Skin, Hair & Nails

Hair: Hair grows from structures called hair follicles — tiny tubular pockets that extend from the skin surface down into the dermis. The base of each follicle contains actively dividing cells that push the hair upward as they multiply. Hair is made of keratin — the same protein as the outer skin. Hair grows in cycles: - Anagen (growth phase) — active cell division, hair grows ~1 cm/month. Lasts 2–7 years for scalp hair. - Catagen (transition) — growth slows, the follicle shrinks. ~2 weeks. - Telogen (resting phase) — the old hair is shed, the follicle rests before starting a new cycle. ~3 months. At any time, about 85–90% of scalp hairs are in the anagen phase. Losing 50–100 hairs per day is completely normal. Stress, illness, nutritional deficiency, or hormonal changes can push more follicles into the telogen phase simultaneously → excessive shedding (telogen effluvium). Hair colour: determined by the amount and type of melanin in the hair shaft. Dark hair has more eumelanin; red hair has phaeomelanin; blonde hair has less melanin overall. Grey and white hair occur when melanocytes in follicles stop producing melanin — partly genetic, often accelerated by stress and age. Goosebumps: Each hair follicle has a tiny muscle (arrector pili). Cold or fear triggers these muscles to contract → hairs stand up (piloerection). In animals with thicker hair, this traps air for warmth or makes them look bigger. In humans it just gives us goosebumps — a vestigial (leftover evolutionary) response. Nails: Nails are plates of dead cells densely packed with keratin. They grow from the nail matrix at the base. Fingernails grow ~3–4 mm per month; toenails grow more slowly. Nails protect the sensitive fingertips and help with fine manipulation tasks. Nail appearance can be medically useful: clubbing (nail curves over the fingertip like a drumstick) indicates chronic low oxygen or lung disease; pale nails suggest anaemia; yellow nails can indicate fungal infection or lung disease.

Your body core temperature must stay within a narrow range — approximately 36.5–37.5°C — for enzymes to work properly. Even a rise to 40°C can cause dangerous enzyme denaturation; a fall below 35°C causes hypothermia. The skin is the main organ that controls this. When you are too HOT: 1. Blood vessels in the dermis dilate (widen) → more warm blood flows near the skin surface → heat radiates outward. This is why your skin goes red when you are hot. 2. Sweat glands produce sweat → water on skin surface evaporates → evaporation takes heat away from the body. Evaporation is very effective — a single gram of water evaporating removes 2,400 joules of heat. 3. Sweating losses can be large: 1–2 litres per hour in hot exercise. If not replaced, dehydration and heat exhaustion follow. When you are too COLD: 1. Blood vessels in the skin vasoconstrict (narrow) → less blood near the surface → less heat lost. Extremities (fingers, toes, nose, ears) get the least blood and feel coldest first — this is why frostbite affects these areas first. 2. Shivering — rapid involuntary muscle contractions generate heat (muscles generate heat as a byproduct of contraction) 3. Hairs stand up (goosebumps — largely ineffective in humans) The hypothalamus — the body's thermostat: The hypothalamus (in the brain) constantly monitors blood temperature. When temperature drifts too high or low, it triggers the responses above. In fever (pyrexia), infection causes the hypothalamus to reset its "thermostat" to a higher temperature — the body feels cold (chills) and shivers to raise temperature to the new set point. Paracetamol and ibuprofen lower fever by blocking prostaglandins that reset the hypothalamic thermostat. Burns: Burns are classified by depth: - Superficial (1st degree) — only the epidermis damaged. Redness, pain. Heals within a week (sunburn). - Partial thickness (2nd degree) — epidermis and part of the dermis damaged. Blistering, very painful (nerve endings exposed). Can heal if dermis cells survive. - Full thickness (3rd degree) — entire dermis destroyed. Appears white or charred. Painless (nerve endings destroyed). Requires skin grafting — cannot heal by itself.

The sun emits ultraviolet (UV) radiation in three bands — UV-A, UV-B, and UV-C. UV-C is blocked by the atmosphere. UV-A and UV-B reach Earth's surface and affect our skin. UV-B (280–315 nm): - Causes sunburn (damages the outer layers of skin) - The main cause of skin cancer (directly damages DNA in skin cells) - Also triggers Vitamin D synthesis — essential for bone health - Blocked by glass UV-A (315–400 nm): - Penetrates deeper into the dermis - Causes skin ageing (breaks down collagen and elastin → wrinkles) - Also contributes to skin cancer - NOT blocked by most glass — responsible for skin damage through car windows How UV damages DNA: UV radiation causes specific DNA mutations — particularly thymine dimers (where two adjacent thymine bases stick together abnormally). Cells normally repair these quickly using nucleotide excision repair. But with repeated intense UV exposure, some mutations escape repair → accumulate → can eventually cause cancer. Skin cancers — the three types: - Basal cell carcinoma (BCC) — the most common cancer in the world. Grows from basal cells at the bottom of the epidermis. Rarely spreads (metastasises) but can be locally destructive. Pearl-like raised nodule, often on the face. - Squamous cell carcinoma (SCC) — grows from keratinocytes. Can metastasise, especially if on the lip or ear. Appears as a scaly, red, thickened lesion. - Melanoma — the most dangerous. Grows from melanocytes. Can spread to lymph nodes and other organs if not caught early. Recognised by the ABCDE rule: Asymmetry, Border irregularity, Colour variation, Diameter >6mm, Evolution (changing over time). Survival is excellent if detected early; poor if it has spread. Sun protection: SPF (Sun Protection Factor) measures how much a sunscreen reduces UV-B exposure. SPF 30 blocks ~97%; SPF 50 blocks ~98%. Sunscreen should be broad-spectrum (blocking both UV-A and UV-B) and reapplied every 2 hours when outdoors.

When skin is injured, a remarkable repair process begins almost immediately — involving blood clotting, inflammation, new tissue formation, and remodelling. The four phases of wound healing: Phase 1 — Haemostasis (stopping the bleeding): Within seconds to minutes of injury. Damaged blood vessels constrict; platelets rush to the injury site, stick together (aggregate), and form a plug. Clotting factors are activated → fibrin mesh forms → blood clot seals the wound. This is your body's emergency first aid. Phase 2 — Inflammation (24–72 hours): The wound becomes red, warm, swollen, and painful. White blood cells (neutrophils first, then macrophages) flood the area to clean up bacteria and debris. Macrophages also release growth factors that signal the next phase to begin. This inflammation is essential — disrupting it (e.g. with too many anti-inflammatory drugs) can impair healing. Phase 3 — Proliferation (days to weeks): New tissue is built. Fibroblasts (connective tissue cells) flood in and produce large amounts of collagen → forms the scar tissue framework. New blood vessels grow into the area (angiogenesis). The skin edges grow toward each other. A temporary pink, raised scar forms. Phase 4 — Remodelling (months to years): The initial collagen is gradually reorganised into stronger, more organised fibres. The scar slowly fades and flattens. Even the best healed skin never quite reaches 100% of original strength — scar tissue is only about 70–80% as strong as the original. Factors that impair healing: - Diabetes — high blood glucose damages blood vessels and impairs immune function → poor circulation to wound + increased infection risk → wounds in diabetic patients can take weeks to heal (or not heal at all → diabetic foot ulcers) - Poor nutrition — Vitamin C and zinc are essential for collagen synthesis - Infection — bacteria break down new tissue faster than it can form - Smoking — nicotine constricts blood vessels → reduces oxygen delivery to healing tissue