
Q

How could you diagnose Amitraz?

A

no specific pathologic lesions

Tissue analysis. liver, kidney, brain, adipose

48
Q

What are your ddx for amitraz toxicity?

A 
Other CNS depressants
Ethanol
Ivermectin
Ethylene glycol
marijuana
49
Q

How could you treat amitraz?

A 
Alpha 2 antagonists
Yohimbine
Atipamezole (fewer cardioresp. effects than yohimbine) 
Washing/soap
Emesis/activated charcoal/cathartics
Supportive care (IV fluids)
50
Q

What is the prognosis for amitraz toxicity?

A

Pretty good

51
Q

What are macrocytic lactones?

A

Avermectins (Ivermectin, selamectin, moxidectin)

Milbemycins

52
Q

Ivermectin is a common

A

Endoparasiticide

53
Q

Ivermectin labeled for prevention of ____ in dogs and cats

A

Heartworm

54
Q

What breed of dogs are most susceptible to ivermectin toxicity? why?

A

Collies - ABCB1/MDR1 mutation

55
Q

T/F Ivermectin is well absorbed orally, oral absorption is more rapid than SC, its well distributed but does not typically cross the BBB, and dogs may have a lower bioavailability than cats

A

False - cats may have lower bioavailability than dogs. all else is true

56
Q

Why does ivermectin not cross the BBB?

A

kept out of the CNS by p-glycoprotien efflux pump

57
Q

What is the elimination half life of ivermectin in normal dogs?

A

2 days

58
Q

Why is the ABCB1/MDR1 gene important?

A

It encodes the p-glycoprotein which is a component of the BBB (keeps drugs out)

59
Q

What is ivermectin MOA?

A

Acts as GABAa agonist - influx of chloride ions hyper polarizes the cell decreasing firing of the neuron (CNS suppression)

60
Q

What occurs in overdose situations of ivermectin?

A

Binding to glycine and voltage gated chloride channels

61
Q

What may low concentrations of ivermectin cause?

A

may reduce GABA and cause excitatory signs

62
Q

What clinical signs will you see with ivermectin toxicity?

A

CNS depression - disorientation, stupor, ataxia, hyperesthesia, hypersalivation, vocalization, progressive weakness, recumbency, coma and death.
Mydriasis, cortical blindness, hypothermia, vomiting, drooling, seizures

63
Q

What are your ddx for ivermectin toxicity?

A 
Other CNS depressants
Ethanol
Methanol 
ethylene glycol
amitraz
64
Q

How would you treat an animal with Ivermectin toxicity?

A

NO specific antidote
Emesis if not contraindicated
Activated charcoal (more useful than emesis)
Physostigmine (cholinesterase inhibitor)
Supportive care

65
Q

What should you be cautious with when treating Ivermectin toxicity?

A

GABA agonists (diazepam, barbiturates, propofol)

66
Q

What therapy would be useful for fat soluble toxins?

A

Intravenous lipid emulsion (ILE)

67
Q

What is lipid emulsion composed of?

A

Triglycerides and phospholipids

68
Q

What fat soluble toxins will intravenous lipid emulsion help with?

A

Chlorinated hydrocarbons (organochlorines)
Pyrethrins?
Ivermectin
Ionophores
Marijuana, “spice”
Drugs: baclofen, bupivacaine, calcium channel blockers

69
Q

How does IV lipid therapy (ILE) work?

A

Forms chylomicrons in the serum which trap toxins and act as a ‘lipid sink’ for the toxin
May enhance myocardial function

70
Q

How might IV lipid therapy help myocardial function?

A

FFAs are preferred energy source for myocardiocytes - Increased FFA stimulate activation of voltage gated calcium channels, increase cytosolic Ca+ and increase cardiac function - beneficial in certain toxins (calcium channel blockers)

71
Q

What are potential adverse effects of ILE therapy?

A

Bacterial contamination - sepsis
Pyrogenic reaction (fever)
Fat embolism, hyperlipiemia, hepatomegaly, icterus, splenomegaly, thrombocytopenia, hemolysis, neuro signs

72
Q

What animals should you avoid ILE therapy in?

A

Pigs! hypersensitivity reactions

Toxicology (7 decks)

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