Q1. Aminoglycosides such as gentamicin act by binding: A. The 30S ribosomal subunit B. The 50S ribosomal subunit C. DNA gyrase D. Penicillin-binding proteins ANSWER: A — the 30S subunit. Why: aminoglycosides and tetracyclines bind 30S; macrolides, clindamycin, chloramphenicol and linezolid bind 50S. C: fluoroquinolones. D: beta-lactams. LEARNING POINT: "buy AT 30, CCEL at 50."

Q2. Which antibiotic is contraindicated in a 5-year-old because of permanent tooth staining? A. Amoxicillin B. Doxycycline C. Azithromycin D. Cefalexin ANSWER: B — Doxycycline (a tetracycline). Why: tetracyclines chelate calcium and deposit in developing teeth and bone. Avoided in pregnancy and under 8 years. LEARNING POINT: the age cut-off is a standard exam fact.

Q3. A wound swab grows MRSA. A colleague suggests co-amoxiclav because "clavulanate covers resistance". The best response is: A. Agree — clavulanate restores beta-lactam activity B. MRSA resistance is from an altered penicillin-binding protein, so clavulanate does not help C. Double the amoxicillin dose instead D. Add gentamicin to the co-amoxiclav ANSWER: B. Why: clavulanate inhibits beta-lactamase ENZYME. MRSA resistance comes from an altered PBP — the target itself has changed, so there is no enzyme to inhibit and no binding to restore. C: dose does not overcome a changed target. D: gentamicin does not reliably treat MRSA. LEARNING POINT: the mechanism of resistance dictates the answer. Vancomycin or linezolid here.

Q4. A 68-year-old on warfarin with a stable INR is given clarithromycin. Six days later the INR is 7.1. The mechanism is: A. Displacement from albumin B. CYP450 inhibition reducing warfarin metabolism C. Vitamin K malabsorption D. Direct anticoagulant effect of the macrolide ANSWER: B — CYP450 inhibition. Why: macrolides inhibit CYP450, so warfarin is metabolised more slowly and accumulates. Metronidazole and co-trimoxazole do the same. D: macrolides have no intrinsic anticoagulant activity. LEARNING POINT: this is predictable, not idiosyncratic. Check interactions before prescribing to an anticoagulated patient.

Q5. A patient with suspected bacterial meningitis needs empirical therapy. The most appropriate agent is: A. Oral amoxicillin B. Intravenous ceftriaxone C. Oral doxycycline D. Intravenous gentamicin ANSWER: B — IV ceftriaxone. Why: third-generation cephalosporins penetrate the CSF well and cover the likely organisms. A: oral therapy is inadequate, and CSF penetration is poor. C: doxycycline is not appropriate empirical cover here. D: aminoglycosides penetrate the CSF poorly. LEARNING POINT: site of infection governs the choice — reaching the target is a prerequisite for killing anything.

Q6. Why are aminoglycosides ineffective against strict anaerobes? A. Anaerobes lack ribosomes B. Uptake requires an oxygen-dependent transport process C. Anaerobes produce beta-lactamase D. They cannot penetrate the anaerobic cell wall ANSWER: B — oxygen-dependent uptake. Why: aminoglycoside entry depends on an oxygen-requiring transport step, so the drug does not accumulate inside anaerobic bacteria despite having a valid target there. A: all bacteria have ribosomes. C: irrelevant — aminoglycosides are not beta-lactams. LEARNING POINT: a spectrum gap you can derive from mechanism rather than memorise.

Q7. A patient reports that penicillin previously caused lip swelling and breathing difficulty. Which is the safest choice for community-acquired pneumonia? A. Co-amoxiclav B. Cefuroxime C. Clarithromycin D. Piperacillin-tazobactam ANSWER: C — Clarithromycin. Why: the history describes anaphylaxis, a true type-1 hypersensitivity. A structurally unrelated class avoids the beta-lactam ring entirely, and a macrolide covers the likely organisms. A, D: both are penicillins. B: a cephalosporin — cross-reactivity is lower than once believed but not zero, and is best avoided after documented anaphylaxis. LEARNING POINT: distinguish true allergy from intolerance, but after genuine anaphylaxis avoid the whole class.