Derm Flashcards
Layers of Skin
Epidermis is comprised of keratioocytes and has four layers (Fig. 19.1).
- Stratum basalis—regenerative (stem cell) layer
- Stratum spinosum—characterized by desmosomes between keratinocytes
- Stratum granulosum—characterized by granules in keratinocytes
- Stratum corneum—characterized by keratin in anucleate cells
Atopic Dermatitis
Pruritic, erythematous, oozing rash with vesicles and edema; often involves the face
and llexor surfaces
Type 1 hypersensitivity reaction; associated with asthma and allergic rhinitis
Contact Dermatitis
Pruritic, erythematous, oozing rash with vesicles and edem
Arises upon exposure to allergens such as
- Poison ivy and nickel jewelry (type IV hypersensitivity)
- Irritant chemicals (e.g., detergents)
- Drugs (e.g., penicillin)
Treatment involves removal of the offending agent and topical glucocorticoids, if
needed.
Acne Vulgaris
Comedones (whiteheads and blackheads), pustules (pimples), and nodules;
extremely common, especially in adolescents
Due to chronic inflammation of hair follicles and associated sebaceous glands
1. Hormone-associated increase in sebum production (sebaceous glands have
androgen receptors) and excess keratin production block follicles, forming
comedones.
2. Prop ion ibacterium acnes infection produces lipases that break down sebum,
releasing proinflammatory fatty acids; results in pustule or nodule formation
Treatment includes benzoyl peroxide (antimicrobial) and vitamin A derivatives (e.g.,
isotretinoin), which reduce keratin production.
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
Possible autoimmune etiology
- Associated with HLA-C
- Lesions often arise in areas of trauma (environmental trigger).
Histology shows:
1. Acanthosis (epidermal hyperplasia)
2. Parakeratosis (hyperkeratosis with retention of keratinocyte nuclei in the
stratum comeum)
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)
Treatment involves corticosteroids, UV light with psoralen, or immune-modulating
therapy.
Lichen Planus
Pruritic, planar, polygonal, purple papules (Fig. 19.3A), often with reticular white lines on their surface (Wickham striae); commonly involves wrists, elbows, and oral
mucosa
Oral involvement manifests as Wickham striae,
Histology shows inflammation of the dermal-epidermal junction with a ‘saw-tooth’ appearance.
Etiology is unknown; associated with chronic hepatitis C virus infection
Pemphigus Vulgaris
Autoimmune destruction of desmosomes between keratinocytes
Due to IgG antibody against desmoglein (type II hypersensitivity)
Presents as skin and oral mucosa bullae.
- Acantholysis (separation) of s t r a t um spinosum keratinocytes (normally connected by desmosomes) results in suprabasal blisLers.
- Basal layer cells remain attached to basement membrane via hemidesmosomes
- Thin-walled bullae rupture easily (Nikolsky sign), leading to shallow erosions with dried crust.
- Immunofluorescence highlights IgG surrounding keratinocytes in a ‘fish net’ pattern.
Bullous Pemphigoid
Autoimmune destruction of hem idesmo somes between basal cells and the underlying basement membrane
Due to IgG antibody against basement membrane collagen
Presents as blisters of the skin; oral mucosa is spared.
1. Basal cell layer is detached from the basement membrane.
2. Tense bullae do not rupture easily; clinically milder than pemphigus vulgaris
D. Immunofluorescence highlights IgG along basement membrane (linear pattern).
Dermatitis Herpetiformis
Autoimmune deposition of IgA at the tips of dermal papillae
Presents as pruritic vesicles and bullae that are grouped
Strong association with celiac disease; resolves with gluten-free diet
Erythema multiforme
Hypersensitivity reaction characterized by targeloid rash and bullae
1. Targetoid appearance is due to central epidermal necrosis surrounded by erythema.
Most commonly associated with HSV infection: other associations include
Mycoplasma infection, drugs (penicillin and sulfonamides), autoimmune disease (e.g., SLE), and malignancy.
EM with oral mucosa/lip involvement and fever is termed Stevens Johnson syndrome (SJS).
Toxic epidermal necrolysis is a severe form of SJS characterized by diffuse sloughing of skin, resembling a large bum; most often due to an adverse drug reaction
Seborrheic Keratosis
Benign squamous proliferation; common tumor in the elderly
Presents as raised, discolored plaques on the extremities or face; often has a coinlike, waxy, ‘stuck-on’ appearance
- Characterized by keratin pseudocysts on histology
Leser-Trelat sign is the sudden onset of multiple seborrheic keratoses and suggests underlying carcinoma of the G1 tract.
Acanthosis Nigricans
Epidermal hyperplasia with darkening of the skin; often
involves the axilla or groin
Associated with insulin resistance (e.g., non-insulin-dependent diabetes) or malignancy (especially gastric carcinoma)
Basal Cell Carcinoma
Malignant proliferation of the basal cells of the epidermis
1, Most common cutaneous malignancy
Risk factors stem from UVB-induced DNA damage and include prolonged exposure to sunlight, albinism, and xeroderma pigmentosum.
Presents as an elevated nodule with a central, ulcerated crater surrounded by dilated (telangiectatic) vessels; ‘pink, pearl-like papule’
Classic location is the upper lip.
Histology shows nodules of basal cells with peripheral palisading,
Treatment is surgical excision; metastasis is rare.
Squamous Cell Carcinoma
Malignant proliferation of squamous cells characterized by formation of keratin pearls.
Risk factors stem from UVB-induced DNA damage and include prolonged exposure
to sunlight, albinism, and xeroderma pigmentosum.
- Additional risk factors include immunosuppressive therapy, arsenic exposure, and chronic inflammation (e.g., scar from burn or draining sinus tract).
Presents as an ulcerated, nodular mass, usually on the face (classically involving the
lower lip)
Treatment is excision; metastasis is uncommon.
Actinic keratosis is a precursor lesion of squamous cell carcinoma and presents as a hyperkeratotic, scaly plaque, often on the face, back, or neck.
Keratoacanthoma is well-differentiated squamous cell carcinoma that develops
rapidly and regresses spontaneously; presents as a cup-shaped tumor filled with
keratin debris
Melanocytes
Melanocytes are responsible for skin pigmentation and are present in the basal layer
of the epidermis.
1. Derived from the neural crest
2. Synthesize melanin in melanosomes using tyrosine as a precursor molecule
3. Pass melanosomes to keratinocytes
