Anatomy and Physiology of the Skin
Layers you will be tested on
The epidermis, from deep to superficial, is basale (stratum germinativum), spinosum, granulosum, and corneum, with the lucidum sometimes listed for thick skin. Keratinocytes are born in the basal layer and migrate upward; turnover averages roughly four weeks and slows with age. Melanocytes sit in the basal layer and transfer melanin via melanosomes. Langerhans cells handle immune surveillance. Merkel cells are involved in sensation. The epidermis is avascular - it is fed by diffusion from the dermis.
The dermis has a papillary layer (fine collagen, capillaries) and a reticular layer (dense collagen, elastin, ground substance, fibroblasts, glands, follicles, nerves). Collagen type I dominates adult dermis; type III rises early in wound healing. The hypodermis provides insulation and cushioning.
Barrier and pH
The brick-and-mortar model: corneocytes are the bricks, lamellar lipids (ceramides, cholesterol, fatty acids) are the mortar. The acid mantle sits near pH 4.5-5.5 and supports enzyme activity and antimicrobial defense. Barrier damage raises transepidermal water loss, which shows up as tightness, stinging, and flaking - not necessarily dryness.
Healing and pigment
Wound healing proceeds hemostasis, inflammation, proliferation, remodeling. Melanogenesis is stimulated by UV, inflammation, and hormones, which is why aggressive treatments on darker or recently inflamed skin produce post-inflammatory hyperpigmentation.
Traps
- Placing melanocytes in the spinosum, or blood vessels in the epidermis.
- Mixing up Langerhans (immunity) and Merkel (sensation).
- Forgetting the acid mantle number or calling skin alkaline.
- Scrambling the order of wound-healing phases.
Rule of thumb
Everything you can legally and safely influence lives in the epidermis and superficial dermis - and the dermoepidermal junction is where pigment trouble starts.