Dermatopathology - University of Kentucky



| Dermatopathology |

|1. Premalignant & Malignant Epithelial Tumors |

|Actinic Keratosis: epith. dysplasia introduced by UVR; more common in fair skinned people; UVR damages keratinocyte DNA (poss. Langerhans’s cells) |

|Gross: rough, red w/ indistinct borders |

|Micro: epith. dyplasia in lower1/3 of epidermis; solar elastosis in dermis |

|Comment: can become SCC; may regress; treat early b/c of unknown progression |

|Squamous Cell Carcinoma (SCC): most arise from AK’s; carcinogens, chronic ulcers; scars, arsenic, HPV, and radiation can also be factors; individuals w/ DNA |

|repair defects and/or imm.supp. (i.e. transplant) are at greater risk |

|G: flesh colored to red; often scaly; CIS (Bowen’s) often presents as scaly erythematous plaque resembling psoriasis |

|M: Nodular proliferation of dysplastic keratinocytes; “fingers” of tumor may infiltrate derm.; CIS replaces epid. w/ atyp. keratinocyte |

|C: UV induced SCC of skin rarely (5%) metastasizes to regional nodes; other precursors (i.e.scars) = more aggressive; actinic SCC of |

|mucous membrane = more likely to metastasize |

|Basal Cell Carcinoma (BCC): most common cancer; rarely metastasizes but is hematogenous; occurs on sun exposed areas but is not as directly related as SCC |

|G&M: Three presentations: 1. Noduloulcerative: translucent telangiectatic papule +/- ulcer; nodular prolif. of basaloid cells in a |

|fibromucinous stroma, may have infiltrating tumor at the deep aspects of the tumor |

|2. Superficial: scaley red patch; mult. buds of basaloid tumor cells along derm/epiderm jxn |

|3. Sclerosing: scar-like plaque; infiltrating slender strands of basaloid tumor cells in fibrous stroma |

|-all tend to show peripheral nuclear palisading |

|C: Patients w/ basal cell nevus syndrome may have hundreds of tiny BCC’s; some lesions may become quite destructive if ignored; |

|other signs of this phenotype include frontal losing jaw, cysts, and bifid ribs; these pts. have PTC gene mutations. |

|Merkel Cell Carcinoma: rare cutaneous neuroendocrine CA that may be lethal or mistaken for BCC |

|Melanoma: may also occur on mucosal surfaces, leptomeninges, uveal tract of eye; sunlight is only 1 factor; genetics can play a role (i.e. dysplastic nevus |

|syndrome) |

|G: ABCD’s: Asymmetry, Border irregularity, Color heterogenieity, Diameter > 6mm |

|M: Growth phases: Radial (can’t metastasize) 1. Pagetoid – larger cells w/ buckshot scatter of atyp. cells at all levels of epid. |

|2. Lentiginous – cells singly & in nests along derm/epider jxn; extend into appendages |

|Vertical (tumorigenic-can metastasize) – nodule of atypical cells growing into dermis |

|C: 4 classic types: Superficial spreading (Pagetoid) |

|Lentigo maligna |

|Acral Lentiginous |

|Nodular – differs from other 3 b/c it has no radial phase; other have radial to vertical progression |

|2. Malignant Dermal Tumors |

|Dermatofibrosarcoma Protuberans (DFSP): one of many dermal and subcuticular sarcomas |

|G: nodule or plaque (may be several cm’s) w/ nodules in it |

|M: “Storiform” pattern; often infiltrates fat; clear surgical margins difficult, CD34 + |

|C: rarely metastasize but are destructive (even larger than BCC) |

|3. Malignant Tumors of Cellular Immigrants to the Skin |

|Histiocytosis X (Langerhans cells histiocytosis): several variants; book refers to Letterer-Siwe variant |

|G: Letterer-Siwe disease often looks like seborrheic dermatitis with tiny hemangiomas |

|M: Several patterns exist but at least some histiocytes are present (w/ foam cytoplasm); eosinos & Lycs are also present; the |

|characteristic cell contains organelles called “Birbeck Granules” and marks w/ S-100 protein and CD1a |

|Cutaneous T-Cell Lymphoma (CTCL): skin involvement w/ poss. leukemia |

|G: several presentations including: red scaly patches; plaques and nodules; diffuse itchy red scaly skin |

|M: due to clonal prolif. of malignant CD4 positive Lycs (Sezary-Lutzner cells – clusters of these cells = Pautrier micro-abscesses) |

|C: Mycosis fungiodes = CTCL w/ patches or plaques and or nodules(tumors) |

|Erythroderma + Leukemia = Sezary Syndrome |

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|4. Disorders of Pigmentation and Melanocytes |

|Vitiligo: patchy hypo/depigmentation due to malanocyte damage/loss (unknown mech.); albinism = absence of tyrosinose |

|Freckle (ephilis): tan-brown macules on sun-exposed skin |

|M: hyperpigmentation of rete; NO proliferation of melanocytes (unknown mech.) |

|Melasma: patchy facial and neck hyperpigmentation (often mask-like) |

|M: Epidermal type has hyperpigmented basal layer of keratinocytes; Dermal type has incontinent melanin in papillary dermis |

|C: cause = Hm’s?; classically occurs w/ pregnancy (“Mask of Pregnancy”) |

|Lentigo = Melanocytic Nevi |

|5. Benign Epithelial Tumors |

|Seborrheic Keratosis (SK): benign keratinocyte prolif. in mid-older people |

|G: rough (warty); flesh colored to brown/black; on trunk; looks “Stuck on” |

|M: proliferation of basaloid keratinocytes, may be squamoid; cystic foci of lamellated keratin (horn pseudocyst) |

|C: tiny dark SK’s on face of darker skinned people are called “Dermatosis Papulosa Nigra”; rapid occurrence of large #’s of SK’s |

|may be assoc. w/ internal malignancy (Leser-Trelat sign) |

|Acanthosis Nigricans: common in obese young-mid aged people; may signify hyperinsulinemia (->Type II DM); may actually be easier to see on extensor surfaces of |

|joints, elbows, knees, toes, than on neck; skin is folded rather than thickened. |

|Fibroepithelial Polyps (aka skin tag, acrochondron, squamous papilloma): may be assoc. w/ acanthosis nigricans and DM; some on the neck may have thick SK-like |

|epith. while others may have a more fibrous core. |

|Epitheloid Cysts: 90% of all cutaneous cysts; most from follicular infundibulum; epidermal inclusion cysts due to injury do occur; acne cysts are epidermoid cysts|

|G: dome shaped nodule w/ poral opening fixed to epidermis; may be multiple |

|M: wall and cyst keratin look like surface skin |

|Trichilemmal (Pilar) Cysts: about 10% of cysts; mainly on scalp; multiple ones inherited as AD trait (women) |

|G: dome shaped papule fixed to epidermis; NO pore; may be firmer |

|M: lining like middle part of hair follicle; pink homogenous keratin |

|Dermoid Cysts: rare but most common on face of infant; lined like epidermoid cyst but have tiny hair follicle elements (sebaceous) |

|Steatocystoma: single or multiple oily centered w/ sebaceous glands in wall; on trunks of teenagers and older people |

|Keratoancanthoma: “self healing squamous cell carcinoma”; classic type is a rapidly growing nodule w/ a keratin filled center |

|Appendage tumors: flesh colored papules and nodules: table 27-2, p.1183 |

|Nevocellular Nevi: melanocytic “nevi” are benign tumors of melanocytes; may go thru many forms in life cycle; “Mole” is the common term for “melanocytic nevus”; |

|types of nevi have general areas of occurrence; most fair-skinned people get 40 or so moles in a lifetime (few after age 40); UVR seems to play a role |

|G& M: Lentigo simplex = 1-2mm brown/black macule - hyperpig., ( #’s of melanocytes at tips of rete ridges |

|Junctional nevus = 2-3mm “ (distal extremities) – clusters of melanocytes and hyperpig. at tips of rete |

|Compound nevus = 3-5mm brown papule (trunk and prox. extremities) – clusters of same and nests/sheets/strands of nml |

|Intradermal nevus = 3-5mm flesh colored papule (face) – junctional component disappears leaving the dermal component; |

|older lesions may resemble neurofibromas or be fat infiltrated |

|-cytological atypia is absent |

|C: some variants on the theme of melanocytic nevus are on P. 1176 |

|Dysplastic Nevi: poss. a percusor for melanoma esp. in patients w/ dysplastic nevus syndrome (rare AD trait in which people develop large #’s of dysplastic nevi |

|in late childhood); felt to be abbherant differentiation of common nevi; sporadic occurences mean nothing. |

|G: predominately on trunk and prox. extremities; larger than common nevi and have some border and color irregularities |

|M: may be junctinal or compound; lentiginous proliferation of melanocytes singly and in nests; lateral bridging of one rete to another; |

|concentric and lamellar dermal fibrosis; patchy lymphocytic infiltrate at base of melanocytic proliferation; +/- cellular atypia |

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|6. Benign Dermal Neoplasms |

|Benign Fibrous Histiocytoma (Dermatofibroma, DF) – may not be a true neoplasm |

|G: Firm dermal papule that indents when pressed on sides (dimple sign); reddish tan to brown/black; most commonly occur on |

|women’s legs; may be mult.; assymp. |

|M: more or less circumscribed proliferation of spindled fibroblasts; may appear to trap normal collagen bundles; some foamy macros; |

|CD 34 neg. |

|Xanthomas: not neoplasms but collections of foamy macrophages often assoc. w/ hyperlipidemia; types include eruptive(fleshy), tuberous and tendinous(yellow |

|nodules), plane(streaks), xanthelasma (eyelids – may not be assoc. w/ hyperlipidemia) |

|Cherry Angiomas: common tiny capillary hemangiomas in adults; no indication of internal disease |

|Strawberry Hemangiomas: rapidly growing capillary hemangiomas in infants; may involute; particularily likely to have internal organ involvement if mult. lesions |

|aare present |

|Benign Tumor of Cellular Imigrants to the Skin |

|Mastocytosis: Variants: 1. Mastocytoma: one or a few lesions; localized dermal nodule of mast cell infiltration; urticate, blister if |

|rubbed (Darier sign); involutes eventually |

|Urticaria pigmentosa: lesions like mastocytomas but usually slightly smaller/more numerous; |

|tachycardia & diarrhea may occur to due release of hist. if rubbed vigorously |

|Diffuse intracutaneous mastocytosis: diffuse skin infiltration w/ mast cells; diffuse edema causes skin |

|to look like leather; concern exists for mast cell leukemia and organ involvement. |

|Telangiectasia macularis eruptiva perstons: minimal ( in mast cells about dermal vessels; often no |

|Derier sign; tan macules that may have telangiectasias on trunk; middle aged adults; |

|most cells stain melachromatically (w/ Giesma and Toluidine blue) |

|7. Inflammatory Cutaneous Disorders |

|Ichthyosis: not really inflammatory; most are congenital/inherited |

|-X-linked is due to def. of steroid sulfatase and prevents normal skin shedding; Acquired ichthyosis may be paraneoplastic |

|Urticaria (Hives): allergic(Type I – IgE mediated hypersensitivity) and non-allergic forms exist |

|G: lesion is an edematous plaque that is called a “wheal”; usually w/ intense pruritus; usually gone w/in 24hrs; swelling of lip or |

|eyelid = “angioedema” |

|M: edema of the upper reticular dermis w/ minimal inflamm. infiltrate (if chronic may see eosinophils) |

|C: all wheels are not urticaria; vasculitis, bullous impetigo, etc. also present w. wheals |

|Dermatitis: 3 clinical presentations: 1. Acute = erythema, blisters, pruritus |

|2. Subacute = erythema, oozing, crustying, early scale formation, pruritus |

|3. Chronic = erythema, scaling, pruritus |

|- other dermatitis are on table 27-3 (p. 1195) |

|- allergic contact dermatitis is Type IV (cell mediated immunity); blisters are due to extreme spongiosis (intercellular edema) in epid. |

|Erythema Multiforme (EM): EM minor assoc. w/ herpes simplex; |

|EM major: Stevens Johnson Syn (SJS) – wide spread severe disease w/ mucus membrane involvment |

|and assoc. w/ allergic rxn to drugs or mycoplasma infxns (7-10 days) |

|Toxic Epidermal Necrolysis – explosive severe skin and mm damage w/ same causes |

|(overnight) |

|G: all three variants characterized by wheals, target lesions (true wheals w/ necrotic blistered center) and blisters; mm damage-major |

|M: minimal cellular (Lyc) infiltrate; vacuolar alteration along the BM zone; Dead keratinocytes in the epid. sometimes to the point |

|of full thickness epith. necrosis; similar histopathology occurs in GVHD and fixed drug eruption |

|Psoriasis: common scaling dermatosis; may be assoc. w/ arthritis; Variants include: classic plaque (mica-like silvery); guttate (eruptive process w/ small scaly |

|papules – assoc w/ strep pyogenes); erythrodermic (red scaly skin); pustular (pustules in red plaques); pinpoint bleeding when scale is removed is Auspitz sign; |

|nail dystrophies = 30% of patients |

|M: regular acanthosis w/o spongiosis; parakeratotic scale; collections of PMN’s in the epidermal living layer (spongiform pustule) |

|and stratum corneum (Munro’s microabscesses) are pathognomonic. |

|C: the Koebner phenomenonon = development of psoriasis at a site of non-specific trauma; psoriasis tend to be AD inheritance |

|Lichen Planus: pruritic self-limited but potentially protracted disorder of skin and mm |

|G: Violaceous papules (irregular, purple); fine grey-white lines on papules are called Wichham stria; mm has lacey white lesions |

|M: dense band-like lymphocytic infiltrate obscures dermal-epid. jn (DEJ); irregular (saw-tooth) rete ridges; dead keratocysts |

|(Civatte bodies) at DEJ; orthokeratotic hyperkeratosis |

|C: may be assoc. w/ Hep C; malignant degeneration (SCC) may develop in chronic mm lesions; Koebner pheno. (lines) may occur |

|Lupus Erythematosus: autoimmune connective tissue d/o; Localized (cutaneous) and multiorgan (SLE) forms exist |

|G: sharply demarcated hyperkeratotic lesions (DLE); can be widely spread mainly on malar eminences (sun-exposed) w/ SLE |

|M: superficial and deep periappendageal and pervascular lymphocytic infiltrate; vacuolar alteration along DEJ w/ BMZ thickening; |

|necrotic keratinocytes in epidermis; varying amounts of mucin; granular DEJ band of Ig and complement on direct IMF |

|C: positive lupus band on direct IMF; if band positive on non-sun exposed areas = more severe; ANA not pos. in skin-only cases |

|Bullous Diseases: many skin diseases have a blistering component, some characteristic depending on site of blister cleavage plane; may be induced by autoimmune, |

|friction, UVR, etc. |

|Pemphigous group of Disorders: group of blistering d/o that may affect skin or mm; blisters are intraepidermal w/ acantholysis; |

|due to antibodies to substances that hold cells together; several variants exist |

|Vulgaris (80%): due to antibody to Desmoglein 3 (adhesin); mm lesions often proceed skin lesions; flaccid blisters on trunk, |

|face, and prox. extremities; suprabasal blister; may become lethal |

|Foliaceous: endemic in S. America, but also sporadic cases; crusty (intact blisters rare); mm almost never involved |

|Vegetans: hyperplastic lesions in intertriginous areas (axilla & groin); oozing and crusting w/o obvious blistering |

|Erythematous: localized foliaceous; mainly on face; may be assoc. w/ SLE |

|M: all have pos. direct IMF – “net wire” pattern in epidermis on indirect; acantholytic keratinocytes float in blisters |

|Bullous Pemphigoid (BP): Sub-epidermal blisters; tense blisters; patients older; mm involvement rare; due to antibodies to BMZ |

|M: sub-epidermal blisters often contain eosinophils; fine BMZ band of complement and sometimes Ig |

|Dermatitis Herpetiformis (DH): a blistering disease assoc. w/ gluten sensitivity but only rarely w/ enteropathy (GSE) |

|G: grouped vesicles or erosions on an erythematous base on extensor surfaces; very pruritic |

|M: micro abscesses of PMN’s destroy dermal papillae; direct IMF shows granular deposits of IgA in dermal papillae |

|C: HLA-B8 and HLA-DRw3 are often assoc. |

|8. Non-inflammatory Blistering Diseases |

|Friction Blisters: common; subcorneal split; high heat and moisture are predisposing factors |

|Mechanobullous Disorders (Epidermolysis bullosa): diseases w/ genetic defects in elements nec. to hold skin together; several variants; blister w/ minimal |

|frictional trauma |

|Porphyria: due to genetic or acquired deficits in genes for enzymes,etc.; Porphyria Cutanea Tarda is the most common = blistering and scarring w/ milial cyst |

|formation in sun-exposed areas (esp. hands), hypertrichosis of temples ((hair), often assoc. w/ hemochromatosis |

|9. Disorders of Epidermal Appendages |

|Acne Vulgaris: inflammatory d/o of sebaceous follicles; effects 80% of teenagers; initial lesions are non-inflamm. (comedomes); but papules, pustules, nodules, |

|cysts, and scarring may ensue |

|10. Panniculitis: inflamm. of fat lobules or fibrous connective tissue septae in sub cutis (often on legs) |

|Erythema Nodosum: really a “septitis” of unknown etiology commonly on skin; may be assoc. w/ strep., birth control pills, sarcoid, TB, etc.; lesions somewhat |

|painful but almost never drain thru skin surface |

|Erythema Induratum: more of an inflammation of fat lobules, commonly on post. legs; assoc. w. TB or unknown; may ulcerate |

|11. Infection and Infestation |

|Warts: benign keratinocyte neoplasms cause by HPV (esp. types 16, 18, 31, 33, 35 – assoc. w/ rare AR d/o called Epidermodysplasia Verruciformis); several variants|

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|Common: verrucous papules on most surfaces; may grow rapidly and bleed w/ minor trauma; show filiform epidermal projections w/ parakeratosis, dilated papillary |

|capillaries and areas of large keratohyaline granules; few koilocytes possible |

|Moist: occur on mm’s and in intertriginous areas; less verrucous; show a proliferation of keratinocytes w/ kocloyctosis |

|Flat: slightly raised; maybe hyperpigmented; legs and face are common; may be spread by scratching; show min. keratinocyte proliferation w/ obvious koilocytosis |

|Plantar: often show massive keratohaline-like granules |

|Molluscum Contagiousum: caused by Pox virus (DNA); spread by physical contact and fomites |

|G: 2-4mm papules w/ central dell (opening to a hair follicle); may be much larger if immunosuppressed |

|M: can see cytoplasmic inclusion (molluscum bodies) in material expressed from lesion (35 microns); also present on biopsy |

|C: topical steroids may actually encourage spreading in patients w/ atopic dermatitis |

|Impetigo: Bullous from caused by Staph. aureus; group A Strep may also be present (erythema at edges of crusted lesion seen); cutaneous strains of strep have been|

|known to be nephritogenic also; Bullous form has acantholytic dermal cells, staph., and PMN’s in a sub-corneal blister |

|Superficial Fungal Infections: 3 genera: Dermatophytes = Trichophyton, Epidermophyton, and Microsporum |

|-Onchomycosis = infxn of nails; but includes all genera not just these 3 |

|-Tinea versicolor is caused by Malassezia furfur (hyper and hypo-pigmented patches on trunk) |

|-Fungal wall stains w/ PAS are usefuls (as is KOH) |

|Arthopod Bites, Stings, and Infestations (see book) |

|Pediculosis: louse infestation due to Head-capitis, Body-Vagabond’s disease, or Pubic-crabs; lice are blood feeders and bites may become infected |

|Scabies (Sarcoptes scabiei var hominis): burrows in skin at stratum corneum; spreads by repeated physical contact; not a blood feeder; intense pruritus due to |

|type IV hypersensitivity to mite parts |

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