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Flashcards in Dermatology Deck (134)
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Allergic contact dermatitis

Form of Spongiotic dermatosis

Pruritic, well-demarcated, erythematous, edematous papules and plaques with vesicle formation
- Blisters in 1-2 days (Often linear lesions)
- Epicutaneous contact (Poison ivy)
- Scaly with chronicity

- Type IV reaction= cell-mediated or delayed hypersensitivity
- Antigen taken up by LC; LC to draining LN; present to T helper cells (MHC class II); becomes sensitized
- Sensitization/challenge

- Intercellular edema between keratinocytes: May form vesicles
- Langerhans cells in vesicles
- Perivascular infiltrate of lymphocytes, histiocytes, and eosinophils



Acanthotic process: hyperplasia of epidermis

Erythematous plaques with silvery scale
- Pustules (early)
- Silvery scale (late)
- Often symmetric, B/L: Elbow, knees, scalp, intertriginous, or generalized
- Koebner phenomenon (damage--> lesion)
- Auspitz sign (scale lifted--> bleeding)
- HLA types : Cw6, B13, B17, Bw57

Psoriatic arthritis: seen in 5-8% of psoriasis patients
- higher association with nail bed changes

- “Regular” acanthosis
- Parakeratosis
- Neutrophils in scale
- Loss of granular layer
- Thin suprapapillary dermal plate
- Prominent, dilated capillaries

- Lymphocytes
- Autoreactive T cell
- Keratinocytes
- Shortened epidermal cell cycle (28x nl production)
- Vessel alterations: abnormal post-capillary vessels (dilated)


Lupus erythematosis

Interface changes in epidermis/dermis:

Acute Form:
- Facial erythema (malar rash)
- Generalized erythema: Face, arms, neck, dorsal hands
- Bullae

Subacute Form
- Psoriasiform
- Annular vesicular

Chronic Forms
- Discoid lesions (5-10% have systemic disease)
- Scaling, atrophic plaque
- Hypo/hyperpigmentation
- Follicular plugging
- Alopecia
- Panniculitis (50% have systemic disease)

Discoid lupus (confined to skin, may develop systemic disease in 5-10%):
- Localized to skin
- Scaling atrophic plaques
- Pigmentary changes
- Telangiectasia
- Alopecia
- Follicular plugging

Discoid lupus histology:
- Hyperkeratosis (scale)
- Epidermal atrophy= Lymphocytes attacking DEJ (interface)
1. Basal cell vacuolization due to interface
2. Necrotic keratinocytes (attacked by lymphocytes- pyknotic keratinocytes)
3. Pigment incontinence: dump melanin)
- Superficial & deep perivascular & perifollicular: Follicular destruction
- Dilated vessels
- Positive ‘Lupus Band’= Granular IgG & C3 along thickened BM


Lichen planus

Interface process
Scaly, flat-topped, violaceous papules and plaques

The 5 Ps:
1. Pink to purple
2. Pruritic
3. Polygonal
4. Papules
5. Plaques
- Often wrists and ankles; Can occur anywhere including oral mucosa
- Most cases idiopathic

Histo: interface process=
- Superficial band-like lymphocytic infiltrate (DEJ)
- Necrotic keratinocytes
- Hyperkeratosis
- Hypergranulosis (wedge-shaped)
- Irregular acanthosis
- Saw-toothing of rete edges


Pemphigus vulgaris

Vesiculobullous process
- Flaccid blisters; Easily ruptured
- Erosions
- Scalp, mucosa, intertriginous sites
- Nikolsky sign: press lateral edge of blister, it will spread
- Genetic predisposition
- Commonly 40s-50s
- Autoimmune disease

- Blistering is Supra-basal (Tombstone pattern where basal keratinocytes still attached to dermis)
- Acantholysis
- Autoantibodies to Desmoglein 3--> destruction of Desmosomes

** vs Bullous pemphigous= entire epidermal layer lifts from dermis (no keratinocytes still resting on basement membrane= sub-basal)
- Sub-epidermal blistering also seen in dermatitis herpetiformis


Erythema nodosum

Tender erythematous nodules on extensor surfaces of lower legs
- Dome-shaped, firm erythematous nodules
- Self-limited, constitutional symptoms
- Seen in young women

Immunologic response to foreign antigens
- Can be due to distal infection (bacterial, viral, TB, fungi), drugs (sulfa, OCPs), sarcoid, IBD, tumors, etc.

- Septal
- Mostly chronic inflammation
- Granulomas
- Fibrosis
- Mimicry: Infection, Factitia


Seborrheic keratiosis

Benign Epidermal neoplasia
- Middle age and older
- Oval or round “stuck on” papule or plaque
- Flesh-colored to brown or black
- Rough surface
- Symmetrical, sharp margins
- Sign of Leser-Trélat: multiple developed over short period of time--> underlying malignancy (release of growth factors)
- Cause???- genetics, sun exposure, viral

- Basaloid keratinocytes (follicular infundibulum): can grow up or invaginate
- “Horn cysts”= invagination, gives rough appearance
- No melanocytic derivation (keratinocytes!)


Verrucae (warts)

Benign epidermal neoplasia; Also, an infection (HPV)!
- Seen at Sites of inoculation
- Malignant transformation with immunosuppression
- “Black dots” when peeled away
- Verruca vulgaris
- Verruca palmaris/plantaris
- Verruca plana
- Condyloma acuminatum

- Benign squamoid proliferation
- Crown-like with vascularized spires; irritation--> bleeding--> black hemorrhagic spots
- Koilocytosis: nucleus with glassy appearance (intranuclear virus)--> crinkled with halo
- Keratohyaline granules within keratinocytes
- HPV genome (typing): immunohistochem, FISH (high or low risk)
- Cell-mediated immune response--> resolution (unless immune suppressed)


Actinic Keratosis

Pre-malignant epidermal changes:
- Rough, scaling, reddish, ill-defined patch or plaque (can see cutaneous horn; may also be wart, carcinoma--> biopsy!)
- Occurs on sun-exposed skin
- UV-radiation induced keratinocyte DNA damage
- Can spontaneously regress (up to 25%)
- May progress to squamous cell carcinoma

- Variable atypia; Less than full epidermal thickness
- Hyperkeratosis
- Parakeratosis
- Solar elastosis
- Chronic dermal inflammation


Squamous cell carcinoma

Malignant epidermal neoplasia
- Scaling, erythematous to flesh-colored plaque or nodule
- May be scaly, ulcerated or crusted
- Occurs most often on sun-exposed skin (75% on head and neck)
- Also on mucous membranes and sites of chronic injury (burn scars, irradiated sites, sinus tracts)

2nd most common skin cancer
- UV radiation induced immunosuppression
- Locally invasive

Potential to metastasize
- 2-5% of SCCs related to sun exposure
- Up to 20% of SCCs arising in sites of chronic injury (draining sinuses, burn scars) and mucous membranes

- Atypical keratinocytes
- Growth into underlying dermis
- Keratin pearls (altered, denser homogenous keratin formation)
- Hyperkeratosis
- Parakeratosis


Basal cell carinoma

Malignant epidermal neoplasia
- Erythematous patch with central erosion/ulceration and rolled, pearly border OR a pearly papule or nodule
- Telangiectasia
- Seen on sun-exposed skin, most common on face
- Most common skin cancer; most common human malignancy
- Rarely metastasizes but may be locally aggressive

- Enlarged basaloid keratinocytes (increased mitoses)
- Individual cell necrosis= malignancy
- Bud and extend into dermis
- Peripheral palisading
- Separation artifact on histologic preparation: due to mucinous stroma- washed away after processing


Melanocytic nevus

Benign melanocytic neoplasia
- Most acquired after age 6 months and before age 35
Variable (but uniform) appearance:
- Macular or papular
- Brown to flesh-colored
- Usually <5 mm in diameter

Junctional: present as nest in epidermal-dermal junction

Compound: involves dermis and epidermis

Dermal: neval cells only seen in dermis

- Derived from neural crest origin
- Maturation with descent into dermis


Dysplastic nevus

Melanocytic dysplasia
- Controversial entitiy
Abnormal: clinical appearance, architecture, cytology, stroma

Isolated vs dysplastic nevi syndrome
- Clinical phenotype
- Personal and family history
- 100% lifetime risk

Premalignant potential, markers for increased melanoma risk

- Irregular nests: bridging (nests coalesce), shoulder (epidermal component descends beyond dermis)
- Cytologic atypia
- Stromal fibrosis, lamellar fibroplasia (collagen, onion-skin layering around rete ridges)


Melanoma prognosis

TNM stage:
1. Measured Depth (mm)= thickness (#1 prognostic feature)
2. Ulceration (bad sign)
3. Mitotic rate (more mitoses, worse prognosis)

- Clark level (obsolete finding- how deep)
- TIL Response (tumor-infiltrating lymphocyte response= good prognosis)
- Regression (bad prognosis: body eradicates part of melanoma)
- Vascular Invasion (mets)
- Microscopic Satellites (bad)
- Gender (F fare better than M)
- Site (extremities except hand and feet do better)
- Stage (metastasized= prognostic indicator)