Derm Flashcards
Clark levels
II: Melanoma present but does not fill/expand papillary dermis
III: Fills and expands papillary dermis
IV: Invades reticular dermis
V: Invades subcutis
Melanoma T staging
a: no ulceration
b: ulceration
pT1: <0.8 cm (0.8-1.0)
pT2: 1-2.0cm
pT3: 2-4.0 cm
pT4: >4cm
Low CSD Melanoma
Superficial spreading
Nodular
Nevoid
Lentiginous
High CSD Melanoma
Lentigo maligna
Desmoplastic
Melanoma in sun shielded areas or without known UV association
Spitz
Acral
Mucosal
Arising in congenital nevus
Arising in blue nevus
Uveal
Merkle cell CA T-staging
Merkle cell CA N-staging
pN1: clinically undetected met
pN2: in-transit met without LN
pN3: in-transit met with LN
Histopathological features of lichen planus
Confluent orthokeratosis without parakeratosis
Wedge shaped hypergranulosis
Epidermal acanthosis with saw-toothed rete ridges
Band-like lymphocytic infiltrate in the superficial dermis
Vacuolar degen of basal keratinocytes with necrotic keratinocytes (Civatte bodies) in the epidermis and papillary dermis (colloid bodies)
4 histopathological variants of lichen planus
Bullous lichen planus
Hypertrophic lichen planus
Lichen planopilaris
Atrophic lichen planus
IF findings of lichen planus
Colloid bodies stain with IgM, occasionally with IgG, IgA, and C3
Fibrinogen deposits are present in the dermoepidermal junction
Types, timing, and histopathological manifestations of cutaneous GvHD
Acute - onset first 3 months posttransplant - vacuolar interface dermatitis
Chronic (lichenoid) - >3 months posttransplant (can follow acute) - lichenoid interface dermatitis
Chronic (sclerodermoid) - up to 18 months posttransplant - morphea-like fibrosing dermatitis
Grading scheme for cutaneous GvHD
Grade 1: basal vacuolar change
Grade 2: dyskeratotic keratinocytes
Grade 3: subepidermal cleft and microvesicle formation
Grade 4: Dermoepidermal split +/- epidermal necrosis
Causes of erythema multiforme
Variety of triggers:
Infection - HSV, mycoplasma
Drugs - NSAIDs
Histopathological findings in erythema multiforme
Early: vacuolar interface dermatitis
More advanced: bullous lesions with subepidermal vasiculation
Severe: resemble toxic epidermal necrolysis with marked epidermal necrosis
Variants and histopathological patterns of lupus skin disease
Cutaneous manifestation of active SLE
* - Superficial and deep perivascular dermatitis, vacuolar interface change
* - Subepidermal blister with neutrophils
Subacute cutaneous lupus erythemattosus
* - Superficial perivascular dermatitis, vacuolar interface change
Discoid lupus erythematosus
* - Superficial and deep perivascular dermatitis, vacuolar interface change
Tumid lupus erythematosus
* - Superficial and deep perivascular dermatitis
Lupus profundus
* - Lobular panniculitis
Histochemical stains with utility in diagnosis of cutaneous lupus
Stains for increased dermal mucin - AB, Colloida iron
Stains for BM thickening - PAS
Significance and diagnostic value of “lupus band” on DIF
Incidence of positivity related to lesion site and duration
Lupus band test has high incidence of positive in systemic SLE in both lesional and nonlesional sun-exposed skin
Lower incidence of + in SLE if nonlesional sun-protected skin sampled
May be falsely pos in chronically sun-exposed skin or normal controls
What to tell a clinician about to sample a pt with bullous disease
Lesional skin for routine sections and perilesional skin for DIF
FFPE for routine sample and saline or Miche;’s medium for IF sample
Normal saline if transport time <24h
Michel’s medium if transport time >24h
No formalin contamination for IF specimen or false neg
Conditions requiring lesional over perilesional tissue for DIF
Lupus
Vasculitis
Lichen planus
Classification of vesiculobullous diseases
Based on 3 features:
- location of split (subepi vs intraepi)
- mechanism of split (intraepi spong, acantholysis, ballooning)
- dermal inflammatory infiltrate
4 disorders characterized by intraepidermal acantholysis, histopath features and IF
**Pemphigus vulgaris ** - suprabasal acantholysis with tombstoning, mixed infiltrate, net-like or intercellular IgG +/- C3 on DIF
Hailey-Hailey - Acantholysis in dilapidated brick wall pattern, minimal dyskeratosis. No IF
Darier disease - Acantholysis with prominent dyskeratosis, neg DIF
**Grover disease **- focal acantholysis and variable dyskeratosis, neg DIF
6 disorders character by subepidermal blisters and histopathological findings, IF
Epidermolysis bullosa acquista - cell poor blister, linear IgG/C3 staining along basement mebrane zone, immune deposits to dermal side of blister (salt split skin)
Porphyria cutanea tarda - cell poor blister with projection of dermal papillae into cavity, caterpillar bodies in roof. IgG/C3 along BMZ and within thickened pap derm vessels
Bullous pemphigoid - eosinophil-rich blister and dermal infiltrate, sometimes with neuts, eosinophilic spong. DIF linear IgG/C3 along BMZ. Salt split skin to roof
Pemphigoid (herpes) gestationalis - indistinguishable from bullous pemphigoid, occurs in pregnancy
Dermatitis herpetiformis - neutrophil rich blisters and microabscesses at tips of dermal papillae, Granular IgA along BMZ, celiac association
Linear IgG dermatosis - similar to dermatitis herpetiformis, association with IBD, LPDs, drugs
Histopathologic features of leukocytoclasic vasculitis
- Fibrinoid necrosis of small vessel walls with extravasated RBCs
- Angiocentric neutrophilic infiltrate with nuclear dust
- DIF: der,al vessel staining with IgG/C3/fibrinogen +/- IgM
- Secondary changes - necrosis/ulceration or subepidermal blister formation
Possible causes of lekocytoclasic vasculitis
- Infection - bacterial, rickettsial, fungal, viral
- Autoimmunity - immune complex diseeases, ANCA-associated
- Drugs
- Malignancy
- Idiopathic (40%)
Clinical findings and histopathology of Sweet syndrome
Clinical
* Pts with sudden eruptions of painful plaques and papules on face/extremities, often following infection
* fever and leukocytosis
* Unknown etiology but assocation with malignancy (esp AML), autoimmunity, infection, drugs
Histopath
* Dense diffuse dermal neutrophilic infiltrate
* subepidermal edema
* Usually no true vasculitis
Histopathological deatures of plaque-type psoriasis
- Regular acanthosis of epidermis with elongated, club-shaped rete ridges and thinned suprapap plates
- Prominent dilated capillaries in pap dermis
- Confluent dry parakeratosis overlying diminished granular layer
- Kogoj microabscess - neut collection in spinous layer
- Munro microabscess - mounds of parakeratosis with neuts
Patterns of cutaneous granulomatous inflammation with relevant disease associations
Tuberculoid: Nodular epithelioid histiocytes with central necrosis and periphera lymphocyte rim - tuberculosis, leprosy, rosacea
Sarcoidal: naked granulomata without necrosis - sarcoidosis, berylliosis, zirconium granulomas, Crohn’s disease
Foreign body: abdundant irregularly distributed forgei-body giant cells - suture granuloma, keratin, tattoo
Xanthomatous: foamy histocytes - xanthogranuloma, infections (leprosy, syph)
Suppurative and granulomatous: aggregations of neuts with interspersed histiocytes - ruptured follicular cyst/unit, deep funal infection, atypical myobacterial infection
Palisading: geographic pattern with histiocytic rims - granuloma annulare, rheumatoid nodule, necrobiosis lipoidica
Clinical and histopathological features of granulama annulare, rheumatoid nodule, necrobiosis lipoidica
GA: young adults, acral sites
* usually foca involvement of upper anf mid reticular dermis, palisading histiocyters, increased dermal mucin
RN: bony prominence of forearms, elbows, hands, feet, knees
* deep in dermis and/or subcutis
* Palisading and sometimes serpiginous granulomas surrounding fibrinoid change, lack of sig dermal mucin
NL: assocation with diabetes
* diffuse dermal involvement and extnding into superficial subcutis
* palisaded, interstitial or tiered inflammatory infiltrate with intervening sclerotic collagen (layer cake appearance)
* mixed infiltrate of histiocytes lymphs, plasma cells
* lack of sig dermal mucin
Histopathologic features of erythema nodosum
Predominantly septal panniculitis with some overflow into fat lobules
* early phase - predominance of neuts
* late phase - predominance of lymphs, eos, multinucleated giant cells
* chronic recurrent EM prominant septal fibrosis with inflammation
5 conditions associated with erythema nodosum
- Drug reaction (eg oral contraceptive)
- Infection
- Sarcoidosis
- IBD
- Malignancy (eg hematolymphoid)
5 key causes of lobular panniculitis
- Infection
- Nodular vasculitis
- Lupus profundus
- alpha-1 antitrypsin deficiency
- Pancreatic panniculitis
Clinical and histopathologic features of fixed drug eruption
Clinical
* ovoid or annular erythematous lesions in response to drug exposure and recur in same location upon reexposure
* Common sites: lipds, face, hands, genitalia
Histopath
* vacuolar interface dermatitis with superficial and deep perivascular infiltrate
* acute phase resembles EM
* pigment incontinece can be observed in quiescent phase
Features of pityriasis rosea
- Self limited papulosquamous eruption in children and young adults
- starts as salmon-coloured herald path on trunk developing into multiple smaller scaly papules on truck and extremities in Christmas tree pattern
- clinically similar to secondary syph
- Histopath - subacute spong derm w superficial perivasc lymph infiltrate with overlying mounds of parakeratotic scale
What is cornoid lamella and where is it found
Angulated pillar of parakeratosis arising from epidermal invagination with loss of granular layer and localized dyskeratosis
Seen in porokeratosis
Cinucal and histopathological features of morphea
Clinical
* localized/plaque-like, linear, or generalized
* Indurated plaques present on trunk and extremities with shiny white centres urrounding by violaceous border
Histopath
* early - superficial and deep perivasc and interstitial lymphplasmacytic infiltrate
* late - thickened dermal collagen resulting in biopsy specimen with square edges, atrophy of adnexal structures with loss of periadnexal fat, diminished inflammation
* may be associated lichen sclerosis type changes