OSCE — assessment of patchy alopecia areata with trichoscopy and treatment counselling

An 8-minute OSCE station on recognition of non-scarring patchy alopecia areata, trichoscopic signs (exclamation-mark hairs, yellow dots), nail and autoimmune associations, prognosis counselling, and stepwise therapy from intralesional corticosteroids to JAK inhibition for extensive disease.

Prompt

Brief (to candidate)

A 19-year-old student has two smooth, round bald patches on the scalp for 3 months, sudden onset, without scale or scarring. He notices pits on several fingernails and high anxiety about appearance before exams. You have 8 minutes to confirm the diagnosis, assess extent and prognosis, and counsel on treatment options including intralesional steroids.

Candidate instructions

Confirm non-scarring patchy alopecia and list key differentials.
Use/describe trichoscopic findings of active AA.
Examine nails, body hair, and ask about autoimmune history.
Stratify extent (patchy / ophiasis / totalis / universalis) and prognosis factors.
Outline stepwise therapy and psychological support.

^[12]

Examiner checklist (mark each domain / 10)

Domain	Key actions expected
Recognition	Sudden smooth non-scarring round/oval patches; exclamation-mark hairs at periphery; positive hair-pull in active disease; skin of patch often normal colour without scale (vs tinea)^[1]
Trichoscopy	Yellow dots, black dots, broken hairs, exclamation-mark hairs — supports AA activity and helps exclude scarring alopecias/tinea when combined with clinic^[7]
Extent & variants	Documents patchy vs ophiasis (band-like occipital — worse prognosis) vs alopecia totalis/universalis; checks eyebrows/beard/body hair
Associations	Nail pitting/trachyonychia; personal/family atopy and autoimmune disease (thyroid, vitiligo); massive psychosocial burden
Pathophysiology brief	Collapse of hair-follicle immune privilege; CD8+ T-cell / IFN-γ / JAK–STAT axis — rationale for corticosteroids and JAK inhibitors in severe disease^[5]
Treatment ladder	Limited patchy: intralesional triamcinolone (typical dilute scalp concentrations; avoid atrophy) ± potent topical steroid; contact immunotherapy/topical immunotherapy or systemic options for extensive disease; JAK inhibitors for severe refractory AA in appropriate settings; spontaneous regrowth possible^[10]^[11]
Communication	Honest prognosis (relapsing); no scarring expected in classic AA; address exam stress/body image; safety-net if rapid total scalp loss

Model key actions

Diagnose patchy alopecia areata using clinical + trichoscopy signs; examine nails.^[1]^[7]
Offer intralesional corticosteroid for limited disease; discuss uncertainty and relapse.^[11]
For extensive disease, outline systemic/JAK pathway options with specialist referral; support mental health.^[5]^[10]

Common errors

Missing tinea capitis (scale, lymphadenopathy, KOH) — wrong steroids alone.
Calling it scarring alopecia without trichoscopy/exam of follicular ostia.
Not examining nails or counselling psychosocial impact.
Over-promising permanent cure; ignoring ophiasis/totalis poor prognostic patterns.
Using high-concentration IL steroid causing dermal atrophy without technique counselling.

^[1] ^[7] ^[11]

References6Show

[1]Fukuyama M, Ito T, Ohyama M. Alopecia areata: Current understanding of the pathophysiology and update on therapeutic approaches, featuring the Japanese Dermatological Association guidelines. The Journal of Dermatology, 2022.PMID 34709679
[5]Xing L, Dai Z, Jabbari A, et al. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nature Medicine, 2014.PMID 25129481
[7]Al-Dhubaibi MS, Alsenaid A, Alhetheli G, et al. Trichoscopy pattern in alopecia areata: A systematic review and meta-analysis. Skin Research and Technology, 2023.PMID 37357664
[10]Mateos-Haro M, Novoa-Candia M, Sánchez Vanegas G, et al. Treatments for alopecia areata: a network meta-analysis. The Cochrane Database of Systematic Reviews, 2023.PMID 37870096
[11]Yee BE, Tong Y, Goldenberg A, et al. Efficacy of different concentrations of intralesional triamcinolone acetonide for alopecia areata: A systematic review and meta-analysis. Journal of the American Academy of Dermatology, 2020.PMID 31843657
[12]Herrera-Rivero M, Gossmann Y, Awasthi S et al. Genome-wide association study of atopic and autoimmune comorbidities in alopecia areata Front Immunol, 2026.PMID 42079583

OSCE — assessment of patchy alopecia areata with trichoscopy and treatment counselling

Brief (to candidate)

Candidate instructions

Confirm non-scarring patchy alopecia and list key differentials.

Use/describe trichoscopic findings of active AA.

Examine nails, body hair, and ask about autoimmune history.

Stratify extent (patchy / ophiasis / totalis / universalis) and prognosis factors.

Outline stepwise therapy and psychological support.

Examiner checklist (mark each domain / 10)

Domain	Key actions expected
Recognition	Sudden smooth non-scarring round/oval patches; exclamation-mark hairs at periphery; positive hair-pull in active disease; skin of patch often normal colour without scale (vs tinea)^[1]
Trichoscopy	Yellow dots, black dots, broken hairs, exclamation-mark hairs — supports AA activity and helps exclude scarring alopecias/tinea when combined with clinic^[7]
Extent & variants	Documents patchy vs ophiasis (band-like occipital — worse prognosis) vs alopecia totalis/universalis; checks eyebrows/beard/body hair
Associations	Nail pitting/trachyonychia; personal/family atopy and autoimmune disease (thyroid, vitiligo); massive psychosocial burden
Pathophysiology brief	Collapse of hair-follicle immune privilege; CD8+ T-cell / IFN-γ / JAK–STAT axis — rationale for corticosteroids and JAK inhibitors in severe disease^[5]
Treatment ladder	Limited patchy: intralesional triamcinolone (typical dilute scalp concentrations; avoid atrophy) ± potent topical steroid; contact immunotherapy/topical immunotherapy or systemic options for extensive disease; JAK inhibitors for severe refractory AA in appropriate settings; spontaneous regrowth possible^[10]^[11]
Communication	Honest prognosis (relapsing); no scarring expected in classic AA; address exam stress/body image; safety-net if rapid total scalp loss

Common errors

Missing tinea capitis (scale, lymphadenopathy, KOH) — wrong steroids alone.

Calling it scarring alopecia without trichoscopy/exam of follicular ostia.

Not examining nails or counselling psychosocial impact.

Over-promising permanent cure; ignoring ophiasis/totalis poor prognostic patterns.

Using high-concentration IL steroid causing dermal atrophy without technique counselling.

References6Show

[1]Fukuyama M, Ito T, Ohyama M. Alopecia areata: Current understanding of the pathophysiology and update on therapeutic approaches, featuring the Japanese Dermatological Association guidelines. The Journal of Dermatology, 2022.PMID 34709679
[5]Xing L, Dai Z, Jabbari A, et al. Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition. Nature Medicine, 2014.PMID 25129481
[7]Al-Dhubaibi MS, Alsenaid A, Alhetheli G, et al. Trichoscopy pattern in alopecia areata: A systematic review and meta-analysis. Skin Research and Technology, 2023.PMID 37357664
[10]Mateos-Haro M, Novoa-Candia M, Sánchez Vanegas G, et al. Treatments for alopecia areata: a network meta-analysis. The Cochrane Database of Systematic Reviews, 2023.PMID 37870096
[11]Yee BE, Tong Y, Goldenberg A, et al. Efficacy of different concentrations of intralesional triamcinolone acetonide for alopecia areata: A systematic review and meta-analysis. Journal of the American Academy of Dermatology, 2020.PMID 31843657
[12]Herrera-Rivero M, Gossmann Y, Awasthi S et al. Genome-wide association study of atopic and autoimmune comorbidities in alopecia areata Front Immunol, 2026.PMID 42079583