4/21 Skin Diseases2 - Corbett Flashcards
pemphigus vulgaris
autoimmune blistering disorder
loss of keratinocyte-keratinocyte adhesion due to IgG antibodies against desmosome components (desmoglein-1 and -3)
most common type of pemphigus but still RARE
M=F, age 40-60
- almost all pt have MUCOSAL INVOLVEMENT
- oral cavity ulcerations (also conjunctiva, nose, esoph, vulva, vagina, cervix, anus)
- skin blisters (flaccid blisters on nl skin) → positive Nikolsky sign
- blisters break easily
tx: hi dose oral steroids for life
Nikolsky sign
bullous pemphigoid
chronic autoimmune subepidermal blistering
- entire epidermal layer lifted off dermis due to antibodies targeting BPA2 (hemidesmosome component)
M=F, onset about 65yo
prodrome phase w pruritis eczematous, papular, urticaria-like skin lesions (wks to months)
clinical sx
- trunk, extremity flexures, skin folds
- bullae usually under 2cm diameter, TENSE
- → DON’T RUPTURE EASILY (unlike blisters in pemphigus)
- heal without scarring
- much less common involvement of mucous membranes
bullous pemphigoid
vs
pemphigus vulgaris
dermatitis herpetiformis
assoc w Celiac disease
- IgA abs against gluten cross react w reticulin in basement membrane → granual IgA deposition at tips of dermal papillae
M > F, 30-40yo
clinical:
- grouped lesions on extensor surfaces of elbows, knees, buttocks
- occasional vesicles
- subepidermal blisters evident
comparisons of PV, BP, DH
erythema multiforme
young adults (20-40yo)
strong association with infection (90%) - also meds, malignancy, autoimmune disease, immunizations
due to cell-mediated immune response against antigens deposited in skin
target lesions!
SJS
TEN
Stevens Johnson Syndrome
Toxic Epidermal Necrolysis
causes
- usually drugs (80% of time; usually in first 3wk)
- allopurinol, carbamazepine, phenobarbital, sulfonamides
- infection (mycoplasma in kids)
- risk factors: HIV, HLA-A, HLA-B
skin detachment
- SJS: under 10% body SA
- TEN: over 30% body SA
affects mucous membranes in 90%+, usually 2 or more distinct sites (ocular, oral, genital)
30% mortality
drugs/causes activate CD8 cytotoxic T cells → release enzymes
- granulysin
- granzyme B
- perforin
enzymes target keratinocytes and kills them
urticaria
type 1 HSR
all ages, but more 20-40yo
lesions (usually trunk, extremities) transient, usually resolving in 24hr BUT episode can last for days
eczema types
- contact dermatitis
- atopic dermatitis
- drug eczema
- photoeczema
- primary irritant dermatitis
clinically:
- red papules and vesicles
- persistent? acanthosis and hyperkeratosis → raised, scaling plaques
cause: exposure to an antigen
tx: stop exposure
histo (vs urticaria) :
- lots of edema!
- perivascular lymphocytic infiltrate
eczema pathogenesis
type IV hypersensitivity rxn to an antigen
acne vulgaris
disease of pilosebaceous follicles
pathophys
- puberty results in glandular hypertrophy
- Propionibacterium acnes within follicle makes pro-infl FAs → secondary infl of follicle
acne vs rosacea
psoriasis
polygenic predisposition + triggering environmental factors (trauma, meds)
HLA-Cw (70%)
- well-demarcated, pink to salmon-colored plaque covered by loosely aherent silver-white scale
- histo: uniform elongation of rete ridges (pathognomonic) w dilated blood vessels, thinning of suprapapillary plate, intermittent parakeratosis
- epidermal and perivascular dermal infiltrates of lymphocytes w neutrophils occasionally aggregated in epidermis
pathophys
- role for Th17 cells, IL17A, IL23, dendritic cells
psoriasis
*remove scales? BLEED - AUSPITZ SIGN
lichen planus
6purples
- pruritic
- purple
- polygonal
- planar
- papules
- plaques
*see a line or band of infl cells (lymphocytic infiltrate)
erythema nodosum
typically lower extremities (tibial surfaces)
raised red/purp nodules
v painful
panniculitis involving infl of septa in subcut fat tissue
erythema migrans
erythema marginatum
verruca plana
molluscum contagiosum
herpes zoster
don’t cross midline!
keloid vs hypertrophic scars
keloid extends beyond borders of original scar
