Dermatology

Psoriasis

Chronic immune-mediated skin disease with well-demarcated erythematous plaques and silvery scale; IL-17/IL-23 axis driven, ~30% develop psoriatic arthritis.

Last reviewed 2 May 2026 - MedicoMedics editorial team

Pathophysiology

Th17 cells release IL-17, driving keratinocyte hyperproliferation. Genetic HLA-Cw6, obesity, streptococcal infection, drugs (lithium, beta-blockers) can trigger.

Sources: AAD Psoriasis 2021; NEJM Secukinumab 2014;371:326

Presentation

Plaque type most common on extensor surfaces, scalp, umbilicus; Auspitz sign; nail pitting and onycholysis; guttate after strep; inverse in flexures.

Diagnosis

Clinical; biopsy shows parakeratosis, neutrophilic microabscesses (Munro), acanthosis. Screen for arthritis and metabolic comorbidities.

Management

Topical corticosteroids + vitamin D analogues (calcipotriol) for limited disease. Moderate-severe: phototherapy, methotrexate, biologics (IL-17 - secukinumab, ixekizumab; IL-23 - guselkumab, risankizumab; TNFi - adalimumab).

Sample USMLE-style MCQs

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Question 1

A 35-year-old has well-demarcated silvery plaques on elbows and scalp with nail pitting. Best initial therapy?

Question 2

Which biologic targets IL-17?

Question 3

Which HLA is associated?

Question 4

Which triggers guttate psoriasis?

Question 5

Systemic drug to avoid in psoriasis?

References

Primary guidelines and peer-reviewed sources used for this entry. Reviewed 2 May 2026 by MedicoMedics editorial team.

Frequently asked

What is the Koebner phenomenon?

New plaques at sites of trauma.

Best biologic for concomitant PsA?

TNF or IL-17 inhibitor.

Which drugs can worsen psoriasis?

Lithium, beta-blockers, antimalarials, abrupt steroid withdrawal.

Related conditions

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