Hives;  localized mast cell degranulation with resultant dermal microvascularhyperpermeability.

Pruritic, edematous plaques - wheals.  IgE is released

w or w/o asthma and allergic rhinitis

dry skin and eczema

self-limiting immunological rxn involving CD8+ cells and their attack on epithelial cells

most severe manifestation would be stevens johnsons disease

inflammatory lesion of subQ fat more common in women than men

usually erythmatous nodules which are painful on anterior shin

Increased epidermal cell turnover causes marked epidermal thickening (acanthosis) with downward elongation of rete ridges

leads to test tube like appearance.  what disease are we referring to?

psoriasis

stratus granulosum is thinned or non-existent

if nuclei are still present in stratus corneum, this is abnormal

strong HLA-C correlation

activated CD4+ and CD8+ cell accumulate in the epidermis and release cytokines

1-2% of normal population but up to 83% of HIV population

occurs in large area of sebaceous glands and hair covered areas

dandruff from a greasy based that dried

what is LICHEN PLANUS?

what are some of its major Ps?

histologic findings?

self-limiting flat topped papules highlighted by white tops or lines.  WICKHAM STRIAE (hyperplasia of stratum granulosum)

common on wrists and ankle

associated with HEP C

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histologic findings, lymphocytes attack basale layers and histo looks saw-toothed along this layer; an anucleated basale layer may start to become confluent wtih a papillary dermis

warts; caused by human papilloma virus

-caused by poxvirus

-transmitted p2p

-multiple lesions of trunk and anogenital areas

-puritic lesions which can have molluscum material squeezed out of the center

-superfiscial bacterial infection

-very contagious

-commonly caused by strep and staph

-mainly involves face and hands

-accumulation of neutrophils beneath the stratum corneum forming subcorneal pustule; bacteria are present; superficial dermal inflammation

1.Bacteria in epidermis evoke immune response which is locally destructive and leads to serous exudate with formation of scale crust. If blister forms, bacteria produces a toxin which specifically cleaves desmoglein 1, protein responsible for cell-to-cell adhesion in uppermost epidermal layers

TINEA VERSICOLOR

 – upper trunk,

Caused by Malassezia furfur, a yeast

Not a dermatophyte - spaghetti and meatballs

dissolution of intracellular attachments (known as acantholysis) caused by autoantibodies, IgG; a suprabasal acantholytic blister (as if vulgaris) resembles a row of tombstones

vulgaris is most common.  blisters easily rupture and immunosupressive reagents are warrented

desmosomes between cells are attacked

a type II rxn

these blisters rupture less easily than those in pemphigus

they are NONancantholytic

eosinophils are found directly below the cell layer

may be generally found beneath the epidermal basal layer

NEGATIVE NIKOLSKY

the Ag response mainly affects hemidesmosomes in pemphigoid unlike in pemphigus vulgaris; the Ags to BPAG2 are the ones the cause the blistering a linear pattern of this Ig laying down is how you can determine it to be bullous pemphigoid

celiac disease

IgA forms to gluten and discontinuous deposits of the Ag can be see on immunofluoresence

excessive keratin buildup, may be genetic

compacted stratus corneum is observed leaving a scaly like appearance.  due to a defect in desquamousation, the scales are retained

open comedones - black head (black keratin plug)

closed comedones - whitehead, no central plug

pts. have a high level of cathaliciden, and important mediator of immune response.

it is usually structurally different, however, and this may cause inappropriate perifollicular lymphocyte infiltration