Dermatology

A disorder of the pilosebaceous unit in which follicular hyperkeratinisation blocks the pore, androgen-driven sebum feeds Cutibacterium acnes, and the resulting inflammation produces comedones, papules, pustules and, in severe disease, scarring.

A defective skin barrier, often driven by filaggrin deficiency, lets water escape and irritants and allergens penetrate, triggering a Th2 immune response, so treatment restores the barrier first and calms the inflammation second.

Dermatophyte fungi digest keratin in the stratum corneum and spread outward as they consume it, producing a scaly lesion with an actively advancing, inflamed edge and a clearing centre, the ring that gives ringworm its name.

A malignant proliferation of melanocytes that, unlike a benign naevus, grows asymmetrically and eventually invades vertically into the dermis, and it is the depth of that invasion at diagnosis, the Breslow thickness, that is the single strongest predictor of survival.

Basal cell carcinoma and squamous cell carcinoma both arise from UV-driven DNA damage to epidermal keratinocytes, but their different cell of origin means BCC grows slowly and almost never metastasises while SCC can invade and spread, a distinction that dictates how urgently each is referred.

A chronic immune-mediated disease in which a self-sustaining T-cell/keratinocyte loop drives massive epidermal overproliferation, producing well-demarcated scaly plaques that respond to therapies aimed at that loop.

Mast-cell degranulation releases histamine into the superficial dermis, causing local vasodilation and fluid leak that produce short-lived, itchy, blanching weals: the same mechanism that, in deeper tissue or on a larger scale, becomes angioedema or anaphylaxis.