Rodenticides Flashcards
(32 cards)
Cholecalciferol
2 active forms of Vit D: plant derived (ergocalicerol/D2) and animal derived (cholecaciferol/ D3)
2 synthetic forms
Most common ways of cholecalciferol toxicity
Ingestion of rodenticides
Human medicine ingestion
Pet foods
Toxic dose of cholecalciferol
Vit D3 10x more potent than D2
Single oral lethal dose: 13 mg/kg
Mechanism of toxicity for cholecalciferol
Enhances Ca and P absorption from the gut
Enhances renal absorption
Mobilizes Ca from bone (hypercalcemia)
What are the differentials for hypercalcemia
Hyperparathyroidism
Addison’s dz
Renal dz
D- vitamin D
Idiopathic
Osteolytic
Neoplasia
Spurious
CS of cholecalciferol toxicity
Secondary to hypercalcemia (GI, renal, cardiovasc. and neuromuscular)
Depression, weakness and anorexia
36-48 hr after ingestion
Progressive signs of cholecalciferol toxicity
V, PU/PD, constipation and dehydration
Acute kidney injury, oliguria/ anuria
Calcification of renal tubules
Hematemesis/ melena
Minimum database for cholecalciferol toxicity
Monitor ionized Ca, P, BUN and creatinine
↑ total calcium (15-18 mg/dL)
Isothenuria
TX of cholecalciferol toxicity
GI decontamination
Reduce hypercalcemia
Supportive care (IV NaCl→ calciuresis and volume expansion)
Tx for acute ingestion for cholecalciferol toxicity
<6 hr
Induce emesis, AC
How do you tx the hypercalcemia associated with cholecalciferol toxicity?
Directed @ reducing blood Ca levels
Prevent acute kidney injury
Tx arrhythmias and supportive care (antiemetics and tx GI ulcers)
Medical tx for cholecalciferol toxicity
Glucos: after other causes of hypercalcemia rule out
Furosemide (lasix): after fluid deficits corrected
Salmon calcitonin: inhibits osteoclast activity, reduces resorption of Ca from bones
Bisphosphonate (pamidronate): Inhibits osteoclastic bone resorption, reduce Ca conc. within 48hr
Bromethalin
Used in warfarin- resistant in mice/ rats
Neurotoxic and accidental ingestion
Toxic dose of bromethalin
Cats sensitive (0.5 mg/kg) and dogs (5mg/kg)
CS seen @ lower doses
Toxicokinetics for Bromethalin
Rapidly absorbed from GI tract (peak plasma levels within 4 hrs)
Metabolized by liver to desmetheylbromethalin (more toxic)
High conc. in body fat
MOA of Bromethalin
Uncoupling of oxidative phosphorylation → ↓ ATP and reduced activity of Na and K ATP → brain electrolyte imbalances → fluid movement to the brain and SC
Bromethalin primary target
CNS primary target
↑ intracranial pressure/ cerebral edema
CS of Bromethalin
2-24 hr after ingestion: severe muscle tremors, hyperthermia, seizures and hyperesthsia (mortality 100%)
Delayed 1-2w: ataxia, patellar hyperreflexia, CNS depression, seizure then coma
Electroencephalographic (EEG) for bromethalin toxicity
Seizure foci
Cerebral edema and hypoxia
Postmortum confirmatory tests of Bromethalin
Diffuse vacuolization of white matter
In fat, liver, kidney and brain tissue
Tx for Bromethalin
Emesis within 1 hr (no CNS signs)
Providing symptomatic and supportive care
AC (every 4-6 hrs, @ least 2-3x)
How do you control cerebral edema and ↑ intracranial pressure associated with bromethalin?
Mannitol, hypertonic saline
Keep head elevated 30 degrees
No jug venipuncture
Controlling seizures associated with bromethalin toxicity
Phenobarbitol, keppra, midazolam/ diazepam/ lorazepam
Anticoagulant rodenticides generations
1st gen: warfarin based products (rats becoming resistant)
2nd gen: More toxic, longer duration (more common)
Brodifacoum, bromadiolone, etc
