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Toxicology Exam 2 > Tox Exam 2 Pesticides > Flashcards

Tox Exam 2 Pesticides Flashcards

1
Q

Strychine is used to control what animals?

A

gophers, deer mice, moles, prairie dogs, rats, porcupines, chipmunks, rabbits, pigeons

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2
Q

What pesticide is linked to the 2008 rabies outbreak in Bali where 130,000 dogs were killed using it?

A

strychnine

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3
Q

Chemical properties of strychnine?

A

Alkaloid from strychnos nun vomica seeds. Bitter taste, white powder, moderately water soluble. In bait form–poorly water soluble & adheres to soil particles.

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4
Q

How long does strychnine persist in soil?

A

up to 40 days

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5
Q

What animals are susceptible to strychnine?

A

ALL! dogs most frequently poisoned but cats are most sensitive

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6
Q

Where is strychnine metabolized & excreted?

A

metabolized in the liver, excreted in urine as both metabolites & unchanged toxin

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7
Q

Most of strychnine dose is eliminated within ____ hrs.

A

24 hrs

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8
Q

Distribution of strychnine?

A

does not accumulate in any particular tissue, DOES cross the BBB, not highly protein bound

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9
Q

Absorption of strychnine?

A

in GIT readily, vomiting decreases toxicity, food may increase/decrease absorption

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10
Q

MOA of strychnine?

A

Blocks the post-synaptic effect of glycine in the spinal cord–glycine important inhibitory NT to motor neurons & interneurons in spinal cord, brainstem, thalamus. Leads to exaggerated reflex arcs, muscle spasms, severe muscle rigidity, tonic seizures.

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11
Q

Clinical signs of strychnine?

A

early signs–>apprehension, panting, nausea/V+, mydriasis, stiffness, muscle twitching, hyperthermia
progresses to–>tonic seizures & opisthotonos
May exhibit sardonic grin and rapid death d/t resp failure.

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12
Q

Onset of action of strychnine?

A

RAPID–10 min to 2 hrs

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13
Q

T/F Seizures caused by strychnine are not elicited by external stimuli such as light, sound, touch.

A

FALSE! seizures are elicited by external stimuli

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14
Q

Preferred postmortem specimens for strychnine diagnosis.

A

stomach contents and liver

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15
Q

Lesions seen postmortem in strychnine poisoning.

A

few or no lesions–hemorrhage, congestion, cyanosis
rapid rigor mortis
stomach contents may still contain bait

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16
Q

Preferred antemortem specimens for strychnine poisoning.

A

stomach contents, bait, serum, urine

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17
Q

Available test for strychnine toxicity?

A

IDEXX TC1030–takes 5-7 working days, around $140

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18
Q

What can you use for decontamination for strychnine poisoning?

A

Emesis if not contraindicated, gastric lavage (NO bicarb or antacids in lavage fluid), activated charcoal w/ cathartic, enhance renal excretion w/ ammonium chloride or methionine–if patient not acidotic.

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19
Q

What drugs should be avoided in animals with strychnine poisoning?

A

opioids, phenothiazines, neuromuscular blockers, dissociative anesthetics

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20
Q

Prognosis for strynchine poisoning?

A

early, aggressive therapy within 24-72 hrs good outcome

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21
Q

Treatment options for the muscle tremors/rigidity caused by strychnine poisoning?

A

methocarbamol, diazepam

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22
Q

T/F Stychnine poisoning may require sedation for 24-72 hours.

A

TRUE!

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23
Q

Treatment options for the seizures caused by strychnine poisoning?

A

diazepam CRI, propofol, barbiturates, avoid stimuli–keep in a quiet, dark place

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24
Q

Zinc phosphide are used to control what species?

A

rats, mice, squirrels, gophers, voles, moles

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25
Q

What other phosphide formulations have similar toxic effects to zinc phosphide?

A

aluminum and magnesium phosphide

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26
Q

T/F Relay (secondary) zinc phosphide toxicosis has not been reported or seen in the field.

A

FALSE. It has not been reported but it has been seen in the field.

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27
Q

How are caged birds commonly exposed to zinc phosphide?

A

rodents tracking it onto their food

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28
Q

Odor and appearance of zinc phosphide?

A

acetylene, garlic, dead fish smell—grey-black powder

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29
Q

How long until zinc phosphide decomposes in the environment?

A

within 2 weeks

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30
Q

What happens with zinc phosphide is exposed to acid?

A

pH less than 4 liberates phosphine gas (PH3)–phosphine gas release is slower when zinc phosphide is exposed to water

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31
Q

Is acute toxicity due to phosphine gas or zinc phosphide?

A

phosphine gas

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32
Q

Is chronic toxicity due to phosphine gas or zinc phosphide?

A

may be due to BOTH!

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33
Q

Lethal dose of zinc phosphide is lowest in what species?

A

caged birds

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34
Q

T/F Stomach acid increases toxicity of zinc phosphide.

A

TRUE! dogs on an empty stomach can handle higher than the lethal dose of zinc phosphide & survive

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35
Q

Properties of phosphine gas?

A

irritant, flammable & toxic

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36
Q

MOA of zinc phosphide toxicity?

A

Direct irritation of GI mucosa from zinc phosphide. Toxicity primarily due to phosphine gas—inhibits oxidative phosphorylation & cellular energy production resulting in cell death & causes increased oxygen radicals.

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37
Q

Zinc phosphide toxicity has the greatest effects on what tissues?

A

Tissues with high oxygen demands (heart, brain), kidneys, liver, tissues with high phosphine (lungs).

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38
Q

ADME of zinc phosphide toxicity?

A

A=zinc phosphide & phosphine gas via GIT & phosphine gas via inhalation
D=serum/tissue zinc levels may be elevated
M=oxidized to less toxic compounds
E=in urine

39
Q

Onset of clinical signs of zinc phosphide toxicity?

A

within minutes to hours–death can result in 3-48 hrs

40
Q

Clinical signs of zinc phosphide toxicity?

A

anorexia, V+ sometimes with blood, increased rate/depth of respiration, wheezing, dyspnea

41
Q

Specific clinical signs of zinc phosphide toxicity associated with cattle?

A

abdominal pain & bloat

42
Q

Specific clinical signs of zinc phosphide toxicity associated with dogs?

A

CNS excitation–>compulsive hypermotility, ‘mad dog run’, yelping, convulsions (like strychnine)

43
Q

Pathology of zinc phosphide toxicity?

A

acetylene, garlic, fishy odor to stomach contents, vomit or bait–gastroenteritis, V+ (+/- blood), congested liver, kidneys, lungs

44
Q

Lab Dx of zinc phosphide toxicity?

A

metabolic acidosis, dehydration, hypocalcemia, elevated serum zinc

45
Q

What tests are available to diagnose zinc phosphide toxicity?

A

Drager detector tubes, silver nitrate impregnated paper. paper turns black held above diluted & heated stomach contents for 15-20 minutes.

46
Q

Prognosis of zinc phosphide toxicity?

A

no signs by 8-12 hrs post ingestion or 12-24 hrs after vomiting–good prognosis
severe signs of tissue damage–guarded to poor

47
Q

T/F Zinc phosphide toxicity can cause rare delayed injury. Explains why you should monitor kidney/liver values after 3-5 days in all symptomatic survival patients.

A

TRUE!

48
Q

Is there is specific antidote for zinc phosphide?

A

NO!

49
Q

What can you use to decontaminate an animal with zinc phosphide toxicity?

A

emetics, gastric lavage w/ dilute K permanganate, antacids, mineral oil, activated charcoal

50
Q

Another name for fluoroacetate?

A

compound 1080, “sodium monofluoracetate”

51
Q

What kind of pesticide is fluoroacetate?

A

rodenticide

52
Q

Currently the only use of compound fluoroacetate?

A

livestock protection collar for controlling coyotes preying on sheep & goats
only used as a pesticide in NZ & Australia

53
Q

The plants that contain fluoroacetate are found in what continents of the world?

A

Africa & South America

54
Q

Chemical properties of fluoroacetate?

A

irritant, odorless, water soluble, relatively insoluble in organic solvents, yellow in color

55
Q

T/F Fluoroacetate remains undegraded in the environment.

A

FALSE–degraded by soil microorganisms & plant enzymes

56
Q

What animals are most sensitive to fluoroacetate?

A

dogs

57
Q

ADME of fluoroacetate?

A

A=readily from GIT, lungs or open wounds–NOT through intact skin
D=throughout body
M=to monofluoracetic acid (toxic) by hydrolysis
E=parent & metabolite are excreted in urine

58
Q

Onset of clinical signs of fluoroacetate?

A

rapid in onset, as early as 30 mins or up to 2-4 hrs post ingestion

59
Q

Clinical signs in dogs w/ fluoroacetate toxicity?

A

CNS–>running in straight line, barking, yelping, intermittent tonic-clonic seizures, opisthotonos
GI–>V+, D+, urination, hyperirritability, hypermotility, tenesmus
death w/in 2-12 hrs d/t to resp failure/anoxia

60
Q

Clinical signs in horses/cattle/sheep/goats w/ fluoroacetate toxicity?

A

CV–>heart failure signs, arrhythmias
CNS–>staggering, terminal convulsions (d/t cerebral anoxia)
horses=mostly cardiac signs, colic
death d/t arrhythmias or resp failure/anoxia

61
Q

Clinical signs in cats/pigs w/ fluoroacetate toxicity?

A

CNS–>depression or excitement, vocalization, hyperesthesia, hypothermia
CV–>bradycardia, arrhythmias

62
Q

T/F CNS signs in dogs d/t fluoroacetate toxicity are NOT as easy to elicit with stimuli as with strychnine.

A

TRUE

63
Q

T/F Fluoroacetate causes a delayed onset of rigor mortis.

A

FALSE–rapid onset of rigor mortis

64
Q

Diagnosis of fluoroacetate toxicity?

A

chem analysis of GI contents, elevated citrate levels in kidney, brain, blood are supportive, hyperglycemia, metabolic acidosis, low ionized calcium (total Ca normal though)

65
Q

Treatment of fluoroacetate toxicity?

A

onset so rapid–may not get to treat
decontamination–>emesis, activated charcoal
supportive/symptomatic–>O2, fluids, IV calcium, Na bicarb for metabolic acidosis
antidote

66
Q

Emesis is sometimes contraindicated in fluoroacetate toxicity in dogs due to?

A

b/c risk of seizures is high in dogs

67
Q

Sodium bicarb is used to treat metabolic acidosis in fluoroacetate toxicity but it can exacerbate this?

A

low levels of ionized calcium

68
Q

List the antidotes that are used in fluoroacetate toxicity.

A

All are acetate donors which compete w/ the toxin to reduce conversion to monofluoroacetic acid.
Glyceryl monoacetate, acetic acid/ethanol, acetamide/dextrose.

69
Q

T/F A higher dose of acetamide/dextrose is necessary for treatment of cats with fluoroacetate toxicity.

A

FALSE–lower dose required

70
Q

Prognosis in fluoroacetate toxicity?

A

guarded to grave

71
Q

MOA of fluoroacetate?

A

Condenses w/ oxaloacetate to fluorocitate–>competes w/ regular citrate as a substrate for aconitase in the TCA cycle–causes slowing of the TCA cycle & decreasing cellular respiration & energy–>high E demand organs hit hardest. Buildup of citrate that is not being used–>citrate to (binding of Ca), inhibition of some enzymes (glutamate, PFK, etc). Inhibition of aconite has variable effects in different species.

72
Q

What type of pesticide is metaldehyde?

A

molluscicides

73
Q

Is metaldehyde a RUP or a GUP?

A

RUP–restricted use pesticide

74
Q

Metaldehyde can be used alone or in combo with these?

A

carbamates

75
Q

Chemical properties of metaldehyde?

A

polymer of acetaldehyde, irritant, flammable, poorly soluble in water

76
Q

What animals are susceptible to metaldehyde toxicity?

A

dogs, cats, livestock, horses

77
Q

T/F Cats are more sensitive to metaldehyde toxicity than dogs.

A

TRUE–but dogs are more likely to ingest it

78
Q

What animals are considered endangered species in the UK due to them feeding on slugs/snails treated with metaldehyde?

A

hedgehogs

79
Q

Which route is more toxic—inhalation or ingestion of metaldehyde?

A

inhalation is more toxic–yet ingestion is the more common route

80
Q

ADME of metaldehyde?

A

A=gastro environment, some MET undergoes acid hydrolysis to ACE–MET abs readily from GIT & also some ACE absorbed
D=both metaldehyde & acetaldehyde cross the BBB
M=MET in liver by microsomal enzymes (p450) & ACE metabolized by hepatic aldehyde dehydrogenase– converted to CO2 & exhaled
E=enterohepatic recycling

81
Q

T/F Enzyme inducers such as phenobarbital may increase toxicity of metaldehyde.

A

FALSE–decrease toxicity!

82
Q

Clinical signs of metaldehyde poisoning?

A

acute neurotoxicosis & hyperthermia–“shake & bake”
GI–>salivation, V+, D+
CNS–>incoordination, muscle tremors, hyperesthesia, convulsive seizures, opisthotonis–seizures eventually lead to CNS depression, resp failure & death w/in 4-24 hrs

83
Q

Onset of signs d/t metaldehyde poisoning?

A

3 hrs–may recover w/in 2-3 weeks

84
Q

T/F Seizures elicited by metaldehyde poisoning may be caused by stimuli in cats & sometimes in dogs.

A

TRUE

85
Q

Specific clinical signs seen in cats d/t metaldehyde poisoning?

A

nystagmus & mydriasis

86
Q

Specific clinical sign seen in dogs d/t metaldehyde poisoning?`

A

reversible blindness

87
Q

MOA of metaldehyde poisoning?

A

in mice–decreases brain GABA, norepinephrine & serotonin. decreased GABA (main inhibitory NT in CNS)–lead to seizures & CNS excitation. decreased NE & serotonin lead to decreased MAO.
also causes direct GI irritation, metabolic acidosis, CNS excitation.

88
Q

What is the cause of death in metaldehyde poisoning?

A

respiratory failure. also dogs that survive acute dz may develop liver failure.

89
Q

Pathology of metaldehyde poisoning?

A

petechiae/ecchymoses in GI mucosa; congestion, edema, hemorrhage in liver, lungs, kidneys
longer survival–degenerative changes in liver & brain

90
Q

Lab diagnosis of metaldehyde poisoning?

A

detection of MET or ACE–stomach contents, bait, serum, urine, liver tissue

91
Q

Differential diagnosis for metaldehyde poisoning?

A

CNS toxicants or dz–severity of hyperthermia & elicitable nature of seizures helps to narrow Ddx

92
Q

Treatment of metaldehyde poisoning?

A

no specific antidote.
decon–>emetics, gastric lavage, charcoal, enema w/ tepid water
fluid therapy to address metabolic acidosis, monitor & manage hyperthermia
tx seizures–>diazepam or pentobarbital
tx muscle relaxers–>methocarbamol or GG
phenobarbital–>enzyme inducer–accelerate elimination of toxin
xylazine & acepromazine in horses

93
Q

Prognosis of metaldehyde poisoning?

A

good if they survive 24 hrs–full recovery may take 2-3 wks

Toxicology Exam 2 (8 decks)

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