Hair and Nail Disorders

Hormonal/genetic (follicular miniaturization)

• Androgenetic alopecia: polygenic inheritance with androgen receptor sensitivity to DHT in frontal/vertex follicles; occipital follicles are androgen-insensitive (the basis for donor-site transplantation). Hyperandrogenic states (PCOS, adrenal or ovarian tumors) accelerate female pattern loss — look for hirsutism, acne, and irregular menses in the stem.

Immune-mediated

• Alopecia areata: loss of hair-follicle immune privilege with CD8+/NKG2D T-cell attack on the anagen bulb. Personal or family history of autoimmune thyroid disease, vitiligo, type 1 diabetes, celiac disease, atopy, and Down syndrome are the classic planted associations.
• Scarring (cicatricial) alopecias: lichen planopilaris, discoid lupus, and central centrifugal cicatricial alopecia destroy the follicular stem-cell bulge, producing permanent loss.

Infectious

• Dermatophytes: Trichophyton rubrum dominates onychomycosis; T. tonsurans dominates US tinea capitis. Candida species affect fingernails in chronically wet hands.

Toxic/metabolic (cycle disruption)

• Anagen effluvium: antimitotic chemotherapy and radiation arrest matrix mitosis within days to weeks.
• Telogen effluvium: febrile illness, major surgery, postpartum state, crash dieting, thyroid disease, and drugs (beta blockers, anticoagulants, retinoids, valproate, lithium).
• Nutritional: iron deficiency (also causes koilonychia), zinc, biotin, and protein-calorie deficiency; hemochromatosis and repetitive occupational wetting also cause koilonychia.

• Disruption of the hair growth cycle: Hair cycles through anagen (active growth, 2-7 years), catagen (transition, 2-3 weeks), and telogen (resting, 2-3 months) phases. Pathological premature entry into catagen/telogen causes telogen effluvium, while dysfunction of hair matrix cells results in anagen effluvium. Androgens (DHT) cause miniaturization of genetically predisposed follicles in androgenetic alopecia via androgen receptor upregulation in dermal papillae.

• Immune-mediated hair follicle destruction: In alopecia areata, CD8+ T lymphocytes breach the hair follicle immune privilege, attacking the hair bulb and surrounding epithelium. This results in acute dystrophy and shedding of hair shaft. The condition is associated with Th1 and Th17 dysregulation.

• Fungal invasion of hair and nail structures: Dermatophytes (particularly Trichophyton tonsurans in North America, Microsporum canis globally) invade the hair shaft and nail plate, causing inflammation and structural compromise. Nail involvement progresses from distal nail plate through to proximal involvement, with keratinolytic enzymes enabling fungal penetration.

• Structural nail apparatus defects: The nail apparatus (matrix, nail bed, nail folds) can be damaged by trauma, inflammation, or systemic disease, leading to onycholysis (separation from nail bed), nail pitting, or leukonychia. Matrix damage during active inflammation produces horizontal ridges (Beau's lines), while lateral matrix damage causes longitudinal ridges.

• Folliculitis and sebaceous gland inflammation: Bacterial colonization (particularly Staphylococcus aureus) combined with follicular occlusion, increased sebum production, and enhanced inflammation causes folliculitis, potentially progressing to scarring alopecia if chronic.

• Androgenetic alopecia: Gradual, progressive hair loss in a pattern distribution (vertex, bitemporal areas in men; diffuse thinning in women per Ludwig scale). Patients report noticing increased hairs on pillow/shower drain. Men typically present in 20s-40s; female presentation often postmenopausal. Hamilton-Norwood scale classifies male pattern severity; Ludwig scale for females.

• Telogen effluvium: Acute shedding of 100-400 hairs daily (normal is 50-100), occurring 2-3 months after stressor (fever, surgery, severe illness, medications like beta-blockers, iron deficiency, crash dieting). Hair loss is diffuse and non-scarring. Patients often report first noticing hair in shower or on pillowcase.

• Alopecia areata: Sudden onset of well-demarcated, round/oval patches of hair loss without scaling or inflammation on scalp, beard, eyebrows, or body. Affected hairs are easily pluckable. "Exclamation mark hairs" (thicker proximally, thinner distally) are pathognomonic. Nails may show pitting (geometric pattern of small depressions). Can progress to alopecia totalis (total scalp loss) or alopecia universalis (total body hair loss).

• Tinea capitis (scalp ringworm): Presents as scaly patches with hair loss, often with scaling and erythema. Non-inflammatory type presents as fine scale ("gray patch" variant, common in children). Inflammatory type presents with pustules, crusting, and drainage ("black dot" variant with broken-off hairs). Kerion (severe host inflammatory response) resembles bacterial infection with suppuration and lymphadenopathy.

• Onychomycosis: Discoloration (white, yellow, or brown), thickening, and crumbling of nails, typically starting at distal free edge. Subungual hyperkeratosis (debris accumulation under nail). Lateral involvement progresses to total nail dystrophy. Toenails more commonly affected than fingernails (85% of cases). Risk increases with diabetes, immunosuppression, age >60.

• Nail psoriasis: Pitting (small punctate depressions in nail surface, highly specific for psoriasis), onycholysis (distal separation), subungual hyperkeratosis, oil spots (yellow-brown discoloration), and nail dystrophy. Often precedes or accompanies cutaneous psoriasis.

• Lichen planus involving nails: Longitudinal ridging, thinning (pterygium formation—pterygoid fusion of nail folds), onycholysis, and nail destruction. Can cause permanent scarring alopecia of scalp if severe.

• Clinical morphology and distribution pattern: Diagnosis of androgenetic alopecia is primarily clinical based on pattern distribution, family history, and gradual progression. Alopecia areata is diagnosed by characteristic round patches, exclamation mark hairs, and nail pitting. Telogen effluvium is confirmed by pull test (>3 hairs extracted easily from 60-hairs pulled) showing telogen-phase hairs.

• Dermoscopy: Magnified visualization reveals specific patterns—androgenetic alopecia shows variable hair diameter (vellus and terminal hairs mixed), perifollicular hyperpigmentation, and decreased hair density. Alopecia areata shows "yellow dots" (pigmented follicles), "cadaver hairs" (remnants), and increased white spaces between hairs.

• KOH preparation and fungal culture: Pluck test or scale collection with KOH (potassium hydroxide) preparation reveals fungal elements for tinea capitis and onychomycosis. Wood's lamp examination (may show blue-green fluorescence with Microsporum canis, though many dermatophytes are non-fluorescent). Fungal culture on Sabouraud dextrose agar identifies organism and permits antifungal susceptibility testing. In onychomycosis, nail clippings or debris under nail is cultured.

• Nail biopsy: Indicated when diagnosis is unclear or to differentiate psoriasis, lichen planus, or tumor. Histology shows specific changes (psoriasis with parakeratosis/clubbing; lichen planus with band-like lymphocytic infiltrate).

• Scalp biopsy: Reserved for scarring alopecia or when diagnosis unclear. Horizontal sections show number of follicles/unit area and hair cycle distribution; vertical sections assess follicle and sebaceous gland involvement. Lichen planopilaris and discoid lupus erythematosus (DLE) show distinct patterns.

• Serological testing: In alopecia areata with extensive involvement, assess for associated autoimmune conditions (thyroid, celiac). DLE-related alopecia warrants ANA and anti-Ro/La testing.

• Androgenetic alopecia—First-line: Minoxidil (topical) 2% solution or 5% foam applied bid for 3-6 months minimum (onset of benefit may take 3-6 months); halts progression and promotes regrowth in ~40% of patients. Finasteride 1 mg daily orally (5-alpha reductase inhibitor reducing DHT) shows efficacy in men; decreases DHT by 70%. Women of childbearing potential must avoid (teratogenic). Combination therapy shows superior results. First-line in men only.

• Androgenetic alopecia—Second-line and adjunctive: Dutasteride (dual 5-alpha reductase inhibitor) 0.5 mg daily; slightly more effective than finasteride but with higher cost. Low-level laser therapy (LLLT) shows modest benefit. Hair transplantation for refractory cases. Topical estrogens or oral contraceptives in women.

• Telogen effluvium: Primarily supportive—address underlying cause (nutritional supplementation for

Disease-related

• Permanent scarring alopecia: untreated kerion, lichen planopilaris, discoid lupus, and late-stage traction alopecia destroy the follicular bulge stem cells. The signal finding is loss of follicular ostia on dermoscopy — a smooth, shiny scalp with no visible pores. This is the one time hair loss is time-sensitive; treat before follicles are lost.
• Progression of alopecia areata to alopecia totalis/universalis, with ophiasis pattern and extensive nail pitting/trachyonychia predicting poorer regrowth.
• Psychiatric morbidity: depression, anxiety, and social withdrawal are common and are the reason treatment is offered even though alopecia is not medically dangerous. Screen with PHQ-9.
• Secondary bacterial infection: onychomycosis creates fissures and subungual portals of entry. In diabetes or peripheral arterial disease this seeds cellulitis, foot ulceration, and osteomyelitis — spreading erythema, fever, or probe-to-bone is an emergency requiring admission, imaging, and IV antibiotics.
• Systemic nail signs missed as cosmetic: splinter hemorrhages with fever and a new murmur mean infective endocarditis (draw blood cultures before antibiotics, per AHA); koilonychia means iron deficiency requiring a search for occult GI blood loss.

Treatment-related

• Terbinafine: idiosyncratic hepatotoxicity and cholestatic injury; jaundice, dark urine, or RUQ pain is an emergency — stop the drug and check LFTs. Baseline transaminases are recommended before oral therapy. Also causes dysgeusia/ageusia and, rarely, DRESS and drug-induced subacute cutaneous lupus.
• Itraconazole: negative inotropy with an FDA boxed warning against use in ventricular dysfunction/heart failure, plus potent CYP3A4 inhibition causing QT prolongation and statin toxicity.
• Finasteride/dutasteride: sexual dysfunction, gynecomastia, and roughly 50% suppression of PSA — double the measured value when interpreting prostate cancer screening. Teratogenic; pregnant women must not handle broken tablets.
• Topical minoxidil: initial telogen shedding that frightens patients, facial hypertrichosis, and irritant/allergic contact dermatitis from propylene glycol.
• Corticosteroids: intralesional injection causes dermal atrophy, telangiectasia, and hypopigmentation; potent topicals under occlusion risk HPA-axis suppression in children.
• Oral JAK inhibitors for severe alopecia areata carry class boxed warnings for serious infection, thrombosis, MACE, and malignancy; screen for latent TB and hepatitis first.

• Exclamation point hairs and dermoscopic yellow dots in a smooth, well-circumscribed patch with intact follicular ostia = alopecia areata. The association examiners test most is autoimmune thyroid disease — check TSH, and remember vitiligo and Down syndrome.
• Scarring versus non-scarring is the first branch point. Visible follicular openings = non-scarring (alopecia areata, telogen effluvium, androgenetic, tinea) and potentially reversible. Absent ostia with a shiny scalp = cicatricial — the best next step is a scalp biopsy and prompt dermatology referral, because lost follicles do not return.
• Tinea capitis always requires an oral antifungal; topicals cannot reach the intrafollicular hyphae. Griseofulvin is preferred for Microsporum, terbinafine for T. tonsurans (AAP Red Book). Adjunctive selenium sulfide or ketoconazole shampoo reduces spore shedding to household contacts.
• Confirm onychomycosis before treating. The AAD recommends mycologic confirmation (KOH, PAS-stained clipping, or culture) prior to oral antifungals, because nail psoriasis, lichen planus, and trauma mimic it and oral therapy carries real hepatic risk. The distractor is starting terbinafine on appearance alone.
• Nail pitting: coarse, irregular, deep pits with oil-drop onycholysis point to psoriasis; fine, regular, geometric pitting points to alopecia areata. Nail-plate pterygium is lichen planus.
• Koilonychia (spoon nails) means iron deficiency until proven otherwise. The next step is not a nail biopsy — it is CBC and ferritin, then a source hunt (endoscopy/colonoscopy in adult men and postmenopausal women).
• Telogen effluvium follows the stressor by 2–3 months, is diffuse, spares the hairline, and yields club-shaped telogen bulbs on the pull test. Management is reassurance plus correcting the trigger; it resolves within months. Anagen effluvium after chemotherapy starts within weeks and shows tapered, fractured shafts.
• Finasteride halves PSA — double a measured value before calling screening normal. And it is teratogenic: never give it to a woman who could become pregnant.