Skin Anatomy Lab

Fifteen to twenty layers of anucleate corneocytes, flattened and packed in a lipid matrix of ceramides, cholesterol and fatty acids. It is shed continuously as invisible scale and renewed from below about every two weeks.

Visible scale is stratum corneum shed too fast or held too long. Barrier failure underlies atopic dermatitis and irritant contact dermatitis; a subcorneal split is the blister of impetigo.

Psoriasis Atopic dermatitis Impetigo Pityriasis versicolor

Keratinocytes here fill with keratohyalin granules (profilaggrin, which becomes filaggrin) and lamellar bodies that pour lipid into the intercellular space above, building the barrier of the stratum corneum.

Filaggrin loss-of-function mutations weaken the barrier and predispose to atopic dermatitis and ichthyosis vulgaris. The granular layer is lost under a psoriatic plaque, one of its histological signatures.

Atopic dermatitis Psoriasis

Five to ten layers of keratinocytes maturing upward, held to one another by desmosomes that appear as spines on a slide. Langerhans cells sit among them.

Pemphigus vulgaris is an autoantibody against desmoglein 3, the desmosome protein, so the cells fall apart here (acantholysis): flaccid blisters and a positive Nikolsky sign. Squamous cell carcinoma arises from these cells.

Pemphigus vulgaris Squamous cell carcinoma Actinic keratosis

A single layer of columnar keratinocytes anchored to the basement membrane by hemidesmosomes. Their divisions supply every cell above; the journey to the surface takes about four weeks.

Basal cell carcinoma, the commonest cancer of all, arises from these cells. Vitiligo and post-inflammatory pigment change are read at this level, where the melanocytes sit.

Basal cell carcinoma Vitiligo Melasma

Born in the basal layer, a keratinocyte differentiates as it moves up: it makes keratin filaments, forms desmosomes, fills with granules, loses its nucleus and finally flakes away. It also signals: cytokines from keratinocytes drive much of inflammation in the skin.

Psoriasis is keratinocytes cycling in days instead of weeks. Viral warts are keratinocytes hijacked by HPV; molluscum by a poxvirus. Sunburn is keratinocyte apoptosis.

Psoriasis Viral warts Molluscum contagiosum Actinic keratosis

Neural crest cells seated among the basal keratinocytes, about one in ten cells there, each sending dendrites up to some thirty-six keratinocytes and handing them melanosomes. Skin colour is decided by how much melanin they make and how it is packaged, not by how many there are.

Melanoma is their malignancy; naevi are their benign nests. Vitiligo is their loss, melasma their overactivity, and post-inflammatory hyperpigmentation their response to injury, which is why skin tone changes how every rash looks.

Melanoma Vitiligo Melasma Seborrheic keratosis

The dermo-epidermal junction: hemidesmosomes, the lamina lucida, the lamina densa of type IV collagen, and anchoring fibrils of type VII collagen hooking into the dermis. It undulates as rete ridges and dermal papillae, which interlock the layers and bring capillaries close to the surface.

Bullous pemphigoid is an autoantibody against its hemidesmosome proteins (BP180, BP230): tense blisters, because the whole epidermis lifts as a roof. Lichen planus attacks the basal layer along it. Epidermolysis bullosa is an inherited weakness of one of its parts.

Bullous pemphigoid Lichen planus Cutaneous lupus erythematosus

The thin upper dermis that fills the dermal papillae: fine collagen and elastic fibres, the capillary loops, free nerve endings and Meissner corpuscles. It is the busiest part of the dermis.

Urticaria is oedema here, which is why a wheal is pale and evanescent. The perivascular infiltrate of most rashes sits here. Melanoma is staged by how far below this it reaches.

Urticaria Melanoma Lichen planus

The bulk of the dermis: coarse bundles of type I collagen woven with elastic fibres, fibroblasts between them, and the adnexa, deep vessels and nerves running through. It gives the skin its tensile strength and recoil.

Scars and keloids are reticular dermis repaired badly. Morphoea and systemic sclerosis thicken it; striae are its tears. Photoageing is elastic fibre degeneration here (solar elastosis).

Keloids & hypertrophic scars Stasis dermatitis

Made by fibroblasts and laid down as wavy bundles that straighten under load. Type III predominates in the papillary dermis and in new scar; type I in the reticular dermis. They turn over slowly, over years.

Wound healing is collagen laid down in a hurry. Ehlers-Danlos syndromes are its faults: hyperextensible skin and poor scars. Steroid atrophy is its loss.

Keloids & hypertrophic scars

A network of elastin cored fibres, finest in the papillary dermis (oxytalan) and thickest in the reticular dermis, that returns the skin to shape after it is stretched.

Sun damage degrades them into the amorphous clumps of solar elastosis, the yellow, wrinkled skin of the neck and face. Cutis laxa and pseudoxanthoma elasticum are elastic fibre diseases.

Actinic keratosis

Spindle-shaped cells scattered between the bundles, synthesising collagen, elastin and ground substance, and remodelling them after injury. Activated, they become myofibroblasts that contract a wound.

Keloids and hypertrophic scars are fibroblasts that do not stop. Dermatofibroma is a benign fibroblastic nodule; dermatofibrosarcoma protuberans its rare malignant cousin.

Keloids & hypertrophic scars

Cuticle, cortex and medulla of hard keratin, pigmented by melanocytes in the bulb. It leaves the skin through the infundibulum, the funnel-shaped top of the follicle that the epidermis lines.

Hair breakage and shaft disorders are read here. A comedone is the infundibulum plugged with keratin and sebum; folliculitis is its inflammation.

Acne vulgaris Furuncles, carbuncles & cutaneous abscess

An invagination of epidermis into the dermis: infundibulum, isthmus (where the sebaceous duct and arrector pili attach, and where the stem cells of the bulge live), and the lower segment ending in the bulb. It cycles: anagen growth for years, catagen regression, telogen rest.

Alopecia areata attacks the anagen bulb; androgenetic alopecia miniaturises the follicle; scarring alopecias destroy the bulge. Acne, folliculitis, furuncles and hidradenitis are follicular diseases.

Acne vulgaris Furuncles, carbuncles & cutaneous abscess Rosacea

The swollen base of the follicle, where matrix keratinocytes divide fastest of any cell in the body and melanocytes pigment the growing shaft, all fed by the dermal papilla, a knot of vessels and specialised fibroblasts that instructs the cycle.

Chemotherapy and telogen effluvium act on the matrix. Alopecia areata's lymphocytes surround the bulb like a swarm of bees. Grey hair is the bulb's melanocytes retiring.

A band of smooth muscle attached to the follicle at the bulge and inserting just under the epidermis. Sympathetic stimulation contracts it, raising the hair and dimpling the skin: piloerection.

Keratosis pilaris and the follicular papules of pityriasis rubra pilaris are read at the follicular opening it pulls on. Piloerection in a cold, frightened or withdrawing patient is a sympathetic sign.

Pityriasis rubra pilaris

Lobules of lipid-laden cells that disintegrate whole to release sebum into the follicle's isthmus. Largest and densest on the face, chest and back, and switched on by androgens at puberty.

Acne is the pilosebaceous unit: excess sebum, a plugged infundibulum, Cutibacterium and inflammation. Seborrhoeic dermatitis follows the sebaceous areas. Sebaceous hyperplasia and rhinophyma are its overgrowth.

Acne vulgaris Seborrheic dermatitis Rosacea Perioral dermatitis

Two to four million of them, all over the body, each a tight coil of secretory cells at the dermal-subcutaneous junction under cholinergic sympathetic control. Their sweat is water, salt and little else, and it cools by evaporating.

Hyperhidrosis is their overdrive; anhidrosis after nerve injury or in some ectodermal dysplasias risks heat stroke. Neutrophilic eccrine hidradenitis is a chemotherapy reaction here.

A straight duct climbs from the coil, then corkscrews through the epidermis as the acrosyringium to open on the surface as a sweat pore, independent of any hair follicle.

Miliaria (heat rash) is this duct blocked at different levels: crystallina in the stratum corneum, rubra in the epidermis, profunda at the dermis. Syringomas are benign tumours of it.

The epidermis has no vessels of its own; each papilla carries a capillary loop from the superficial plexus that feeds it by diffusion across the basement membrane.

These loops dilate and tortuous under a psoriatic plaque, which is why scraping it bleeds in pinpoints (Auspitz sign). Dermoscopy reads their patterns: dotted, hairpin, arborising.

Psoriasis Basal cell carcinoma

Arterioles, capillaries and postcapillary venules running horizontally just under the papillae. Its venules are where leucocytes leave the blood in inflammation, so most rashes begin around it.

Erythema is this plexus dilated; blanching on pressure proves the blood is still inside it. Purpura and petechiae are blood outside it. Urticaria, morbilliform drug eruptions and vasculitis are its diseases.

Urticaria Morbilliform drug eruption Cutaneous small-vessel vasculitis Rosacea

Arteries and veins at the dermal-subcutaneous junction that feed the hair bulbs and sweat coils and send branches up to the superficial plexus. Arteriovenous shunts here regulate heat loss.

Livedo reticularis is this plexus seen through the skin when flow slows. Deep vasculitis (polyarteritis nodosa) and cellulitis involve it; stasis dermatitis follows venous hypertension in it.

Cellulitis Stasis dermatitis Cutaneous small-vessel vasculitis

Blind-ended capillaries in the papillary dermis collect interstitial fluid and carry it, with Langerhans cells and their antigens, through deeper collecting vessels to the regional nodes.

Lymphangitis is the red streak toward the node in a spreading infection. Lymphoedema follows their loss. Melanoma spreads along them to the sentinel node.

Cellulitis Melanoma

Oval cells in the basal layer, densest on the fingertips and lips, each in contact with a nerve terminal. Together they form the slowly adapting receptor for fine touch and edges.

Merkel cell carcinoma is a rare, aggressive tumour of sun-exposed skin in older people, often a fast-growing painless red nodule.

Sensory and autonomic fibres enter with the deep vessels, branch through the reticular dermis and end in receptors or as free endings. Each dermatome is one spinal nerve's territory.

Herpes zoster travels down these fibres from a dorsal root ganglion, which is why it stops at the midline; postherpetic neuralgia is their injury. Leprosy thickens them and numbs their territory.

Herpes zoster

Unmyelinated C fibres and thin A-delta fibres that lose their sheath in the papillary dermis and run up between the keratinocytes. Itch has its own dedicated C fibres, driven by histamine and by non-histamine pathways.

Itch begins here, in eczema, urticaria, scabies and lichen simplex, and scratching feeds it back. Neuropathic itch and pain follow their damage.

Atopic dermatitis Scabies Lichen simplex chronicus Urticaria

Stacked lamellae of Schwann cells around a coiled nerve ending, sitting in the dermal papillae of glabrous skin, densest on the fingertips. A rapidly adapting receptor for light touch and low-frequency vibration.

Their loss underlies the impaired fine touch of peripheral neuropathy, tested at the fingertips.

The largest receptor, up to a millimetre across: dozens of concentric lamellae round a single nerve ending, in the deep dermis and subcutis of the palms, soles and joints. Rapidly adapting, tuned to vibration.

Vibration sense, tested with a tuning fork, is the first modality lost in many neuropathies, including diabetic neuropathy of the feet.

Bone-marrow-derived dendritic cells that patrol the spinous layer, catch antigens that cross the barrier and carry them to the lymph node to start an immune response.

Allergic contact dermatitis is a Langerhans cell presenting nickel or urushiol to T cells; the rash arrives a day or two later. Ultraviolet light depletes them, part of why the sun suppresses skin immunity.

Contact dermatitis

Resident cells clustered round the superficial plexus and nerves, their granules full of histamine, tryptase and heparin, released when IgE on their surface is cross-linked or by direct triggers.

Urticaria and angio-oedema are mast cell degranulation: wheals within minutes, gone within a day. Urticaria pigmentosa is mast cells in excess (Darier's sign). Antihistamines act one step downstream.

Urticaria

Skin-resident memory T cells and recruits from the blood that leave the postcapillary venules of the superficial plexus. Most inflammatory dermatoses are, under the microscope, a lymphocyte infiltrate somewhere specific.

Psoriasis (Th17), atopic dermatitis (Th2), lichen planus (cytotoxic T cells at the basal layer) and drug eruptions are T cell diseases. Mycosis fungoides is a lymphoma of these cells, living in the epidermis.

Psoriasis Atopic dermatitis Lichen planus Mycosis fungoides & cutaneous T-cell lymphoma DRESS (drug hypersensitivity syndrome)

The subcutis is mostly adipocytes packed in lobules, each cell a single lipid droplet. It insulates, cushions, stores energy and, as an endocrine organ, secretes leptin and adiponectin.

Lobular panniculitis inflames the fat itself (pancreatic panniculitis, lupus profundus). Lipomas are benign lobules run wild. Insulin and steroid injections leave lipoatrophy or lipohypertrophy here.

Erythema nodosum

Sheets of collagen that partition the fat into lobules and tether the dermis to the fascia beneath; the larger vessels and nerves travel in them.

Erythema nodosum is a septal panniculitis: tender red nodules on the shins, the septa inflamed and the lobules spared. Cellulite is fat lobules pushing between tethering septa.

Erythema nodosum

Perforating arteries from the fascia branch in the septa and rise to form the deep plexus; veins and lymphatics return the same way; cutaneous nerves enter alongside.

Necrotising fasciitis spreads along the fascia beneath and thromboses these vessels, which is why the skin above looks deceptively normal until it dies. Deep vein thrombosis and venous insufficiency present through them.

Necrotizing fasciitis Stasis dermatitis