Test 4: 55 rodenticides part 2 Flashcards
— are rodenticides with no antidotes
- Zinc and Aluminum Phosphide
- Cholecalciferol
- Aldicarb
- Bromethalin
- Strychnine
ZCABS
— is vitamin D3
cholecalciferol
cholecalciferol will cause
↑ calcium and phosphorus
metabolized in liver and kidney into calcitriol that can cause GI to ↑ absorption of Ca and Phos, will tell bones to ↑ osteoclast
↑ calcium and phosphorus can lead to mineralization/ stone formation
ADME of cholecalciferol
- Rapidly absorbed– often clinical signs within 12- 18 hours
- Undergoes enterohepatic recirculation
- Fat soluble– giving a very long terminal half life (days to weeks)
clinical signs of cholecalciferol exposure
- Acute kidney injury: PU/PD, impaired action of ADH, reduced tubular sodium absorption
- Anorexia
- Weakness
- Depression
- Vomiting
- Diarrhea
diagnosis of cholecalciferol
- Hyperphosphatemia– often increases 12 hours before calcium
- Hypercalcemia
- Hyposthenuria
- Azotemia
- PTH levels are low
treatment for early cholecalciferol ingestion
- Emesis if ingested within 2 hours
- Activated charcoal
- Monitor Ca/Phos/BUN/Creat for 4 days
treatment for clinical cholecalciferol ingestion
Fluids: 0.9% NaCl
- High sodium content competes with calcium and reduces calcium resorption
- Increases GFR and increases filtered load of calcium
- Contains no additional calcium
Furosemide
- Inhibits calcium resorption in the thick ascending loop of Henle
- Need to hydrate the patient first
- DO NOT use thiazide diuretics → increase Ca resorption
Glucocorticoids
- Reduce osteoclastic bone resorption of Ca, GI absorption of Ca, and promotes calciuresis
Bisphosphonates
Calcitonin
Phosphate binders
May require hemodialysis if anuric renal failure develops
prognosis of cholecalciferol ingestion
- Depends on severity of hypercalcemia and side effects
- Hematemesis is associated with poor outcomes
- Very long half life so may continue to absorb Vitamin D3 for weeks
- May develop long term CKD
how does bromethalin work
uncouple oxidative phosphorylation → decreased ATP production
Na/K pump can’t work → ↑Na in the cell →↑ water into the cell = cell swells and ruptures
cerebral edema and increased ICP
ADME of bromethalin
- Rapidly absorbed from the GI tract (< 1.5 hours)
- Peak plasma concentration in 4-6 hours
- Highly lipophilic, distributes within the brain, fat, liver, kidney
- Hepatic metabolism to N-demethylated intermediates via cytochrome P450 system is required for
toxicity to occur - Excreted in bile → undergoes enterohepatic recirculation
- Cats are much more sensitive than dogs!! Can relay toxicity from ingestion of poisoned rodents
↓ATP production= ↑Na and water in cell = cell swells → cerebral edema and ↑ICP
clinical signs of bromethalin ingestion
Nervous system: Depression, ataxia, seizures, paresis/paralysis, hyperthermia, coma
* Can be very acute (2 hours) in high doses (>LD50)
Delayed syndrome (< LD50) can see signs in 2-7 days
* Anorexia, ataxia, paresis, paralysis, CNS depression, tremors, seizures, abnormal PLR, anisocoria, nystagmus
* Clinical signs may resolve in 1-2 weeks
treatment of bromethalin ingestion
Decontamination
* Early emesis in asymptomatic animals
* Activated charcoal for 2-3 days (enterohepatic recirculation)
* Consider IV Lipid Emulsion in severe intoxication
* Gingko Biloba??
Supportive care
* Intubation +/- mechanical ventilation
* Seizures → Benzodiazepines, Keppra, Phenobarbital
* High ICP → Mannitol
* Tremors → Methocarbamol
MOA of strychnine
Reversibly binds glycine
* Inhibitory neurotransmitter in the dorsal horn of the spinal cord
* Loss of inhibition in the nervous system leads to unchecked spinal reflexes and nerve excitability
ADME of strychnine
- Absorbed rapidly in the small intestines and widely distributed
- Actively metabolized in the liver and excreted in the urine
- Rapid onset of clinical signs in 10 minutes to 2 hours
- Complete elimination within 48-72 hours
- Enterohepatic recirculation
clinical signs of strychnine posioning
- Rapid onset
- Violent seizures, extensor rigidity (sawhorse stance), opisthotonos, tachycardia, hyperthermia, metabolic acidosis, apnea
- Sardonic grin
- Death can be rapid
treatment of strychnine
- Detoxification: if no clinical signs → emesis, activated charcoal
- Keep in a dark, dimly lit room to avoid stimulation
Supportive care
* IV Fluids
* Control seizures → Benzodiazepines, Keppra, Phenobarbital
* Control tremors → Methocarbamol
Prognosis poor if seizures can not be controlled.
Good prognosis if they have normal neurologic function after 48-72 hours
MOA of phosphides
Mechanism of Action
* Phosphide is hydrolyzed into phosphine gas in a moist or acidic environment
* Phosphine gas is a direct irritant to the GI tract and is rapidly absorbed across the GI mucosa and systemically distributed
* Cytotoxic to pulmonary cells
* Inhibits oxidative phosphorylation and enzyme/protein function
ADME of phosphides
- Poorly understood
- Absorption affected by amount of food ins stomach, gastric acid level, product formulation
- Acute emesis can self-limit toxicity
clinical signs of phosphides ingestion
- Acute vomiting (within 15 minutes of ingestion)
- Hematemesis, anorexia, bloating,
abdominal pain, melena - Respiratory distress, ataxia, seizures, coma, death
phosphine gas in cytotoxic to pulmonary cells and inhibits oxidative phos and enzyme/protein function
treatment of phosphides
- DO NOT feed– can increase phosphine gas production
- Decontamination → only induce emesis in a well ventilated area to prevent human exposure
- Acid suppression → Magnesium hydroxide or gastric lavage with bicarbonate
- Supportive care →GI protectants, IN fluids, oxygen, ventilation, seizure management
Prognosis is guarded if clinical signs are present
MOA of aldicarb
Reversibly binds acetylcholinesterase(AcHE) at synaptic and neuromuscular junction
- Prevents breakdown of acetylcholine
- Produces severe muscarinic signs and occasionally nicotinic signs
clinical signs of aldicarb ingestion
block AcHE
muscarinic: DUMBBELLS
Nicotinic: HTN, tremors, respiratory failure, death
nictotinic: tension, weakness, paralysis: MT WTF (mydraisia tachycardia, muscle weakness, twitching, fasiculations) high BP, paralysis
muscarinic: diarrhea, urinartion, miosis, bradycardia, bronchospasm, emesis, lacrimation, lethargy, salivation
treatment for aldicarb
- VERY RAPID ONSET
- If no clinical signs consider emesis, activated charcoal, gastric lavage
- Parasympatholytic therapy: Atropine
- Supportive care
- IV fluids, oxygen, ventilation
Prognosis is grave
