Clinical Pharmacology and Therapeutics Flashcards
6 cards from real Pharm.D. Doctor of Pharmacy practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 6 Clinical Pharmacology and Therapeutics flashcards as text
Which class of medications is contraindicated in patients with hyperkalemia and is known to cause hyperkalemia as a side effect?
Answer: Potassium-sparing diuretics (e.g., spironolactone)
Potassium-sparing diuretics like spironolactone block aldosterone, retaining potassium and causing hyperkalemia, making them contraindicated when potassium is already elevated.
Naloxone reverses opioid overdose by acting as a:
Answer: Opioid receptor competitive antagonist
Naloxone competitively displaces opioids from mu, kappa, and delta receptors, reversing respiratory depression, sedation, and analgesia within minutes.
A patient with gout presents with an acute attack. Which medication is most appropriate for acute treatment?
Answer: Colchicine or NSAIDs or corticosteroids
Acute gout is treated with anti-inflammatory agents (colchicine, NSAIDs, or corticosteroids); urate-lowering drugs like allopurinol are not started during acute attacks.
Which antibiotic class works by inhibiting bacterial cell wall synthesis through binding to penicillin-binding proteins (PBPs)?
Answer: Beta-lactams (penicillins, cephalosporins, carbapenems)
Beta-lactam antibiotics inhibit transpeptidase enzymes (PBPs) required for cross-linking peptidoglycan in bacterial cell walls, causing lysis and death.
Which medication requires regular monitoring of thyroid function tests (TFTs) due to its known thyroid toxicity?
Answer: Amiodarone
Amiodarone contains ~37% iodine by weight and can cause both hypothyroidism and hyperthyroidism; TFTs should be monitored every 6 months during therapy.
Corticosteroids exert their anti-inflammatory effect primarily by:
Answer: Binding to intracellular glucocorticoid receptors to suppress inflammatory gene expression
Corticosteroids bind cytosolic glucocorticoid receptors; the complex enters the nucleus and suppresses transcription of inflammatory cytokines and mediators.