Rodenticides Flashcards

1
Q

What are the possible sources of anticoagulant rodenticides?

A
  • used as prepared baits, or powders for mixing with bait material
  • some used as medical anticoaguants
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2
Q

How can animals be exposed to anticoagulant rodenticides?

A
  • ingestion of baits or eating contaminated food
  • relay toxicosis (secondary)
  • malicious poisoning
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3
Q

What are the properties of anticoagulant rodenticides?

A
  • odorless and tasteless
  • resistant in environment for weeks to months
  • slow action
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4
Q

What factors can enhance the toxicity of anticoagulant rodenticides?

A
  • vitamin K deficiency
  • pre-existing liver disease
  • enzyme inhibitors
  • concurrent factors causing hemorrhage
  • drugs displacing anticoagulant from binding sites
  • steroids or thyroxine may increase receptor site affinity
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5
Q

Describe the mechanism of action of anticoagulant rodenticides

A
  • inhibit vitamin K epoxide reductase
  • leads to depletion of reduced vitamin K
  • reduced carboxylation and activation of precursors of clotting factors
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6
Q

Which are the precursor clotting factors?

A

II, VII, IX, X

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7
Q

When is the onset and what are the clinical signs of anticoagulant rodenticide toxicosis?

A
  • onset in 1-5 days
  • hemorrhage signs: epistaxis, bloody discharge, hematuria, weakness, shock, hematomas, anorexia
  • abortion in cattle
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8
Q

How do you diagnosis anticoagulant rodenticide toxicosis?

A
  • detection in blood, serum, or plasma in live animal

- postmortem: liver, GI contents, vomitus, sample of bait

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9
Q

How would you treat anticoagulant rodenticide toxicosis if exposure is recent and the animal has a normal coagulation panel?

A

decontamination

- emesis, charcaol

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10
Q

How would you treat anticoagulant rodenticide toxicosis if there are no clinical signs, but prolonged coagulation?

A
  • give vitamin K1 orally

- consider giving clotting factors

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11
Q

How would you treat anticoagulant rodenticide toxicosis if the animal is bleeding, but PCV is > 15-20% and stable?

A
  • start with vitamin K therapy
  • give clotting factors
  • consider giving RBCs
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12
Q

How would you treat anticoagulant rodenticide toxicosis if the animal is bleeding, and PCV is < 15% and unstable?

A
  • give clotting factors and RBCs

- start vitamin K therapy

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13
Q

What are possible sources of/ways of exposure to Cholecalciferol?

A
  • ingestion of pesticides for rats/mice
  • relay toxicosis
  • vitamin D toxicosis: large doses, poisonous plants, ingestion of psoriasis medications
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14
Q

What are the properties of Cholecalciferol?

A
  • Cholecalciferol = vitamin D3
  • insoluble in water
  • soluble in most organic solvents/oil
  • no bait shyness
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15
Q

Describe the mechanism of action of cholecalciferol

A
  • absorbed from GI tract
  • binds to vitamin D binding protein in plasma and transported to liver
  • metabolized in liver to calcidiol
  • calcidiol transported to kidneys and metabolized to calcitriol
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16
Q

What are the effects of cholecalciferol toxicity?

A
  • increased serum Ca
  • causes hypercalcemia and hyperphosphatemia
  • deposition of Ca in soft tissues
  • tissue damage, hemorrhage, increased capillary permeability, and renal ischemia
  • increased loss of Na and K
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17
Q

When is the onset and what are the clinical signs of Cholecalciferol toxicity?

A
  • onset is 24-36 hours
  • depends on tissues affected
  • GI: anorexia, vomiting, ab pain, constipation
  • Renal: PU/PD
  • CV: arrhythmias, hypertension
  • CNS: depression, weakness, seizures
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18
Q

What are the lesions of Cholecalciferol toxicosis?

A
  • hemorrhagic gastroenteritis

- mineralization in affected tissues

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19
Q

How is Cholecalciferol toxicosis diagnosed?

A
  • elevated serum Ca/P
  • elevated calidiol and calcitriol
  • radiographs: mineralization
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20
Q

How is Cholecalciferol toxicosis treated?

A
  • emesis and activated charcoal if recent
  • IV lipid therapy
  • restrict Ca/P in diet
  • avoid sunlight
  • supportive therapy
  • treat the hypercalcemia
21
Q

How can you treat hypercalcemia?

A
  • saline diuresis
  • furosemide
  • sodium bicarbonate
  • glucocorticoids
22
Q

What are the properties of Bromethalin?

A
  • effective against warfarin-resistant rodents

- no bait shyness

23
Q

What are the toxicokinetic features of Bromethalin?

A
  • highly lipophilic
  • rapidly absorbed orally
  • widely distributed
  • lethal synthesis in liver
  • excreted in bile
24
Q

Describe the mechanism of action of Bromethalin

A
  • uncoupling of oxidative phosphorylation
  • lack of adequate ATP
  • insufficient energy for Na/K pumps
  • leads to fluid imbalance, edema, and increased pressure (brain and spinal cord)
25
Q

What are the acute clinical signs of Bromethalin toxicosis?

A
  • severe muscle tremors, hyperthermia
  • extreme hyperexcitability
  • generalized seizures
26
Q

What are the subacute clinical signs of Bromethalin toxicosis?

A
  • hind-limb ataxia, proprioceptive deficits, and paresis (can progress)
  • CNS depression
  • focal motor or generalized seizures
  • death due to respiratory failure
27
Q

What are the lesions of Bromethalin toxicosis?

A
  • cerebral edema

- diffuse white matter vacuolization

28
Q

How is Bromethalin toxicosis treated?

A
  • emesis (if within 1 hour)
  • activated charcoal with cathartic
  • supportive care
  • treat cerebral edema, seizures
29
Q

What are the properties of Strychnine?

A
  • bitter taste, white powder
  • moderately water soluble
  • persists in environment up to 40 days
30
Q

What are the toxicokinetic features of Strychnine?

A
  • rapidly absorbed from the GI tract
  • crosses the BBB
  • metabolized in liver
  • excreted in urine
31
Q

What is the mechanism of action of Strychnine?

A
  • blocks post-synaptic effect of glycine in the spinal cord

- leads to: exaggerated reflexes, muscle spasms, extensor rigidity, and tonic seizures

32
Q

When is the onset and what are the clinical signs of Strychnine toxicosis?

A
  • rapid onset of 10 min - 2 hours
  • early: apprehension, panting, nausea
  • stiffness, muscle twitching, hyperthemia
  • progresses to tonic seizures and opisthotonos
  • death due to respiratory failure
33
Q

What are the properties of zinc phosphate?

A
  • grey-black powder
  • acetylene, garlic, or “dead fish” odor
  • stable when dry, decomposes in environment within 2 weeks
  • when exposed to acid, liberates phosphine gas
34
Q

When is the onset, and what are the clinical signs of zinc phosphate toxicosis?

A
  • rapid onset (min-hrs)
  • anorexia, vomiting
  • ab pain and bloat in cattle
  • increased RR, wheezing, dyspnea
  • dogs may show CNS excitation
  • death due to tissue anoxia
35
Q

Where is zinc phosphate absorbed?

A
  • zinc phosphate and phosphine gas absorbed in GI tract

- gas can also be inhaled

36
Q

What lesions are caused by zinc phosphate toxicosis?

A
  • gastroenteritis

- congestion of liver/kidneys/lungs

37
Q

How is zinc toxicosis treated?

A
  • emesis, gastric lavage, antacids, mineral oil

- supportive care

38
Q

What are the properties of Fluoroacetate?

A
  • odorless
  • water soluble
  • degraded by soil microbes and plant enzymes
  • irritant
39
Q

What are the toxicokinetic features of Fluoroacetate?

A
  • absorbed from GI tract, lungs, or open wounds (not intact skin)
  • distributed throughout the body
  • excreted in urine
40
Q

What is the mechanism of action of Fluoroacetate?

A
  • competes with citrate in citric acid cycle
  • slows TCA cycle and decreases cellular respiration and energy
  • build up of unused citrate
41
Q

When is the onset, and what are the clinical signs of Fluoroacetate toxicosis in dogs?

A
  • 30 min to 22-4 hours
  • CNS stimulation: seizures, yelping, running
  • GI signs: diarrhea, vomiting
  • hyperthermia
  • death from respiratory failure/anoxia
42
Q

What are the clinical signs of Fluoroacetate toxicosis in horses, cattle, and goats?

A
  • cardiac signs in horses
  • heart failure, staggering, arrhythmias
  • colic and terminal convulsions
43
Q

What are the clinical signs of Fluoroacetate toxicosis in sheep?

A
  • disoriented running, blindness, weakness, ataxia, coma, death
44
Q

What are the clinical signs of Fluoroacetate toxicosis in cats and pigs?

A
  • bradycardia and other arrhythmias

- CNS depression or excitement, vocalization, hyperesthesia, hypothermia

45
Q

What are the properties of Metaldehyde?

A
  • irritant, flammable

- poorly soluble in water

46
Q

What are the toxicokinetics features of Metaldehyde?

A
  • absorbed from GI tract
  • cross the BBB
  • metabolized in liver by enzymes
47
Q

What is the mechanism of action of Metaldehyde?

A
  • decreases brain GABA, NE, and serotonin
  • causes direct GI irritation
  • causes metabolic acidosis
  • CNS excitation
48
Q

When is the onset and what are the clinical signs of Metaldehyde toxicosis?

A
  • onset within 3 hours
  • acute neurotoxicosis and hyperthermia
  • salivation, vomiting, diarrhea
  • incoordination, muscle tremors, seizures
  • nystagmus, mydriasis in cats
49
Q

What are lesions of Metaldehyde toxicosis?

A
  • formaldehyde odor in stomach contents
  • petechiae/ecchymosis in GI mucosa
  • congestion, edema, hemorrhage in lungs, liver, and kidneys