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Diseases of Skin

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  • 1. Diseases of the Skinby Noel C. Santos, M.D.
  • 2. Definition of Terms Macroscopic Macule: flat, circumscribed, discoloration Papule: elevated solid area  5 mm. Nodule: elevated solid area > 5 mm. Plaque: elevated flat-topped > 5mm. Vesicle: elevated fluid-filled  5 mm. Bulla: elevated fluid-filled > 5 mm. Blister: common term for vesicle or bulla Pustule: discrete, pus-filled raised area
  • 3. Wheal: pruritic, erythematous elevated area resulting from dermal edema.Scale: dry, plate-like excrescence resulting from aberrant cornification.Lichenification: thick, rough skin with prominent skin markings, usually 2o repeated rubbing.Excoriation: linear, traumatic lesion resulting in epidermal breakage.Onycholysis: loss of nail substance.
  • 4. Microscopic Hyperkeratosis: stratum corneum hyperplasia, with aberrant keratinization. Parakeratosis: retention of nuclei in stratum corneum, normal in mucous membranes. Acanthosis: epidermal hyperplasia Dyskeratosis: abnormal keratinization below the stratum granulosum.
  • 5. Papillomatosis: elongation or widening of the dermal papillae.Lentiginous: linear pattern of melanocyte proliferation within the epidermal basal cell layer, reactive or neoplastic.Spongiosis: epidermal intercellular edema.Exocytosis: inflammatory cells infiltrating the epidermis.
  • 6. Erosion: focal, incomplete loss of epidermis.Ulceration: focal complete loss of epidermis, may include dermis and subcutaneous fat.Vacuolization: vacuoles within or adjacent to cells.
  • 7. ACUTE INFLAMMATORY DERMATOSES short-lived, mononuclear cell infiltrates with edema, local tissue damage URTICARIA (HIVES) ACUTE ECZEMATOUS DERMATITIS ERYTHEMA MULTIFORME ERYTHEMA NODOSUM and ERYTHEMA INDURATUM
  • 8. URTICARIA (HIVES)focal mast cell degranulation – histamine release: pruritus, edema & whealAngioedema: dermal & SC fat edemaPerivascular mononuclear infiltrates and edemaMediated by Ag-specific IgE or IgE-independent (chemical-induced, PG’s suppression)Persistent – inability to clear the inciting Ag, cryptic collagen-vascular disorders, Hodgkin/s disease
  • 9. Hereditary Angioneurotic EdemaRecurrent attacksWith GIT and laryngeal involvementDeficient C1 esterase inhibitorUnregulated activation of the early complement components
  • 10. ACUTE ECZEMATOUS DERMATITIS Pathogenetically different w/ same histologic features Cutaneous delayed-type HS response Cytokine release and nonspecific recruitment of inflammatory cells Gross: pruritic, red, papulovesicular to blistered, oozing and subsequently crusted, and may evolve into psoriasis-like scaling plaques Micro: spongiosis, progressive fluid accumulation, intraepidermal vesicles; dermal perivascular lymphocytic infiltrate, mast cell degranulation, papillary dermal edema; eosinophils (drug); progressive acanthosis & hyperkeratosis (chronic)
  • 11. 5 Primary Types of EczemaCONTACT DERMATITISATOPIC DERMATITISDRUG-RELATED ECZEMATOUS DERMATITISPHOTO-ECZEMATOUS ERUPTIONPRIMARY IRRITANT DERMATITIS
  • 12. Type Cause Histology Clinical FeaturesContact Dermatitis Topically applied Spongiotic dermatitis Itchy or burning; chemicals; delayed antecedent exposure HSAtopic Dermatitis Unknown; heritable ? Spongiotic dermatitis Erythematous plaques (flexors); + family HxDrug-related Systemically Spongiotic dermatitis; Eruption after exposure & administered eosinophils remits when discontinuedPhoto-eruption UV light Spongiotic dermatitis Sun-exposed skin; phototesting help in diagnosisPrimary irritant Repeated trauma Spongiotic dermatitis Localized to site of trauma (rubbing) (early stage)
  • 13. ERYTHEMA MULTIFORMEUncommon, self-limited HS response (drugs, infections, systemic disorders)Extensive epidermal degeneration and necrosisDue to cell-mediated immune injury (CD8+ cytotoxic T-cells)Gross: “multiform” – macules, papules, vesicles, and bullae; “targets” – red maculopapular with central vesicular or eroded pallor; symmetric involvement of extremities
  • 14. ERYTHEMA MULTIFORME (Cont.)Steven-Johnson syndrome: severe, febrile, erosions and hemorrhagic crustingToxic Epidermal Necrolysis: diffuse mucocutaneous epithelial necrosis and sloughing; analogous to 30 burnsMicro: dermoepidermal junction & superficial perivascular lymphocytic infiltrates; dermal edema, focal basal keratinocyte degeneration and necrosis; Exocytosis with epidermal necrosis, blistering and shallow erosions; Target lesions – central epidermal necrosis w/ perivenular inflammation
  • 15. ERYTHEMA NODOSUM/INDURATUMPanniculitis or inflammation of SC fat Connective tissue septa – NODOSUM Fat lobules – INDURATUMmay be Acute or ChronicEarly lesions: necrotizing vasculitis in deep dermis and subcutisEventually develop granulomatous inflammation and necrosis
  • 16. Erythema NodosumMost common, acute onsetIdiopathic or Secondary (drugs, infections, sarcoidosis, IBD, visceral malignancy)Ill-defined, tender erythematous nodules with fever and malaiseOld lesions flatten, ecchymotic without scarring while new lesions developBx: early septal widening - edema, fibrin deposition, neutrophil infiltration (giant cells & eosinophils) w/o vasculitis
  • 17. Erythema InduratumUncommon, unknown causeAdolescent and menopausal womenPrimary vasculitis of SC fat with subsequent inflammation and necrosis of adipose tissueErythematous, slightly tender nodule that ulcerates and scarsEarly: necrotizing vasculitis in deep dermis and subcutisLate: fat lobules develop granulomatous inflammation and necrosis
  • 18. Weber-Christian disease (Relapsing Febrile Nodular Panniculitis) Rare form of panniculitis; crops of erythematous plaques or nodules, mainly on the legs Deep lymphohistiocytic infiltrates and giant cellsFactitial Panniculitis Self-administered foreign substances Deep mycotic infections in immunocompromised Others: SLE
  • 19. CHRONIC INFLAMMATORY DERMATOSESPersistent inflammatory disordersScaling and shedding (desquamation)PSORIASISLICHEN PLANUSLUPUS ERYTHEMATOSUSACNE VULGARIS
  • 20. PSORIASISCommon, HLA types (genetic)New lesions at sites of trauma (Koebner’s phenomenon) – exogenous stimuliDamage to stratum corneum – deposition of complement- fixing Ab’s with 20 complement-mediated injuryPsoriatic endothelium – sensitive to cytokine-induced expression of adhesion molecules with subsequent enhanced neutrophil recruitmentAssociated with other disorders: myopathies, enteropathies, AIDS, arthritis
  • 21. PSORIASIS (Cont.)Gross: well-demarcated salmon pink plaques with silvery scaling; elbows, knees, scalp, lumbosacral area, intergluteal cleft, glans penisAnnular, linear, gyrate or serpiginousERYTHRODERMA - total body scaling and erythemaNail changes: discoloration, pitting, onycholysisPustular psoriasis: rare, life-threatening
  • 22. PSORIASIS (Cont.)Micro: marked acanthosis with rete elongation, mitoses above the basal layer; thin or absent stratum granulosum; extensive overlying parakeratosisThin epidermis overlying dermal papillae with dilated vessels – pinpoint bleeds when overlying scale is removed (Auspitz sign)Aggregates of neutrophils in epidermis within small spongiotic foci in the stratum spinosum (spongiform pustules) or within the parakeratotic stratum corneum (Munro’s microabscesses); large, abscess-like
  • 23. LICHEN PLANUSUnknown cause, self-limited, after 1 to 2 yrs. Leaves postinflammatory hyperpigmentationOral may persist, may become malignantCell-mediated immune injury to basal cellsWith Koebner’s phenomenonGross: pruritic, purple, polygonal papules that may coalesce into plaques; highlighted by white dots or lines (Wickham’s striae)Multiple, symmetrically distributed; hair follicle epithelium (lichen planopilaris)
  • 24. LICHEN PLANUS (Cont.)Micro: dense, bank-like dermoepidermal junction lymphocytic infiltrate with basal cell degeneration and necrosis; jagged rete “saw- toothing”Necrotic basal cells may be sloughed into inflamed papillary dermis forming colloid or Civatte bodiesWith chronic changes: acanthosis, hyperkeratosis, thick granular cell layer
  • 25. LUPUS ERYTHEMATOSUSDiscoid LE – localized cutaneous form w/o systemic manifestationImmune complex-mediated and cell-mediated injury to pigment-containing basal cellsSun exposure exacerbates the lesionGross: ill-defined malar erythema; sharply demarcated “discoid” erythematous scaling plaques with zones of irregular pigmentation and small keratotic plugs in hair follicles
  • 26. LUPUS ERYTHEMATOSUS (Cont.)Micro: dermoepidermal junction perivascular & periappendiceal lymphocytic infiltratesPreferential involvement of SC fat – lupus profundusBasal cell vacuolization, epidermal atrophy, variable hyperkeratosisImmunofluorescence: granular band along the dermoepidermal and dermal-follicular junctions (lupus band test)
  • 27. ACNE VULGARISCommon, chronic, inflammatory dermatosis affecting hair folliclesMiddle to late teens, males>femalesHormonal changes, alteration in hair follicle maturations, infection (P. acnes)Sex hormones, corticosteroid, occupational exposure, occlusive conditions, heritable componentLipase degradation of sebaceous oils to highly irritating fatty acidsAntibiotics and vit. A (retinoic acid)
  • 28. ACNE VULGARIS (Cont.)Gross: Non-inflammatory – follicular papules with central black keratin plugs (open comedo); follicular papules w/ central plugs trapped beneath the epidermis (closed comedo)Rupture – Inflammatory: erythematous papules, nodules, pustulesMicro: lipid & keratin at the midportion of hair follicles, follicular dilatation; epithelial and sebaceous gland atrophyLymphohistiocytic infiltrates; acute & chronic inflammation with scar formation
  • 29. BLISTERING (BULLOUS) DERMATITISPrimary conditions; level of blister involvement within the skin SUBCORNEAL: impetigo, p. follaceus SUPRABASAL: p. vulgaris SUBEPIDERMAL: bullous pemphigoid, dermatitis herpetiformisPEMPHIGUSBULLOUS PEMPHIGOIDDERMATITIS HERPETIFORMIS
  • 30. PEMPHIGUSRare, autoimmune, 4th to 6th decadesCirculating Ab’s to keratinocyte intercellular cement components that bind and trigger release of plasminogen activator by keratinocytesFOUR variants: P. vulgaris P. vegetans P. foliaceus P. erythematosus
  • 31. Pemphigus vulgaris80%; oral mucosa, scalp, face, intertriginous zones, trunk, pressure pointsSuperficial and easily ruptures that leave shallow & crusted erosionsUntreated – uniformly fatalPemphigus vegetansRare; large, moist verrucous plaques studded with pustulesFlexural and intertriginous zones
  • 32. Pemphigus foliaceusMore benign, epidemic in S. AmericaFace, scalp and upper trunkExtremely superficial bullae leaving only slight erythema and crusting after rupturePemphigus erythematosusLocalized, milder variant of P. foliaceusMalar zone on the face
  • 33. PEMPHIGUS (Cont.)Micro: acantholysis leading to intercellular clefting and broad-based intraepidermal blistersP. vulgaris & vegetans: immediately above the basal layer (suprabasal blisters)P. foliaceus: stratum granulosumImmunofluorescence staining around each keratinocyte (anti-Ig and anti-complement)
  • 34. BULLOUS PEMPHIGOIDCommon, autoimmune, elderlyCirculating Ab’s, with complement activation and granulocyte recruitment, against Ag’s of the lamina lucida in the epidermal BMunderlying lymphoreticular neoplasmGross: tense bullae (up to 8 cm) w/ clear fluid, do not rupture easily and heal w/o scarringMicro: subepidermal nonacantholytic blister; linear dermoepidermal junction fluorescence; superficial perivascular infiltrates
  • 35. DERMATITIS HERPETIFORMISRare, 3rd to 4th decade, m>fspecific HLA types & celiac diseaseSkin & GI lesions respond to gluten-free dietImmune complex deposition in the skinAnti-gliadin Ab’s cross reacting with junction anchoring components (reticulin)Granular IgA deposits dermal papillae tipsGross: pruritic, urticarial plaques & vesicles, symmetric (extensors, upper back & buttock)
  • 36. DERMATITIS HERPETIFORMIS (Cont.)Micro: neutrophils & fibrin accumulate in the tips of dermal papillae (microabscesses) with overlying basal vacuolization; microscopic blisters coalescing to large subepidermal blisters
  • 37. NONINFLAMMATORY BLISTERING DISEASESPrimary disorders with vesicles and bullae NOT mediated by inflammatory mechanismsPORPHYRIAEPIDERMOLYSIS BULLOSA
  • 38. PORPHYRIAInborn or acquired disturbances of porphyrin metabolismUnknown pathogenesisUrticaria and vesicles exacerbated by sun exposure; heals w/o scarringSubepidermal vesicles with marked superficial dermal vascular thickening
  • 39. EPIDERMOLYSIS BULLOSABlistering at pressure sites and traumaTYPES: JUNCTIONAL: blistering at the lamina lucida DYSTROPHIC: scarring, blistering beneath the lamina lucida due to defective anchoring fibrils SIMPLEX: epidermal basal cell degeneration
  • 40. INFECTION and INFESTATIONVERRUCAE (WARTS)MOLLUSCUM CONTAGIOSUMIMPETIGOLEPROSYSUPERFICIAL FUNGAL INFECTIONSARTHROPOD-ASSOCIATED LESIONS
  • 41. VERRUCAE (WARTS)Common, HPV, direct contactV. Vulgaris: most common, dorsum of hand; gray-white to tan, flat to convex, up to 1 cm. papules with rough pebbly surfaceV. plana (flat wart): face or dorsum of hand; flat, smooth, small, tan papulesV. plantaris or palmaris: rough, scaly, up to 2 cm; may coalesce, confused with callousCondyloma acuminatum (Anogenital and Venereal Warts): soft, tan, cauliflower-likeMicro: undulant (verrucous) epidermal hyperplasia and koilocytosis
  • 42. MOLLUSCUM CONTAGIOSUM Common, poxvirus, direct contact Gross: firm, pruritic, pink to skin-colored, umbilicated papules, up to 2 cm, trunk & anogenital regions Cheezy material with molluscum bodies expressed from central umbilication Micro: cuplike verrucous epidermal hyperplasia with molluscum bodies (large eosinophilic cytoplasmic inclusions in the stratum granulosum or corneum)
  • 43. IMPETIGOStreptococcal & Staphylococcal infectionerythematous macule progressing to small papules and eventually shallow erosion with honey-colored crustMicro: subcorneal pustules filled with neutrophils and Gm+ cocci; dermal inflammationPustule rupture releases serum and necrotic debris to form the crust
  • 44. LEPROSYSlowly progressive, unsightly & disabling deformities, peripheral neural sensory deficitsAerosol transmission, bipolar disease TUBERCULOID: granulomas, (+) 48-hr lepromin test LEPROMATOUS: anergic to lepromin, nodular lesions with macrophages stuffed with bacilli, may coalesce – leonine facie
  • 45. SUPERFICIAL FUNGAL INFECTIONSDermatophytes; confined to nonviable stratum corneum; by locationReactive epidermal changes similar to mild eczematous dermatitis Tinea capitis: asymptomatic hairless patches, mild erythema, crusting and scales Tinea barbae: beard area among adult men Tinea corporis: excessive heat & humidity, infected animals, chronic infection of the feet/nails; expanding erythematous plaque with elevated scaling border – “ringworm”
  • 46. FUNGAL INFECTIONS (Cont.)Tinea cruris: inguinal areas among obese, warm weather; moist patches with raised scaling bordersTinea pedis (Athlete’s foot): erythema & scaling in the webbed spaces, 2O bacterial infectionsOnychomycosis: discoloration, thickening and deformity of the nail plateTinea versicolor: Malassezia furfur, upper trunk, vari- sized hyper- or hypopigmented macules with peripheral scale
  • 47. ARTHROPOD-ASSOCIATED LESIONSBites, stings, infestationsReactions: trivial to fatalGross: urticarial, inflamed papules or nodules, expanding erythematous plaques (erythema migrans) Direct irritant effect Immediate IgE-mediated or delayed cell- mediated HS Rxn Specific effects of venom Associated with secondary invaders
  • 48. SCABIESPruritic caused by mite Sarcoptes scabieiFemale burrows beneath the stratum corneum – linear, poorly defined furrows: interdigital skin, palms, wrists, periareolar area, scrotal folds
  • 49. PEDICULOSISPruritic, caused by louse: insect or eggs attach to hair shaftsMay be complicated by impetigo with lymphadenopathy; urticaria-likeExcoriations and hyperpigmentationMicro: wedge-shaped dermal perivascular lymphohistiocytic and eosinophilic infiltrates; central zone of epidermal necrosis w/ birefringent insect mouth parts; florid inflammatory infiltrates or spongiosis – intraepidermal blisters
  • 50. DISORDERS OF PIGMENTATION ANDMELANOCYTESVITILIGOFRECKLE (EPHELIS)MELASMALENTIGONEVOCELLULAR NEVUS (PIGMENTED NEVUS, MOLE)DYSPLASTIC NEVIMELANOMA
  • 51. VITILIGOIrregular, well-demarcated macules devoid of pigmentationAutoimmunity (melanocyte autoAb’s, T-cell abnormalities); neurohormonal factors; toxic intermediates in melanin synthesisMicro: loss of melanocytes
  • 52. FRECKLE (EPHELIS)Pigmented lesions: tan-red to brown macules occurring after sun exposure, fading and recurring with subsequent cycles of winter and summerMicro: normal melanocyte number, ?slight hypertrophy; increased melanin within basal keratinocytes
  • 53. MELASMAMasklike facial hyperpigmentationHyperestrogenic states, fades postpartumGross: blotchy, irregular, ill-defined macules; accentuated by sunlightEnhanced melanin transfer from melanocytes to other cell types w/ subsequent accumulationMicro: increased melanin deposition in basal layers (epidermal type); papillary dermal macrophage phagocytosis of melanin released from the epidermis – pigment incontinence (dermal type)
  • 54. LENTIGOBenign, hyperpigmented macules, do not darken with sun exposureUnknown etiology and pathogenesisMicro: linear basal hyperpigmentation due to melanocyte hyperplasia; with elongation and thinning of rete ridges
  • 55. NEVOCELLULAR NEVUSGroup of congenital or acquired melanocyte neoplasmWell-demarcated, tan-brown papulesMelanocytes derive from basal dendritic cells that differentiate into round-to-oval cells with uniform nuclei and prominent nucleoliNatural History: Begin as well-defined nests along the dermoepidermal junction (junctional nevi); lentigo-like (lentiginous) melanocyte proliferation Extension of melanocytes forms nests within both dermis and epidermis (compound nevi)
  • 56. NEVOCELLULAR NEVUS (Cont.) Lost epidermal component resulting in dermal nevi Progressive dermal downgrowth, nevus cells undergo maturation to resemble neural tissueVariants: Congenital nevus Blue nevus Spindle & Epithelioid cell (Spitz) nevus Halo nevus Dysplastic nevus
  • 57. Nevus Variant Diagnostic Architectural Features Diagnostic Cytologic Clinical Significance FeaturesCongenital nevus Deep dermal, SC growth around Same as ordinary acquired At birth; large variants adnexae, neuro-vascular bundles nevi have increased melanoma & blood vessel walls riskBlue nevus Non-nested dermal infiltration, Highly dendritic, heavily Black-blue nodule; often with fibrosis pigmented nevus cells confused with melanomaSpitz’s nevus Fascicular growth Large, plump cells with Children; red-pink nodule; pink-blue cytoplasm; confused with fusiform hemangiomaHalo nevus Lymphocytic infiltration Identical to ordinary Immune response vs surrounding nevus cells acquired nevus nevus cells & surrounding normal melanocyteDysplastic nevus Large, coalescent intraepidermal Cytologic atypia Potential precursor of nests malignant melanoma
  • 58. DYSPLASTIC NEVUSAutosomal dominant or sporadicLarger than acquired nevi; as hundreds of irregular macules/plaques with pigment variegation in both sun-exposed and nonexposed skinMicro: cytologic and architectural atypia; enlarged & fused epidermal nevus cell nests, lentiginous hyperplasia, linear dermo- epidermal junction fibrosis, pigment incontinence
  • 59. MELANOMASun exposure, lightly pigmented individuals, hereditary componentPruritic, variegated, irregular maculopapular lesions; CHANGE IN COLORATIONInitially extends horizontally within the epidermis and superficial dermis (RADIAL GROWTH PHASE); don’t metastasize – LENTIGO MALIGNA and SUPERFICIAL SPREADINGVERTICAL GROWTH PHASE – extension into the deep dermis, loss of cellular maturation, dev’t of the capacity to metastasize
  • 60. MELANOMA (Cont.)Clinical behavior & probability of metastasis – characteristics and depth of invasion of the vertical growth; mitotic rates and degree of lymphocytic infiltratesMicro: melanoma cells – larger than nevus cells, irregular nuclei, prominent eosinophilic nucleoli; grow as loose nests lacking melanocyte maturation
  • 61. BENIGN EPITHELIAL TUMORSbiologically inconsequential lesions derived from keratinocytes or skin appendagesSEBORRHEIC KERATOSISACANTHOSIS NIGRICANSFIBROEPITHELIAL POLYPEPITHELIAL CYST (WEN)KERATOACANTHOMAADNEXAL (APPENDAGE) TUMORS
  • 62. SEBORRHEIC KERATOSISSpontaneous lesions; trunk, smaller facial lesions (dermatosis papulosa nigra)Large number as part of paraneoplastic syndrome (sign of Leser-Trelat) due to tumor elaboration of growth factors]Gross: uniform, tan-brown, velvety/granular, round plaques, keratin-filled plugsMicro: exophytic, hyperplasia of basaloid cells, hyperkeratosis, keratin-filled “horn cysts”
  • 63. ACANTHOSIS NIGRICANSThick hyperpigmented zones in flexural areasAssociated with benign or malignant conditions elsewhere in the bodyBENIGN: 80%, childhood through puberty, autosomal dominant, obesity or endocrine disorders, part of rare congenital disordersMALIGNANT: middle-aged & older, occult adenocarcinomaMicro: hyperkeratosis, prominent rete ridges, basal hyperpigmentation w/o melanocyte hyperplasia
  • 64. FIRBOEPITHELIAL POLYPAcrochordon, squamous papilloma, skin tagSoft, flesh-colored attached by slender stalk with fibrovascular core covered by benign epidermisAssociated with pregnancy, diabetes or intestinal polyposis
  • 65. EPITHELIAL CYSTSWell-circumscribed, firm, SC nodulesDowngrowth and cystic expansion of the epidermal and follicular epitheliumMicro: based on cyst wall characteristic Epidermal Inclusion Cyst: normal epidermis Pilar (Trichilemmal) Cyst: follicular epithelium w/o granular cell layer Dermoid Cyst: epidermis w/ multiple skin appendages, hair follicles Steatocystoma multiplex: sebaceous gland ductal epithelium w/ numerous compressed sebaceous lobules
  • 66. KERATOACANTHOMASpontaneously heal, rapidly growing, sun-exposedGross: flesh-colored, superficial, with central keratin-filled craters, face/handsMicro: cup-shaped epithelial proliferations w/ atypical cells, enclose central keratin-filled plug.Pattern of keratinization recapitulates hair follicle (no granular cell layer)Minimal inflammation during rapid proliferative phase; evolves – dermal inflammation and fibrosis; eventually regress & disappear
  • 67. ADNEXAL (APPENDAGE) TUMORSBenign neoplasms, few malignant variants; Mendelian pattern; indicate visceral malignancy (Cowden’s syndrome – multiple trichilemmomas with breast Ca)Single or multiple, nondescript papules and nodules, site predilectionEx: Cylindromas, Syringomas, Trichoepitheliomas, Trichilemmomas, Sebaceous Gland Adenoma/Adenocarcinoma
  • 68. PREMALIGNANT AND MALIGNANT EPIDERMATUMORSACTINIC KERATOSISBOWEN’S/BOWENOID LESIONS and ERYTHROPLASIA OF QUEYRATSQUAMOUS CELL CARCINOMABASAL CELL CARCINOMAMERKEL CELL CARCINOMA
  • 69. ACTINIC KERATOSISPremalignant dysplastic lesion, chronic sun exposure; ionizing radiation, hydrocarbons, and arsenicalsGross: tan-brown, red or flesh-colored, rough consistency, cutaneous hornsMicro: cytologic atypia in the lower epidermis, parabasal cell hyperplasia, dyskeratosis; hyperkeratosis, parakeratosis; epidermal atrophy; dermis is thick with blue-gray elastic fibers (elastosis)
  • 70. CARCINOMA IN-SITUFull thickness epidermal cytologic atypia (Bowen’s disease; Bowenoid papulosis; Erythroplasia of Queyrat)Perineal/groin area with erythematous patches; leukoplakia; well-demarcated, red, scaling plaquesMicro: entire thickness of epidermis exhibits cytologic nuclear atypia
  • 71. SQUAMOUS CELL CARCINOMAMost common; sunlight/UV light directly damages DNA & exerts immuno-suppressive effect to Langerhans’ cells; industrial carcinogens, chronic skin ulcers, old burn scars, draining osteomyelitis, ionizing radiation, tobacco or betel nut chewingImmunosuppression; xeroderma pigmentosum; HPV infection
  • 72. SQUAMOUS CELL CARCINOMA (Cont.)Gross: nodular, variably hyperkeratotic, ulcerates; leukoplakia (mucosal surface)May metastasize to regional LNMicro: from well differentiated to highly anaplastic with necrosis & abortion keratinization
  • 73. BASAL CELL CARCINOMACommon, slow-growing, sun-exposed and rarely metastasizeImmunosuppression & xeroderma pigmentosumGross: pearly papules or expanding plaques; may be pigmented; ulcerate with extensive local invasion “rodent ulcer”Micro: basal cell proliferation extending deeply into the dermis; superficial or nodular
  • 74. MERKEL CELL CARCINOMARare, neural crest derived Merkel cells (tactile sensation)Potentially lethal; small, round malignant cells containing neurosecretory type cytoplasmic granulesResemble small cell Ca of the lung
  • 75. TUMORS OF THE DERMISBENIGN FIBROUS HISTIOCYTOMADERMATOFIBROSARCOMA PROTUBERANSXANTHOMASDERMAL VASCULAR TUMORS
  • 76. BENIGN FIBROUS HISTIOCYTOMAIndolent neoplasms of dermal fibroblasts & histiocytesUnknown cause, antecedent trauma and aberrant healingGross: tan-brown, firm papules, may be tender; lateral compression exert dimplingMicro: dermatofibroma – spindle shaped fibroblasts, unencapsulated in the mid-dermis extending to SC fat
  • 77. DERMATOFIBROSARCOMA PROTUBERANSWell-differentiated, slow-growing fibrosarcoma; locally aggressive but rarely metastasizeGross: firm solid nodules arising as protuberant, ulcerated aggregates within an indurated plaqueMicro: radially oriented (storiform) fibroblasts; scanty mitosis; thin overlying epidermis with extension into SC fat
  • 78. XANTHOMASNot true neoplasm, focal accumulation of foamy histiocytesIdiopathic or Secondary (familial or acquired hyperlipidemias, lymphoproliferative disorders)Types (gross & hyperlipidemia): Eruptive Xanthoma: sudden showers of yellow papules that wax & wane w/ plasma triglycerides & lipid levels Tuberous Xanthoma: yellow, flat-to-round nodules over the joints
  • 79. XANTHOMAS (Cont.) Tendinous Xanthoma: yellow nodules over the Achilles tendon and finger extensor tendons Plane Xanthoma: linear yellow lesions in skin folds (palmar creases); 1O biliary cirrhosis Xanthelasma: soft yellow plaques on the eyelidsMicro: dermal aggregates of macrophages with vacuolated cytoplasm containing cholesterol, phospholipids, and triglycerides
  • 80. DERMAL VASCULAR TUMORSHemangiomas, vascular malignant tumors, Kaposi’s sarcoma and angiomatosis
  • 81. TUMORS OF CELLULAR IMMIGRANTS TO THESKIN Proliferative disorders of cells arising elsewhere but which homed to the skin HISTIOCYTOSIS X MYCOSIS FUNGOIDES (CUTANEOUS T-CELL LYMPHOMA) MASTOCYTOSIS
  • 82. HISTIOCYTOSIS XCutaneous form – solitary or multiple papules or nodules; scaling erythematous plaques resembling seborrheic dermatitisHisto: variable numbers of eosinophils and different patterns: Diffuse dermal infiltrates of mononuclear cells with bland, indented nuclei Similar cells clustered to resemble granulomas Dermal infiltrates composed of mononuclear cells with foamy cytoplasmBirbeck granules, CD1 Ag’s – Langerhans’ cell derivation
  • 83. MYCOSIS FUNGOIDESCutaneous T-cell Lymphoma, 3 patterns Mycosis Fungoides (MF) MF d’emblee: nodular eruptive variant Adult T-cell leukemia or lymphoma: aggressive course, HTLV-1Lymphoproliferative disorder arising from the skin & eventually seed the blood (Sezary’s syndrome) and evolve into more generalized T- cell leukemia or lymphoma
  • 84. MYCOSIS FUNGOIDESGross: eczema-like lesions evolving into scaly, red- brown patches or plaques; to nodules (nodular cutaneous growth – deep dermal invasion; onset of LN & visceral involvement)Micro: Sezary-Lutzner cell – malignant CD4-positive (T-helper) cell with hyperconvoluted or “cerebriform” nucleus; band-like dermal infiltrates with invasion of single cells or small clusters into the epidermis (Pautrier’s microabscess)
  • 85. MASTOCYTOSISRare, cutaneous (visceral) mast cell proliferation; degranulation (histamine and heparin)Pruritus & flushing – specific foods, temperature, alcohol, certain drugsDermal edema & erythema (wheal) when skin (Darier’s sign) or normal skin (dermatographism) is rubbedEpistaxis or GI bleeding
  • 86. MASTOCYTOSIS (Cont.)Urticaria pigmentosa (50%) exclusively cutaneous, favorable prognosis, children; 10% adults, systemic, poorer prognosisGross: multiple, round-to-oval, nonscaling, red- brown papules & plaquesMicro: dermal fibrosis, edema, eosinophils and mast cells
  • 87. That’s all folks!!! Thank you very much!!! Good morning!!!

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