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PA33.1-4 | Skin — PBL Case

CLINICAL SETTING

Meenakshi Rajan, a 44-year-old schoolteacher from Madurai, Tamil Nadu, comes to the dermatology outpatient clinic of the district government hospital with her husband. She is self-conscious about a pigmented lesion on her right upper arm that she has had 'all her life' — but she says it has been 'changing' over the past four months. She grew up in a farming family and spent many years outdoors before taking up teaching. She has moderately fair skin for the region (Fitzpatrick skin type III) and no family history of skin cancer. She does not use sunscreen regularly. She is otherwise well, with no weight loss, fever, or systemic symptoms. The dermatologist examines the lesion and notes it is approximately 14 mm in diameter, with a notched and irregular border, variegated colour (areas of tan, dark brown, and a small zone of pink), and slight asymmetry. Alongside it are two smaller flat brown lesions, each uniformly coloured, well-bordered, and less than 5 mm. On the dorsum of her right hand, the dermatologist also notes a rough, scaly, erythematous plaque approximately 8 mm in diameter at the base of the thumb — an area of maximum sun exposure.

Trigger 1: The Changing Lesion

The dermatologist applies the ABCDE assessment systematically to the three lesions on the arm. He documents: Lesion 1 (14 mm, upper arm) — Asymmetric: YES, Border: Irregular/notched: YES, Colour: Variegated tan-dark-brown-pink: YES, Diameter: 14 mm (>6 mm): YES, Evolution: Changing over 4 months: YES. Lesion 2 and Lesion 3 (both <5 mm, flat, uniform): all ABCDE criteria: NO. The rough dorsal hand plaque is described separately as an 8 mm erythematous, hyperkeratotic plaque with fine scale, tender on scraping. The dermatologist decides to refer Lesion 1 for urgent biopsy.

DISCUSSION POINTS

  • Apply the ABCDE framework systematically. Why does Lesion 1 score positive on all five criteria while Lesions 2 and 3 do not? What is the significance of 'E' (evolution) as the single most clinically actionable criterion in a patient who presents with a lesion she has had 'all her life'?
  • The rough, hyperkeratotic dorsal hand plaque is suspicious for a premalignant lesion. Name this lesion, describe its histological features (focusing on which epidermal layers show atypia and what the dermis shows), and explain the molecular mechanism by which chronic ultraviolet exposure drives progression to invasive carcinoma.
  • Meenakshi has three melanocytic lesions. Using your knowledge of the junctional, compound, and intradermal classification of benign melanocytic naevi, predict which type Lesions 2 and 3 most likely represent based on their clinical appearance, and contrast the microscopic appearance of a benign naevus with the early changes expected in Lesion 1.
  • The dermatologist is deciding between an excision biopsy, a punch biopsy, and a shave biopsy for Lesion 1. Explain why the choice of biopsy technique is critical for this type of lesion, with specific reference to the single most important prognostic measurement that must not be compromised.
Click to reveal Trigger 2: The Biopsy Report (discuss previous trigger first!)

Trigger 2: The Biopsy Report

The excision biopsy report of Lesion 1 is received one week later. The pathologist writes: 'Sections show a 13 mm melanocytic proliferation. The epidermis shows atypical melanocytes spreading along the basal layer and into the upper epidermis (pagetoid spread), with evidence of early invasion into the papillary dermis. Breslow thickness: 0.85 mm. Clark Level III. No ulceration. Mitotic rate: 1/mm². No satellite lesions. Excision margins: clear by 1 mm radially. No regression zones.' Sentinel lymph node biopsy is planned. The pathologist also separately notes regarding the dorsal hand plaque biopsy: 'Full-thickness atypia of the squamous epithelium with preservation of the basement membrane.'

DISCUSSION POINTS

  • The pathologist reports pagetoid spread and early dermal invasion. Define pagetoid spread, identify which growth phase this histology represents, and explain the transition from radial to vertical growth phase in terms of tumour biology — why does vertical growth phase herald a dramatically worse prognosis?
  • The Breslow thickness is 0.85 mm. Explain what this measurement represents, why it is the primary prognostic determinant for thin melanomas, and how it determines T-stage in the AJCC staging system. How would the prognosis change if the Breslow thickness were 2.5 mm with ulceration?
  • The dorsal hand plaque biopsy shows 'full-thickness atypia with preservation of the basement membrane.' What is this lesion (give the specific eponym for full-thickness intraepidermal SCC), and what distinguishes it from actinic keratosis histologically? What is the risk of progression to invasive SCC?
  • Sentinel lymph node biopsy is planned. Explain the anatomical and pathophysiological basis for this procedure in melanoma staging. If the sentinel node is positive, how does this change staging, prognosis, and management compared to a node-negative result?
Click to reveal Trigger 3: A New Patient in the Same Clinic (discuss previous trigger first!)

Trigger 3: A New Patient in the Same Clinic

While Meenakshi's results are being discussed, the tutor draws the group's attention to the next patient: Mr. Krishnamurthy, a 70-year-old retired postal worker presenting with two facial lesions. Lesion A (inner canthus of left eye, 1 cm) is a pearly, translucent papule with rolled telangiectatic edges and a central ulcer. Lesion B (right cheek, 1.5 cm) has raised, irregular, everted edges and an ulcerated centre with surrounding induration; a small satellite cervical lymph node is palpable. The tutor also displays a histology slide of a benign lesion from a 62-year-old patient — a warty, 'stuck-on' plaque from the trunk with pseudohorn cysts and a basaloid proliferation pattern on microscopy.

DISCUSSION POINTS

  • Lesion A (pearly rolled nodule, inner canthus) and Lesion B (everted edges, satellite node, sun-damaged cheek) represent two distinct skin cancers with very different natural histories. Identify each, describe the key histological feature that distinguishes them, and explain why Lesion A 'almost never metastasises' while Lesion B has significant metastatic potential.
  • Explain the molecular pathogenesis of Lesion A. What signalling pathway is constitutively activated, what gene is mutated, and why does UV radiation cause this specific mutation? How does this differ from the BRAF V600E pathway that drives the majority of melanomas?
  • For Lesion B (SCC), identify at least four risk factors that increase the probability of metastasis beyond the baseline rate of 5–10%. Which specific clinical sub-type of SCC arising in chronic scars or ulcers carries a particularly aggressive course and what is its eponym?
  • The histology slide of the benign trunk lesion shows pseudohorn cysts and basaloid proliferation in a 'stuck-on' pattern. Name this lesion, state its origin, confirm that it has no malignant potential, and identify the rare paraneoplastic syndrome in which a sudden eruption of multiple such lesions signals an occult visceral malignancy.

Group Task Assignments

Group 1: ABCDE and biopsy technique

  • Prepare a structured one-page clinical decision tool (formatted for use in a PHC or district hospital setting) that guides a non-specialist to correctly apply the ABCDE criteria and decide when to refer versus watch.
  • Summarise in a table the three biopsy techniques (excision, punch, shave) for suspected melanoma: indication, advantage, critical disadvantage, and which one should NEVER be used for a lesion where Breslow thickness is the key measurement.

Competencies: PA33.3, PA33.4

Group 2: Melanoma pathogenesis and staging

  • Draw a flowchart of melanoma pathogenesis from chronic UV exposure to BRAF V600E mutation to uncontrolled MAPK signalling to vertical growth phase invasion, labelling each molecular step.
  • Construct a Breslow thickness staging table with the corresponding T-stage, 5-year survival estimate, and recommended surgical margin for each tier. Mark Meenakshi's lesion on the table.

Competencies: PA33.3

Group 3: BCC vs SCC — distinguish and compare

  • Using Mr. Krishnamurthy's two lesions as the anchor, create a comparison table for BCC and SCC covering: cell of origin, carcinogenic pathway (key mutation), macroscopic appearance, histological hallmark, metastatic potential, and prognosis.
  • Identify and describe the two histological features unique to BCC (peripheral palisading + retraction clefts) and the two unique to SCC (keratin pearls + intercellular bridges) using annotated sketch diagrams.

Competencies: PA33.1, PA33.2

Group 4: Skin tumour morphology identification

  • Using the master recognition table from SDL2, prepare a rapid identification card for the practical exam listing seven skin tumours (seborrheic keratosis, dermatofibroma, BCC, SCC, actinic keratosis, Bowen disease, melanoma) with the one or two histological features that make each unmistakable.
  • For each tumour on the card, state whether a biopsy is mandatory, optional (if growing/changing), or not required (entirely benign), with a brief justification for the clinical decision.

Competencies: PA33.4

Learning Issues

Research these questions and bring your findings to the discussion.

  1. [PA33.1] What are the risk factors and molecular mechanisms (UV → TP53 mutation → keratinocyte atypia) that drive the progression from normal skin to actinic keratosis to invasive squamous cell carcinoma? What is Marjolin's ulcer, how does it differ from UV-induced SCC in biological behaviour, and which risk factors predict metastasis?
  2. [PA33.2] What is the cell of origin, molecular pathway (UV → PTCH1 loss → constitutive Hedgehog signalling), macroscopic subtypes, and histological hallmarks (peripheral palisading, retraction clefts) of basal cell carcinoma? Why does BCC almost never metastasise despite being locally destructive?
  3. [PA33.3] What are the distinguishing clinical and histological features between a benign melanocytic naevus and melanoma? Describe the ABCDE criteria, molecular pathogenesis (UV → BRAF V600E → MAPK cascade), radial vs vertical growth phases, Breslow thickness measurement, Clark levels, routes of metastasis, and the five-year survival impact of staging. What is the single most important prognostic factor in primary melanoma?
  4. [PA33.4] What are the clinical and histological features that allow identification of seborrheic keratosis (pseudohorn cysts, basaloid cells, stuck-on appearance), dermatofibroma (spindle fibroblasts, collagen entrapment, Fitzpatrick sign), actinic keratosis (basal layer atypia, solar elastosis), and Bowen disease (full-thickness intraepidermal atypia, basement membrane intact) as distinct entities? Which are premalignant and require follow-up?