Papulosquamous Diseases Flashcards
Lichen planus clinical presentation
- acute or chronic inflammation of mucous membranes or skin, especially on flexural surfaces
- morphology: pruritic, well-demarcated, violaceous, polygonal, flat-topped papules
- common sites: wrists, ankles, mucous membranes in 60% (mouth, vulva, glans), nails, scalp
- distribution: symmetrical and bilateral Wickham’s striae: reticulate white-grey lines over surface; pathognomonic but may not be present
- mucous membrane lesions: lacy, whitish reticular network, milky-white plaques/papules; increased risk of SCC in erosions and ulcers
- nails: longitudinal ridging; dystrophic; pterygium formation
- scalp: scarring alopecia with perifollicular hyperkeratosis
- spontaneously resolves but may last for weeks, months or years (mouth and skin lesions)
- rarely associated with hepatitis C
- Koebner phenomenon
The 6 Ps of Lichen Planus Purple Pruritic Polygonal Peripheral Papules Penis (i.e. mucosa)
Lichen planus pathophysiolgoy
- autoimmune, antigen unknown
* lymphocyte activation leads to keratinocyte apoptosis
Lichen planus epi
- 1%
* 30-60 yr old, F>M
Lichen planus investigations
- consider a skin biopsy
* hepatitis C serology if patient has risk factors
Lichen planus management
- topical or intralesional corticosteroids
- short courses of oral prednisone (rarely)
- phototherapy or oral retinoids or systemic immunosuppressants (e.g. azathioprine, methotrexate, cyclosporine) for extensive or recalcitrant cases
Pityriasis Rosea clinical presentation
- acute, self-limiting eruption characterized by red, oval plaques/patches with central scale that does not extend to edge of lesion
- long axis of lesions follows skin tension lines (i.e. Langer’s Lines) parallel to ribs producing “Christmas tree” pattern on back
- varied degree of pruritus
- most start with a “herald” patch which precedes other lesions by 1-2 wk
- common sites: trunk, proximal aspects of arms and legs
Pityriasis Rosea etiology
suspected HHV-7 or HHV-6 reactivation
Pityriasis Rosea investigations
none required
Pityriasis Rosea management
- none required; clears spontaneously in 6-12 wk
* symptomatic: topical glucocorticoids if pruritic, cool compresses, emollients
Psoriasis presentation and pathophysiology
Pink papules/Plaques/Pinpoint bleeding (Auspitz sign)/Physical injury (Koebner phenomenon)
Silver scale/Sharp margins
Nail findings: pitting/onycholysis/Oil spots/ subungual hyperkeratosis/red lunula/ Itching (sometimes)
Immunologic with Th 1 and Th 17 helper cells being actively involved in the pathogenesis
Psoriasis triggers
- Physical trauma (Koebner phenomenon)
- Infections (acute streptococcal infection precipitates guttate psoriasis)
- Stress (can be a major factor in flares)
- Drugs (rebound from stopping systemic glucocorticoids, lithium, antimalarial drugs, interferon)
Smoking and heavy alcohol consumption
Psoriasis classification
- plaque psoriasis
- guttate psoriasis
- erythrodermic psoriasis
- pustular psoriasis
- inverse psoriasis
Psoriasis pathophys
• not fully understood, genetic and immunologic factors shortened keratinocyte cell cycle leads to Th1 and Th17-mediated inflammatory response
Psoriasis epi
- 1.5-2%, M=F
- all ages: peaks of onset: 20-30 and 50-60
- polygenic inheritance: 8% with 1 affected parent, 41% with both parents affected
- risk factors: smoking, obesity, alcohol, drugs, infections
Psoriasis ddx
• AD, mycosis fungoides (cutaneous T-cell lymphoma), seborrheic dermatitis, tinea, nummular dermatitis, lichen planus
Psoriasis investigations
• biopsy (if atypical presentation, rarely needed)
Plaque psoriasis clinical presentation
- chronic and recurrent disease characterized by well-circumscribed erythematous papules/plaques with silvery-white scales
- often worse in winter (lack of sun and humidity)
- Auspitz sign: bleeds from minute points when scale is removed
- common sites: scalp, extensor surfaces of elbows and knees, trunk (especially buttocks), nails, pressure areas
Plaque psoriasis management
• principles of management depends on severity of disease, as defined by BSA affected or less commonly Psoriasis Area and Severity Index (PASI)
• mild (<3% BSA)
■ topical steroids, topical vitamin D3 analogues, or a combinations of the two are first line
■ topical retinoid ± topical steroid combination, anthralin, and tar are also effective but tend to be less tolerated than first line therapies
■ emollients
■ phototherapy or systemic treatment may be necessary if the lesions are scattered or if it involves sites that are difficult to treat such as palms, soles, scalp, genitals
• moderate (3-10% BSA) to severe (>10% BSA)
■ goal of treatment is to attain symptom control that is adequate from patient’s perspective
■ phototherapy if accessible
■ systemic or biological therapy based on patient’s treatment history and comorbidities
■ topical steroid ± topical vitamin D3 analogue as adjunct therapy
topical treatments for chronic plaque psoriasis - corticosteroids vs vitamin D
Corticosteroids perform at least equally w ll to vitamin D analogues and are associated with fewer local adverse events. The risk of skin dermal atrophy with long-term use of corticosteroids for people chronic plaque psoriasis remains unclear
Calcipotriol is a Vitamin D Derivative Dovobet® - compsed of…
calcipotriene combined with betamethasone dipropionate and is considered to be one of the most potent topical psoriatic therapies
Emollient mechanism in psoriasis
reduce fissure formation
salicyclic acid 1-12% mechanism in psoriasis
remove scales
Tar (LCD: liquor carbonic detergens) mechanism in psoriasis
Inhibits DNA synthesis, increases cell turnover
Tar (LCD: liquor carbonic detergens) downside
poor long-term compliance
