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POD > 4.5 Pesticides and Rodenticides > Flashcards

4.5 Pesticides and Rodenticides Flashcards

1
Q

what is the definition of pesticides

A

conventional chemical substances, as well as pheremones, organisms and devices that can be used to control a pest or lessen the detrimental effects of a pest

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2
Q

T/F pesticides are usually selective to the pest

A

F

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3
Q

what two types of insecticides share the same MOA

A

carbamates and organophosphates (OPs)

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4
Q

what is the MOA of OPs and carbamates

A

inhibit cholinesterase

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5
Q

how are OPs and carbamates metabolized and excreted

A

metabolized in the liver to the active form (toxication) and excreted in urine

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6
Q

how do OPs versus carbamates bind to acetylcholinesterase

A

OPs: irriversible
carbamates: reversible

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7
Q

by inhibiting acetylcholinesterase, what effect do OPs and carbamates have on the nervous system

A

activation of nicotinic, muscarinic and CNS cholinergic receptors

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8
Q

what are the clinical signs of OP/carbamate poisoning

A

SLUDGEM

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9
Q

how is OP/carbamate toxicosis diagnosed

A

history, clinical signs, plasma/whole blood and brain testing for AChE activity, testing of suspect materials, stomach contents, tissues

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10
Q

describe the interpretation of the following AChE activity results:
< 50% of normal:
< 25% of normal:

A

< 50% of normal: suspect, possible
< 25% of normal: diagnostic

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11
Q

how do we treat OP/carbamate poisoning

A

supportive care, detoxification (lavage, charcoal), atropine, pralidoxime chloride

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12
Q

T/F OPs and carbamates can negatively affect RBC AChE and plasma BChE activity in agricultural workers, prompting staff relocation

A

T

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13
Q

what is a very important organochloride historically that is still used today

A

DDT

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14
Q

what does DDT do to eggs and what is a consequence

A

thins shell -> decline in bird populations (ex. raptors)

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15
Q

what is the MOA of organochlorides

A

endocrine disruptors

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16
Q

why were organochlorides mostly banned

A

they persist in the environment and bioaccumulate

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17
Q

which is more stable and which is more unstable, which is more allergenic?

a) pyrethrins
b) pyrethroid

A

pyrethrins are more unstable and more allergenic

pyrethroids are more stable

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18
Q

what plant are pyrethrins derived from

A

Chrysanthenum

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19
Q

what is the MOA of pyrethrins and pyrethroids

A

slow opening/closing of neuronal Na channels -> continued depolarization -> hyperexcitability

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20
Q

where is there an abundance of Na channels in the body (3)

A

muscle, salivary gland, CNS

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21
Q

what are some clinical signs of pyrethrin and pyrethroid toxicosis

A

related to the muscle, salivary gland and CNS (where there is Na channels:

hypersalivation, vomiting, diarrhea, hyperexcitability, ataxia, tremors, seizures, hypo or hyperthermia, paresthesia, hypersensitivity

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22
Q

how do we diagnose pyrethrins/pyrethroid toxicosis

A

history of exposure, clinical, signs, tissue residues on chromatography

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23
Q

T/F pyrethrin/pyrethroid poisoning produces specific clinical signs

A

F

24
Q

how do we treat pyrethrin and pyrethroid toxicosis

A

manage clinical signs, remove source, monitor complications (tremors, seizures)

25
Q

neonicotinoids:
- MoA
- affinity for what animals

A
  • nAChR agonist -> paralysis
  • high affinity for insects and not for mammals
26
Q

bromethalin, cholecalciferol, zinc phosphide and strychnine are all examples of

A

rodenticides (non-anticoagulant types)

27
Q

what is the active ingredient in anticoagulant rodenticides

A

bromadiolone

28
Q

what is the MOA of anticoagulant rodenticides

A

inhibit Vitamin K epoxide reductase, which inhibits reduction of vitamin K epoxide to Vitamin K -> no metabolism of vitamin K dependent coagulants

29
Q

what is the clinical sign of anticoagulant rodenticide toxicity

A

hemorrhage (cranium, pericardium, thorax, GI tract, joints, lungs)

30
Q

how long does it take to notice clinical signs of anticoagulant rodenticide ingestion

A

2-3 days (depletion of activated clotting factors takes time)

31
Q

how is anticoagulant rodenticide toxicosis diagnosed

A

clinical signs (hemorrhage, anemia), prolonged PT/PTT/ACT, anticoagulant screen of blood and liver

32
Q

T/F the GI tract contents are reliable for testing for an anticoagulant screen

A

F - use blood or liver instead

33
Q

where does bromethalin accumulate and why

A

fat, liver, brain, kidney (it is lipophilic)

34
Q

where are the highest concentrations of bromethalin

A

kidney and fat

35
Q

bromethalin is metabolized in the ______ to its active metabolite _________________

A

liver; desmethylbromethalin

36
Q

what animals are resistant to bromethalin toxication and why

A

guinea pigs, have limited metabolism into desmethylbromethalin

37
Q

what is the MOA of bromethalin

A

uncouples oxidative phosphorylation -> decreased ATP production -> inhibits Na/K ATPase -> increased intracellular sodium -> edema

affects the CNS

38
Q

what are the clinical signs of bromethalin toxicosis

A

Acute: CNS signs -> coma, seizures, CNS stim/depression, hyperesthesia, abnormal behaviour

Chronic: hind limb paresis/paralysis

39
Q

how do we treat bromethalin poisoning

A

supportive care, decontamination, IV fluids

40
Q

what is cholecalciferol

A

vitamin D3

41
Q

what is the MOA of cholecalciferol and the net effect (3)

A

1) stimulates bone resorption of Ca and P
2) stimulates GI absorption of Ca and P
3) stimulates renal tubular absorption of Ca

Net effect: soft tissue mineralization (kidneys, GI, lungs, cardiovascular)

42
Q

what are signs of cholecalciferol toxicosis

A

lethargy, weakness, diarrhea, cardiac arrythmia, ECG changes, acute renal failure, death

43
Q

how do we diagnose cholecalciferol toxicosis

A

hypercalcemia, hyperphosphatemia, X-rays of calcifications, quantification of Vitamin D3 in tissue

44
Q

how do we treat cholecalciferol toxicosis

A

decontamination, fluids, GI support, monitor Ca, P, creatinine, urea

drugs: prednisone, furosemide, biphosphonates (dec. Ca); phosphate binders (dec. P)

45
Q

what happens to zinc phosphide when it is exposed to
1) acidic conditions
2) water

A

1) quickly becomes phosphine gas
2) slowly becomes phosphine gas

46
Q

why would we fumigate feed with phosphine gas

A

to control insects and rodents during storage

47
Q

what is the MOA of zinc phosphide

A

thought to inhibit cytochrome oxidase -> cellular asphyxiation

48
Q

what is a unique concern with zinc phosphide toxicosis for veterinarians and staff and how can we be exposed (2)

A

exposure to phosphine gas on:
- post mortem
- emesis

49
Q

T/F relay toxicosis occurs with zinc phosphide poisoning

A

T

50
Q

what are the clinical signs of zinc phosphide poisoning

A

anorexia, depression, bloat, colic, rapid/deep respiration, vomiting, ataxia, convulsions, hyperesthesia

51
Q

strychnine is a naturally occuring:

A

alkaloid

52
Q

what is the MOA of strychnine toxicosis

A

blocks binding of glycine in the CNS -> unchecked nerve reflexes -> hyperexcitability to muscles

53
Q

what are clinical signs of strychnine poisoning

A

hyperextension of limbs, tetanic seizures, muscle spasms, respiratory failure, hyperthermia, tachycardia, opisthotonus

54
Q

how do we diagnose strychnine poisoning

A

history of exposure and chromatography

55
Q

how do we treat strychnine poisoning

A

keep quiet, reduce absorption, IV fluids, anticonvulsants (diazepam, pentobarbitol), methocarbamol to relax mm.

56
Q

tons of suicides and accidental poisonings with what drug prompted new the EPA to produce new regulations to include colour change and emetic agents

A

paraquat

57
Q

what is the MOA of paraquat

A

induces production of free radicals in the lungs -> lipid peroxidation, NADPH oxidation to NADP+, mitochondrial damage

POD (31 decks)

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