-no acanthosis

-no hyperkaratosis

-epidermal spongiosis

-intraepidermal vesicles

-mixed perivascular inflamm infiltrate of lymphocytes and some eosinophils

-hyperkeratosis

-acanthosis

-mild spongiosis, no vesicles

-mixed perivascular infiltrate

thickening of dermal collagen, vertical streaking with chronic scratching

-dermal edema causing collagen bundles to separate

-may look like normal skin or only subtle changes

-normal epidermis

-perivascualr infiltrate

-epidermal and dermal junction vacuolization (damage to basal cells with intracytoplasmic vacuole formation)

-vacuoles can lead to subdermal blister

-inflamm infiltrate at the junction and perivascular

-necrotic keratinocytes/epidermis (worse in SJS, TEN)

-hyperkaratosis

-parakaratosis

-acanthosis

-muno microabscesses-- neutrophils in the stratum corneum

-decreaed granular layer

-thinning of epidermis over the dermal papillae (Auspitz's sign for diagnosis)

-dilated vessels in papillae

-hyperkaratosis

-focal, wedge-shaped hypergranulosis

-"saw tooth" pattern of irregular acanthosis

-lichenoid infiltrate- dense band-like dermal infiltrate ofmainly lymphocytes "hugging" underside of epidermis

-basal cell layer damage (vacuolization)-> pigment incontinence

-civatte bodies-necrotic keratinocytes

Pemphigous vulgaris- histopath

-intraepidermal blister with "tombstoning effect

-intact basal layer

-acantholysis (loss of intercellular adhesion)

-superficial dermal perivascular eosinophils

-DIF:  intercellular IgG throughout epidermis forming "chicken wire" pattern

-subepidermal blister (deeper than pemphigous vulgaris)

-no acantholysis

-perivascular infiltrates with eosinophils (like pemphigous vulgaris)

-DIF-- linear depostis of IgG and C3 at the basement membrane zone (positive in almost 100%)

-neutrophils, eosinophils and fibrin at tips of dermal papillae ("microabscesses")

-multiloculated microabscesses become a subepidermal blister

-intense papillary dermal infiltrate

-DIF- granular deposits of IgA at tips of dermal papillae

Macule

Patch

Papule

Plaque

Macule- flat lesion different color than skin < 5 mm

Patch- Flat lesion different color than skin > 5 mm

Papule- raised lesion, solid, < 5mm

Plaque- raised flat topped lesion > 5mm

Vesicle

Bulla

Pustule

Nodule

Vesicle- circumscribed, elevated collection of fluid < 5 mm

Bulla- circumscribed collection of fluid > 5 mm

Bulla and vesicle can be located within intraepidermal or below epidermis

Pustule- pus varies in size

Nodule- solid, palpable lesion below epidermis

scale=

crust=

scale- abnormal shedding or proliferation of stratum corneum

crust- dried serum, pus, blood on skin

hyperkeratosis with pyknotic nuclei in the cornified layer

usually with decreased granular layer

seen in disease with rapid cell turnover

Spongiosis

Dyskeratosis

Acantholysis

spongiosis- edema b/w spinous cells = widened intercellular spaces

dyskeratosis- premature abnormal keratinization of cells having eosinophilic cytoplasm and small dark nuclei

acantholysis- loss of cohesion between epidermal cells that leads to intraepidermal celfts and vesicles

• type 4 delayed hypersensitivity reaction in person sensitized and the re-exposed to antigen
• Acute- pruitic, erythematous oozing papules or vesicle
• may be linear as in poison ivy or specific pattern

- Nonallergic reaction w/ no prior sensitization

-caused by chemical agents

-dry skin and thick skin less likely to react

Eczematous dermatitis- atopic dermatitis

In infants

In adults

- common pruiritic disease- genetic predisposition

infants- acute eczema with oozing/crusting papules on head, neck or extensor

Adults- chronic eczema with scaling and lichenification in flexural areas

Eczematous dermatitis-

Photodermatitis

and

Drug-related eczematous dermatitis

Photodermatits- rxn in sunexposed areas. Different mechanisms, seen w/ drugs (nsaids)

Drug related eczematous dermatitis- spongiotic rxn coinciding with use of medication. systemic contact dermatitis

Urticaria

Type of rxn

Appearance

most common cause in kids

acute vs chronic

• vascular reaction causing pruiritic red or white wheals and possibble subcutaneous swelling- angioedema of eyes and lips
• IgE type 1 reaction.
• Mast cell degranulation release of histamine and heparin causing increased permeability of capillaries and fluid extravasation into tissue
• On covered areas acute <6 wks and chroni >6 wks
• in kids- strep infections
• Clearing of central region of lesion= annular lesion

The spectrum of disease for Erythema Multiforma?

Which one is associate w/ infections?

Which one is associated most w/ drugs?

Spectrum=

• Erythema Mulitforma
• Steven's johnson syndrome
• toxic epidermal necrolysis TEN

Erythema multiforma is most associated with infections- HSV and mycoplasma

SJS and TEN assoc w/ drugs- NSAIDS, antibiotics etc

- usually no or mild prodrome

- "target" with three zones (central dusky purpura or vesicle, erythematous raised pale ring, peripheral rim of macular erythema)

- symmetric distribution of hands and feet

- maybe mild oral involvement

Dx

• biopsy erythematous rim of target lesion

• febrile prodrome
• * mucous membrane prominent
• atypical target lesion that are diffuse and confluent
• SJS about 10% body
• TEN>30%

Dx

• biopsy erythematous skin adjacent to sloughing skin

• isomorphic response- appearance of lesions at sites of trauma
• IN psoriasis

abnormal differentiation, keratinocyte hyperplasia, and inflammation

males= females

Average age onset- 27 years old

• well demaracated erythematous plaque with white scale
• on nails, scalp, knees, elbows etc
• asymptomatic, itching, or burning

• 2-5 mm erythematous papule
• diffusely distributed
• abrupt onset after acute infection- usually strep pharyngitis. Usually pts <30 yo

• may be intial sign
• nail pitting
• oil spots- oncholysis- separation of nail plate from nail bed
• subungual debris-

oil spots- separation of nail plate from nail bed

seen in psoriasis

adalimumab

infliximab

etanercept

side effects- TB reactivation, Lupus like, demyelinating disease

alefacept

side effect lymphopenia

Drug for psoriasis that is off market but still in our packet.

Binds LFA -1 and ICAM-1

efalizumab

side effects- Thrombocytopenia and exacerbates psoriasis- rebound flare

Lichus Planus

5 Ps= pruiritic, planar, purple, polygonal papules

Lesions on flexor surfaces and above ankles, lumbar region

Koebnerization

Characterized by immun rxn of helper T cells at basal layer

Age of onset 30-70's Women increase in incidence as age

Lichus planus has a higher incidence in what patients

Describe the course of Lichus planus

Patient with Hep C!

The course of the disease if unpredictable. 2/3 of pts have lesions for <1 yr, 50 % have recurrences, mucous membrane is usually chronis

50% have mucous membrane disease. (may have genital involvement)

Oral involvement:

• Ulcerative- have increased risk squamous cell cancer
• Reticulate- most common
• or
• Atrophic

Rare autoimmune disorder.

Antibodies cause loss intercellular cohesion and blister formation secondary to antibodies

Antigen- Desmoglein-1 and 3

Common in jewish ppl

may be drug induced

How does pemphigus vulgaris heal?

Describe blisters of Pemphigus vulgaris

Pemphis vulgaris heals with hypermentation but no scarring

Its a superficial blistering disease. Flaccid blisters and erosion on skin and mucous membranes. Blisters can be clear or hemorrhagic

Can have esophageal involvement in pemphigus vulgaris

Positive in Pemphis vulgaris. indicates superrficial blistering

 pressure on skin near blister causing the epidermis to shear off

Positive in pemphigus VUlgaris. To indicate superifical blistering.

gentle pressure on an intact blister will force fluid under adjacent skin away from pressure site

- biopsy of intact blister

punch biopsy perilesional skin for DIF

Or IIF os serum

autoimmune suubepidermal blistering disorder

IgG antibodies to basement membrane antigens= hemidesmosomal proteins

average age- 65-75 male=female

Clinical characteristics of Bullous pemphigoid

Appearance of blisters

Location

Healing

• Large tense bullae and erythematous patches and urticarial plaques
• pruiritis
• like groin, axillae, and flexor surfaces of forearm
• Rupture and heal spontaneously
• rare muscoal involvement

Dermatitis herpetiformis

Associated with what condition

Genetic predisposition?

description of skin rash

healing

Dermatitis Herpetiformis

• Is associated with gluten sensitive enteropathy. Also increased incidence of thyroid disorders and lymphomas
• genetic predisposition- HLA  B8. Rare in blacks and asias. Males >females
• Chronic, relapsing, bilaterally symmetrical papulovesicular lesions on red base. If bullae present they are tense.
• Spontaneous remissions by a week and then new crop of lesions

skin biopsy- punch of blister or skin for DIF

Serum- IIF negative. SHould be negatvie for antibodies to rule out bullous pemphigoid