Pharmacology and Pharmacotherapy
This domain tests whether you can predict what a drug will do - wanted and unwanted - from its mechanism, and then apply that prediction to a specific patient. Expect mechanism-to-adverse-effect reasoning, interaction mechanisms, monitoring parameters, and dose adjustment in renal or hepatic impairment.
Mechanism drives effect and toxicity
Most toxicity questions reduce to where the drug acts. ACE inhibitors accumulate bradykinin → dry cough and angioedema. Beta-blockers block β2 in the lung → bronchospasm. NSAIDs inhibit prostaglandin synthesis → gastric ulceration, reduced renal perfusion and blunted antihypertensive effect. Aminoglycosides concentrate in cochlea and proximal tubule → ototoxicity and nephrotoxicity. Metformin does not cause hypoglycaemia but accumulates as eGFR falls → lactic acidosis.
Monitoring is drug-specific
Therapeutic drug monitoring earns marks when you name the right parameter: INR for warfarin, aPTT or anti-Xa for unfractionated heparin, trough or AUC for vancomycin, potassium plus drug level for digoxin toxicity, and free phenytoin in hypoalbuminaemia. Lithium needs level, renal function and thyroid checks.
Worked example
A 68-year-old stabilised on warfarin 5 mg daily is prescribed trimethoprim–sulfamethoxazole for a urinary tract infection. Three mechanisms converge: sulfamethoxazole inhibits CYP2C9 (slower S-warfarin metabolism), trimethoprim displaces warfarin from albumin, and the antibiotic suppresses gut flora that make vitamin K. INR climbs over 3–5 days. The safe action is an alternative antibiotic if possible; otherwise check INR within 3–5 days, counsel on bleeding signs, and adjust the warfarin dose to the result.
Traps
- Assuming every member of a class shares the same adverse effects (atenolol versus propranolol).
- Missing non-prescription interactions: St John's wort, ginkgo, cranberry, grapefruit.
- Ignoring renal function in an older patient whose creatinine looks normal because muscle mass is low.