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Drug Interactions Flashcards

7 cards from real PSA practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.

Read the first 7 Drug Interactions flashcards as text
  1. A patient on ramipril is prescribed spironolactone for heart failure. What electrolyte abnormality is the primary concern?

    Answer: Hyperkalemia from dual potassium-retaining mechanisms

    Both ACE inhibitors and potassium-sparing diuretics independently reduce renal potassium excretion; their combination creates additive hyperkalemia risk, particularly in those with renal impairment.

  2. Which drug combination carries the highest risk of serotonin syndrome?

    Answer: SSRI with a monoamine oxidase inhibitor

    MAOIs prevent serotonin degradation while SSRIs block its reuptake; together they cause massive serotonergic excess, presenting as hyperthermia, tremor, clonus, and autonomic instability.

  3. A patient on digoxin 125 mcg daily starts amiodarone for atrial fibrillation. Which mechanism best explains the increased digoxin toxicity risk?

    Answer: Amiodarone inhibits P-glycoprotein, reducing renal and biliary digoxin elimination

    Amiodarone inhibits P-glycoprotein-mediated secretion of digoxin in the kidney and bile duct, causing plasma digoxin concentrations to approximately double.

  4. Which drug combination constitutes the renal 'triple whammy' associated with acute kidney injury?

    Answer: NSAIDs + ACE inhibitors (or ARBs) + loop or thiazide diuretics

    NSAIDs reduce efferent arteriolar dilation, ACE inhibitors blunt angiotensin II-mediated efferent constriction, and diuretics cause hypovolemia — together these mechanisms collapse glomerular filtration pressure.

  5. Which drug combination creates the greatest additive risk of QT prolongation and torsades de pointes?

    Answer: Amiodarone and sotalol

    Both amiodarone and sotalol independently prolong the cardiac action potential by blocking potassium channels; combining them markedly amplifies QT prolongation and arrhythmia risk.

  6. Naloxone reverses opioid-induced respiratory depression via which interaction mechanism?

    Answer: Competitive pharmacodynamic antagonism at mu-opioid receptors

    Naloxone has very high affinity for mu-opioid receptors and rapidly displaces opioid agonists by competitive antagonism, reversing analgesia, sedation, and respiratory depression.

  7. A patient prescribed an opioid analgesic is also taking a benzodiazepine for anxiety. The most dangerous pharmacodynamic interaction produces:

    Answer: Additive CNS and respiratory depression with risk of fatal apnea

    Opioids and benzodiazepines both suppress central respiratory drive through distinct but complementary mechanisms; their combination multiplicatively increases the risk of fatal respiratory arrest.