Skin Pathology

Front 1

Atopic (eczematous) dermatitis

Back 1

• Pruritic, erythematous, oozing rash with vesicles and edema
• Often involves face and flexor surfaces
• Type I hypersensitivity reaction; associated with asthma and allergic rhinitis

Front 2

Contact dermatitis

Back 2

• Pruritic, erythematous, oozing rash with vesicles and edema
• Arises upon exposure to allergens such as poison ivy and nickel jewelry (type IV hypersensitivity reaction), irritant chemicals (e.g. detergents), drugs (e.g. penicillin)
• Topical glucocorticoids may be used if needed

Front 3

Acne vulgaris

Back 3

• Comedones (whiteheads and blackheads), pustules (pimples), and nodules; extremely common, especially in adolescents
• Due to chronic inflammation of hair follicles and associated sebaceous glands
• Treatment includes benzoyl peroxide (antimicrobial) and vitamin A derivatives (e.g. isotretinoin), which reduce keratin production

Front 4

Propionibacterium acnes infection

Back 4

Produces lipase's that break down sebum, releasing pro inflammatory fatty acids; results in in pustule or nodule formation

Front 5

Psoriasis

Back 5

• 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

Front 6

Possible autoimmune etiology of psoriasis

Back 6

• Associated with HLA-C
• Lesions often arise in areas of trauma (environmental trigger)

Front 7

What does histology show in psoriasis?

Back 7

• Acanthosis (epidermal hyperplasia)
• Parakeratosis (hyperkeratosis with retention of keratinocyte nuclei in the stratum corneum)
• Collections of neutrophils in the stratum corneum (Munro microascesses)
• Thinning of epidermis above elongated dermal papillae; results in bleeding when scale is picked off (Auspitz sign)

Front 8

Treatment of psoriasis

Back 8

Corticosteroids, UV light with psoralen, or immune-modulating therapy

Front 9

Lichen planus

Back 9

• Pruritic, planar, polygonal, purple papules, often with white reticular white lines on their surface (Wickham striae); commonly involves wrists, elbows, and oral mucosa
• Histology shows inflammation of dermal-epidermal junction with 'saw-tooth' appearance
• Etiology unknown; associated with chronic hep C virus infection

Front 10

Pemphigus vulgaris

Back 10

• Autoimmune destruction of desmosomes between keratinocytes
• Due to IgG antibody against desmoglein (type II hypersensitivity)
• Presents as skin and oral mucosa bullae
• Immunofluorescence highlights IgG surrounding keratinocytes ('fish net' pattern)

Front 11

What causes suprabasal blisters in pemphigus vulgaris?

Back 11

Acantholysis (separation) of stratum spinosum keratinocytes (normally connected by desmosomes)

Front 12

What causes the 'tombstone' appearance in pemphigus vulgarism?

Back 12

Basal layer cells remain attached to basement membrane via hemidesmosomes

Front 13

Nikolsky sign

Back 13

Thin-walled bullae rupture easily, leading to shallow erosions with dried crust in pemphigus vulgaris

Front 14

Bullous pephigoid

Back 14

• Autoimmune destruction of hemidesmosomes between basal cells and the underlying basement membrane
• Due to IgG antibody against hemidesmosome components (BP180) of the basement membrane
• Presents as blisters of skin, usually in the elderly; oral mucosa is spared
• Immunofluorescence highlights IgG along basement membrane (linear pattern)

Front 15

Dermatitis herpetiformis

Back 15

• Autoimmune deposition of IgA at tips of dermal papillae
• Presents as pruritic vesicles and bullae that are grouped (herpetiform)
• Strong association with celiac disease; resolves with gluten-free diet

Front 16

Erythema multiforme

Back 16

• Hypersensitivity reaction characterized by targeted rash and bullae
• Targetoid appearance is due to central epidermal necrosis surrounded by erythema

Front 17

What causes erythema multiforme?

Back 17

HSV infection; other associations include Mycoplasma infection, drugs (penicillin and sulfonamides), autoimmune disease (e.g. SLE) and malignancy

Front 18

Stevens-Johnson syndrome

Back 18

• EM with oral mucosa/lip involvement and fever
• Toxic epidermal necrolysis is a severe form os SJS characterized by diffuse sloughing of skin, resembling a large burn; most often due to adverse drug reaction

Front 19

Seborrheic keratosis

Back 19

• Benign squamous proliferation; common tumor in elderly
• Presents as raised, discolored plaques on extremities or face; often has a coin-like, waxy, 'stuck-on' appearance
• Characterized by keratin pseudocysts on histology

Front 20

Leser-Trelat sign

Back 20

The sudden onset of multiple seborrheic keratoses and suggests underlying carcinoma of GI tract

Front 21

Acanthosis nigricans

Back 21

• Epidermal hyperplasia with darkening of skin ('velvet-like' skin); often involves axilla or groin
• Associated with insulin resistance (e.g. non-insulin-dependent diabetes) or malignancy (especially gastric carcinoma)

Front 22

Basal cell carcinoma

Back 22

• Malignant proliferation of basal cells of epidermis
• Most common cutaneous malignancy
• Risk factors include sun exposure, albinism, and xeroderma pigmentosa
• Treatment is surgery; metastasis is rare

Front 23

How does BCC present?

Back 23

• As an elevated nodule with a central, ulcerated crater surrounded by dilated (telangiectatic) vessels
• 'pink, pearl-like papule'
• Classic location is upper lip

Front 24

What does histology show in BCC?

Back 24

Nodules of basal cells with peripheral palisading

Front 25

Squamous cell carcinoma

Back 25

• Malignant proliferation of squamous cells characterized by formation of keratin pearls
• Presents as ulcerated, nodular mass, usually on face (lower lip is classic)
• Treatment is excision; metastasis uncommon

Front 26

Risk factors for squamous cell carcinoma

Back 26

• sunlight, albinism, xeroderma pigmentosum
• immunosuppressive therapy
• arsenic exposure
• chronic inflammation (eg scar from burn of draining sinus tract)

Front 27

Actinic keratosis

Back 27

Precursor lesion of squamous cell carcinoma and presents as hyperkeratotic, scaly plaque, often on face, back or neck

Front 28

Keratoacanthoma

Back 28

Well-differentiated squamous cell carcinoma that develops rapidly and regresses spontaneously; presents as a cup-shaped tumor filled with keratin debris

Front 29

Vitiligo

Back 29

• Localized loss of skin pigmentation
• Due to autoimmune destruction of melanocytes

Front 30

Albinism

Back 30

• Congenital lack of pigmentation
• Due to enzyme defect (usually tyrosinase) that impairs melanin production
• May involve eyes (ocular form) or both the eyes and skin (oculocutaneous form)

Front 31

Melasma

Back 31

• Mask-like hyper pigmentation of cheeks
• Associated with pregnancy and oral contraceptives

Front 32

Growth phases of melanoma

Back 32

1. Radial growth horizontally along epidermis and superficial dermis; low risk of metastasis
2. Vertical growth into the deep dermis; increased risk of metastasis; depth of extension (Breslow thickness) is the most important prognostic factor in predicting metastasis

Front 33

Dysplastic nevus syndrome

Back 33

Autosomal dominant disorder characterized by formation of dysplastic nevi that may progress to melanoma

Front 34

Superficial spreading melanoma

Back 34

• Most common subtype
• Dominant early radial growth results in good prognosis

Front 35

Lentigo maligna melanoma

Back 35

• Lentiginous proliferation (radial growth)
• good prognosis

Front 36

Nodular melanoma

Back 36

Early vertical growth; poor prognosis

Front 37

Acral lentiginous melanoma

Back 37

Arises on palms or soles, often in dark-skinned individuals; not related to UV light exposure

Front 38

Impetigo

Back 38

• Superficial bacterial skin infection, most often due to S aureus or S pyogenes
• Commonly affects children
• Presents as erythematous macules that progress to pustules, usually on face; rupture of pustules results in erosions and dry, crusted, honey-colored serum

Front 39

Cellulitis

Back 39

• Deeper (dermal and subcutaneous) infection, usually due to S aureus or S pyogenes
• Presents as red, tender, swollen rash with fever
• Risk factors include recent surgery, trauma, or insect bite
• Can progress to necrotizing faciitis with necrosis of subcutaneous tissues due to infection with anaerobic 'flesh-eating' bacteria

Front 40

Verruca (wart)

Back 40

• Flesh-colored papules with rough surface
• Due to HPV infection of keratinocytes; characterized by koilocytic change
• Hands and feet are common location

Front 41

Molluscum contagiosum

Back 41

• Firm, pink, umbilicated papules due to poxvirus; affected keratinocytes show cytoplasmic inclusions (molluscum bodies)
• Most often in children
• Also occur in sexually active adults and immunocompromised individuals

Front 42

Staphylococcal scalded skin syndrome

Back 42

• Sloughing of skin with erythematous rash and fever; leads to significant skin loss
• Due to S aureus infection; exfoliative A and B toxins results in epidermolysis of stratum granulosum

Front 43

How is staphylococcal scalded skin syndrome distinguished histologically from toxic epidermal necrolysis?

Back 43

by level of skin separation; separation in TEN occurs at the dermal-epidermal junction

Front 44

Freckles occur due to an increased number of ____________

Back 44

Melanosomes (not melanocytes!)