Clinical Pharmacy and Therapeutics: Guidelines, Monitoring and Interactions
Think in algorithms
Most therapeutic questions test first-line choice and the reason a drug is not used. Anchor yourself to common pathways: hypertension (ACE inhibitor/ARB, calcium channel blocker or thiazide, often two agents at diagnosis), type 2 diabetes (metformin plus a cardiorenal-protective agent when indicated), asthma (inhaled corticosteroid-containing therapy, never a long-acting beta-2 agonist alone), heart failure with reduced ejection fraction (the four pillars: ARB/ACE inhibitor or ARNI, beta-blocker, mineralocorticoid receptor antagonist, SGLT2 inhibitor), and anticoagulation (direct oral anticoagulants for most non-valvular atrial fibrillation; warfarin with INR target usually 2–3).
Monitoring is examinable
Know therapeutic drug monitoring basics: trough sampling for vancomycin and aminoglycosides, AUC-guided vancomycin dosing, digoxin levels, lithium, phenytoin (total vs free), and the fact that assay timing relative to the last dose determines interpretation. Renal dosing uses estimated creatinine clearance; remember metformin needs review at low eGFR and is held around iodinated contrast.
Interaction traps
- "Triple whammy": NSAID + ACE inhibitor/ARB + diuretic → acute kidney injury.
- NSAIDs blunt antihypertensives and increase bleeding with anticoagulants.
- Macrolides/azoles + statins → myopathy.
- ACE inhibitor + potassium-sparing diuretic or potassium supplement → hyperkalaemia.
- Beta-blockers worsen asthma; non-selective ones mask hypoglycaemia.
- ACE inhibitor cough or angioedema → switch to ARB.
Worked example
A patient on ramipril and spironolactone develops vomiting and is started on ibuprofen. The highest-yield answer is not "add a PPI" but "stop the NSAID and recheck renal function and potassium" - you are correcting the cause of a predictable interaction. Rule of thumb: before answering any therapeutics question, list the patient's comorbidities, renal function and interacting drugs.