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Toxicology > Unit 1 - Other Insecticides, Avicides, Herbicides, and Fungicides > Flashcards

Unit 1 - Other Insecticides, Avicides, Herbicides, and Fungicides Flashcards

1
Q

What are the sources of rotenone?

A

Restricted use pesticide and old products out of use

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2
Q

Rotenone is extremely toxic to what species?

A

fish

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3
Q

Are dogs or cats more sensitive to rotenone?

A

Cats are more sensitive

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4
Q

What is the MOA of rotenone?

A

It interferes with electron transport synthesis resulting in decreased ATP synthesis

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5
Q

What does rotenone interact with?

A

It is synergistic with pyrethrins/pyrethroids

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6
Q

What clinical signs are associated with rotenone toxicosis?

A

Vomiting, lethargy, tremors, seizures, hypoglycemia

Mass die off in fish populations

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7
Q

What samples are used to detect rotenone toxicosis?

A

Vomitus, blood, and urine

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8
Q

How is rotenone toxicosis treated?

A

Decontamination and supportive care (diazepam, oxygen, and dextrose IV)

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9
Q

What type of drug is imidacloprid?

A

It is a neonicotinoid - very safe

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10
Q

What is the MOA of imidacloprid?

A

It blocks post synaptic receptors in insects

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11
Q

Should there be any concern for imidacloprid use?

A

There is environmental concern because pollinating species are susceptible

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12
Q

What are the sources of fipronil?

A

Frontline, max force bait station, and seed corn products

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13
Q

What is the MOA of fipronil?

A

It inhibits GABA which increases excitation

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14
Q

What is the MOA of hydramethylon?

A

It inhibits metabolism which decreases ATP synthesis

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15
Q

What is danger with hydramethylon associated with?

A

Trauma from eating the containers are more problematic than the drug itself - the drug itself isn’t really a concern

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16
Q

T/F: Insect growth regulators like Methoprene and Luferon are very safe products.

A

True

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17
Q

What is 4-Aminopyridine (Avitrol) used for?

A

It is an avicide that is used to ward off pest birds from certain areas

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18
Q

Avitrol has ____ oral absorption and ____ dermal absorption.

A

rapid, low

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19
Q

What is the MOA of Avitrol?

A

It blocks K channels and increases the release of ACh at synapses

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20
Q

When does the onset of clinical signs due to Avitrol toxicosis occur?

A

15 minutes

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21
Q

What clinical effects does Avitrol cause?

A

Hyperexcitability, tremors, convulsions, salivation, and cardiac and respiratory arrest

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22
Q

What may happen in birds when they are exposed to Avitrol?

A

They become disoriented and emit a distress cry to scare others away

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23
Q

What samples can Avitrol be detected in?

A

Vomitus, stomach content, liver, and bait

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24
Q

What does the canine CNS panel at ISU screen for?

A

Strychnine, nicotine, caffeine, 4-aminopyrindine

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25
Q

How is Avitrol toxicosis treated?

A

Decontamination, fluids, treat acidosis, and supportive care

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26
Q

What are the environmental and human health considerations for Avitrol?

A

All species are susceptible
It can cause mass deaths in bird populations
Potential for relay toxicosis
Food safety impact is unknown

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27
Q

What species is the intended use for Starlicide?

A

Starlings, gulls, and other unwanted birds

28
Q

What is the MOA for Starlicide?

A

It is unknown - nephrotoxic

29
Q

When is the onset of clinical signs for Starlicide toxicity?

A

Hours to Days

30
Q

What samples are used for diagnosis of Starlicide?

A

Stomach/Crop contents, liver, and kidney

31
Q

How is Starlicide treated?

A

Supportive

32
Q

What is the prognosis for Starlicide toxicity?

A

Guarded

33
Q

What is an herbicide?

A

A substance that kills plants

34
Q

What is the difference between a selective and a non-selective herbicide?

A

A selective herbicide targets specific plants whereas a non-selective herbicide kills everything

35
Q

What type of herbicide is Paraquat?

A

A non-selective herbicide

36
Q

What degrades paraquat?

A

Sunlight - 3 days

37
Q

What inactivates paraquat?

A

Soil and clay

38
Q

Paraquat is ____ soluble, concentrates in the ______, and is excreted in the ______ unmetabolized.

A

water, lungs, urine

39
Q

What is the MOA of paraquat?

A

It is taken up by alveolar cells and then is reduced into a free radical when O2 is present

40
Q

What clinical signs due to paraquat toxicosis are early onset?

A

Vomiting, ataxia, and seizures

41
Q

When do respiratory clinical signs onset due to paraquat toxicosis?

A

2-7 days

42
Q

What respiratory clinical signs does paraquat toxicosis cause?

A

Tachypnea, dyspnea, moist rales, hypoxia, cyanosis, and death

43
Q

What gross lesions are associated with paraquat toxicosis?

A

Congestion, hemorrhage, emphysema

44
Q

What microscopic lesions are associated with Paraquat toxicosis?

A

Necrosis of alveolar epithelium, emphysema, fibrosis, and renal tubular necrosis

45
Q

What samples are used to detect paraquat?

A

Lung, urine, stomach contents, and bait

46
Q

What sample is used for histopath in cases of paraquat toxicosis?

A

lung

47
Q

How is paraquat toxicosis treated?

A

Early decontamination and supportive care (antioxidants, fluid diuresis, and ventilation

48
Q

What is the preferred decontaminant for paraquat toxicosis?

A

Bentonite clay

49
Q

What is the prognosis for paraquat toxicosis?

A

hopeless if signs are present

50
Q

What is the difference between diquat and paraquat?

A

Diquat does not concentrate in the lung

The affected tissues are the GI tract, liver, and kidney

51
Q

Phenoxy herbicide poisonings are rare unless what happens?

A

Concentrate or tank mix is ingested

52
Q

Phenoxy herbicides are an indirect cause of what?

A

nitrate poisoning

53
Q

Phenoxy herbicides have ____ distribution, _____ accumulation, _____ metabolism, and is excreted in ______.

A

Wide, little, little, and urine

54
Q

What is the MOA of phenoxy herbicides?

A

Dogs - decreased chloride conductance
Decreased ribonuclease synthesis which decreases proteins
Uncoupling of oxidative phosphorylation

55
Q

What clinical effects does phenoxy herbicide toxicosis cause in cattle?

A

Anorexia, diarrhea, rumen stasis and bloat, and oral ulceration

56
Q

What clinical effects does phenoxy herbicide toxicosis cause in dogs?

A

Vomiting, diarrhea, posterior weakness, and seizures

57
Q

What will you see on chemistry in patients with herbicide toxicosis?

A

Increased ALP and CPK

58
Q

What samples will you use for diagnosis of phenoxy herbicide toxicosis?

A

Forage, rumen, and urine

59
Q

How is phenoxy herbicide toxicosis treated?

A

Decontamination (emesis and AC) and supportive care

60
Q

What clinical signs can roundup (glyphosate) cause?

A

Ocular irritation, contact dermatitis, and GI irritation

61
Q

What is the MOA of dinitro compounds?

A

Uncouples oxidative phosphorylation which decreases ATP

62
Q

What concerns do we have with Atrazine toxicosis?

A

reproductive concerns

63
Q

What are the sources of fungicides?

A

Seed protectants
Fruit, vegetable, crop, and grass applications
Wood preservatives

64
Q

Why is toxic chemical is in CCA treated wood?

A

25% arsenic which presents a hazard to livestock

65
Q

What are the most toxic herbicides overall?

A

Dipyridyl products

Toxicology (32 decks)

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