MPharm Master of Pharmacy Master of Pharmacy: Pharmacology and Therapeutics 2 — Questions and Answers
Question 1: A patient on warfarin is started on rifampin. What is the expected pharmacokinetic interaction?
- Rifampin inhibits CYP2C9, increasing warfarin levels
- Rifampin induces CYP2C9, decreasing warfarin levels (Correct answer)
- Rifampin displaces warfarin from plasma proteins
- Rifampin inhibits warfarin renal excretion
Correct answer: Rifampin induces CYP2C9, decreasing warfarin levels
Rifampin is a potent CYP2C9 inducer that accelerates warfarin metabolism, reducing its anticoagulant effect and requiring dose increases.
Question 2: Which receptor mechanism explains morphine-induced constipation?
- Activation of mu-opioid receptors in the enteric nervous system (Correct answer)
- Blockade of delta-opioid receptors in the colon
- Antagonism of kappa-opioid receptors in the gut
- Stimulation of serotonin 5-HT4 receptors in the intestine
Correct answer: Activation of mu-opioid receptors in the enteric nervous system
Mu-opioid receptors in the enteric nervous system mediate decreased GI motility and secretion, causing opioid-induced constipation.
Question 3: A patient with atrial fibrillation and CrCl of 30 mL/min requires anticoagulation. Which DOAC requires the most significant dose adjustment?
- Apixaban
- Rivaroxaban
- Dabigatran (Correct answer)
- Edoxaban
Correct answer: Dabigatran
Dabigatran is ~80% renally eliminated and is contraindicated or requires major dose reduction at CrCl <30 mL/min due to accumulation risk.
Question 4: The narrow therapeutic index of lithium requires monitoring for toxicity. Which early sign indicates toxicity?
- Hypertension and tachycardia
- Coarse tremor, nausea, and diarrhea (Correct answer)
- Dry mouth and urinary retention
- Hypoglycemia and diaphoresis
Correct answer: Coarse tremor, nausea, and diarrhea
Early lithium toxicity (serum level >1.5 mEq/L) presents with coarse tremor, GI disturbances, and drowsiness before progressing to seizures.
Question 5: Which mechanism accounts for resistance to beta-lactam antibiotics in MRSA?
- Overexpression of beta-lactamase enzymes
- Acquisition of mecA gene encoding altered PBP2a (Correct answer)
- Efflux pumps reducing intracellular antibiotic concentration
- Modification of lipopolysaccharide in the outer membrane
Correct answer: Acquisition of mecA gene encoding altered PBP2a
MRSA expresses PBP2a (encoded by mecA), a modified penicillin-binding protein with low affinity for beta-lactams, conferring resistance.
Question 6: A patient develops serotonin syndrome after adding linezolid to fluoxetine. What is the pharmacodynamic basis?
- Linezolid inhibits MAO, increasing synaptic serotonin alongside SSRI (Correct answer)
- Linezolid blocks serotonin reuptake synergistically with fluoxetine
- Linezolid activates 5-HT1A receptors directly
- Linezolid inhibits serotonin degradation via COMT
Correct answer: Linezolid inhibits MAO, increasing synaptic serotonin alongside SSRI
Linezolid has weak MAO inhibitory activity; combined with fluoxetine's SERT inhibition, it causes excessive serotonergic activity leading to serotonin syndrome.
Question 7: In heart failure with reduced ejection fraction, why are ACE inhibitors considered first-line?
- They increase preload by promoting sodium retention
- They reduce afterload and prevent ventricular remodeling via angiotensin II blockade (Correct answer)
- They increase cardiac contractility by blocking phosphodiesterase
- They reduce heart rate via beta-adrenergic antagonism
Correct answer: They reduce afterload and prevent ventricular remodeling via angiotensin II blockade
ACE inhibitors reduce angiotensin II-mediated vasoconstriction and aldosterone release, decreasing afterload and preventing maladaptive cardiac remodeling.
A patient on warfarin is started on rifampin.
What is the expected pharmacokinetic interaction?