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Toxicology > Exam I - Rodenticides and Molluscicides > Flashcards

Exam I - Rodenticides and Molluscicides Flashcards

1
Q

What type of rodenticides are there?

A 
Anticoagulant rodenticides
Cholecalciferol 
Bromethalin
Strychnine 
Zinc phosphide
Fluoroacetate (compound 1080)
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2
Q

What type of molluscicides are there?

A

Methaldehyde

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3
Q

What are the first generation anticoagulant rodenticides?

A

Warfarin
Pindone
Chlorphacinone

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4
Q

What are the second generation anticoagulant rodenticides?

A

Brodifacoum
Diphacinone
Bromadialone

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5
Q

What is relay toxicosis?

A

Secondary toxicosis - animal being poisoned by eating an animal that ate the poison.

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6
Q

What animals can be poisoned by relay toxicosis?

A

Pigs, cats and dogs

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7
Q

T/F Anticoagulant rodenticides are odorless and tasteless, they are resistant in the environment for weeks to months and action is fast

A

False - action is slow - generally not less than 24-36 hrs

Over 1 week for first generation

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8
Q

When are first generation anticoagulant rodenticides most toxic?

A

When ingested daily for about a week

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9
Q

When are second generation anticoagulant rodenticides most toxic?

A

effective after one dose

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10
Q

What is the order of sensitivity to anticoagulant rodenticides in other species?

A 
Pigs
Dogs/Cats
Ruminants
horses
chickens
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11
Q

What enhances the anticoagulant rodenticide effects?

A

Vitamin K deficiency (oral sulfonamide therapy)
Liver disease
Enzyme inhibitors (cimetidine)
Anything that causes hemorrhage, anemia, hemolysis
Drugs that displace the anticoagulant from protein binding sites - (Phenylbutazone, salicylates, sulfonamides, corticosteroids)

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12
Q

What would the administration of steroids or thyroxine in an animal with anticoagulant rodenticide poisoning cause?

A

Increase receptor site affinity

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13
Q

What factors decrease anticoagulant rodenticide toxicity?

A 
Pregnancy
Enzyme inducers (phenytoin)
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14
Q

T/F Anticoagulant rodenticide absorption is complete, largely bound to plasma protein, achieve higher concentrations in the liver, cross the placenta, and reach peak blood level in 6-12 hrs

A

True

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15
Q

T/F first generation anticoagulant rodenticides have longer plasma half lives than second generation

A

False - second generation have long half lives
Diphenadione - 4.5 days
Brodifocoum - 6 days
Warfarin - 19 hrs (1st generation)

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16
Q

What is the MOA of anticoagulant rodenticides?

A

Inhibit vitamin K epoxide reductase

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17
Q

What does the vitamin K epoxide reductase do? and what does the inhibition of this enzyme lead to?

A

Converts vitamin K epoxide to reduced form
Leads to depletion of reduced vitamin K, which leads to reduced carboxylation and activation of precursors of clotting factors II, VII, IX, X

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18
Q

How long does it take to see onset of clinical signs with anticoagulant rodenticides?

A

1-5 days

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19
Q

What clinical signs will you see on an animal with anticoagulant rodenticide?

A

Epistaxis, bloody discharge from orifices, hematuria, bleeding from venipuncture site, hematoma, weakness, shock, tachypnea/dyspnea, anorexia, lethargy

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20
Q

What coagulation parameters are prolonged when anticoagulant rodenticide toxicity occurs?

A

Activated clotting time (ACT)
One stage prothrombin time (OSPT, PT)
Activated partial thromboplastin time (APTT)
Proteins induced by vitamin K antagonist (PIVKA)

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21
Q

What laboratory findings will you see in an animal with anticoagulant rodenticide toxicity?

A

Anemia
thrombocytopenia
Hypoproteinemia
Radiographic changes (hemorrhage)

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22
Q

What are your ddx for anticoagulation rodenticide toxicity?

A 
Spoiled sweet clover (cattle, horses)
Vitamin K deficiency (swine, poultry) 
Other toxins that cause hemorrhage - 
Ricin (caster beans)
Saponis (coffee weeds)
Monocrotaline (crotalaria)
Gossypol (cotton seed)
Aflatoxins
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23
Q

What vitamin K should be used to give in an animal with anticoagulant rodenticide toxicity?

A 
Vitamin K1 (phytonadione) orally
Vit. K3 not effective
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24
Q

Why don’t you want to give vitamin K IV?

A

risk of anaphylaxis

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25
Q

How would you treat an animal with anticoagulant rodenticide toxicity?

A 
Emesis/activated charcoal 
Vitamin K
Clotting factors (FFP, cryoprecipitate)
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26
Q

What is cholecalciferol?

A

Early form of vitamin D3

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27
Q

Is cholecalciferol soluble in water or oil?

A

Insoluble in water, soluble in most organic solvents/oil

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28
Q

T/F More bioavailable forms of cholecalciferol are toxic at higher doses

A

False - more bioavailable forms are toxic at far lower doses

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29
Q

Cholecalciferol is absorbed from the GI tract, binds to vitamin D binding protein in plasma for transportation to the liver, its metabolized and turned into

A

Calcidiol - main form in circulation

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30
Q

Calcidiol is transported to the kidney and metabolized to

A

Calcitriol - very potent!

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31
Q

Where are highest concentrations of cholecalciferol found?

A

Plasma, liver, kidneys, fat (very fat soluble)

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32
Q

Could cholecalciferol under enterohepatic recirculation?

A

yes

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33
Q

What may predispose an animal to cholecalciferol toxicity?

A

Renal disease
Hyperparathyroidism
High calcium/phos in the diet

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34
Q

What is the MOA of cholecalciferol rodentocides?

A

Causes hypercalcemia and hyperphosphatemia

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35
Q

What does the increase in calcium cause?

A

deposition of calcium in soft tissues (mineralization), tissue damage, increased capillary permeability, renal ischemia, renal loss of Na and K

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36
Q

What does calcitriol do?

A

Causes increase absorption of Ca from the GI tract,
decreases Ca storage in bone,
decreased of Ca excretion from the kidneys

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37
Q

T/F When there is a cholecalciferol rodenticide overdose, calcidiol itself, instead of calcitriol, has effects on the GI, bone and kidneys, which continues to increase Ca levels

A

True

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38
Q

When will you start to see clinical signs of cholecalciferol rodenticide toxicity?

A

within 24-36 hrs

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39
Q

What GI clinical signs will you see with cholecalciferol rodenticide toxicity?

A

GI - anorexia, vomiting, +/- HEMATEMESIS (vomiting blood), abdominal pain, constipation (+/- MELENA - dark stool - blood in stool)

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40
Q

What renal, CV, neurologic clinical signs will you see with cholecalciferol rodenticide toxicity?

A

PU/PD (hyposthenuria)
Arrhythmias, hypertension
Depression, weakness, muscle twitching, seizures, coma/death

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41
Q

What lesions might you see on an animal with cholecalciferol rodenticide toxicity?

A

Hemorrhagic gastroenteritis

Mineralization of kidneys, myocardium, lungs stomach, major vessels

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42
Q

what lab findings will you see on animal with cholecalciferol rodenticide toxicity?

A 
Hypercalcemia
Hyperphosphatemia
Increased Calcidiol and Calcitriol 
Decreased PTH
Azotemia
proteinuria
Glucosuria
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43
Q

What are your ddx for cholecalciferol rodenticide toxicity?

A 
HARD IONS
Hyperparathyroidism
Addison disease, aluminum, Vitamin A toxicity,
Renal disease, Raisins
D - Vit. D toxicosis
Idiopathic
Osteolytic 
Neoplasia
Spurious
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44
Q

How would you treat cholecalciferol rodenticide?

A

Treat hypercalcemia -
In hospital -saline diuresis, furosemide, sodium bicarb
At home - Glucocorticoids, salmon calcitonin, bisphosphonates

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45
Q

Bromethalin is a GUP, what does that mean?

A

General use pesticide

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46
Q

T/F Bromethalin is effective agains warfarin resistant rodents, has no bait shyness, and has possible secondary (relay) toxicosis of non target animals (even though its not been reported)

A

True

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47
Q

What animal is resistant to bromethalin?

A

Guinea pigs - lack correct metabolic enzymes

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48
Q

What animal is most sensitive to bromethalin and what animal is more susceptible?

A

Cats are more sensitive

Dogs are more susceptible

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49
Q

What are the toxicokenetics of bromethalin?

A

Highly lipophilic
Rapidly absorbed orally
Highly distributed

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50
Q

What tissue would have the highest concentration of bromethalin?

A

fat and brain

51
Q

Bromethalin is metabolized in the liver by N-demethylation to a metabolite _____

A

desmethylbromethalin - which is more toxic

52
Q

What is the half life of bromethalin in the rat?

A

5-6 days

53
Q

What is the MOA for bromethalin?

A

Uncoupling of oxidative phosphorylation
Lack of adequate ATP
Insufficiency energy for Na+/K+ ion pumps

54
Q

What are primary organ targets for bromethalin?

A

Brain and spinal cord

55
Q

What does ion pump dysfunction with bromethalin toxicity lead to?

A

fluid imbalance, edema and increased pressure

56
Q

Bromethalin may have acute or delayed (subacute) signs, which one is more common?

A

Delayed - subacute signs (2-3 days to onset)

57
Q

What signs might you see on a subacute bromethalin toxicity case?

A

Hind limb ataxia, proprioceptive deficits and paresis, paralysis, loss of deep pain response, patellar hyperreflexia, UMN bladder

58
Q

What lesions will you see on an animal with bromethalin toxicity?

A

Cerebral edema

Diffuse white matter vacuolization through CNS

59
Q

What should you avoid giving an animal with bromethalin toxicity?

A

Magnesium containing cathartics - CNS depressive

60
Q

How could you treat bromethalin toxicity?

A 
No specific antidote
Decontamination - emesis/activated charcoal with sorbitol 
Supportive care - 
Cerebral edema - mannitol, furosemide
Seizures - diazepam, phenobarbitol
61
Q

Strychnine is a RUP, what does that stand for?

A

Restricted use pesticide

62
Q

Strychnine is used to control what animals?

A 
Gophers
Squirrels
Deer mice
Moles
Prairie dogs
Rats
Porcupines 
Chipmunks
Rabbits
Pigeons
63
Q

T/F Strychnine is a weak base, has a bitter taste, moderately water soluble, and persist in the environment up to ~40 days

A

True

64
Q

What animals are susceptible and what animus are more sensitive to strychnine?

A

All animals are susceptible

Dogs are most sensitive and most frequently poisoned than cats

65
Q

T/F Strychnine is rapidly absorbed from the GI tract, dose not accumulate in tissue, its highly protein bound, does cross the BBB, and undergoes enterohepatic recirculation

A

False- its not highly protein bound, all else is true

66
Q

What is the MOA for Strychnine?

A

Block post synaptic effect of glycine in the spinal cord
Glycine is an important inhibitory neurotransmitter to motor neurons and interneurons in the spinal cord/brainstem/thalamus

67
Q

What does strychnine lead too?

A

Highly exaggerated reflex arcs
Muscle spasms
Severe extensor rigidity
Tonic seizures

68
Q

How long does it take to see clinical signs with strychnine toxicity?

A

Rapid onset - 10mins - 2hrs and rapid death

69
Q

What clinical signs will you see with strychnine poisoning?

A

Mydriasis, stiffness, muscle twitching, hyperthermia, tonic seizures and opisthotonos,

70
Q

How do animals die from strychnine poisoning?

A

Respiratory failure

71
Q

How would you treat strychnine poisoning?

A

Decontaminate - emesis if not contraindicated, activated charcoal
Enhance renal excretion with ammonium chloride or methionine (if patient is not acidotic)

72
Q

What do you want to avoid in strychnine toxic patients?

A

Bicarbonate or antacids in the lavage fluid - will cause them to absorb it faster
Opioids, phenothiazines, neuromuscular blockers and dissociative anesthetics

73
Q

What is the most important thing to do with a strychnine patient?

A

KEEP IN A QUIET PLACE, avoid stimulation

74
Q

What is the prognosis for strychnine toxic animals?

A

Reasonably good if alive, early and aggressive therapy for 24-72 hrs

75
Q

Is Zinc phosphide a GUP or RUP?

A

RUP - restricted use pesticide

76
Q

What is a grey/black powder, has a acetylene, garlic or dead fish odor and its stable when dry and decomposes in environment within 2 weeks

A

Zinc phosphide

77
Q

What does zinc phosphide do when exposed to acid?

A

liberates phosphine gas

78
Q

T/F zinc phosphide is relatively insoluble in water, phosphine liberation is slower in water, and the gas is toxic, flammable and a irritant

A

True

79
Q

What is the acute toxicity of zinc phosphine due to?

A

the phosphine gas

80
Q

What is the chronic toxicity of zinc phosphine due to?

A

Both zinc phosphine and phosphine gas

81
Q

What enhances zinc phosphide toxicity?

A

Acid (gastric)

Dogs have been reported to eat large amounts of it on an empty stomach (more alkaline) and survive

82
Q

Hydrolysis and liberation of phosphine gas occurs at a pH of ___

A

4 or lower

83
Q

Why would you not want to induce emesis on an animal that consumed zinc phosphide?

A

Its corrosive (GI irritant)

84
Q

What is the MOA for zinc phosphide?

A

Exact mechanism unknown
Direct irritation of GI mucosa
Toxicity primarily due to phosphine

85
Q

What effects does phosphine have?

A

May inhibit oxidative phosphorylation and cellular energy production, leading to cell death
increases oxygen radicals resulting in peroxidation and cell damage

86
Q

How fast is the onset of clinical signs with zinc phosphide toxicity?

A

rapid (mins to hrs)

87
Q

What clinical signs will you see with zinc phosphide?

A

anorexia, vomiting (hematemesis), abdominal pain and bloat in cattle, increase resp. CNS excitation, compulsive hyper motility (mad dog running), yelping, convulsions,

88
Q

How will an animal die from zinc phosphide and how fast?

A

Death within 3-48 hrs due to tissue anoxia

89
Q

How would you be able to tell an animal has zinc phosphide toxicity?

A

Acetylene, garlic or fishy odor to vomitus/GI content
Gastroenteritis (hemorrhagic)
Congestion of liver/kidneys/lungs

90
Q

If you want to test for zinc phosphide and send samples to a lab, what should you do?

A

Send specimens in an airtight container and frozen ASAP. they could release gas!

91
Q

You should be cautious when dealing with zinc phosphide toxicities because phosphine gas is easily liberated, what is the EPA safe limit exposure for 15 min?

A

1 ppm

8 hrs = 0.3ppm

92
Q

What should you tell an owner that calls with a concern of pet ingesting zinc phosphide?

A

DO NOT MAKE THEM VOMIT. gas could escape and affect them.

If pet vomits in the car, make sure to open the windows and dispose of the vomit properly

93
Q

How could you treat zinc phosphide toxicity?

A

No specific antidote
Decontaminate - Emesis (No H2O2)
Antacids - raise gastric pH above 4 with combination Mg.
Supportive care - IV fluids, trat seizures, hypomagnesemia, hypocalcemia,

94
Q

What should you not use to make an animal vomit with zinc phosphide toxicity?

A

Hydrogen peroxide

95
Q

What yellow toxin is used in livestock protection collar (LPC) for controlling coyotes preying on sheep and goats?

A

Fluoroacetate (compound 1080)

96
Q

T/F Fluoroacetate is odorless, water soluble, relatively insoluble in organic solvents, its an irritant, and degraded by soil microorganisms and plant enzymes

A

True

97
Q

How are fluoroacetate compounds absorbed?

A

GI tract, lung or open wound

98
Q

Will you see fluoroacetate relay (secondary) toxicosis?

A

Yes, because doses to kill rodents are soo high and doses for dogs are so low

99
Q

Fluoroacetate is metabolized to monofluoroacetic acid by hydrolysis, is this toxic?

A

Yes, its also toxic

100
Q

What is the mechanics of action for Fluoroacetate?

A

condenses with oxaloacetate to fluorocitrate and competes with regular citrate as a substrate for aconite in the TCA cycle

101
Q

What does fluoroacetate cause?

A
  • Slowing of the TCA cycle and decreasing cellular respiratory and energy
  • Build up of citrate - citrate toxicity binds Ca_
  • inhibits enzymes (glutamate, PFK)
102
Q

How long before you start seeing clinic signs when an animal has fluoroacetate toxicity?

A

Clinical signs are rapid in onset - 30 mins- 2-4 hrs

103
Q

What signs will you see on a dog?

A

CNS stimulation and GI signs
GI - V/D, Urination, hyperirritability, tenesmus
CNS - running in a straight line, barking, helping, opisthotonos
Hyperthermia, mydriasis, coma
Death within 2-12 hrs

104
Q

What signs will you see on horses, cattle, sheep and goats with fluoroacetate toxicity?

A

Cardiac signs predominate in horses!
heart failure, staggering, arrhythmias
Colic, terminal convulsions, death

105
Q

What signs will you see on cats and pigs with fluoroacetate toxicity?

A

BOTH CNS sings and cardiac sings in cats
Bradycardia/arrhythmias
vocalization, hyperesthesia, hypothermia

106
Q

What lab findings will you see on an animal with fluoroacetate?

A

Elevated citrate levels
Hyperglycemia
Metabolic acidosis
Low ionized Ca+

107
Q

How would you treat an animal with fluoroacetate toxicity?

A 
Onset rapid, may not get to treat
Emesis? 
Activated charcoal 
Glyceryl monoacetate (IV/IM)
Acetic acid/ethanol (PO)
Acetamide/dextrose
108
Q

T/F Metaldehyde is a restricted use pesticide, used as fuel camp stoves outside of NA, Soluble in water, and products can release Metaldehyde for 10-14 days under moderately moist conditions

A

False - its poorly soluble in water

109
Q

What animals are susceptible to metaldehyde poising? which ones are most sensitive? which are more likely to ingest?

A

Dogs, cats, livestock and horses are susceptible
Cats are more sensitive
Dogs more likely to ingest

110
Q

Hedgehogs are considered an endangered species in the UK why?

A

because they feed on slugs/snails and they are being killed with metaldehyde

111
Q

What routes could metaldehyde be absorbed? which one is more toxic?

A

Inhalation is more toxic

Ingestion is more common

112
Q

What occurs to metaldehyde in the gastric environment?

A

Undergoes acid hydrolysis to acetaldehyde

113
Q

T/F metaldehyde is readily absorbed from the GI tract, both metaldehyde and acetaldehyde cross the BBB, and may undergo enterohepatic recirculation

A

True

114
Q

Metaldehyde is metabolized in the liver by a microsomal enzyme (P450 enzymes), what could decrease the toxicity of metaldehyde?

A

Phenobarbital - enzyme inducer

115
Q

Acetaldehyde is also metabolized by hepatic aldehyde dehydrogenase, what is it converted into?

A

CO2 and exhaled

116
Q

What is the MOA of metaldehyde?

A

In mice, metaldehyde decreases brain GABA, norepinephrine and serotonin (5-HT) - may lead to seizures/CNS excitation,

117
Q

What does metaldehyde cause?

A

GI irritation
Metabolic acidosis
CNS excitation lead to HYPERTHERMIA

118
Q

What is the cause of death in animals with metaldehyde toxicity?

A

Respiratory failure

119
Q

What may occur to dogs that survive the acute disease of metaldehyde?

A

Liver failure may develop (not reported in cats)

120
Q

What clinical signs will you see on an animal with metaldehyde toxicity?

A

Acute neurotoxicosis/hyperthermia
“shake and bake”
Salivation, V/D.
Incordination, muscle tremors, hyperesthesia, convulsions, opisthotonos

121
Q

What signs might you see in cats with metaldehyde toxicity?

A

Nystagmus, mydriasis

122
Q

How would you treat an animal with metaldehyde toxicity?

A 
Decontaminate - emesis (1-2 hrs) 
Activated charcoal 
Enemas
Fluid therapy
Mange hyperthermia 
Phenobarbital - enzyme inducer
Methocarbamol (muscle relaxant)
123
Q

How could you treat horses with metaldehyde toxicity?

A

Xylazine and acepromazine

Toxicology (7 decks)

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