Skin Pathology Flashcards
Skin
A. Functions as a barrier against environmental insults and fluid loss
B. Composed of an epidermis and dermis
What are the layers of the epidermis? Features of each layer?
Epidermis is comprised ofkcratinocytes and has four layers
- Stratum basalis- regenerative (stem cell) layer
- Stratum spinosum- characlerized by desmosomes between keratinocytes
- Stratum granulosum-characterized by granules in keratinocytes
- Stratum corneum- characterized by keratin in a nucleate cells
What important structures are in the dermis?
Dermis consists of connective tissue, nerve endings, blood and lymphatic vessels, and adnexal structures (e.g., hair shafts, sweat glands, and sebaceous glands).
ATOPIC (ECZEMATOUS) DERMATITIS
A. Pruritic, erythematous, oozing rash with vesicles and edema; often involves the face and flexor surfaces
B. Type l hypersensitivity reaction; associated with asthma and allergic rhinitis
CONTACT DERMATITIS
Pruritic, erythematous, oozing rash with vesicles and edema
B. Arises upon exposure to allergens such as
1. Poison ivy and nickel jewelry (type IV hypersensitivity)
2. Irritant chemicals (e.g., detergents)
3. Drugs (e.g., penicillin)
C. Treatment involves removal of the offending agent and topical glucocorticoids, if needed.
ACNE VULGARIS
A. Comedones (whiteheads and blackheads), pustules (pimples), and nodules; extremely common, especially in adolescents
B. Due to chronic inflammation of hair foil ides and associated sebaceous glands
l. Hormone-associated increase in sebum production (sebaceous glands have
androgen receptors) and excess keratin production block follicles, forming
comedones.
2. Propionibacterium acnes infection produces lipases that break down sebum, releasing proinflammatory fatty acids; results in pustule or nodule formation
PSORIASIS
- Well-circumscribed, salmon-colored plaques with silvery scale, usually on extensor surfaces and the scalp, pitting of nails may also be present.
- Due to excessive keratinocyte proliferation
- Associated with HLA-C
D. Histology (fig. 19.2B) shows
1. Acanthosis (epidermal hyperplasia)
2. Parakeratosis (hyperkeratosis with retention of keratinocyte nuclei in the
stratum corneum)
3. Collections of neutrophils in the stratum corneum (Munro microabscesses)
4. Thinning of the epidermis above elongated dermal papillae; results in bleeding when scale is picked off (Auspitz sign)
LICHEN PLANUS
A. Prurit ic, planar, polygonal, purple papules (Fig. l9.3A), often with reticular while lines on their surface (Wickham striae); commonly involves wrists, elbows, and oral mucoa
1. Oral involvement manifests as Wickham striae.
$ B. Histology shows inflammation of the dermal-epidermal junction with a ‘saw-tooth’ appearance (Fig. l9.3B).
$ C. Etiology is unknown; associated with chronic hepatitis C virus infection
PEMPHIGUS VULGARIS
- Autoimmune destruction of desmosomes between keratinocytes
- Due to TgG antibody against desmoglein (type IT hypersensitivity)
C. Presents as skin and oral mucosa bullae (Fig. 19.4A).
1. Acantholysis (separation) of stratum spinosum keratinocytes (normally connected by desmosomes) results in suprabasal blisters.
2. Basal layer cells remain attached to basement membrane via hemideslnosomes
(‘tombstone’ appearance, Fig. 19.4B).
3. Thin-walled bullae rupture easily (Nikolsk’)’ sign), leading to shallow erosions with dried crust.
4. Immunofluorescence highlights IgG surrounding keratinocytes in a ‘fish net’ pattern.
involves oral mucosa
BULLOUS PEMPHIGOID
A. Autoimmune destruction of hemidesmosomes between basal cells and the underlying basementmembrane
B. Due to lgG antibody against basement membrane collagen
C. Presents as blisters of the skin (Fig. l9.5A); oral mucosa is spared.
l. Basal cell layer is detached from the basement membrane (Pig. 19.5B) .
2. Tense bullae do not rupture easily; clinically milder than pemphigus vulgaris
D. Immunofluorescence highlights lgG along basement membrane (linear pattern).
DERMATITIS HERPETIFORMIS
A. Autoimmune deposition of IgA at the tips of dermal papillae
B. Presents as pruritic vesicles and bullae that are grouped (herpetiform, Fig. 19.6)
C. Strong association with celiac disease; resolves with gluten-free diet
ERYTHEMA MULTIFORM£ (EM)
A. Hypersensitivity reaction characterized by targetoid rash and bullae (Fig. 19.7)
l. Targetoid appearance is due to central epidermal necrosis surrounded by
erythema.
B. Most commonly associated with HSV infection; other associations include Mycoplasma infection, drugs (penicillin and sulfonamides), autoimmune disease (e.g., SLE), and malignancy.
C. EM with oral mucosa/lip involvement and fever is termed Stevens-Johnson syndrome {SJS).
l. Toxic epidermal necrolysis is a severe form of SJS characterized by diffuse
sloughing of skin, resembling a large bLtrn; most often due to an adverse drug
reaction
SEBORRHEIC KERATOSIS
A. Benign squamous proliferation; common tumor in the elderly
B. Presents as raised, discolored plaques on the e:x.-tremities or face; often has a coinlike,
waxy, ‘stuck-on’ appearance (Fig. 19.8A)
l. Characterized by keratin pseudocysts on histology
Leser-Trelat sign is the sudden onset of multiple seborrheic keratoses and suggests
underlying carcinoma ofthe GI tract
ACANTHOSIS NIGRICANS
Epidermal hyperplasia with darkening of the skin (‘velvet-like’ skin, Fig. 19.9); often involves the axilla or groin
Associated with insulin resistance (e.g., non-insulin-dependent diabetes) or malignancy (especially gastric carcinoma)
BASAL CELL CARCINOMA
A. Malignant proliferation of the basal cells of the epidermis
1. Most common cutaneous malignancy
B. Risk factors stem from UVB-induced DNA damage and include prolonged exposure
to sunlight, albinism, and xeroderma pigmentosum.
