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Q1: Definition and clinical presentation (2 min)
Question: Define actinic keratosis and describe its typical clinical presentation.
Model answer: Actinic keratosis is a premalignant intraepidermal keratinocyte dysplasia arising on chronically sun-damaged skin. It is the commonest premalignant skin lesion. Clinically it presents as rough, scaly, erythematous macules or patches, typically 2–10 mm, on sun-exposed sites such as the bald scalp, face, ears, dorsal hands, forearms, and lower lip. The lesions are often described as "easier felt than seen" because the gritty scale is palpable.
[2] [4]Q2: Pathophysiology (2 min)
Question: What is the key molecular event in AK, and what is field cancerization?
Model answer: The key molecular event is UV-induced DNA damage producing characteristic mutations, most notably in the TP53 tumour-suppressor gene. UV signature mutations (C→T and CC→TT transitions at dipyrimidine sites) inactivate p53, allowing damaged keratinocytes to survive and proliferate. Field cancerization is the presence of multiple independent premalignant clones within a broad area of sun-damaged skin, which explains why patients develop multiple AKs and why field-directed therapy is often required.
[3]Q3: Differential diagnosis (3 min)
Question: How would you distinguish AK from SCC in situ, invasive SCC, and seborrhoeic keratosis?
Model answer:
- SCC in situ (Bowen's disease): Sharply demarcated, persistent, scaly red patch; histology shows full-thickness epidermal atypia without dermal invasion.
- Invasive SCC: Indurated, nodular, or ulcerated plaque; biopsy shows atypical keratinocytes breaching the basement membrane into the dermis.
- Seborrhoeic keratosis: Waxy, "stuck-on" papule or plaque with milia-like cysts and comedo-like openings; not restricted to sun-exposed sites; benign.
Q4: Dermoscopy (2 min)
Question: What is the classic dermoscopic pattern of facial AK?
Model answer: The "strawberry pattern" is the classic dermoscopic finding in non-pigmented facial AK. It consists of an erythematous pseudonetwork (background vessels between follicles), white-yellow surface scale, and white circles surrounding follicular openings. Polymorphic vessels or erosion suggest progression to SCC.
[2]Q5: Management (3 min)
Question: Outline your stepwise approach to managing a patient with multiple AKs on the scalp and a single thickened, indurated lesion.
Model answer:
- Biopsy the thickened, indurated lesion first to exclude invasive SCC.
- For the remaining thin, discrete AKs, use cryotherapy (liquid nitrogen, 5–10 second freeze-thaw).
- For multiple confluent scalp lesions, use field-directed therapy such as topical 5-FU 5% cream for 2–4 weeks, imiquimod 5% 2–3 times weekly for up to 16 weeks, or photodynamic therapy.
- If invasive SCC is confirmed on biopsy, arrange definitive excision.
- Provide sun protection advice and consider nicotinamide 500 mg twice daily for chemoprevention in immunocompetent patients.
Q6: Complications and prognosis (2 min)
Question: What is the risk of malignant progression, and what is the prognosis?
Model answer: The risk of any single AK progressing to invasive SCC is low, though published estimates vary widely; it is clinically significant because patients usually carry multiple lesions within a sun-damaged field. Many AKs remain stable or regress spontaneously. Prognosis is excellent with treatment, but patients require ongoing surveillance because new lesions continue to arise from the field.[3]
References4ShowHide
- [1]Chen AC, Martin AJ, Choy B, et al. A Phase 3 Randomized Trial of Nicotinamide for Skin-Cancer Chemoprevention N Engl J Med, 2015.PMID 26488693
- [2]Zalaudek I, Giacomel J, Argenziano G, et al. Dermoscopy of facial nonpigmented actinic keratosis Br J Dermatol, 2006.PMID 17034524
- [3]Willenbrink TJ, Ruiz ES, Cornejo CM, et al. Field cancerization: Definition, epidemiology, risk factors, and outcomes J Am Acad Dermatol, 2020.PMID 32387665
- [4]Dianzani C, Conforti C, Giuffrida R, et al. Current therapies for actinic keratosis Int J Dermatol, 2020.PMID 32012240