Dermatology and Clinical Pharmacology
Core framework
For dermatology, describe the lesion morphology and distribution first, then decide whether the process is inflammatory, infective, autoimmune or neoplastic, and whether a biopsy is needed. For pharmacology, link every drug to its mechanism, its key adverse effects, and its interactions; the exam frequently tests adverse drug reactions and prescribing in organ impairment.
Concepts examiners test
Dermatology: recognition of drug eruptions (morbilliform, urticarial, bullous, severe cutaneous adverse reactions such as Stevens–Johnson syndrome and toxic epidermal necrolysis), psoriasis and its systemic associations, eczema and its management ladder, skin infections, and melanoma recognition using the ABCDE rule. Pharmacology: first-order versus zero-order kinetics (phenytoin, warfarin, alcohol), enzyme inducers and inhibitors, the cytochrome P450 system, therapeutic drug monitoring, prescribing in renal and hepatic impairment, and common interactions (warfarin, statins, macrolides, azoles, rifampicin).
Traps
- Do not miss severe cutaneous adverse reactions - stop the culprit drug immediately; these are emergencies.
- Topical steroids differ in potency by site and thickness of skin; avoid potent agents on the face.
- Zero-order kinetics means small dose increases cause large level rises - phenytoin toxicity is a classic.
- Enzyme inducers reduce drug levels (rifampicin, carbamazepine, phenytoin); inhibitors raise them (macrolides, azoles, grapefruit).
- Renal impairment requires dose adjustment for many drugs, including some antibiotics and anticoagulants.
Worked rule of thumb
A patient on warfarin started on a macrolide with a rising INR: the macrolide inhibits cytochrome P450, reducing warfarin metabolism. Check the INR, reduce the warfarin dose if needed, and consider an alternative antibiotic. Apply the same inductive logic to rifampicin, which lowers warfarin effect.