• papillary dermis
• reticular dermis
• adnexal structures
  • pilosebaceous unit
  • apocrine and eccrine glands

• formation of anuclear keratin layer

• modes of keratinization characterized by retention of the nuclei in the stratum corneum

• epidermal hyperplasia
• marked thickening of epidermins due to increase in number and size of epithelial cells

• premature keratinization in cells that are not in the keratinizing surface layer of the skin
• faulty and premature keratinization of individual keratinocytes
• microscopic features
  • usually intensly eosinophilic
  • small, dense, basophilic nuclear remnant

• loss of intercellular cohesion between keratinocytes
• intercellular connections are broken, producing rounded cells that are dissociated from each other

• surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae
• marked increase in length of dermal papillae and rete ridges

• intercellular edema of epidermis
• fluid accumulates between cells, pulling them apart while keeping the intercellular connections largely in tact
• microscopic appearance
  • cell surounded by broad white band w/ tiny dark cross strips = closed zipper

• small discolored patch or spot on skin
• FLAT (not elevated or depressed from skin surface)

• slightly larger circumscribed elevation (greater than 0.5 cm)

• small, circumscribed, solid elevation on skin (less than 0.5 cm)

• small circumscribed elevation of skin containing fluid

• large blister appearing as circumscribed area of separation of epidermis from subepidermal structure (subepidermal bulla) or 
• circumscribed area of separation of epidermal cells (intraepidermal bulla) caused by presence of serum, and sometimes an injected substance

• inflammatory conditions of skin, particularly w/ vesculation in acute stage
• typically erythematous, oedematous, papular and crusting
• often followed, by lichenification, scaling, occasionally by duskiness of erythema, and, infrequently hyperpigmentation

• urticaria
• acute eczematous dermatitis
• erythema multiform

• appearance- circumscribed, evanescent, erythematous, usually pruritic, area of edema
• lesion lasts several hours
• mechanism of action
  • IgE dependent (exposure to different antigens) or IgE independent (chemical)
  • local mast cell degranulation
  • results in dermal microvascular hyperpermeability
  • deficiency in C1 leads to hereditary angioneurotic edema, due to uncontrolled activation of early components of complement system, producing vasoactive mediators

• superficial dermal edema and sparase inflammatory infiltrate in acute urticaria
• variable perivascular and interstitial infiltrate consisting of mast cells, lymphocytes, eosinophils, neutrophils

• allergic contact dermatitis
• atopic dermatitis
• drug related eczematous dermatitis
• photoeczematous dermatitis
• primary irritant dermatitis

• immune dysfunction resulting in IgE sensitization and secondary epithelial barrier disturbance
• defect in epithelial cells leading to defective barrior problems with immunological aspects being epiphenomena

• adults, youths- flexural surfaces
  • antecubital fossae
  • sides of necks
• infancy (first few months of life)- head, neck, diaper area, extensor surfaces of extremities
• appearance in blacks- may appear papular

1. Ag's uptaken at epidermal surface by dendritic Langerhans cells
2. Langerhan cells migrate to dermal lymph nodes via lymphatcs
3. Ag's presented to naive CD4 T cells
4. CD4 cells activated and develop into effector and memory cells
5. upon re exposure to Ag, the memory T cells migrate to affected skin site of Ag localization
6. CD4 T cells adhere to post capillary venules, extravasate into tissue
7. CD4 T cells release cytokines and chemokines to recruit inflammatory cells characteristic of eczema

account for initial erythema and pruritus of delayed hypersensitivity

• chronic UV light exposure
  • injures Langerhans cells, preventing sensitization to contact Ag's
• neuropetide release from nerve endings that terminate near Langerhans cell body

• inflammatory rxns
• epidermal spongiosis (swelling)
• progressive acanthosis (thickening of epidermis due to increase size and number of cells)
• perivascular inflammatory infiltrates in dermis
• you will be able to see bridging/desmosomes between cells

• usually become milder and often resolve after puberty
• in adults, severe cases rarely evolve into erythroderma
• in rare carss, adults may develop keratosis pilariis

• individuals with personal and family history of atopy
  • inherited disorder characterized by:
    • urticaria
    • asthma
    • hay fever

• pruritic
• erythema
• scaling
• excoriation
• occasional vesiculation
• secondary bacterial infection (esp. in infants because they scratch)

• symptomatic discrete blanchable erythematous macules and papules aka target lesions
• often associated with itching and burning sensation

Acute self limited dermatosis characterized by varying clinical manifestations

• infections
  • histoplasmosis
  • coccidioidomycosis
  • typhoid
  • leprosy
• administration of certain drugs
  • sulfonamides
  • penicillin
  • barbituates
  • salicylate
  • hydantoins
  • antimalarials
• malignant disease (carcinoma, lymphoma)
• collagen vascular disease
  • SLE
  • dermatomyositis
  • polyarteritis nodosa

• inflammatory rxn characterized by interface or vacuolar alteration along basal layer of epidermis
• individual keratinocyte death
• dermal edema
• scant superficial dermal lymphoid infiltrates

• hypersensitivity reaction characterized by immunologically mediated epidermal cell injury
• epithelial cells killed by CD8 T cells
• when looking at lesions:
  • CD8 T cells are more prominant in the central portion of the lesion
  • CD4 T cells and Langerhans cells are more common in the raised, erythematous periphery