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Nail Clubbing — SCE Dermatology MCQ

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HardNail DisordersNail ClubbingSCE Dermatology

A patient with an intrathoracic malignancy develops new bilateral clubbing. Which mechanism most plausibly links the thoracic disorder to nail-bed enlargement?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: DVEGF and prostaglandin-E2 signalling drives distal fibrovascular tissue expansion

Explanation lettering: C = shown as B · D = shown as C · B = shown as D

B is correct. The prevailing model proposes that megakaryocytes and platelet clumps escape normal fragmentation in the pulmonary circulation, reach distal digital vessels and release mediators including platelet-derived growth factor and VEGF; increased PGE2 signalling also contributes. Vascular permeability and fibroblast proliferation expand the nail bed, increase fluctuation and abolish the normal Lovibond angle. Hypoxaemia alone is insufficient to explain the range of associated pulmonary, cardiac, hepatic and gastrointestinal conditions. Melanocytes cause pigmentation, dermatophytes cause onychomycosis, and matrix-destructive inflammation produces dystrophy rather than symmetrical bulbous enlargement.

Reference: GatewayC finger-clubbing clinical resource: https://www.gatewayc.org.uk/cancer-keys/finger-clubbing-an-easily-forgotten-red-flag/