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23 spring: pharm > Test 4: 55 rodenticides part 2 > Flashcards

Test 4: 55 rodenticides part 2 Flashcards

1
Q

— are rodenticides with no antidotes

A
  • Zinc and Aluminum Phosphide
  • Cholecalciferol
  • Aldicarb
  • Bromethalin
  • Strychnine

ZCABS

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2
Q

— is vitamin D3

A

cholecalciferol

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3
Q

cholecalciferol will cause

A

↑ 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

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4
Q

ADME of cholecalciferol

A
  • Rapidly absorbed– often clinical signs within 12- 18 hours
  • Undergoes enterohepatic recirculation
  • Fat soluble– giving a very long terminal half life (days to weeks)
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5
Q

clinical signs of cholecalciferol exposure

A
  • Acute kidney injury: PU/PD, impaired action of ADH, reduced tubular sodium absorption
  • Anorexia
  • Weakness
  • Depression
  • Vomiting
  • Diarrhea
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6
Q

diagnosis of cholecalciferol

A
  • Hyperphosphatemia– often increases 12 hours before calcium
  • Hypercalcemia
  • Hyposthenuria
  • Azotemia
  • PTH levels are low
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7
Q

treatment for early cholecalciferol ingestion

A
  • Emesis if ingested within 2 hours
  • Activated charcoal
  • Monitor Ca/Phos/BUN/Creat for 4 days
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8
Q

treatment for clinical cholecalciferol ingestion

A

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

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9
Q

prognosis of cholecalciferol ingestion

A
  • 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
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10
Q

how does bromethalin work

A

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

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11
Q

ADME of bromethalin

A
  • 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

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12
Q

clinical signs of bromethalin ingestion

A

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

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13
Q

treatment of bromethalin ingestion

A

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

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14
Q

MOA of strychnine

A

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

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15
Q

ADME of strychnine

A
  • 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
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16
Q

clinical signs of strychnine posioning

A
  • Rapid onset
  • Violent seizures, extensor rigidity (sawhorse stance), opisthotonos, tachycardia, hyperthermia, metabolic acidosis, apnea
  • Sardonic grin
  • Death can be rapid
17
Q

treatment of strychnine

A
  • 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

18
Q

MOA of phosphides

A

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

19
Q

ADME of phosphides

A
  • Poorly understood
  • Absorption affected by amount of food ins stomach, gastric acid level, product formulation
  • Acute emesis can self-limit toxicity
20
Q

clinical signs of phosphides ingestion

A
  • 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

21
Q

treatment of phosphides

A
  • 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

22
Q

MOA of aldicarb

A

Reversibly binds acetylcholinesterase(AcHE) at synaptic and neuromuscular junction

  • Prevents breakdown of acetylcholine
  • Produces severe muscarinic signs and occasionally nicotinic signs
23
Q

clinical signs of aldicarb ingestion

A

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

24
Q

treatment for aldicarb

A
  • 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

23 spring: pharm (46 decks)

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