Skin structure

Work down the layers. Staphylococcal scalded skin syndrome, bullous impetigo and pemphigus foliaceus split subcorneally at the granular layer, because all three disable desmoglein 1. Pemphigus vulgaris splits immediately above the basal layer, because it disables desmoglein 3, which predominates deeply and in mucosa. Bullous pemphigoid, linear IgA disease and junctional epidermolysis bullosa split within the lamina lucida. Epidermolysis bullosa acquisita and dystrophic epidermolysis bullosa split below the lamina densa, where the type VII collagen anchoring fibrils are — which is why only these last two heal with scarring and milia.

Pemphigus vulgaris is intraepidermal, so the blister roof is thin: blisters are flaccid, rupture early leaving painful erosions, Nikolsky sign is positive, and painful oral erosions typically come months first. Bullous pemphigoid is subepidermal, so the roof is full-thickness epidermis: blisters are tense, Nikolsky is negative, mucosa is usually spared, the patient is elderly, and weeks of intense itch often precede any blister. Direct immunofluorescence separates them definitively — intercellular IgG and C3 throughout the epidermis in pemphigus, a linear band along the basement membrane in pemphigoid.

Because re-epithelialisation comes from surviving epithelium, and the appendages carry epithelium deep into the dermis. A superficial partial-thickness burn spares the hair follicles, sebaceous glands and sweat glands, so new epidermis spreads outwards from thousands of adnexal islands across the wound and it closes in 7-14 days. A full-thickness burn destroys every one of them, leaving only the wound margin, so the wound can close only by contraction and grafting is mandatory. A deep dermal burn sits between the two: a few deep follicles and sweat coils survive, healing takes more than three weeks, and anything taking longer than three weeks scars hypertrophically — which is the argument for early excision and grafting.

Melanocytes and Merkel cells are both in the stratum basale; Langerhans cells sit mainly in the stratum spinosum. Melanocytes are neural crest derived and supply melanin to about 30-40 keratinocytes each, at a ratio of roughly one melanocyte per ten basal keratinocytes that is the same in every skin colour. Merkel cells are keratinocyte-lineage neuroendocrine cells coupled to an A-beta afferent as the slowly adapting type I mechanoreceptor. Langerhans cells are bone-marrow-derived dendritic cells, CD1a and langerin positive, that carry antigen to the draining node and initiate allergic contact dermatitis.

The eccrine secretory coil produces an isotonic primary secretion, and the duct then reabsorbs sodium through ENaC and chloride through CFTR without reabsorbing water, so normal surface sweat is hypotonic. In cystic fibrosis, CFTR cannot reabsorb chloride, sweat leaves the duct with its salt still in it, and pilocarpine iontophoresis measures a sweat chloride above 60 mmol/L (30-59 mmol/L being intermediate). The same defect explains hyponatraemic, hypochloraemic salt-loss crises in hot weather.

Both are full-thickness losses; the difference is the deepest tissue exposed. In stage 3 the loss extends into the hypodermis so adipose tissue is visible, often with granulation tissue, rolled edges, slough or undermining, but fascia, muscle, tendon, ligament, cartilage and bone are not exposed. In stage 4 one of those deeper structures is exposed or directly palpable, and underlying osteomyelitis should be assumed when bone is reached. If slough or eschar obscures the base so the depth cannot be determined, the injury is unstageable rather than a lower stage.