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RUSVM Toxicology Summer 2019 > Rodenticides > Flashcards

Rodenticides Flashcards

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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
Who is more sensitive to bromethalin toxicosis?
Cats (1.8mg/kg) > Dog ( 4.7mg/kg) Highly toxic
26
What speices is resistant to bromethalin rodenticide?
Guinea pigs
27
Is bromethalin hydrophilic or lipophilic?
Highly lipophilic | -> rapidly absorbed orally and reaches high concentrations in fat and brain
28
Where is bromethalin metabolized and excreted?
Liver: metabolized to desmethylbromethalin (more toxic) Excreted in bile (possible enterohepatic circulation) Small amount excreted in urine
29
What is the MOA of bromethalin?
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
Severe muscle tremors, hyperthermia, extreme excitability, running fits, generalized seizures that are triggered by light/noise DDX?
Bromethalin Neurotoxins - Zinc phosphide Strychnine Organic aresenic, lead, organophosphate, metaldehyde, urea
31
What are the subacute signs that can develop with bromethalin toxicosis ?
Hindlimb ataxia and paresis that progress to hindlimb paralysis, loss of deep pain response, patellar hyper-reflexive ,severe CNS depression and vomiting
32
What lesions are seen in bromethalin toxicosis?
Cerebral edema | Diffuse white matter vacuolization in the CNS
33
What is the treatment for bromethalin toxicosis?
Decontaminate: Emetic, activated charcoal, saline cathartic Mannitol and dexamethasone for cerebral edema Diazepam and phenobarbital to control seizures
34
T/F: cats are more sensitive to strychnine toxicosis than dogs
False Dogs 0.75mg/kg -extremely toxic Cats 2.0mg/kg - highly toxic Horses, cattle, and pig also very sensitive
35
T/F: small amounts of strychnine ingested over time may not cause poisoning
True Rapid elimination
36
Where is strychnine distributed in the body?
Does not accumulate, but significant amounts can be found in liver and kidney Crosses BBB Metabolized in liver
37
Where is strychnine metabolized and excreted?
Met: liver Ex: urine
38
What is the MOA of strychnine?
Blocks the post synaptic effect of glycine in the spinal cord Stimulation of spinal cord causes tonic seizures
39
What are clinical signs seen with strychnine poisoning ?
Early - apprehension, panting, possible nausea and vomiting Mydriasis, stiffness, muscle twitching, tonic seizure, and opisthotonos Animal dies from respiratory failure
40
What sample is used or detection of strychnine?
Urine | Stomach contents
41
What is the treatment of strychnine toxicosis?
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
What drugs are contraindicated in strychnine toxicosis?
``` Opioid Phenothiazine Butyrophenones NMBD Dissociative anesthetics ```
43
What are the properties of zinc phosphide?
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
What is the legal dose for zinc phosphide?
20-40mg/kg | Gastric acid increases toxicity, vomiting decreases toxicity
45
Gastric acid causes hydrolysis of zinc phosphide to ____________ which is absorbed across the GI tract
Phosphide gas
46
What is the MOA of zinc phosphide ?
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
What are the main tissues affected by zinc phosphide toxicosis?
``` Brain Heart Liver Kidney Lung ```
48
What are the clinical signs associated with zinc phosphide toxicosis?
``` Anorexia Vomiting Incresed rate and empty of respiration Wheezy Abdominal pain Bloat (cattle) “Mad dog running”, hyperexcitabiltiy ```
49
What lesions are associated with zinc phoside toxicosis?
Odor of acetylene (dead fish) Gastroenteritis Congestion of liver and kidney Pulmonary congestion and edema
50
What specimens should be collected and how are they handled for testing zinc phosphide?
Stomach content, vomitus, or bait Rapidly frozen
51
What lab abnormalities would you see with zinc phosphide toxicosis?
Elevated serum zinc Metabolic acidosis Dehydration Hypocalcemia
52
What is the treatment of zinc phosphide toxicosis?
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
Prognosis of zinc phosphide?
Animals that vomit may recover Signs of tissue damage have guarded to poor prognosis
54
What is currently the onl used of flouroacetate ?
Currently it is only used in the livestock protection collar Controls coyotes preying on sheep and goats
55
What are the properties of flouroacetate?
Odorless and water soluble Insoluble in most organic solvents Degraded in soil by microorganisms Irritant
56
What is the LD50 for flouroacetate in dogs
0.05mg/kg | Extremely toxic
57
T/F: flouroacetate is readily absorbed from GI tract, lung, wounds, and intact skin
False Cannot be absorbed across intact skin
58
Where does flouroacetate accumulate?
Trick question.. it does not accumulate in any particular tissue
59
How is flouroacetate metabolized?
Acid hydrolysis makes flouroacetate —> monofluoroacetic acid
60
What is the MOA of flouroacetate?
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
What signs do you see for flouroacetate toxicosis in dogs?
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
What clinical signs do you see in flouroacetate toxicosis in horse, cattle, sheep, and goat?
Signs of heart failure Colic, staggering, arrhythmia, Vfib Terminal convulsions due to cerebral anoxia
63
What clinical signs do you see in cats and pigs due to flouroacetate toxicosis?
CNS and cardiac signs
64
Death due to flouroacetate toxicosis is a result of?
Convulsions and respiratory failure that causes cyanosis, hemorrhage on the heart, pulmonary changes, dark blood, and organ congestion
65
What specimens are best to run lab diagnostics for flouroacetate ?
Gastric contents and vomitus
66
What is the treatment for flouroacetate toxicosis?
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
Prognosis for flouroacetate toxicity?
Grave

RUSVM Toxicology Summer 2019 (10 decks)

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