Pathogenesis
This is the immune pathway is most strongly associated with plaque psoriasis.
What is the IL-23/Th17 pathway?
These are the two active components of first-line defense cream.
What are calcipotriene + betamethasone?
This is the primary anti-inflammatory effect of topical corticosteroids.
What is suppress local inflammatory cytokine/immune activity?
This is generally the first-line treatment for mild, localized plaque psoriasis.
What is topical therapy?
This is why OTC dandruff shampoo might fail to adequately treat plaque psoriasis.
Dandruff shampoos often target dermatitis rather than the immune-mediated psoriasis.
This cytokine produced by dendritic cells promotes Th17 activity in psoriasis.
What is IL23?
This is how calcipotriene reduces psoriatic plaque formation.
What is decreasing keratinocyte proliferation and promoting differentiation?
These are two local adverse effects of prolonged high-potency topical steroid use.
What are atrophy, striae, telangiectasias, hypopigmentation, bruising, etc.
A patient has persistent psoriasis despite appropriate topical therapy. This is one possible next-step treatment option.
What are phototherapy, systemic therapy, or biologic therapy, etc.?
A patient applies a high-potency steroid twice as often as prescribed. This is why this is potentially harmful.
What are (some adverse effects)?
This is how activation of the IL-23/Th17 pathway ultimately produces psoriatic plaque.
IL-23 → Th17 → IL-17/IL-22 → keratinocyte proliferation/inflammation
This is how ustekinumab interferes with the pathogenesis of psoriasis.
What is ustekinumab blocks the shared p40 subunit of IL-12/IL-23?
This is why high-potency topical steroids should generally be used for limited durations.
What are minimize skin atrophy and systemic absorption?
This type of therapy uses controlled ultraviolet exposure to treat more widespread psoriasis.
What is Narrowband UV-B?
This is why tacrolimus may be preferred over a high-potency steroid for psoriasis involving the face or skin folds.
What is tacrolimus avoids skin atrophy that extended corticosteroid use can result in?
A patient has erythematous plaques with silvery scale. List the sequence from dendritic-cell activation to keratinocyte hyperproliferation.
Dendritic cell activation → IL-23 → Th17 cells → IL-17/IL-22 → keratinocyte hyperproliferation → psoriatic plaque.
Compare the targets and mechanisms of ustekinumab and tacrolimus.
Targets monoclonal antibodies; IL-12/23 p40; blocks signaling.
Targets calcineurin inhibitor; Blocks T-cell activation and IL-2 production.
A patient develops thin, fragile skin and visible superficial blood vessels after prolonged steroid use. Explain the pathophysiology of these adverse effects.
Steroids lower glucocorticoid receptors, lowers fibroblasts and collagen.
A patient has moderate-to-severe plaque psoriasis that remains uncontrolled with topical therapy. What broad categories of treatment should be considered next?
What are phototherapy, systemic treatments, or biologics?
A patient cannot afford a biologic medication despite having severe psoriasis. Identify two healthcare-access barriers and explain how they could affect treatment.
What are SES status, coverage, poor physical access, etc.?