Example FRCS Plast questions
Skin: FRCS(Plast) example questions
Our skin coverage spans the whole JCST curriculum - from dermoscopy and excision margins through to sentinel lymph node biopsy, flap reconstruction and scar management - with illustrated questions and referenced explanations throughout.
Skin assessment & dermoscopy
Melanoma & NMSC
Recurrent & metastatic disease
Reconstruction & flaps
Scars & complex wounds
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The contemporary evidence base places the annual risk of an individual AK lesion progressing to invasive SCC at approximately 0 to 0.075% per lesion-year in patients without prior non-melanoma skin cancer. The figure of 0.1% is the conventional rounded value quoted in current guidelines.
B (0.5%) - is the per-lesion annual progression rate in patients with a prior history of non-melanoma skin cancer (up to 0.53% per lesion-year). The stem specifies no prior cutaneous malignancy, so this does not apply.
C (8%) - originates from Glogau's 2000 review (Br J Dermatol), which extrapolated an average per-lesion annual progression rate of approximately 8% across five heterogeneous studies (range 0.025–16%). This figure is now regarded as a substantial overestimate driven by methodological variability and is not the contemporary answer.
D (10%) - is the commonly quoted per-patient cumulative risk over approximately 10 years of follow-up, a fundamentally different denominator. A patient with multiple AKs has a meaningful cumulative risk of developing at least one invasive SCC, but this is not the per-lesion annual rate the question asks for. This is the most common cognitive trap.
E (25%) - is the approximate annual spontaneous regression rate of individual AK lesions (≈20–25%), not the progression rate - the reverse concept!
The clinical picture: multiple crateriform lesions with spontaneous regression and pitted scarring, autosomal dominant family history, and Scottish ancestry, is characteristic of Ferguson-Smith syndrome (multiple self-healing squamous epithelioma, MSSE).
The lesions are histologically indistinguishable from sporadic keratoacanthomas, but regress over weeks to months, often leaving disfiguring depressed scars. Onset is usually in the second or third decade. MSSE is caused by heterozygous loss-of-function mutations in TGFBR1 (transforming growth factor β receptor 1) on chromosome 9q22.3, inherited as an autosomal dominant trait with high penetrance. Although lesions typically self-heal, excision may be offered both to limit scarring and to exclude SCC, which is histologically very difficult to distinguish.
APC - Gardner syndrome (FAP variant with epidermoid cysts, osteomas, desmoid tumours, colonic polyposis)
MLH1 (or MSH2) - Muir-Torre syndrome (sebaceous neoplasms and KA-like lesions with internal malignancy, classically colorectal)
PTCH1 - Gorlin syndrome (multiple BCCs, odontogenic keratocysts, palmar/plantar pits, falcine calcification)
PTEN - Cowden syndrome (trichilemmomas, oral papillomas, raised breast, thyroid, and endometrial cancer risk)
frcs(plast) part 1 question bank
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