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POD from G > 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

24
Q

how do we treat pyrethrin and pyrethroid toxicosis

A

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

25
neonicotinoids: - MoA - affinity for what animals
- nAChR agonist -> paralysis - high affinity for insects and not for mammals
26
bromethalin, cholecalciferol, zinc phosphide and strychnine are all examples of
rodenticides (non-anticoagulant types)
27
what is the active ingredient in anticoagulant rodenticides
bromadiolone
28
what is the MOA of anticoagulant rodenticides
inhibit Vitamin K epoxide reductase, which inhibits reduction of vitamin K epoxide to Vitamin K -> no metabolism of vitamin K dependent coagulants
29
what is the clinical sign of anticoagulant rodenticide toxicity
hemorrhage (cranium, pericardium, thorax, GI tract, joints, lungs)
30
how long does it take to notice clinical signs of anticoagulant rodenticide ingestion
2-3 days (depletion of activated clotting factors takes time)
31
how is anticoagulant rodenticide toxicosis diagnosed
clinical signs (hemorrhage, anemia), prolonged PT/PTT/ACT, anticoagulant screen of blood and liver
32
T/F the GI tract contents are reliable for testing for an anticoagulant screen
F - use blood or liver instead
33
where does bromethalin accumulate and why
fat, liver, brain, kidney (it is lipophilic)
34
where are the highest concentrations of bromethalin
kidney and fat
35
bromethalin is metabolized in the ______ to its active metabolite _________________
liver; desmethylbromethalin
36
what animals are resistant to bromethalin toxication and why
guinea pigs, have limited metabolism into desmethylbromethalin
37
what is the MOA of bromethalin
uncouples oxidative phosphorylation -> decreased ATP production -> inhibits Na/K ATPase -> increased intracellular sodium -> edema affects the CNS
38
what are the clinical signs of bromethalin toxicosis
Acute: CNS signs -> coma, seizures, CNS stim/depression, hyperesthesia, abnormal behaviour Chronic: hind limb paresis/paralysis
39
how do we treat bromethalin poisoning
supportive care, decontamination, IV fluids
40
what is cholecalciferol
vitamin D3
41
what is the MOA of cholecalciferol and the net effect (3)
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
what are signs of cholecalciferol toxicosis
lethargy, weakness, diarrhea, cardiac arrythmia, ECG changes, acute renal failure, death
43
how do we diagnose cholecalciferol toxicosis
hypercalcemia, hyperphosphatemia, X-rays of calcifications, quantification of Vitamin D3 in tissue
44
how do we treat cholecalciferol toxicosis
decontamination, fluids, GI support, monitor Ca, P, creatinine, urea drugs: prednisone, furosemide, biphosphonates (dec. Ca); phosphate binders (dec. P)
45
what happens to zinc phosphide when it is exposed to 1) acidic conditions 2) water
1) quickly becomes phosphine gas 2) slowly becomes phosphine gas
46
why would we fumigate feed with phosphine gas
to control insects and rodents during storage
47
what is the MOA of zinc phosphide
thought to inhibit cytochrome oxidase -> cellular asphyxiation
48
what is a unique concern with zinc phosphide toxicosis for veterinarians and staff and how can we be exposed (2)
exposure to phosphine gas on: - post mortem - emesis
49
T/F relay toxicosis occurs with zinc phosphide poisoning
T
50
what are the clinical signs of zinc phosphide poisoning
anorexia, depression, bloat, colic, rapid/deep respiration, vomiting, ataxia, convulsions, hyperesthesia
51
strychnine is a naturally occuring:
alkaloid
52
what is the MOA of strychnine toxicosis
blocks binding of glycine in the CNS -> unchecked nerve reflexes -> hyperexcitability to muscles
53
what are clinical signs of strychnine poisoning
hyperextension of limbs, tetanic seizures, muscle spasms, respiratory failure, hyperthermia, tachycardia, opisthotonus
54
how do we diagnose strychnine poisoning
history of exposure and chromatography
55
how do we treat strychnine poisoning
keep quiet, reduce absorption, IV fluids, anticonvulsants (diazepam, pentobarbitol), methocarbamol to relax mm.
56
tons of suicides and accidental poisonings with what drug prompted new the EPA to produce new regulations to include colour change and emetic agents
paraquat
57
what is the MOA of paraquat
induces production of free radicals in the lungs -> lipid peroxidation, NADPH oxidation to NADP+, mitochondrial damage

POD from G (46 decks)

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