Dermatopathology
| 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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