Clinically, mild defined as <3 % BSA, moderate 3–10 %, severe >10 %

Extent of psoriasis can be measured by different indices; one of the most commonly used is the PASI (Psoriasis Area and Severity Index), based on redness, thickness, and scaliness of lesions

Nail findings include nail pitting, oil spots, onycholysis, thickened nails

Associated with systemic inflammatory comorbidities (e.g., increased risk of cardiovascular disease)

Pathogenesis = T-cell activation with cytokine mediated keratinocyte proliferation (Th1 and Th17), mostly CD8+ T-cells

Path: psoriasiform hyperplasia, parakeratosis, neutrophils in the epidermis (pathognomonic for psoriasis and AGEP) = “Munro’s microabscesses” in stratum corneum, “Spongiform pustule of Kogoj” in stratum spinosum

Koebner phenomenon = recurrence at site of trauma (also see in lichen planus, lichen nitidus)

Auspitz sign = lesions bleed when scale is removed, from thinned suprapapillary plates and dilated papillary dermal vessels

“Woronoff ring” = hypopigmented halo/ ring around plaques caused by inhibition of prostaglandin E2 (PGE-2)

Can be triggered by meds (SIR BLAM): Steroid rebound, interferon and ribavirin, beta blockers, lithium, anti-malarials

Early-onset psoriasis associated with HLA-Cw6

Unlike atopic dermatitis, psoriasis plaques rarely impetiginized (perhaps because no decrease in antimicrobial peptides)

Geographic tongue (benign migratory glossitis) can be associated; is psoriasiform on path

Treatment: topical steroids, vitamin D analogs, phototherapy, acitretin, methotrexate, cyclosoporine, anti-TNF biologics, others

Treatment with prednisone discouraged given apparent risk of flare of pustular psoriasis upon withdrawal