Medicine chapters
Pigmentary, hair and nail disorders
The common causes of pale and dark patches, the types of hair loss and excess hair, and the nail changes that point to skin or systemic disease, with the key test and treatment for each.
- Vitiligo is autoimmune loss of melanocytes giving chalk-white, well-defined, non-scaly patches (face, hands, genitals) linked to thyroid disease; melasma is symmetrical brown facial pigment in women triggered by pregnancy, the pill and sun.
- Hair loss is non-scarring (alopecia areata with exclamation mark hairs, androgenetic, telogen effluvium, tinea capitis) or scarring (lichen planus, discoid lupus, kerion), where follicles are destroyed for good.
- Nail signs: pitting (psoriasis, alopecia areata), koilonychia (iron deficiency), leuconychia (low albumin), Beau lines (past severe illness), clubbing and onycholysis (psoriasis, thyrotoxicosis).
On this page
Overview
Colour, hair and nails are where many systemic diseases first show. In Pakistan, patients worry greatly about white patches (fear of leprosy or social stigma), facial pigmentation and hair loss, so these are common clinic problems and common MCQs.
Melanin is made by melanocytes in the basal layer from tyrosine (enzyme tyrosinase) and handed to keratinocytes. Two types: eumelanin (brown-black) and phaeomelanin (red-yellow). Skin colour depends mainly on how much melanin is made, not the number of melanocytes.
Hypopigmentation and depigmentation
Depigmented means melanin is absent (chalk-white, as in vitiligo). Hypopigmented means reduced (paler than normal, as in pityriasis alba). A Wood's lamp makes depigmented areas stand out sharply.
Vitiligo
- Affects about 1–2% of people worldwide; about a third start in childhood.
- Autoimmune, T-cell-mediated destruction of melanocytes.
- Associations: autoimmune thyroid disease (most common), type 1 diabetes, Addison disease, pernicious anaemia, alopecia areata.
- Clinical: symmetrical, well-defined, milky-white (depigmented) macules with no scale and no inflammation; normal sensation. Typical sites: face (around eyes and mouth), hands, wrists, genitals, knees, elbows and bony points. Hair in patches may turn white (leucotrichia). Köbner phenomenon occurs.
- Patterns: generalised (non-segmental, commonest), segmental (one side, stable), acrofacial, universal.
- Wood's lamp accentuates the white areas.
- Treatment:
- Potent topical steroids or topical tacrolimus for limited patches (tacrolimus for face).
- Narrowband UVB phototherapy for widespread disease.
- Repigmentation begins as dots around hair follicles ("perifollicular" speckles).
- Hands, feet and long-standing patches respond poorly.
- Sunscreen, camouflage cosmetics and psychological support.
- Surgical grafting for stable segmental disease.
- Check thyroid function at diagnosis.
Vitiligo is depigmentation (melanocytes gone), so patches are milky-white and glow brightly under a Wood's lamp; there is no scale and no loss of sensation.
A pale patch with loss of sensation and thickened nearby nerves is leprosy, not vitiligo. Vitiligo is chalk-white with normal sensation; leprosy patches are hypopigmented (not white) and anaesthetic.
Other causes of pale patches
| Condition | Clue |
|---|---|
| Pityriasis alba | Children with atopic tendency; ill-defined, slightly scaly, hypopigmented patches on the cheeks and arms; emollients and mild steroid |
| Pityriasis versicolor | Young adults, upper trunk, fine scale; KOH shows Malassezia |
| Post-inflammatory hypopigmentation | After eczema, psoriasis or burns; recovers slowly |
| Tuberculoid or indeterminate leprosy | Hypopigmented, anaesthetic, dry patches; thick nerves |
| Oculocutaneous albinism | Autosomal recessive; tyrosinase fault; white hair, pale skin, pink-grey irides, photophobia, nystagmus, poor vision; very high risk of skin cancer; strict sun protection |
| Piebaldism | Autosomal dominant; white forelock and stable white patches from birth |
| Tuberous sclerosis | Ash-leaf macules (seen best with Wood's lamp), with seizures and angiofibromas |
| Mycosis fungoides (hypopigmented) | Persistent pale patches on the trunk, especially in dark skin |
Hyperpigmentation
Melasma (chloasma)
- Symmetrical brown patches on the cheeks, forehead, upper lip and nose.
- Mostly women; triggered by pregnancy ("mask of pregnancy"), the contraceptive pill and sunlight; very common in South Asian skin.
- Treatment: strict broad-spectrum sunscreen, stop hormonal triggers if possible, hydroquinone 2–5%, azelaic acid, topical retinoids (often as a triple combination with a mild steroid for short periods). It recurs easily with sun.
Prolonged use of strong hydroquinone or "fairness" creams containing steroids or mercury is common in Pakistan and can cause exogenous ochronosis, steroid damage and mercury toxicity.
Other causes of dark skin
| Condition | Key features |
|---|---|
| Post-inflammatory hyperpigmentation | After acne, eczema, lichen planus, injury; very common in dark skin; fades over months |
| Freckles (ephelides) | Small brown spots in fair-skinned children; darken in summer, fade in winter |
| Lentigines | Persistent brown macules that do not fade in winter; solar lentigines in older people; multiple lip and mouth lentigines in Peutz–Jeghers syndrome |
| Café-au-lait macules | Uniform light-brown patches; multiple suggest neurofibromatosis type 1 (with axillary freckling); also McCune–Albright syndrome |
| Acanthosis nigricans | Velvety, dark, thickened skin in the axillae, neck folds and groin; commonest with obesity and insulin resistance (type 2 diabetes, PCOS); sudden, extensive or mucosal disease in an older adult suggests cancer, especially gastric adenocarcinoma |
| Addison disease | Generalised darkening, worst in palmar creases, scars, knuckles and buccal mucosa (excess ACTH/MSH) |
| Haemochromatosis | Bronze or grey skin with diabetes and liver disease |
| Drugs | Minocycline (blue-grey), amiodarone (slate-grey on sun-exposed skin), antimalarials, chemotherapy, oral contraceptives (melasma) |
| Arsenic poisoning | Raindrop pigmentation, palm and sole keratoses, and white transverse nail bands |
| Mongolian blue spot | Blue-grey patch over the sacrum in infants (deep dermal melanocytes); very common in Asian babies; usually fades by about 7 years; not a bruise from abuse |
| Urticaria pigmentosa | Brown macules in children that urticate when rubbed (Darier sign); excess mast cells |
Dark, velvety skin in the neck and axillae of an obese patient points to insulin resistance. In a thin older adult with weight loss it is a paraneoplastic sign.
Hair disorders
Hair loss (alopecia): first decide scarring or non-scarring
| Non-scarring (follicles intact; regrowth possible) | Scarring (follicles destroyed; permanent) |
|---|---|
| Androgenetic alopecia | Discoid lupus erythematosus |
| Alopecia areata | Lichen planus (lichen planopilaris) |
| Telogen effluvium | Kerion (severe tinea capitis) |
| Tinea capitis (non-inflammatory) | Dissecting cellulitis, folliculitis decalvans |
| Trichotillomania (hair pulling) | Radiation, burns, morphoea |
| Early traction alopecia | Late traction alopecia |
| Iron deficiency, hypothyroidism, drugs (chemotherapy, heparin, isotretinoin) | Idiopathic (pseudopelade) |
In scarring alopecia the scalp looks shiny and smooth with no follicle openings.
Alopecia areata
- Autoimmune attack on hair follicles; lifetime risk about 2%; often children and young adults.
- Associations: thyroid disease, vitiligo, atopy, Down syndrome.
- Clinical: one or more round or oval, smooth, completely bald patches with normal-looking skin (no scale, no scarring).
- Exclamation mark hairs at the edge (short broken hairs narrower at the base than the tip) are diagnostic.
- Nail pitting may be present.
A child with a smooth, round bald patch, normal scalp skin and exclamation mark hairs at the edge has alopecia areata; scaling, broken hairs and a boggy swelling would point instead to tinea capitis or kerion.
- Severe forms: alopecia totalis (whole scalp), alopecia universalis (all body hair), ophiasis (band-like loss around the back and sides).
- Course: small patches often regrow on their own within months; regrowth may be white at first.
- Treatment: intralesional or potent topical steroids; contact immunotherapy (diphencyprone) for extensive loss; JAK inhibitors for severe disease; wigs and support.
Androgenetic alopecia (male- and female-pattern hair loss)
- The commonest cause of hair loss; genetic sensitivity of follicles to dihydrotestosterone, causing miniaturisation of hairs.
- Men: frontal recession and vertex thinning. Women: diffuse thinning of the crown with the frontal hairline kept.
- Women with acne, hirsutism and irregular periods need tests for PCOS or another androgen excess.
- Treatment: topical minoxidil (both sexes); oral finasteride (5-alpha-reductase inhibitor) in men; antiandrogens (spironolactone, cyproterone) in some women. Benefit lasts only while treatment continues.
Pregnant women should neither swallow nor touch crushed finasteride, because it can feminise a male fetus.
Telogen effluvium
- Diffuse shedding of many hairs at once, starting about 2–3 months after a trigger: childbirth, high fever, major surgery, severe illness, crash dieting, stopping the pill, or some drugs.
- The trigger pushes many hairs into telogen together.
- Hair pull test is positive; scalp looks normal.
- Usually recovers within months once the trigger is gone; check ferritin and thyroid function.
Other hair problems
- Tinea capitis: scaly patches with broken hairs in children; kerion if inflamed. Needs oral antifungal.
- Trichotillomania: irregular patches of broken hairs of different lengths; linked to anxiety and obsessive-compulsive behaviour.
- Traction alopecia: loss at the hair margins from tight braids, ponytails or buns; becomes permanent if continued.
Excess hair
| Feature | Hirsutism | Hypertrichosis |
|---|---|---|
| Definition | Male-pattern terminal hair in a woman (beard, chest, lower abdomen) | Excess hair anywhere, in either sex, not androgen-dependent |
| Causes | PCOS (commonest), idiopathic, congenital adrenal hyperplasia, androgen-secreting tumours, Cushing syndrome, drugs (anabolic steroids) | Drugs (minoxidil, ciclosporin, phenytoin), porphyria cutanea tarda, anorexia nervosa, malnutrition, cancer (acquired hypertrichosis lanuginosa) |
Red flags in hirsutism (rapid onset, deep voice, clitoromegaly, raised testosterone) suggest an androgen-secreting tumour and need urgent endocrine work-up. Treatment of hirsutism includes weight loss, the combined pill with cyproterone, spironolactone, laser or electrolysis, and eflornithine cream.
Nail disorders
Nail signs and what they mean
| Nail sign | Description | Main causes |
|---|---|---|
| Pitting | Small depressions in the nail plate | Psoriasis (commonest), alopecia areata, eczema |
| Onycholysis | Nail separates from the bed from the tip | Psoriasis, thyrotoxicosis (Plummer nails), trauma, fungal infection, photosensitising drugs (tetracyclines) |
| Koilonychia | Thin, spoon-shaped nails | Iron deficiency anaemia (also Plummer–Vinson syndrome) |
| Leuconychia | White nails | Hypoalbuminaemia (cirrhosis, nephrotic syndrome); white spots from minor trauma |
| Beau lines | Transverse grooves | A past episode of severe illness or chemotherapy that briefly stopped growth |
| Clubbing | Loss of the angle between nail and nail fold; bulbous fingertip | Lung cancer, bronchiectasis, lung abscess, empyema, fibrosing alveolitis, cyanotic heart disease, infective endocarditis, IBD, cirrhosis |
| Splinter haemorrhages | Thin red-brown lines | Infective endocarditis, vasculitis, trauma |
| Yellow nail syndrome | Thick, yellow, slow-growing nails | With lymphoedema and pleural effusion or bronchiectasis |
| Subungual hyperkeratosis | Thick debris under the nail | Fungal infection, psoriasis |
| Onychogryphosis | Thick, curved "ram's horn" nail | Elderly, neglect, poor footwear (big toe) |
| Pterygium | Scar joining nail fold to nail bed | Lichen planus |
| Half-and-half nails | Pale base, dark tip | Chronic kidney disease |
| Terry nails | White nail with a narrow pink tip | Cirrhosis, hypoalbuminaemia |
| Mees lines | White transverse bands | Arsenic poisoning, chemotherapy |
Koilonychia = "Iron" spoon. Pitting = Psoriasis. Beau = Bad illness Before.
Infections of the nail
- Onychomycosis (tinea unguium): thick, yellow-white, crumbling nails starting at the distal edge; Trichophyton rubrum; confirm with clippings; oral terbinafine for 3–6 months (fingernails need less time than toenails).
- Acute paronychia: painful red swollen nail fold with pus; usually Staph. aureus; drain and give flucloxacillin.
- Chronic paronychia: swollen nail folds with loss of the cuticle in people with wet work (cooks, cleaners, housewives); Candida and irritant dermatitis; keep hands dry, topical azole and steroid.
Pigmented nails
- Longitudinal melanonychia (brown stripes) in several nails is normal in dark-skinned people.
- A single, widening, dark streak, especially with pigment spreading onto the nail fold (Hutchinson sign), suggests subungual melanoma and needs biopsy.
- Subungual haematoma after trauma grows out with the nail.
Nails grow slowly: about 6 months for a fingernail and 1 year for a toenail to regrow, so changes take a long time to clear after treatment.
Expect: features and associations of vitiligo (thyroid), how to separate vitiligo from leprosy, pityriasis alba and pityriasis versicolor, albinism genetics, melasma triggers and treatment, acanthosis nigricans (insulin resistance or gastric cancer), Addison pigmentation, scarring versus non-scarring alopecia, exclamation mark hairs of alopecia areata, telogen effluvium after pregnancy, androgenetic alopecia treatment, hirsutism versus hypertrichosis, and the nail signs (pitting, koilonychia, leuconychia, Beau lines, onycholysis, clubbing, Hutchinson sign).
Quick revision
- Vitiligo: autoimmune loss of melanocytes; chalk-white, non-scaly, normal sensation; thyroid link.
- Leprosy patch: hypopigmented, anaesthetic, thick nerve.
- Pityriasis alba: scaly pale cheeks in atopic children.
- Albinism: autosomal recessive, tyrosinase; nystagmus and skin cancer.
- Melasma: pregnancy, pill, sun; sunscreen and hydroquinone.
- Acanthosis nigricans: insulin resistance; sudden onset suggests gastric cancer.
- Alopecia areata: exclamation mark hairs; nail pitting; steroids.
- Telogen effluvium: 2–3 months after childbirth or illness; recovers.
- Hirsutism: PCOS commonest; hypertrichosis: drugs such as minoxidil.
- Koilonychia: iron. Leuconychia: low albumin. Beau lines: past illness. Pitting: psoriasis.
- Hutchinson sign: subungual melanoma.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
How can vitiligo be told apart from leprosy?
Vitiligo patches are chalk-white with normal sensation, while leprosy patches are hypopigmented, dry and numb, often with a thickened nerve nearby.
What are exclamation mark hairs?
Short broken hairs at the edge of an alopecia areata patch that taper towards the scalp; they are diagnostic of the condition.
Why does hair fall out a few months after childbirth?
The stress of delivery pushes many hairs into the resting phase together, and they shed two to three months later (telogen effluvium); it usually recovers.
What does koilonychia indicate?
Spoon-shaped nails most often indicate iron deficiency anaemia.
When is acanthosis nigricans worrying?
When it appears suddenly and extensively, involves the mouth, or occurs in a thin older adult, because it may signal an internal cancer, usually of the stomach.