• Hives-pruritic edematous elevation of skin
• Type 1 hypersensitivity= release of histamine from mast cell. Dermatographism. 

1. initial sensitization to allergen
2. CD4 TH2 activated--> release IL-4, IL-5--> IL-4 activate IgE production by B cell, IL-5 activate eosinophil production--> IgE Ab bind to allergen on re-exposure and to the Fc receptor on mast cell
3. mast cell activation releases histamine and other mediator--> itchy, red , puffy reaction

• IgE dependent: Ag induces releases of mediators from mast cell via sensitization with IgE.
• IgE independent: Ag directly incite mast cell degranulation
• complement mediateD: hereditary angioneurotic edema- inherited deficiency of C1 inhibitor resulting in uncontrolled activation of early component of complement system and production of vasoactive mediators (lost of control lead to wide spread of mediators)

• type I HS-IgE mediated
• A/w asthma and allergic rhnitis
• children-dry skin/eczema on cheek and extensors.
• adult: dry skin/eczema on hands, eyelids, elbows and knees.

• type IV Hs rxn
• poison Ivy, nickle in jewelry

• Type I: immediate IgE ab mediated action of mast cells
• Type II: ab dependent (complement dependent, complement independent, etc)
• Type III: deposition of Ag-Ab complexes
• Type IV: Ab independent T cell mediated rxn (cell mediated toxicity)

ag at epidermal surface taken up by dendritic langerhan cell--> langerhan cell get to lymph node via lympathic-->present Ag to CD4+ T cell-->T cells proliferate into effector and memory cell.

Upon re-exposure, Memory T cell migrate to affected site, adhere to post-capillary venules-->extravasate into tissue and release cytokines and chemokines-->recruit inflammatory cells--->itch, and redness (within 24 hr)

• some kind of hypersensitivity rxn to drug or infection.
• self-limiting immunologic rxn that involve CD8+ T cell's attack in epithelial cells to infection (herpes, simplex, mycoplasma, etc) ,drugs (sulfonamides, PNC, barbiturates, salicylates, antimalarial) , and malignant disease (lupus, dermatomyositis, polyarteritis nodosa). 
• presentation: macule, papule, vescile, bullae ( target lesion red macule with pale and eroded center)
• Stevens-Jonhson Syndrome=severe erythema multiforme--> hemorrhagic crust.

• epithelial cells killed by skin-homing (CLA+) CD8+ cytotoxic T lymphocytes
• these cytotoxic cells are prominent in the central portion of the lesion, whereas CD4+ helper cells and langerhan cells are more common in the raised, erythematous periphery.

• inflammatory lesio of subQ fat (panniculitis)
• women>men
• A/w coccidiodomycosis, histoplasmosis, tb, leprosy, strep, sarcoidosis, ulcerative colitis, pregancy
• presentation: raised, erythematous, painful nodules on the anterior portion of the shins.

• a/w arthritis, myopathy, spondylitic joint dz, AIDS
• salmon-colored plaque covered by loose silver-white scale.
• Auspitz sign: bleeding when scales are scraped away.
• onycholysis, pitting, discoloration of nails
• CD4+ and CD8+ accumulate in epidermis, facilitate release of cytokines that act as growth factor for keratinocytes (T cell mediated dz)
• acanthosis w/ parakeratotic scaling (nuclei still in stratum corneum)

• "test tube in a rack" appearance
• increased epidermis cell turnover caused ancanthosis (epidermal thickening)
• stratum granulosum is thinned or abscent; extensive overlying of parakeratotic scale.
• autspits sign: due to thining of epidermal cell layer overlying dermal papillae where blood vessels are.
• neutrophils form small aggregates w/in parakeratotic stratum corneum-->munro microabscesses.

• genetic, environmental
• strong HLA-C association particularly HLA-Cw 0602
• sensitized CD4+ TH1 and TH7 cells and activated CD8+ effector T Cell enter the skin and acumulate in the epidermis; cytokines released included IL-12, Interferon gamma, TNF and IL-17

• 83% rise incidence in HIV pats.
• skin regions with high desnity of sebaceous glands
• macule and papule on erythematous-yellow, greasy base a/w scaling and crusting
• unknown etiology
• dandruff in adult, cradle cap in infant.
• spongiosis and acanthosis,
• superficial perivascular inflammatory infiltrate
•  may see parakeratosis containing neutrophils and serum present at ostia of hair fillicles- "follicular lipping"

• 6 P's= pruritic, purple, polygonal, planar, papules, plaques
• flat topped papules, highlighted with white dots or line known as wickham striae (hypergranulosis-hyperplasia of the stratum granulosum)
• common on wrist and ankles; oral mucosa
• a/w hep C

• dense, infiltrate of lymphocytes in the dermoepidermal junction lead to degeneration and necrosis of basal keratinocytes.
• "saw toothed" dermoepideral inferface caused by infiltration of destructive lymphocytes
• anucleated, necrotic basal cells become incorporated into inflammed papillary dermis--> colloid (civatte) bodies (apoptotic keratinocyte)

more histology of lichen panus

this show hypergranulosis of stratum granulosum

presence of apoptotic keratinocytes (Civatte bodies) in the basal layer

lymphocytic infiltration against undersurface of epidermis (dermoepidermis junction)

• caused by HPV
• direct contact transmission
• self-limited, regress within 2 year
• verruca vulgaris-esp on hands, papules with pebble like surface
• verruca plana (flat)-face or dorsal hands
• verruca plantaris/palmaris
• condyloma accuminatum-venereal wart

• epidermal hyperplasia (papillomatous)
• cytopasmic vacuolization (koilocytosis) of more superficial epidermal layers which produce haloes of pallor around infected nuclei-viral cytopathic effect.
• different HPV subtypes: HPV 16 a/w dysplasia, in situ carcinoma in genital; HPV 5 and 8 a/w squamous cell carcinoma.

• viral skin infection, caused by poxvirus via direct contact
• pruritic, pink to flesh clored, umbilicate dpapules-"curdy" material can be squeezed out of center-contain molluscum bodies (viral particles seen as homogenous cytoplasmic inclusion in cells of stratum granulosum and corneum)
• microscopically, cuplike verrucous epidermal hypeplasia.

• superficial bacterial skin infection, highly contagious
• "honey crusted color"
• impetigo contagiosa (group A, beta-hemolytic strep) and bullosa (straph aureus)
• now both contagiosa and bullosa usually caused by staph aureus.
• presentation: in face/hand. macule, pustule, erosion. bullae may form.
• mirco-accumulation of neutrophils beneath the stratum corneum forming subcorneal pustule; bacterial are present->superficial derma inflammation.
• bacteria in epidermis-->evoke immune response-->destruction lead to serous exudate--> formation of scale crust.
• if blister formed, bacterial produces a toxin which cleaves desmoglein 1 (pt responsible for cell to cell adhesion in uppermost epidermis layers).

what are the superficial fungal infection of skin? give some characteristics pertain to them.

• tinea capitis (scalp)
• tinea barbae (beard AND M'stach, Ryan!)
• tinea corporis (body)
• tinea cruris (inguinal region)
• tinea pedis (foot)
• tinea versicolor (upper trunk, malassezia furfur-,a yeast- show x-mas tree pattern or meatball and spaghetti)

What's Superficial fungal skin infection? appearance? histology

• confined to stratum corneum
• caused by dermatophytes (grow in soil and animal)

• a bullous (blistering) disease
• Autoimmune result in dissolution of intercellular attachments within epidermis.
• variant includes pemphigus vulgaris (most common-on skin scalp- can rupture and leave shallow eriosion and crusting), vegetans, foliaceus, erythematosus, and paraneoplastic.

• acantholysis-lysis of intercellylar adhesion btw keratinocytes; cells become rounded.
• suprabasal acantholytic blister forms (pemphigus vulgaris) with a single layer of intact basal cells resembling a row of tombstone. 
• superficial dermal infiltration by lymphs, histiocytes, and eosinophils.

• bullous dz, pt 30-50s
• autoimmune: IgG ab against intercellular attachment sites, desmosomes, between keratinocytes (type II HS rxn). target desmogleins.
• presentation: invov. mucosa and skin of scalp, face, axilla, groin, trunk. may present as oral ulcer. positive nikolsky sign (outer epidermis separates from basal layer within minimal pressure)

What's bullous pemphigoid? presentation? histology? differences from pemphigus vulgaris??

• common in elderly
• oral lesion is common
• tense bullae that do not rupture easily as in pemphigus.
• autoimmune: IgG ab against hemidesmosome (bullous pemphigoid ag 1 and 2---BPAG1 & 2) at the basal cell-basement membrane interface.
• only ab to BPAG2 cause blister. ab to BPAG2 result in continuous, linear deposition of IgG along basement membrane and fixation of complement, and recuitment of eos and neutros
• Veiscles are SUBEPIDERMAL, NO ACANTOLYTIC CELLS in vesicle fluid. no tombstone clinging on basal layer like pemphigus
• basal layer vacuolization--> fluid filled blister
• early lesion show superficial and deep pervasion of eosinopgils and lymphocytes.
• Presentation: tense bullae, clear fluid, mostly occur in flexor surface, inner thighs
• NEGATIVE NIKOLSKY-bullae do not rupture easily.

• urticaria (hives), grouped vesicles, usually symmetrical
• a/w celiac dz
• IgG abs to gluten which cross react with reticulin, a part of anchoring fibrils that hold the epidermal basement membrane to superficial dermis. this injury and inflammation causes a subepidermal blister. 
• fibrin and neutrophils accumulate at tips of dermal papillae forming microabscesses.  Basal cells overlying these microabcesses show vacuolization and focal DE separation-->subepidermal blisters.

• "fish scale"-build up compacted stratum corneum a/w loss of normal basket weave pattern, little if any inflammation.
• chronic excessive keratin build up due to defective dequamation.
• AD or acquired.

• due to hormones, drug-induced, occupation
• noninflammatory:

1. blackheads: open comedones-small follicular papules with a central black keratin plug
2. whitehead: closed comedones, no central plug

• Inflammatory:

1. inflammation of pilosebacoeus cyst present with inflammatory erythematous papules, pustules, nodules, and cysts
2. due to abnormal keratinization of the follicular epithelium and increased sebum production which is androgen-dependent.

process in which acne developed?

1. change in keratinization of lower follicular infundibulum with keratin plug out flow of sebum
2. sebaceous gland hypertropy
3. colonization of hair follicle with lipase-synthesizing bacteria (propionibacterium acnes) which convert lipids in sebum to pro-inflammatory fatty acids.
4. acute inflammation of follicle (release of cytotoxic and chemotactic factors)

• esp women
• phgih skin levels of endogenous antimicrobial peptide cathelicidin (mediator in innate immune response, qualitatively different because of alternative processing by serine protease)
• 4 stages:

1. flushing episodes
2. persistent erythema and telangiectasia
3. pustules and papules
4. rhinophyma-persistent thickening of nasal skin because of confluent erythematous papules and prominence of follicles.

• nonspecific perifollicular infiltration of lymphocytes; sebaceous glad hypertropy and follucular plugging because of keratotic debris.