• psoriasis
• lichen planus
• SLE

• definition- chronic, inflammatory dermatosis char by:
  • sharply demarcated, erythematous papules and plaques w/
  • abundant silvery white scales

• extensor surfaces of the:
  • extremities
  • knees
  • elblows
  • scalp
  • lumbosacral areas
  • sacral area
• nails (cause nail pitting, onycholysis)
• when it involves flexural, intertriginous areas = inverse psoriasis

• complex multifactorial disease influenced by genetic and immune mediated components
• strong association with HLA-C

1. sensitized populations of Th1 cells, Th17 cells, activated CD8 T cells enter skin and accumulate in epidermis
2. interactions between CD4, CD8 T cells, dendritic cells, keratinocytes give rise to a cytokine soup dominated by Th1 type and Th17 type cytokines
   1. IFN gamma, IL-12, IL-17, TNF
3. lymphocytes also produce growth factors for keratinocytes
4. epidermal hyperplasia leads to accelerated cell turnover rate, leading to improper cell maturation
   • epidural turnover goes from 23 days to 3-5 days

• epidermal hyperplasia (acanthosis)
• elongation of rete ridges and clubbing (thickening) of their lower portions
• focal or confluent mounds of parakeratosis
  • exocytosis of neutrophils form small aggregates within them = Munro microabscesses
• decreased or absent granular layer
• elongation and edema of dermal papillae
• dilated and tortous capillary vessels in the papillary
  • if you cut it, it will bleed (Auspitz sign)
• perivascular and interstitial infiltrate of lymphocytes in upper parts of dermis

• lichen planus
• lichnoid drug eruption
• benign lichenoid keratosis
• lichen nitidus
• lichen striatus

• pruritic
• polygonal
• erythematous to violaceous flat topped papules
• lesions can have linear distribution
• hypertrophic lichen planus has hyperpigmentation and hyperkeratotic lesions
• Wickham's striae (visible white lines in lacy pattern) may be vissible in some papules

• preferentially involves flexural surfaces
• nail dystrophy occasionally
  • longitudinal ridging
  • roughening
  • thinning and pterygium formation
• mucosal lesions (most common is oral)
  • can be erosive
• extremities, genitalia

1. expression of altered antigens in basal cell layer and dermoepidermal junction
2. elicits cell mediated cytotoxic immune response
   • proof: see T lymphocyte infiltrates and hyperplasia of Langerhans cells with this disorder

• hyper/orthokeratosis (NO parakeratosis)
• wedge shaped hypergranulosis
• irregular acanthosis with sawtooth rete ridges
• band like lymphohistocytic infiltrate obscuring dermo-epidermal junction
• eosinophilic squamatization of basal layer
• civatte bodies aka apoptotic bodies, colloid bodies- eosinophilic, deyskeratotic cell remnants in epidermis and papillary dermis

• inflammatory
  • pemphigus
  • bullous pemphigoid
  • dermaitis herpetiformis
• noninflammatory
  • epidermolysis bullosa
  • porphyria

• pemphigus foliaceus
• pemphigus vulgaris

IgG autoAb's against desmogleins (show links to specific HLA types)

• gross presentation
  • only involves superficial layers of epidermis (intraepidermal split)
    • much less erosive than vulgaris
  • slowly spreading eczematoid patches with or without vesicles
• common locations (oral lesions uncommon)
• • scalp
  • face
  • upper chest
  • abdomen
  • back
• Ab directed against desmosomal Ag (desmoglein 1)

• gross presentation
  • weeping flaccid bullous lesions that break easily (ulcerate), resulting in large denuded areas of skin (suprabasal split due to acantholysis)
• common location
  • oral mucosa
  • scalp
  • umbilicus
  • intertriginous areas
• usually during 4th and 5th decades of life (but can be at any age)
• Ab against desmosomal plaque protein plakoglobin (desmoglein 3)

• acanthlysis of granular layer or subcorneal, but can be subtle (subcorneal sep.)
• neutrophils, some eosinophils cmay accumulate in blister cavity
• mild to moderate eosinophilc exocytosis
• immunofluorescence shows intercellular IgG and C3 deposits through full thickness of epidermis in majority of cases

• suprabasal acantholysis
• tombstone arangement of basal cells at base of blister
• mixed inflammatory cells infiltrating blister
• indirect immunofluorescence of esophagus of monkey or guinea pig show IgG deposits in intercellular substance

• commonly in elderly persons
• gross appearance
  • subepidermal blisters
  • large, tense blisters
  • arise in either erythematous base or normal skin
• common locations (wide areas)
  • flexor surfaces of limbs
  • groin
  • axillale
  • lower abdomen
  • lower limbs (RARE)

• autoAb's against components of basement membrane BP180 (30-50%), BP230 (97%)
  • major components of hemidesmosomes
  • leads to in situ deposition of IgG, C3 on BM
    • allows for linear immunofluorescent pattern

• imminofluorescent pattern is linear (IgG, C3 on basement membrane)
• subepidermal blister formation associated with inflammatory infiltrates containing lymphocytes, eosinophils, neutrophils

• septal erythema nodosum
• lobular erythema induratam

• lesions may be preceeded by prodrome of:
  • fever
  • malaise
  • leukocytosis
  • arthralgias
• gross appearance
  • sudden onset
  • tender
  • bright or dusky red
  • subQ nodules
• common location (usually bilateral)- pretibial region of leg

• HS rxn to variety of genetic insults (although many times cause cant be IDed)
• genetic insults could include
  • Yersinia enterocolitica
  • deep fungal infection
  • streptococcal infection
  • TB
  • viral infection
  • drugs
    • oral contraception
    • sarcoidosis
    • ulcerative colitis
    • Crohn's disease
    • Behcet's disease
    • pregnancy
    • underlying malignancy

• septal inflammation
• perivascular infiltration of neutrophils (often focal aggregates), lymphocytes, macrophages, some eosinophils

• nodular vasculitis (represents a HS rxn)
  • primary vasculitis affecting deep vessels supplying lobuls of subcutis
  • w/subsequent necrosis and inflammation within fata
• TB (this lesion is considered a facultative tuberculoid)

• gross appearance
  • recurrent, often bilateral
  • tender
  • may evolve into blue-red plaques, often ulcerate
  • after ulcerate, eventually heal with atrophic scars
  • chronic and may persist months or yrs
• common location- calf
• usually in young and middle aged women

• lobular panniculitis
• lobular infiltration of neutrophils
• vasculitis of subQ arteries and veins
• arteries with inflammation, thrombosis, necrosis of vessel wall and infiltration of neutrophils
• epidermal ulceration may be present