Test 4: 53 insecticides Flashcards

1
Q

uses of organophosphorous and carbamate insecticides

A

Topical: plants, animal, soils, household floor

Systemic: absorbed by plants or animals systemically to infect insect upon feeding or via inhalation

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2
Q

sources of exposure to OP’s and carbamate insecticides

A
  • contaminated Livestock feedstuffs with concentrated
  • Improper use on crops or animals
  • Malicious use
  • Secondary or relay toxicosis possible (scavengers eating poisoned animals)
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3
Q

ADME of OP’s and carbamate insecticides

A
  • rapidly absorbed (skin, respiratory and GI tract)
  • Rapid distribution and metabolism (P-450 and hydrolysis) with species dependence
  • Rapid excretion via urine
  • “Sulfone” forms of OP’s are bioactivated to a more toxic “oxon” form
  • Variable toxicity among OP’s and carbamates
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4
Q

“Sulfone” forms of OP’s are bioactivated to a more toxic — form

A

“oxon”

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5
Q

MOA for OPs and carbamates

A

Competitive inhibition of carboxyl ester hydrolases
* Acetylcholinesterase (found in Red blood cells, brain, retina, NMJs) → Responsible for the breakdown of Ach
* Butyrlcholinesterase found in plasma, liver, pancreas, CNS

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6
Q

how do OPs effect AchE?

A

will bind to AchE and doesn’t want to let go = irreversible phosphorylation

aging

this leads to ↑AcH activity= continous stimulation of nervous, glandular, and muscular receptors

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7
Q

how does carbamates effect AcHE

A

reversibly attach to AcHE

will inactivate AcHE for a few minutes (unlike OPs that forever inactive AcHE)

this leads to ↑AcH activity= continous stimulation of nervous, glandular, and muscular receptors

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8
Q

OPs long term effect

A

cause increased AcH activation on NMJ will cause continuous contractions → muscular paralysis, convulsions and death by asphyxiation once the nerve agent spreads to the diaphragm

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9
Q

treat OP

A

2-PAM (pralidoxime chloride) reactivates the AChE if given early

2-PAM ineffective after aging occurs

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10
Q

clinical signs of OP

A

Muscarinic DUMBBELS
* Diarrhea
* Urination
* Miosis
* Bradycardia
* Broncho-constriction
* Emesis
* Lacrimation
* Salivation

Nicotinic: itching, tetany, paralysis → Death generally due to hypoxia (respiratory tract secretions and bronchospasm) or respiratory depression and paralysis.

CNS: dogs and cats: occ seizures, hyperactive and hyperreflexive. LA: hyperactivity, seizures rare

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11
Q

coumaphos

A

OP

  • Systemic insecticide causing a syndrome with slower onset muscarinic and nicotinic signs
  • Tetany and seizures may occur prior to death
  • Linked to neuro dysfunction in bees
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12
Q

chlorpyrifos

A

OP

  • Cattle exhibit anorexia, diarrhea, rumen stasis, dehydration, and death
  • Cats are especially sensitive to chlorpyrifos and develop severe depression, anorexia, tremors, cervical ventroflexion +/- others
  • Intermediate syndrome or chronic, low dose exposures are also possible
  • Commonly used; in-home use banned in 2001
  • Linked to neuro signs, developmental defects and autoimmune disorders in people
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13
Q

how to diagnose OP and carbamates exposure

A

measure AcHE inhibition

< 50% suspicious, < 25% diagnostic

carbamates may have normal activity

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14
Q

treatment of OP exposure

A

atropine
vomit
activated charcoal
bathe if topical exposure
if atropine does not work: pralidoxime (2-PAM)
symptomatic and supportive care: respiratory, control seizures, monitor acid base status

may need high dose atropine, careful in horses

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15
Q

OP and carbamates cause PARA: —
NM: —
CNS:—

A

DUMBELS
tremors → paralysis
coma → seizures

dumbels: Diarrhea, Urination, Miosis, Bradycardia/ Broncho- constriction, Emesis, Lacrimation, Salivation

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16
Q

pyrethrins are —

A

made from chysanthemum

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17
Q

pyrethrins and pyrethroids are used for

A

flea control and as insecticidal spray (raid)

18
Q

MOA of pyrethrins and pyrethroids

A

↑ Na into the cell by effecting volatge gated sodium channels → excitatory

↑NT release: AcH, GABA, catecholamines

19
Q

clinical signs of pyrethrins and pyrethroids exposure

A

Minor:
– Self-limiting
– Hypersalivation, paw flicking, ear twitching, hyperesthesia, reduced activity, single episodes of V/D

Major:
– Protracted vomiting or diarrhea, marked depression or
hyperexcitability, ataxia or muscle tremors
– Rarely seizures and death
– Require immediate veterinary attention!

raid, flea control

20
Q

why are cats more sensitive to pyrethrins and pyrethroids exposure

A

↓ glucuronidase activity= slow hydrolysis/breakdown of toxin

21
Q

treatment for pyrethrins and pyrethroids exposure

A

emesis
bathe
control seizures, muscle tremors +/- hyperexcitability (valium, barbiturates)
 Methocarbamol IV for tremors
 20% Intralipid
Prognosis generally good!

Complications
* hyperthermia
* lactic acidosis
* hypoxia
* +/-myoglobinuric nephropathy

22
Q

— is found in slug and snail baits

A

metaldehyde

23
Q

ADME of metaldehyde

A
  • Rapidly absorbed from GIT
  • Metabolized to acetaldehyde →Promoted by gastric acidity
  • Readily crosses BBB
  • Range of lethal doses 60-600 mg/kg → > 2 mg/kg dangerous
24
Q

MOA of metaldehyde

A

↓ serotonin and NE
↓GABA (inhibitory)
↑MAO activity

crosses the BBB, ↓ in serotinin and GABA → seizures and acidosis

slug and snail bait

25
Q

clinical signs of Metaldehyde exposure

A
  • Anxiety, tachycardia, restlessness
  • Nystagmus > cats
  • Mydriasis, tremors, ataxia (esp cattle and sheep), colic in horses
  • Polypnea, tachycardia, opisthotonus, convulsions, hyperthermia, acidosis
  • Delayed signs: depression and coma
  • Liver failure 2-3 days after exposure
  • Death possible from respiratory failure
26
Q

treatment of metaldehyde exposure

A

vomit
control seizures/tremors
ventilate if needed
control hyperthermia
IV fluids
Sodium bicarbonate (for acidosis): caution
Prognosis: good if treated early

27
Q

amitraz is found in

A

flea collars

should never be used on cats or horses

28
Q

— is a ⍺2 agonist and weak MAO inhibitor

A

amitraz (dog flea collars)

can cause light sedation or death in high doses

29
Q

dog is 15 kg
9.0% amitraz collar
collar weighs 27.5 g
toxic dose is 40 mg/kg

change collar?

A

27.5g → 27500 mg

27500mg (0.09)= 2475 mg
2475mg/15 kg= 165 mg/kg

need to decrease collar

30
Q

clinical signs of amitraz exposure

A

Relate to CNS and cardiovascular effects of toxicant.

  • ataxia, depression, disorientation, polyuria, vocalization, seizures
  • bradycardia
  • some GI signs: emesis, diarrhea, anorexia

⍺2 agonist

31
Q

treatment for amitraz exposure

A

GI: emesis
bathe
intralipid
α-adrenergic antagonists such as yohimbine or atipamizole (antiseden) (less cardiorespiratory effects)

32
Q

what are some macrolide endectocides

A

Ivermectin
Selemectin
Abamectin
Doramectin
Milbemycin

33
Q

how do macrolides work

A

↑ GABA (inhibitory)

34
Q

what animals are more sensitive to macrolides

A

collies

lack p-glycoprotein at BBB so macrolides (ivermectin,selemectin) can cross into BBB

white feet don’t treat

35
Q

citrus oil extracts MOA

A

not really known

central and peripheral vasodilation?

36
Q

clinical signs of citrus oil exposure

A

CNS depression and ↓temp
salivation, skin irritation, tremors
Often resolve in 6 to 12 hours with supportive care and bathing

37
Q

— effect the Na channels and cause hyperexcitability, tremors and seizures

A

pyrethrins and pyethroids

38
Q

ivermectin work on — receptors and overdose causes —

A

GABA

Anxiety Restlessness Mydriasis Tremors Ataxia Polypnea Tachycardia Opisthotonus Convulsions Hyperthermia

39
Q

metaldehyde work on — and cause —

A

↓GABA and serotonin

Anxiety Restlessness Mydriasis Tremors Ataxia Polypnea Tachycardia Opisthotonus Convulsions Hyperthermia

acidosis, nystagmus, liver failure 2-3 days after exposure

40
Q

OPs and carbamates work on — and cause

A

block AcHE

DUMBELS

Muscle Fasiculations Weakness Mydriasis Tachycardia Bradycardia Hypertension Bronchodilation Excitability Lethargy Agitation Coma Seizure

41
Q

amitraz works on — and causes

A

⍺2 agonist

Ataxia Depression Disorientation
Vocalization Seizures Bradycardia Emesis Diarrhea Anorexia