Medicine chapters
Structure and function of the skin
The layers of the epidermis, dermis and subcutis, the cells in each, the skin appendages and the functions of skin, linked to the diseases that PGET questions use them to explain.
- Skin has three layers: epidermis (stratified squamous, made mostly of keratinocytes), dermis (collagen and elastin) and subcutis (fat).
- The stratum basale divides and renews the epidermis; the stratum corneum provides most of the barrier; filaggrin keeps it hydrated.
- Melanocytes (from neural crest) make pigment, Langerhans cells present antigen, and Merkel cells sense touch.
On this page
Overview
The skin is the largest organ of the body. It has three layers: the epidermis on the outside, the dermis beneath it and the subcutis (subcutaneous fat) at the bottom.
Many skin diseases are best understood as a fault in one part of this structure. Eczema is a barrier fault, psoriasis is a fault of turnover, blistering diseases attack the adhesion proteins, and vitiligo destroys melanocytes. Learn the structure and the diseases make sense.
The epidermis
The epidermis is a stratified squamous epithelium. It has no blood vessels; it is fed by diffusion from the dermis. Its thickness varies with site, from about 0.05 mm (eyelids) to 1.5 mm (palms and soles).
Layers of the epidermis (deep to superficial)
| Layer | What happens there | Exam point |
|---|---|---|
| Stratum basale (basal layer) | Single row of dividing cells; keratinocyte stem cells; melanocytes and Merkel cells sit here | Regenerates the epidermis after superficial injury |
| Stratum spinosum (prickle layer) | Cells joined by many desmosomes (the "prickles") | Target of pemphigus antibodies (desmogleins) |
| Stratum granulosum (granular layer) | Keratohyalin granules; lipids made and secreted to seal the gaps between cells | Lost in psoriasis; thickened in lichen planus |
| Stratum lucidum | Thin clear layer | Seen only in thick skin of palms and soles |
| Stratum corneum (horny layer) | Flat, dead cells without nuclei, packed with keratin | Provides most of the barrier; site of dermatophytes and scabies mites |
A keratinocyte takes roughly 30 days to travel from the basal layer to the surface and be shed. In psoriasis this journey is much faster, so cells reach the surface still carrying nuclei (parakeratosis) and pile up as thick scale.
The stratum basale is the germinative layer. A wound that leaves the basal layer (and hair follicles) intact heals without a scar.
Cells of the epidermis
| Cell | Origin | Function | Related disease |
|---|---|---|---|
| Keratinocyte (most numerous) | Ectoderm | Makes keratin and desmosomal proteins; secretes cytokines and antimicrobial peptides | Psoriasis, eczema, SCC |
| Melanocyte | Neural crest | Makes melanin in melanosomes and passes it to nearby keratinocytes to shield DNA from UV | Vitiligo, albinism, melanoma |
| Langerhans cell | Bone marrow (dendritic cell) | Captures antigen and presents it to T lymphocytes | Allergic contact dermatitis; Langerhans cell histiocytosis |
| Merkel cell | Basal layer | Touch receptor, linked to nerve endings | Merkel cell carcinoma |
Skin colour differences between races are due to the amount and type of melanin made, not the number of melanocytes, which is roughly similar.
Barrier proteins
- Keratins (for example K5 and K14 in basal cells) form the cell skeleton. Faults cause epidermolysis bullosa simplex.
- Desmosomes (with desmogleins 1 and 3 and desmoplakin) hold keratinocytes to each other.
- Filaggrin in the outer layers acts as a natural moisturising factor. Loss-of-function filaggrin mutations give dry, cracked, "leaky" skin and are a major risk factor for atopic eczema, food allergy and ichthyosis vulgaris.
Filaggrin deficiency explains why atopic skin is dry and lets allergens and microbes in. That is why emollients are the base of eczema treatment.
The basement membrane zone (dermo-epidermal junction)
This thin protein layer anchors the epidermis to the dermis. From top to bottom: basal cell hemidesmosomes (with BP180 and BP230), the lamina lucida, the lamina densa (type IV collagen) and anchoring fibrils (type VII collagen).
The level of the target protein decides where a blister forms:
| Target | Level of split | Disease |
|---|---|---|
| Desmogleins 1 and 3 | Within the epidermis | Pemphigus vulgaris (flaccid blisters) |
| BP180 and BP230 (hemidesmosome) | Below the epidermis | Bullous pemphigoid (tense blisters) |
| Type VII collagen | Below the lamina densa | Dystrophic epidermolysis bullosa, EB acquisita |
| Keratins 5 and 14 | Basal keratinocytes | Epidermolysis bullosa simplex |
Pemphigus = "in" the epidermis, so the roof is thin and the blister bursts. Pemphigoid = below it, so the roof is thick and the blister stays tense.
The dermis
The dermis is a tough layer of collagen (strength) and elastin (recoil) fibres in a gel-like ground substance.
- Papillary dermis (upper): thin, with finger-like papillae that interlock with the epidermal rete ridges; contains capillary loops.
- Reticular dermis (lower): thicker and denser collagen.
- Resident cells: fibroblasts make collagen; mast cells, lymphocytes and dendritic cells guard against invaders.
- Also contains blood vessels, lymphatics, nerves, the arrector pili muscle and the appendages.
Mast cell degranulation in the dermis releases histamine and causes the weal of urticaria.
Skin appendages
| Structure | Where | Key facts |
|---|---|---|
| Eccrine sweat glands | All over the skin (not mucosa) | Temperature control by sweating; supplied by sympathetic cholinergic nerves |
| Apocrine sweat glands | Axillae and anogenital area | Inactive until puberty; affected in hidradenitis suppurativa |
| Sebaceous glands | Densest on face, scalp, upper chest and back; open into the hair follicle | Inactive until puberty; make sebum under androgen control; central to acne |
| Hair follicles | All skin except palms, soles and mucosa | Stem cells in the bulb; damage to them causes scarring (permanent) hair loss |
| Nails | Fingers and toes | Hard keratin; fingernail grows out in about 6 months, toenail in about 1 year |
The hair cycle
- Anagen (growth): more than 90% of scalp hairs at any time; lasts about 3–5 years on the scalp.
- Catagen (involution): short transition.
- Telogen (resting and shedding).
In telogen effluvium, a large group of hairs is pushed into telogen together by a stress (childbirth, severe illness), so diffuse shedding starts 2–3 months later, not immediately.
The subcutis
Lobules of fat divided by fibrous septa. It insulates, cushions against trauma and stores energy. Inflammation here is panniculitis; the commonest example is erythema nodosum.
Functions of the skin
- Mechanical barrier that resists friction, shearing and trauma.
- Chemical and UV protection (melanin absorbs UV).
- Defence against infection: intact keratin layer, acidic surface, sebum, antimicrobial peptides, normal skin flora and Langerhans cells.
- Prevents water loss (and excess absorption). Loss of skin in burns or toxic epidermal necrolysis causes fluid loss, hypothermia and sepsis.
- Temperature regulation by sweating and changes in skin blood flow.
- Vitamin D synthesis: UVB converts 7-dehydrocholesterol to vitamin D3.
- Sensation: touch, pain, itch, pressure, vibration and temperature.
- Wound healing and immune surveillance.
When the whole skin fails (erythroderma, extensive TEN), patients die of the same problems as a large burn: dehydration, hypothermia, high-output heart failure and infection. This is called acute skin failure.
Describing skin lesions
PGET stems use these words, so learn them exactly.
| Term | Meaning |
|---|---|
| Macule | Flat, non-palpable colour change (a large one is a patch) |
| Papule | Small raised, palpable lesion (standard cut-off under about 1 cm) |
| Nodule | Larger, deeper solid lump |
| Plaque | Raised, flat-topped lesion wider than it is high |
| Vesicle | Small fluid-filled blister |
| Bulla | Large fluid-filled blister (standard cut-off over about 0.5 cm) |
| Pustule | Blister containing pus |
| Weal | Smooth, itchy, short-lived swelling from dermal oedema (urticaria) |
| Lichenification | Thickened skin with exaggerated skin lines from chronic rubbing |
| Excoriation | Scratch mark |
| Purpura / petechiae | Bleeding into skin that does not blanch on pressure |
| Ulcer | Loss of the full epidermis and some dermis |
Useful clinical signs
- Köbner phenomenon: lesions appear at sites of trauma (psoriasis, lichen planus, vitiligo, viral warts, molluscum).
- Nikolsky sign: gentle sideways pressure shears off the epidermis (pemphigus vulgaris, TEN, staphylococcal scalded skin).
- Darier sign: rubbing a lesion makes it urticate (urticaria pigmentosa).
- Diascopy: pressing a glass slide shows "apple jelly" nodules of lupus vulgaris.
- Wood's lamp (UVA): coral-pink in erythrasma, green fluorescence in some Microsporum scalp ringworm, and sharper edges in vitiligo.
Common investigations
- Skin scrapings, hair and nail clippings for fungal microscopy (KOH) and culture.
- Bacterial and viral swabs.
- Skin biopsy (punch, shave or excision) for histology.
- Direct immunofluorescence of skin next to a blister and indirect immunofluorescence of serum in suspected immunobullous disease.
- Patch testing for allergic contact dermatitis (type IV); skin prick tests and specific IgE for immediate (type I) allergy.
Expect: the order and role of the epidermal layers, which layer regenerates skin, which layer forms the barrier, the origin and job of melanocytes and Langerhans cells, filaggrin and atopic eczema, the basement membrane proteins and the level of split in pemphigus versus pemphigoid, the glands that switch on at puberty, the phases of the hair cycle, functions of skin (especially vitamin D and temperature control), and definitions of primary lesions and signs such as Köbner and Nikolsky.
Quick revision
- Three layers: epidermis, dermis, subcutis.
- Epidermis deep to surface: basale, spinosum, granulosum, (lucidum on palms and soles), corneum.
- Basal layer regenerates; corneum is the barrier.
- Melanocytes from neural crest; Langerhans cells present antigen; Merkel cells sense touch.
- Filaggrin mutation: atopic eczema and ichthyosis vulgaris.
- Desmoglein = pemphigus (intraepidermal); BP180/BP230 = pemphigoid (subepidermal).
- Sebaceous and apocrine glands switch on at puberty; sebum is androgen-driven.
- Anagen over 90% of scalp hair; telogen effluvium appears 2–3 months after a stress.
- Skin makes vitamin D3 from 7-dehydrocholesterol under UVB.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
Which layer of the epidermis forms the main barrier?
The stratum corneum, the outer layer of dead keratin-filled cells sealed with lipids.
Where are melanocytes found and where do they come from?
They sit in the basal layer of the epidermis and are derived from the neural crest.
What are Langerhans cells?
Dendritic cells in the epidermis that pick up antigens and present them to T cells; they drive allergic contact dermatitis.
Why does atopic eczema skin become dry?
Many patients carry loss-of-function filaggrin mutations, so the outer layer cannot hold water and the barrier leaks.
Why do pemphigus blisters burst while pemphigoid blisters stay tense?
Pemphigus splits within the epidermis, giving a thin roof, while pemphigoid splits below it, giving a thick roof.