Chronic immune-mediated inflammatory disorder with well-demarcated erythematous plaques and silvery scale; systemic comorbidities.
Also known as: psoriasis, plaque psoriasis, psoriasis vulgaris, guttate psoriasis, inverse psoriasis, pustular psoriasis
Overview
A chronic immune-mediated inflammatory skin disease driven by IL-23/Th17 axis activation, characterized by well-demarcated erythematous plaques with silvery-white scale and frequent involvement of scalp, extensor surfaces, and nails. Systemic disease with cardiometabolic and joint comorbidities.
Epidemiology
Prevalence 2-3% in the US; bimodal onset (16-22 and 57-60 years). Equal sex distribution. ~30% develop psoriatic arthritis (PsA). Strong genetic component — HLA-Cw6 association.
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Question 1DermatologyMedium
A 35-year-old woman has a several-month history of itchy, well-demarcated erythematous plaques topped with thick silvery scale on the extensor surfaces of her elbows and knees and on her scalp. Several fingernails show pitting, and the eruption reliably worsens during the winter months. Which of the following is the most likely diagnosis?
ALichen planus
BSeborrheic dermatitis
CTinea corporis
DPsoriasis vulgaris
Reveal answer & full explanation
Correct answer: D — Psoriasis vulgaris
ALichen planus
BSeborrheic dermatitis
CTinea corporis
DPsoriasis vulgaris✓
Why Psoriasis vulgaris is correct
Well-demarcated erythematous plaques with silvery scale on extensor surfaces (elbows, knees) and the scalp are the classic distribution of chronic plaque psoriasis
Nail pitting is a characteristic associated finding, along with distal onycholysis and oil-drop spots
Winter worsening reflects reduced ultraviolet exposure and drier skin, a typical seasonal pattern
The chronic, sharply marginated, scaly extensor plaques integrate into one coherent diagnosis
Why the others are wrong
Lichen planus — presents with purple, polygonal, flat-topped papules and lacy Wickham striae on flexural surfaces, not silvery extensor plaques (confused-with another papulosquamous disorder)
Seborrheic dermatitis — causes greasy, yellowish scale on the scalp, nasolabial folds, and chest rather than thick silvery plaques on elbows and knees (buzzword-matching scalp scaling)
Tinea corporis — a dermatophyte infection forming annular plaques with central clearing and a scaly advancing border; it does not cause nail pitting or this symmetric extensor pattern (premature closure on a "scaly rash")
Question 2DermatologyMedium
A 45-year-old man with moderate-to-severe plaque psoriasis (PASI 22) and a longstanding history of Crohn disease presents for treatment. He has previously failed methotrexate and adalimumab. His dermatologist wants a biologic that will treat his skin disease without flaring his inflammatory bowel disease. Which of the following biologics is the most appropriate choice for this patient?
ARisankizumab
BSecukinumab
CInfliximab
DBrodalumab
Reveal answer & full explanation
Correct answer: A — Risankizumab
ARisankizumab✓
BSecukinumab
CInfliximab
DBrodalumab
Why Risankizumab is correct
PASI 22 plaque psoriasis with comorbid Crohn disease requires an agent effective for both conditions, and prior failure of methotrexate plus the anti-TNF adalimumab narrows the options
Risankizumab is a selective interleukin-23 (IL-23 p19) inhibitor FDA-approved for both moderate-to-severe plaque psoriasis and Crohn disease (ADVANCE and MOTIVATE trials)
It delivers high skin clearance while inducing and maintaining remission in Crohn disease, so it treats the bowel rather than flaring it
AAD-NPF and gastroenterology (ECCO/AGA) guidance favor IL-23 inhibitors or ustekinumab in psoriasis with coexisting IBD
Why the others are wrong
Secukinumab — an IL-17A inhibitor; IL-17 blockade can precipitate or worsen inflammatory bowel disease, so it is avoided in Crohn disease (right-disease-wrong-pathway)
Infliximab — an anti-TNF agent, but this patient already failed adalimumab, so switching within the same class has lower yield than changing mechanism (confused-with class switch)
Brodalumab — blocks the IL-17 receptor and carries the same IBD-flare risk plus a boxed warning for suicidal ideation (anchoring on psoriasis efficacy)
Additional high-yield points
In psoriasis with IBD, IL-23 inhibitors (risankizumab, guselkumab) and ustekinumab are preferred because they treat both diseases, whereas IL-17 pathway agents should be avoided
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Psychosocial impact, depression, sexual dysfunction
Signs / physical exam
Plaque psoriasis (90%): well-demarcated erythematous plaques with adherent silvery scale on extensor elbows, knees, scalp, lumbosacral area, umbilicus
Guttate psoriasis: sudden eruption of small (<1 cm) drop-shaped plaques on trunk and proximal extremities, 1-3 weeks after streptococcal infection; often in children/young adults
Clinical diagnosis based on lesion morphology and distribution; severity by BSA, PASI, and impact (DLQI). Mild: BSA <3%; moderate: 3-10%; severe: >10% OR involvement of face, palms/soles, genitals, or nails with disability.
Pre-biologic workup: CBC, CMP, hepatitis B/C, TB testing (IGRA or PPD), HIV, pregnancy test; chest X-ray if indicated
PsA screening: PEST or PsAID questionnaire, joint exam at each visit
Imaging
Not routinely indicated for skin disease
Joint X-rays/MRI for suspected PsA: 'pencil-in-cup' deformity, periostitis, ankylosis
Diagnostic algorithm
Subtype
Hallmark
Preferred First-Line
Plaque (vulgaris)
Silvery scale on extensor surfaces, scalp, lumbosacral
Topical steroid + vitamin D analogue; NBUVB or biologic if extensive
Guttate
Drop-shaped lesions post-strep
Treat strep; NBUVB; topical steroid
Inverse
Glossy red plaques in folds
Low-potency steroid, TCI, calcipotriene
Pustular (generalized)
Sheets of sterile pustules, fever
Hospitalize; cyclosporine, infliximab, spesolimab
Erythrodermic
>90% BSA erythema/scale
Hospitalize; cyclosporine, infliximab
Nail
Pitting, oil drop, onycholysis
Intralesional triamcinolone; systemic if associated PsA
Psoriasis subtypes and preferred first-line therapy.
Treatment
First-line
Mild-moderate (limited BSA): topical corticosteroid potency by site — clobetasol 0.05% (high; trunk/extremities, 2 wks then taper), triamcinolone 0.1% (mid), hydrocortisone 1-2.5% (face/folds)
Topical vitamin D analogues — calcipotriene/calcipotriol, calcitriol — often combined with steroid (calcipotriene/betamethasone foam, ointment)
Topical retinoid — tazarotene 0.05-0.1%
Topical calcineurin inhibitors (tacrolimus, pimecrolimus) for face and intertriginous areas
Topical PDE4 inhibitor — roflumilast 0.3% cream daily (FDA-approved, all body areas including folds and face)
Topical AhR agonist — tapinarof 1% cream daily
Coal tar preparations (older) for scalp and plaque psoriasis
Moderate-severe / extensive plaque
Phototherapy: narrowband UVB (first-line for widespread plaque), PUVA (rarely used due to skin cancer risk), targeted excimer laser (308 nm) for localized
Never give systemic corticosteroids for psoriasis flare — withdrawal can precipitate pustular or erythrodermic psoriasis.
Auspitz sign (pinpoint bleeding after scale removal) and Koebner phenomenon (lesions at sites of trauma) are classic.
Nail pitting + onycholysis in a patient with joint pain = think psoriatic arthritis even if skin disease is mild.
Anti-IL-17 biologics (secukinumab, ixekizumab) can worsen or precipitate IBD — choose anti-IL-23 or anti-TNF for IBD overlap.
Check IGRA/PPD and HBV serologies before starting any biologic — TB and HBV reactivation are well-described.
References
AAD-NPF 2020-2021 — AAD-National Psoriasis Foundation Joint Guidelines: Biologics, Phototherapy, Topical Therapy, Pediatric Psoriasis, and Comorbidities (Menter et al., J Am Acad Dermatol)
GRAPPA 2021 — GRAPPA Treatment Recommendations for Psoriatic Arthritis (Coates et al., Nat Rev Rheumatol 2022)
NPF Treat-to-Target — From the Medical Board of the National Psoriasis Foundation: Treatment Targets for Plaque Psoriasis (Armstrong et al., J Am Acad Dermatol 2017)
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