Week 6 more cards

blackhead acne (open comedone)

still able to produce melanin

white head acne (closed comedone)

Altered follicular growth and diff  

Keratin plug blocks outflow of sebum to surface

can cause

acne

Propionibacterium acnes colonization of duct → lipase converts sebum to pro-inflamm fatty acids

can cause

acne

Sebaceous gland hyperplasia from hormonal stim or steroid use 

Inflammation and immune response (release of cytotoxic and chemotactic factors)

Altered follicular growth and diff  can cause

acne

rhus dermatitis can be caused by

Can be caused by eczematous dermatitis

rhus dermatitis sensitization

Sensitization: Ag taken up by dendritic Langerhans cells → lymph → naive CD4 T cell → effector and memory cells → Ab pdn w/ B cells

rhus dermatitis re exp

Re-exp: memory T migrate to affected skin sites → extravasate into tissues → release cytokines and chemokines that activate immune response

Urticaria causes

Ag- induced release of mast cell granules (IgE Ab)

IgE- induced

complement mediated

pollen drugs foods causing urticaria

Ag-induced release of mast cell granules (IgE Ab) ie pollen, foods, drugs

IgE-ind urticaria

substances in certain ind directly incite mast cell degranulation (ie opiates, ABx, contrast media)

Complement - mediated uricaria

hereditary angioedema, inherited def of C1 inh → uncontrolled act of complement   

early psoriasis dominated by

erythematous lesions

secondary phase of psoriasis dominated by

plaques and scales

colors of psoriasis

Red- capillary dilation from inflammation

Silver- parakeratosis scale

what mutation can contribute to psoriasis risk

HLA-Cw*0602 can contribute to risk

psoriasis inflammatory response

CD4 TH1 and TH17, activated CD8 effector T → IL12, IFNy, TNF, IL17

Bandlike infiltrate of lymphocytes @ dermoepidermal junction 

Hyperkeratosis, hypergranulosis, sawtoothing (result of chronic basal cell layer injury)

lichen planus

Linear pattern at dermoepidermal junction

Bullous pemphigoid

NET-LIKE PATTERN OF INTERCELLULAR IgG deposits

Pemphigus vulgaris

tombstone basale layer

Pemphigus vulgaris

Supepidermal, NONACANTHOLYTIC BLISTERS

Bullous pemphigoid

Bullae usually < 2cm

Usually heal w/o scarring, unless secondarily infected 

Bullous pemphigoid

SUBEPIDERMAL blisters

Inner aspects of thighs, flexor surfaces of forearms, axillae, groin, lower abdomen 

Oral (sometimes, would be after cutaneous lesions)

Bullous pemphigoid

Bullous pemphigoid involves what type of Ab

IgG

auto IgG Ab to BP Ag 230 (BPAG1) and BP Ag 180 (BPAG2

BPAG2 can activate

complement → more inflammation

hemidesmosomes are needed for

adherence of basal keratinocytes to basement mem

HEMIDESMOSOMES connect

basal epidermal layer w/ underlying membrane

Dissolution of intercellular attachments w/i epidermis and mucosal epithelium

Pemphigus vulgaris

Acantholysis

dissolution of intercellular bridges that connect squamous epithelial cells → rounded, dissociated cells

Pemphigus vulgaris

Suprabasal acantholytic blister histology

row of tombstones, intact basal cells at base of blister

pemphigus vulgaris

Rupture easily → shallow erosions covered w/ crust

pemphigus vulgaris

positive nikolsky sign

(formation of new blister or extension of current blister w/ slight pressure to skin)

Pemphigus vulgaris

Portion of epidermis (including stratum corneum) forms the roof of bullae

pemphigus vulgaris

 (Dsg1 and Dsg3), parts of

desmosome

pemphigus vulgaris

DESMOSOMES adhesion between

epidermal cells

pemphigus vulgaris

Dsg1: higher exp in

more superficial epidermis (ie stratum corneum)

why you see subcorneal blister in pemphigus foliaceus (Dsg1 only) and lower in pemphigus vulgaris (Dsg1 and Dg3)

Dsg3: higher exp in

deeper epidermis (ie basal lamina)

pemphigus vulgaris

Benign but can be fatal w/o tx

pemphigus vulgaris

endemic to brazil

Pemphigus foliaceus

Pemphigus foliaceus blister location

Superficial subcorneal blisters in STRATUM GRANULOSUM (stratum corneum forms roof of bullae) 

Superficial subcorneal blisters in STRATUM GRANULOSUM (stratum corneum forms roof of bullae) 

pemphigus foliaceus

pemphigus foliaceus Ab type

Auto IgG Ab just against Dsg1 → more superficial subcorneal blisters

pemphigus foliaceus affects

DESMOSOMES (adhesion between epidermal cells)

Large, wart like vegetating plaques

Studded w/ pustules

on Groin, axillae, flexural surfaces

Pemphigus vegetans

Localized version of pemphigus foliaceus

Malar region

Pemphigus erythematous

Assoc w/ various malignancies, non-Hodgkins lymphoma

Paraneoplastic pemphigus

Males 

3rd and 4th decades of life 

Celiac disease

Dermatitis herpetiformis

Dermatitis herpetiformis

Urticaria and grouped vesicles 

Bilateral, symmetric, grouped 

Erythematous

Dermatitis herpetiformis blisters

Subepidermal blisters

Dermatitis herpetiformis antibody

IgA auto Ab to fibrils that anchor hemidesmosomes to dermis

Dermatitis herpetiformis antibody anchors to

fibrils

reticulin (tethers epidermal basement mem to superficial dermis) —> blisters

reticulin

tethers epidermal basement mem to superficial dermis

targeted in dermatitis herpetiformis

In dermatitis herpetiformis, _____ accumulate at _____

Fibrin and neutrophils accumulate at tips of dermal papillae

Fibrin and neutrophils accumulate at tips of dermal papillae —>

→ small microabscesses → subepidermal blisters

dermatitis herpetiformis

tx for dermatitis herpetiformis

GF diet

Non-inflammatory blister disorders:

Epidermolysis Bullosa

Porphyria

Epidermolysis Bullosa starts

soon or after birth

Epidermolysis Bullosa location

Sites of pressure, rubbing, trauma

in epidermolysis bullosa, _____ in struc proteins →

inherited defects in struc proteins —>

mechanical instability of skin

porphyria exacerbated by

sunlight

Urticarial and vesicles assoc w/ scarring exacerbated by exposure to sunlight

porphyria

Subepidermal, adjacent dermis contains vessels w/ walls that are thickened by glassy deposits of serum proteins (ie immunoglobulins)

porphyria