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RUSVM Toxicology Summer 2019 > Rodenticides > Flashcards

Rodenticides Flashcards

1
Q

What type of rodenticide is warfarin?

A

Anticoagulant rodenticide

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2
Q

Are anticoagulant rodenticides environmentally stable?

A

Resistant in environment for weeks and months

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3
Q

What is the order of species susceptibility to anticoagulant rodenticides?

A

Pig > dog > cat > ruminant > horse > chicken

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4
Q

What factors increase toxicity of anticoagulant rodenticides?

A 
Vit K deficiency 
Liver disease 
Enzyme inhibitors 
Presence of drugs that cause hemorrhage, anemia, hemolysis, methemoglobinemia, or increase capillary permeability 
Administration of steroids or thyroxine 
Trauma or surgery 
Renal insufficiency and fever 
Newborn and debilitated animals
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5
Q

What factors decrease anticoagulant rodenticide toxicity?

A

Pregnancy and lactation

Enzyme inducers

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6
Q

Where are anticoagulant rodenticides metabolized?

A

Liver by hydroxylation

Second-generation compounds (brodifacoum or diaphacinone) have long half lives

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7
Q

T/F: anticoagulant rodenticides cross the placenta and are excreted in milk

A

True

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8
Q

What is the MOA of anticoagulant rodenticides?

A

Inhibit vit K epoxied reductase
-> no reduced vitK
Reduced carboxylation and activation of precursors of clotting factor 2,7,9,10

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9
Q

Tachypnea/dyspnea
Anorexia and lethargy
Signs of hemorrhage- epistaxis, bloody discharge, melena, hematuria

DDX?

A

Anticoagulant rodenticide

Spoiled sweet clover (cattle and horse)
Vit K deficiency (swine and poultry)

Other conditions associated with hemorrhage like ricin, saponins, monocrotaline, gossypol, inorganic arsenic, iron, and zinc phosphide

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10
Q

What would you see in laboratory tests with anticoagulant rodenticides and what is the best sample?

A

Blood

Prolonged coagulation parameters

  • activated coagulation time (ACT)
  • activated partial thromboplastin time (APTT)
  • prolonged PT
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11
Q

Treatment of anticoagulant rodenticide toxicity?

A

Symptomatic

  • fresh whole blood/fresh frozen plasma
  • fluid therapy
  • oxygen therapy
  • thoracocentesis

Vit K (oral and bioavailability is increased with fatty meal)

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12
Q

What is cholecalciferol toxicosis?

A

Large dose of vit D —> excessive calcium and phos

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13
Q

What are sources of cholecalciferol toxicosis?

A

Feeding on poisoned rodents
Large doses of vit D
Ingestion of human psoriasis meds with vit D
Poisonous plants containing vit D analogs

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14
Q

What is the oral LD50 of cholecalciferol ?

A 
88mg/kg 
Moderately toxic (50-500mg/kg)
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15
Q

What are predisposing factors to cholecalciferol toxicosis?

A

Renal disease
Hyperparathyroidism
Ingestion of high Ca and Phos in diet

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16
Q

How is cholecalciferol transported in the body?

A

Binds to serous vitD binding protein and transported to the liver

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17
Q

The highest concentrations of cholecalciferol are found where?

A

Plasma, liver, kidney, and fat

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18
Q

How is cholecalciferol metabolized?

A

Liver: cholecalciferol —> 25-hydroxycholecalciferol
Kidney: 25-hydroxycholecalciferol (calcifediol) —> 1,25-dihydroxycholecalciferol (calcitriol)

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19
Q

Where is cholecalciferol excreted?

A

Bile and feces

Can be excreted in milk in toxic levels

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20
Q

What is the MOA of cholecalciferol ?

A

VitD -> increase GI absorption and tubular reabsorption of calcium
Hyperphosphatemia

Deposition in kidney, cardiac, lung, vascular, and stomach tissues

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21
Q

Anorexia, bloody vomit, abdominal pain, dehydration
PU/PD
Cardia arrhythmia and hypertension

DDX?

A

Hypercalcemia

  • lymphoma
  • pseudohyperparathyroidism
  • primary hyperparathyroidism
  • ingestion of calcinogenic plants
  • cholecalciferol (Vit D)

PU/PD

  • diabetes mellitus/insipidus
  • hyper/hypo-adrenocortisism
  • renal disease
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22
Q

Anorexia, bloody vomit, abdominal pain, dehydration
PU/PD
Cardiac arrhythmia and hypertension

You suspect cholecalciferol toxicosis, what would you expect to see on lab data?

A

Hypercalcemia
Hyperphosphatemia

elevated BUN, crea, azotemia
Hyperproteinemia, proteinuria, and glucosuria

Decreased PTH

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23
Q

What is the treatment for cholecalciferol toxicosis ?

A

GI tract decontamination —>emetic, activated charcoal, cathartic
Reduction of serum Ca —> saline IV, furosemide, glucocorticoids, calcitonin

Pamidronate disodium —> inhibitor of bone resorption

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24
Q

T/F: secondary poisoning of non target animals by bromethalin rodenticide may be possible in cats

A

True

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25
Q

Who is more sensitive to bromethalin toxicosis?

A

Cats (1.8mg/kg) > Dog ( 4.7mg/kg)

Highly toxic

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26
Q

What speices is resistant to bromethalin rodenticide?

A

Guinea pigs

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27
Q

Is bromethalin hydrophilic or lipophilic?

A

Highly lipophilic

-> rapidly absorbed orally and reaches high concentrations in fat and brain

28
Q

Where is bromethalin metabolized and excreted?

A

Liver: metabolized to desmethylbromethalin (more toxic)

Excreted in bile (possible enterohepatic circulation)
Small amount excreted in urine

29
Q

What is the MOA of bromethalin?

A

Uncouple oxidative phosphorylation
Lack of ATP
Insufficient energy for Na and K ion pump

Cerebral and spinal cord edema

Cerebral damage due to lipid peroxidation

30
Q

Severe muscle tremors, hyperthermia, extreme excitability, running fits, generalized seizures that are triggered by light/noise

DDX?

A

Bromethalin

Neurotoxins -
Zinc phosphide
Strychnine

Organic aresenic, lead, organophosphate, metaldehyde, urea

31
Q

What are the subacute signs that can develop with bromethalin toxicosis ?

A

Hindlimb ataxia and paresis that progress to hindlimb paralysis, loss of deep pain response, patellar hyper-reflexive ,severe CNS depression and vomiting

32
Q

What lesions are seen in bromethalin toxicosis?

A

Cerebral edema

Diffuse white matter vacuolization in the CNS

33
Q

What is the treatment for bromethalin toxicosis?

A

Decontaminate: Emetic, activated charcoal, saline cathartic

Mannitol and dexamethasone for cerebral edema

Diazepam and phenobarbital to control seizures

34
Q

T/F: cats are more sensitive to strychnine toxicosis than dogs

A

False
Dogs 0.75mg/kg -extremely toxic
Cats 2.0mg/kg - highly toxic

Horses, cattle, and pig also very sensitive

35
Q

T/F: small amounts of strychnine ingested over time may not cause poisoning

A

True

Rapid elimination

36
Q

Where is strychnine distributed in the body?

A

Does not accumulate, but significant amounts can be found in liver and kidney

Crosses BBB
Metabolized in liver

37
Q

Where is strychnine metabolized and excreted?

A

Met: liver
Ex: urine

38
Q

What is the MOA of strychnine?

A

Blocks the post synaptic effect of glycine in the spinal cord
Stimulation of spinal cord causes tonic seizures

39
Q

What are clinical signs seen with strychnine poisoning ?

A

Early - apprehension, panting, possible nausea and vomiting

Mydriasis, stiffness, muscle twitching, tonic seizure, and opisthotonos

Animal dies from respiratory failure

40
Q

What sample is used or detection of strychnine?

A

Urine

Stomach contents

41
Q

What is the treatment of strychnine toxicosis?

A

Phenobarbital (dog) and thiobarbiturates (cat) for seizures
Diazepam effect is variable
Methocarbamol, guaifenesin, and xylazine as alternatives

Apomorphine and gastric lavage -prevent further absorption

Ammonium chloride and fluid therapy - enhance renal excretion

42
Q

What drugs are contraindicated in strychnine toxicosis?

A 
Opioid
Phenothiazine
Butyrophenones 
NMBD 
Dissociative anesthetics
43
Q

What are the properties of zinc phosphide?

A

Gray-black powder with acetylene odor (dead fish)
Liberates phosphine gas under acidic conditions

Phosphine gas is toxic and flammable
Zinc phosphide is insoluble in water
Both gases are irritants

44
Q

What is the legal dose for zinc phosphide?

A

20-40mg/kg

Gastric acid increases toxicity, vomiting decreases toxicity

45
Q

Gastric acid causes hydrolysis of zinc phosphide to ____________ which is absorbed across the GI tract

A

Phosphide gas

46
Q

What is the MOA of zinc phosphide ?

A

Phosphide gas may inhibit oxidative phosphorylation and cellular energy production —> cell death

Irritation of GI tract and respiratory mucosa
Damage of blood vessels and RBC membrane

47
Q

What are the main tissues affected by zinc phosphide toxicosis?

A 
Brain
Heart 
Liver
Kidney 
Lung
48
Q

What are the clinical signs associated with zinc phosphide toxicosis?

A 
Anorexia
Vomiting 
Incresed rate and empty of respiration 
Wheezy 
Abdominal pain 
Bloat (cattle) 
“Mad dog running”, hyperexcitabiltiy
49
Q

What lesions are associated with zinc phoside toxicosis?

A

Odor of acetylene (dead fish)

Gastroenteritis
Congestion of liver and kidney
Pulmonary congestion and edema

50
Q

What specimens should be collected and how are they handled for testing zinc phosphide?

A

Stomach content, vomitus, or bait

Rapidly frozen

51
Q

What lab abnormalities would you see with zinc phosphide toxicosis?

A

Elevated serum zinc
Metabolic acidosis
Dehydration
Hypocalcemia

52
Q

What is the treatment of zinc phosphide toxicosis?

A

Emetic and gastric lavage, sodium bicarbonate, potassium permanganate

Oral antacids
IV anti acidotic agents - sodium bicarb or sodium lactate
Ca gluconate for hypocalcemia
O2 therapy

Symptomatic treatment

53
Q

Prognosis of zinc phosphide?

A

Animals that vomit may recover

Signs of tissue damage have guarded to poor prognosis

54
Q

What is currently the onl used of flouroacetate ?

A

Currently it is only used in the livestock protection collar
Controls coyotes preying on sheep and goats

55
Q

What are the properties of flouroacetate?

A

Odorless and water soluble
Insoluble in most organic solvents

Degraded in soil by microorganisms
Irritant

56
Q

What is the LD50 for flouroacetate in dogs

A

0.05mg/kg

Extremely toxic

57
Q

T/F: flouroacetate is readily absorbed from GI tract, lung, wounds, and intact skin

A

False

Cannot be absorbed across intact skin

58
Q

Where does flouroacetate accumulate?

A

Trick question.. it does not accumulate in any particular tissue

59
Q

How is flouroacetate metabolized?

A

Acid hydrolysis makes flouroacetate —> monofluoroacetic acid

60
Q

What is the MOA of flouroacetate?

A

Enters cells
Condense with oxaloacetate to fluorocitrate that competes with citrate for active site in CAC —> decreased cellular respiration and energy

Brain and heart most affected
Build up of citrate
Ammonia accumulation in brain —> convulsions

61
Q

What signs do you see for flouroacetate toxicosis in dogs?

A

CNS stimulation and GI irritation

Vomiting, diarrhea, urination, hyper irritability, hyper-motility, running in straight line, barking, yelping, intermittent clonic-tonic seizures and opisthotonos

62
Q

What clinical signs do you see in flouroacetate toxicosis in horse, cattle, sheep, and goat?

A

Signs of heart failure

Colic, staggering, arrhythmia, Vfib
Terminal convulsions due to cerebral anoxia

63
Q

What clinical signs do you see in cats and pigs due to flouroacetate toxicosis?

A

CNS and cardiac signs

64
Q

Death due to flouroacetate toxicosis is a result of?

A

Convulsions and respiratory failure that causes cyanosis, hemorrhage on the heart, pulmonary changes, dark blood, and organ congestion

65
Q

What specimens are best to run lab diagnostics for flouroacetate ?

A

Gastric contents and vomitus

66
Q

What is the treatment for flouroacetate toxicosis?

A

Anticonvulsant for seizures
O2 therapy
Charcoal, milk, limewater

Antidote = acetate donors (glycerol monoacetate, ethanol, and acetic acid)

Calcium chloride - protect against arrhythmias
Sodium bicarbonate IV for metabolic acidosis

67
Q

Prognosis for flouroacetate toxicity?

A

Grave

RUSVM Toxicology Summer 2019 (10 decks)

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