Keratinocytic pathology (BCC, SCC, actinic keratosis) — SAQ

Stem

A 68-year-old outdoor worker has multiple scaly forearm papules, a thick scalp plaque, and a pearly telangiectatic nodule on the nasal sidewall. You must use keratinocytic pathology principles to plan sampling, interpret reports, and map next steps.

Questions

a) Contrast the histologic definitions of actinic keratosis, SCC in situ, and invasive cutaneous SCC. (2 marks)

b) List four high-risk pathologic or clinical features of invasive cSCC that change management intensity. (2 marks)

c) Name classic histologic hallmarks of nodular BCC and explain why infiltrative/morpheaform subtype alters surgical planning. (3 marks)

d) State the role and one limitation of Ber-EP4, and define field cancerization in one sentence. (3 marks)

Model answers

a)

• AK: partial-thickness keratinocyte atypia ± parakeratosis on solar elastosis.
• SCCIS/Bowen: full-thickness epidermal atypia without dermal invasion.
• Invasive SCC: tumour breaches basement membrane into dermis/deeper.

b)

Any four: poor differentiation; deep invasion/thickness; perineural invasion; LVI; positive/close deep margins; immunosuppression/transplant host; high-risk site/recurrence context.

c)

• Nodular BCC: basaloid nests, peripheral palisading, stromal retraction clefting.
• Infiltrative/morpheaform: thin strands, ill-defined borders → margin-critical surgery (often Mohs), not casual destruction assumptions.

d)

• Ber-EP4 supports BCC vs SCC but can label Bowen disease — morphology still rules.
• Field cancerization: UV-driven genetically altered keratinocyte clones across a region beyond single visible AKs.