Bromethalin Rodenticide Flashcards

1
Q

Is bromethalin a general use or restricted use pesticide?

A

general use

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2
Q

What species is more sensitive to Bromethalin poisoning?

A

Cats are more sensitive than dogs

Dogs are more susceptible as they are more likely to ingest it

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3
Q

What species are resistant to Bromethalin poisoning?

A

Guinea pigs

they lack the correct metabolic enzymes for lethal synthesis

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4
Q

Is bromethalin lipophilic or water soluble?

A

Lipophilic - readily absorbed orally

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5
Q

Where is Bromethalin distributed in the highest amount in the body?

A

Fat and brain

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6
Q

What is the metabolism of Bromethalin ?

A

metabolized by N-demethylation in the liver to a MORE TOXIC metabolite: Desmethylbromethalin

***lethal synthesis

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7
Q

What is the half life of Bromethalin and how is it excreted?

A

Half life in the rat = 5-6 days

mainly excreted in the bile, small amount in the urine

*likely undergoes enterohepatic recirculation

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8
Q

What is the MOA of Bromethalin ?

A

Uncoupleing of oxidative phosphorylation

= lack of adequate ATE and insufficient energy for Na/K ion pumps

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9
Q

What are the primary targets or tissues affected by Bromethalin toxicosis?

A

Brain and Spinal cord

  • these rely heavily on oxidative phosphorylation
  • further tissue damage may occur through lipid peroxidation
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10
Q

T/F: Signs for Bromethalin toxicosis are always acute

A

FALSE

acute or delayed
*acute is less common

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11
Q

What clinical signs are associated with acute Bromethalin toxicosis?

A

occurs 2-36hrs post ingestion

“convulsant syndrome” - generally a higher dose

CNS excitatory signs - severe muscle tremors, hyperthermia, running fits and hyper excitability - that may be precipitated by light or noise

(may note CNS depression in end stage)

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12
Q

What is the prognosis of Bromethalin Convulsive syndrome?

A

POOR

difficult to treat

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13
Q

What are the clinical signs associated with subacute Bromethalin toxicosis?

A

onset 1-4 days - MORE COMMON - Paralytic syndrome

Develops within the first few days and progresses over 1-2 weeks

hind limb ataxia, proprioceptive deficits, paresis, can progress to paralysis and loss of deep pain

CNS depression
Other: vomiting, anorexia, nystagmus – may progress to sz late stage

Death may occur due to respiratory failure

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14
Q

What lesions are associated with Bromethalin toxicosis?

A
Cerebral edema (intramyelinic edema)
Diffuse white matter vacuolization in the white matter
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15
Q

Paralytic syndrome is usually associated with what kind of Bromethalin dose?

A

Lower dose

Convulsive syndrome = high doses

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16
Q

What are the most important factors for diagnosing Bromethalin toxicosis?

A

History and clinical signs

theres nothing very striking in blood work besides a mild hyperglycemia

Chemical analysis is expensive and takes a long time

17
Q

What is essential to prevent further CNS damage due to Bromethalin ?

A

Decontamination!!

Emetic is only successful if it is done within 1-2hours post ingestion since it is quickly absorbed

  • Activated charcoal with sorbitol - needs to be repeated
  • want to avoid cathartics with magnesium
18
Q

What is sorbitol?

A

A cathartic - will act as an osmotic agent to pull fluid into the colon

Should do one dose of toxiban with sorbitol and repeat doses without sorbitol to prevent hypernatremia

19
Q

What is the treatment for Bromethalin toxicosis?

A

lipid emulsion therapy should be considered

Supportive and symptomatic when signs are present - mannitol, furosemide, anticonvulsants, Gingko biloba

20
Q

What is the prognosis of Bromethalin toxicosis?

A

Mild cases - signs may resolve over several weeks

Severe cases = grave