Exam 1: Pharmaceuticals Flashcards

1
Q

What are the major toxicities associated with the use of NSAIDs in companion animals?

A

Dogs: OTC medications, human prescription meds, veterinary products
Cats: liquid medications, NSAIDs, acetominophen, veterinary medications
GI, renal nervous

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2
Q

Mechanism of Action: NSAIDs

A

Inhibition of cyclooxygenase

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3
Q

Clinical Signs: Ibuprofen [note about cats]

A

Acute: vomiting, diarrhea, nausea, anorexia, gastric ulceration, abdominal pain
Moderate: renal damage
High: seizure, ataxia, coma
Cats are considered to be twice as sensitive due to limited glucoronyl-conjugating capacity

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4
Q

Treatment: Ibuprofen

A

Goal is to prevent gastric ulceration, renal failure, CNS effects
Stabilization (diazepam, IV electrolytes, blood)
Decontamination (enterohepatic circulation)
Prevent renal failure: fluid diuresis
Gastric protection

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5
Q

What phase II metabolizing system are felines deficient in?

A

Cats are deficient in UGT1A6 = glucoronidation = more drug exposure (longer t1/2), toxic forms can accumulate

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6
Q

Mechanism of Action: Acetominophen

A

Inhibits COX enzymes and metabolites may modulate cannabanoid system
Accumulation of reactive N-acetyl benzoquinoneimine metabolite

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7
Q

Clinical Signs: Acetominophen (Dogs)

A

Hepatocellular injury and necrosis - vomiting, anorexia, tachycardia, tachypnea
Methoglobinemia at higher doses

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8
Q

Clinical Signs: Acetominophen (Cats)

A

Predominantly methomoglobinemia - cyanosis, muddy mm, respiratory distress, edema of face and paws
Hepatotoxicosis at higher doses, primarily males

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9
Q

Treatment: Acetominophen

A

Prevent additional drug absorption (emesis, gastric lavage, activated charcoal)
Support (oxygen, fluids)
Administer N-acetylcystein

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10
Q

How does N-acetylcysteine work?

A

Acetominophen toxicity
Serves as thiol source in the face of GSH depletion caused by acetominophen - allows for detoxification of reactive metabolites

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11
Q

Why are dogs generally more likely to be poisoned by pharmaceuticals?

A

Chewing on a bottle and accidentally ingesting it
More inquisitive nature and willingness to eat nonfood items
Powdered drinks and nutrition bars are more attractive to dogs

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12
Q

Why are cats more likely to be poisoned by venlafaxine?

A

They readily eat them

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13
Q

Treatment: Amphetamines

A

Limit absorption (emitics, activated charcoal, cathartics)
Ace, barbiturates, cyproheptadine, propranolol
Increase elimination (acidify the urine)

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14
Q

Mechanism of Action: Pseudophedrine

A

Act as sympathomimetics
PNS: vasoconstriction, cardiac stimulation
CNS: enhanced CNS output

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15
Q

Clinical Signs: Pseudoephedrine

A

Initial: restless, agitation, pacing
Hallucinogenic behavior
Mydriasis, tachycardia, hypertension, seizure
Death due to cardiovascular collapse

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16
Q

Treatment: Pseudoephedrine

A

Decontamination (emesis within 30min)
Ace, chlorpromazine, barbiturates
Not diazepam
Propranolol (tachycardia)

17
Q

What is more likely to cause overdose with thyroid hormone?

A

Chronic overdose

18
Q

Mechanism of Action/Clinical Signs: Thyroid Hormone

A

Hyperthyroidism
Vomiting, diarrhea, hyperactive to lethargic, hypertension, tachycardia, tachypnea, dyspnea, abnormal PLR

19
Q

Treatment: Thyroid Hormone

A

Limit absorption (emetics, activated charcoal, cathartics)
Oxygen, ventilator, cardiac glycosides, beta blockers, fluids

20
Q

Treatment: Venlafaxine

A

Cyproheptadine

21
Q

Clinical Signs: Amphetamines

A

Agitation, hyperthermia, tremors, seizures, tachycardia, hypertension, arrhythmias, coma