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Skin tumours flashcards

15 high-yield MRCP Part 1 cards from the Intellect Medicos Dermatology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. What is the single most important prognostic factor in primary malignant melanoma?

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    Breslow thickness (depth of invasion in mm).

    Why? Deeper tumours are more likely to metastasise.

  2. What is the initial diagnostic step for a suspected melanoma in secondary care?

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    Excision biopsy with a narrow (about 2 mm) clinical margin for histology; wide local excision follows, guided by Breslow thickness.

    Why? Full-thickness histology gives the Breslow depth, which determines the final excision margin and staging.

  3. What is the mechanism of action of vemurafenib in metastatic melanoma?

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    BRAF kinase inhibitor (used in BRAF V600-mutated melanoma).

    Why? About half of melanomas carry an activating BRAF mutation driving the MAPK pathway.

  4. Ipilimumab, used in advanced melanoma, blocks which molecule?

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    CTLA-4 (an immune checkpoint on T cells).

    Why? Blocking this checkpoint releases the brake on T-cell activation against the tumour.

  5. The commonest subtype of malignant melanoma is ______ melanoma.

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    superficial spreading

    Why? It accounts for about 70% of cases. Nodular melanoma is the second commonest; it grows vertically early, so it is often thick at diagnosis and carries a poorer prognosis.

  6. How is a suspected basal cell carcinoma managed?

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    Refer for surgical excision — usually a non-urgent (routine) referral, not the suspected cancer pathway.

    Why? BCC is the commonest skin cancer; it grows slowly and very rarely metastasises.

  7. What is the first-line treatment for a single localised actinic keratosis?

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    Cryotherapy.

    Why? Actinic keratoses are premalignant sun-damage lesions that can progress to SCC.

  8. Which skin cancer shows the greatest increase in incidence in organ transplant recipients?

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    Cutaneous squamous cell carcinoma.

    Why? Long-term immunosuppression (e.g. azathioprine, ciclosporin) raises SCC risk many-fold, so these patients need sun protection and regular skin surveillance.

  9. How should a suspected cutaneous squamous cell carcinoma be referred from primary care?

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    Consider a suspected cancer pathway (urgent) referral, aiming for cancer to be diagnosed or ruled out within 28 days.

    Why? SCC can metastasise, unlike most BCCs (usually a non-urgent referral). Definitive treatment is surgical excision; Mohs surgery for cosmetically important sites.

  10. Pigment spreading from a longitudinal nail streak onto the proximal nail fold (Hutchinson's sign) suggests which diagnosis?

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    Subungual (acral lentiginous) melanoma.

    Why? Acral lentiginous melanoma affects palms, soles and nail beds, is not related to sun exposure, and is the commonest subtype in people with darker skin.

  11. What is the classic triad of Sézary syndrome?

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    Erythroderma, generalised lymphadenopathy and circulating Sézary cells (atypical T cells with cerebriform nuclei).

    Why? It is the leukaemic form of cutaneous T-cell lymphoma. Mycosis fungoides, the commonest CTCL, is a CD4+ T-cell lymphoma that starts as itchy eczema-like patches.

  12. Which two characteristic skin adverse effects occur with BRAF inhibitors such as vemurafenib?

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    Photosensitivity and new cutaneous squamous cell carcinomas/keratoacanthomas.

    Why? BRAF inhibition paradoxically activates the MAPK pathway in BRAF wild-type keratinocytes, driving new squamous tumours; regular skin checks are needed. Adding a MEK inhibitor reduces this.

  13. What is the mechanism of action of pembrolizumab and nivolumab in advanced melanoma?

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    Monoclonal antibodies against PD-1 (programmed cell death protein 1), an immune checkpoint on T cells.

    Why? Blocking PD-1 stops tumour PD-L1 from switching T cells off. Immune-related adverse effects include colitis, hepatitis, pneumonitis and endocrinopathies (thyroiditis, hypophysitis).

  14. Topical 5-fluorouracil, used for multiple actinic keratoses, inhibits ______; imiquimod is an immune response modifier that acts as a toll-like receptor 7 (TLR7) agonist.

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    thymidylate synthase

    Why? Both cause an expected local inflammatory reaction (redness, crusting, soreness) during treatment; warn patients in advance.

  15. Topical 5-fluorouracil, used for multiple actinic keratoses, inhibits thymidylate synthase; imiquimod is an immune response modifier that acts as a ______.

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    toll-like receptor 7 (TLR7) agonist

    Why? Both cause an expected local inflammatory reaction (redness, crusting, soreness) during treatment; warn patients in advance.

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