Skin Pathology Flashcards
Skin Overview
-barrier against <b>environmental insults and fluid loss</b>
- <b>Epidermis</b>: made of keratinocytes and has 4 layers:
- –Stratum Basalis: regenerative
- –Stratum Spinosum: desmosomes between keratinocytes
- –Stratum Granulosum: granules in keratinocytes
- –Stratum Corneum: keratin in anucleate cells
-<b>Dermis</b>: made of CT, nerve endings, blood and lymphatic vessels, adnexal structures (i.e. hair shafts, sweat glands, sebaceous glands)
Inflammatory Dematoses
- Atopic (Eczematous) Dermatitis
- Contact Dermatitis
- Acne Vulgaris
- Psoriasis
- Lichen Planus
Blistering Dermatoses
- Pemphigus Vulgaris
- Bullous Penphigoid
- Dermatitis Herpetiformis
- Erythema Multiforme
Epithelial Tumors
- Seborrheic Keratosis
- Acanthosis Nigrans
- Basal Cell Carcinoma
- Squamous Cell Carcinoma
Disorders of Pigmentations/Melanocytes
- Vitiligo
- Albinism
- Freckle (Ephelis)
- Melasma
- Nevus (Mole)
- Melanoma
Infectious Disorders
- Impetigo
- Cellulitis
- Staphylococcal Scalded Skin Syndrome
- Verruca (Wart)
- Molluscum Contagiosum
Atopic (Eczematous) Dermatitis–> cause, clinical features
<b>-type I hypersensitivity reaction associated with asthma and allergic rhinitis</b>
-causes: pruritis, erythematous, oozing rash with vesciels and edema involving face and flexor surfaces
Contact Dermatitis–> cause, clinical features
<b>-exposure to allergens (could be type IV)</b>
- causes: pruritis, erythematous, oozing rash with vesciels and edema
- treatment: topical glucocorticoids
Acne Vulgaris–> cause, clinical features, treatment
- comedones, pustules, nodules
- chronic inflammation of hair follicles & sebaceous glands
<b>comedones can be formed by hormone-associated increase in sebum production and excess keratin blocking follicles</b>
-treament: benzoyl peroxide & vitamin A derivatives (reduction of keratin production)
Psoriasis–> cause, histology, treatment
-autoimmune association with <b>HLA-C</b> causing lesions in areas of trauma (environmental trigger)
Histology: <b>acanthosis</b> (epidermal hyperplasia), <b>parakeratosis</b> (hyperkeratosis with retention of keratinocyte nuclei in stratum corneum), <b>Munro microabscesses</b> (collections of neutrophils in stratum coreum), <b>thining of epidermis, elongated dermal papillae, Auspitz sign (pinpoint bleeds)</b>
-treatment: corticosteroids, UV light with psoralen (PUVA), immune-modulating therapy</b>
Pemphigus Vulgaris–> cause, clinical features, IF
-<b>autoimmune destruction of desmosomes between ketatinocytes</b> due to IgG Ab against desmoglein
- Clinical features–> skin & oral mucosa bulla:
1. <b>Acantholysis</b>: separation of stratum spinosum keratinocytes causing suprabasal blisters
2. <b>Tombstone appearance</b>: hemidesmosomes keep basal layer cells attached to BM
3. <b>Thin-walled bullae ruptures easily</b> (Nikolsky sign)
4. <b>IF highlights IgG surrounding ketatinocytes in “fish net” pattern</b>
Bullous Pemphigoid–> cause, clinical features, IF
-<b>IgG Ab against hemidesmosome components (BP180) of BM leading to autoimmune destruction of hemidesmosomes</b>
- blisters (basal cell layer is detached from BM, tense bulla do not rupture easily)
- oral mucosa is spared
*IF highlights IgG along BM- “linear pattern”
Dermatitis Herpetiforms
-autoimmune deposition of IgA at tips of dermal papillae presenting as pruritic vesicles and bullae that are grouped
Erythema Multiforme–> causes, clinical features
- hypersensitivity reaction with targetoid rash (central epidermal necrosis surroinded by erythema) & bullae
- associated with <b>HSV infection</b>, Mycoplasma infection, drugs, autoimmune disease and malignancy
- involved in SJS
Stevens-Johnson syndrome
<b>Erythma Multiforme + Oral mucosa/lip involvement & fever</b>
-severe form–> toxic epidermal necrolysis (diffuse sloughing off of the skin probably from drug reaction)