2013 07 12 Plastic-Skin Tumor

8/13/2019 2013 07 12 Plastic-Skin Tumor

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Date July 12Th, 2013

TUMORS OF THE SKINBy Chaschaya Puangpikul, MD.


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contents

! Anatomy of the skin! Disorders of pigmentation and melanocytes!

Benign epithelial tumors

! Premalignant and malignant epidermal tumors


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Anatomy of the skin

Figure Robbins Pathologic Basis of Disease, 8thedition


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Benign epithelial tumors

! Seborrheic keratosis! Acanthosis Nigricans! Fibroepithelial polyp!

Epithelial Cyst(Wen)

! Adnexal (Appendage) tumors! Keratoacanthoma


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Seborrheic keratosis

! Common in middle aged.! Arise spontaneosly on trunk, extremities, head and neck.! Multiple small lesions on the face are termed Dermatosis papulosa

nigra.! Clinical features: uniformly tan to dark brown, round, flat, coinlike,

waxy plaques that vary in diameter and usually show a velvety togranular surface. stuck on and may be easily peeled off.

! Darkly pigmented seborrheic keratosis may look similar toMelanoma(biopsy reveals correct diagnosis)


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Rounded, tan/brown

exophytic plaques withgranular surface

basaloid keratinocytes with 3 features:

acanthosis, hyperkeratosis, keratin-filled horncysts

Acanthosis:

thickened

epidermis

Hyperkeratosis: thickened stratumcorneum

Paraneoplastic syndrome: explosive development of many seborrheic keratoses in

a patient with internal malignant neoplasm producing transforming growth factor-!:

Leser-Trelat sign


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Seborrheic keratosis:Treatment

! Shave excision! Curettage! Superficial electrodesiccation! Cryotherapy


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Acanthosis nigricans

! Thickened(acanthosis= hyperplasia of the stratum spinosum of theepidermis), Hyperpigmented skin with a valvet-like

! Most common involving in flexural areas! The benign type: 80% of all cases develops gradually and usually

occurs in childhood or during puberty. it may occur(as an autosomal

dominant trait or in associated with obesity or endocrineabnormalities.! The malignant type, in which lesions arise in middle-aged and older

individuals, often in associated with an underlying gastrointestinal

adenocarcinoma.


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Hyperpigmented plaque of

thickened skin in flexural

areas (neck, groin, axilla)

Papillomatosis (hills & valleys of keratinocytes with dermal

cores), hyperkeratosis, acanthosis, and increased number of

pigmented basal keratinocytes


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Acanthosis nigricans:Treatment

!

Therapy for underlying cause(weight loss in obese, discontinuation ofoffending drugs)! Topical tretinion!

Dermabrasion! Carbon dioxide laser


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Soft, flesh-colored, bag-like polyp;

occurs on neck, trunk, extremities,

intertriginous areas

Core of loose fibrovascular tissue

covered by essentially normal

epidermis with variable acanthosis


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Fibroepithelial polyp(skin tag, Acrochordon,squamous cell papilloma): treatment

! No treatment is needed.! Scissor excision with or without local anesthesia may be done for

cosmetic reasons or when the skin tag is irritated.


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Epithelial cyst(WEN,Epidermal

inclusion cyst)

!

WEN meaning lump or tumor! Cysts are filled with keratin and variable amounts of lipid-containing

debris derived from sebaceous secretions. Cheeselike, foul-smellingmaterial will exude from.

! Clinical features: they are dermal or subcutaneous, well-circumscribed, firm and often movable nodules.


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Well-demarcated,

soft, malleable,

movable nodule, a

punctum is usually

present

Mechanism of cyst formation:

invagination /cystic expansion of

epidermis

Histopathologyof cyst:

Lining = squamous epithelium with

a distinct granular layer

Cyst contents: laminated keratin

Clinical features: may become painful if

ruptured into dermis, because keratin

elicits a foreign body reaction;

accordingly, the entire cyst wall must

be surgically excised to prevent

recurrence(cant just shell it out)


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Epithelial cyst(WEN,Epidermal

inclusion cyst):treatment

! Excision with narrow margins! Intralesional corticosteriod (for inflamed lesion)! Simple drainage may lead to recurrence


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Adnexal (Appendage) tumors

! Arise from transformed epithelial of hair follicle, eccrine glands,apocrine glands, and sebaceous glands.

! Vast majority are benign( rarely malignant)! Some exhibit Autosomal dominant inheritance: eg. Multiple

cyclindromas! Some are associated with internal malignancy: cowden syndrome


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Hair follicle tumors

Trichofolliculoma Pilomatricoma


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Eccrine tumors

syringomaseccrine hidrocystoma


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Eccrine tumors

Eccrine poromas Cyclindroma


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Apocrine tumors

Apocrine Cystadenoma Syringocystadenoma papilliferum


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Sebaceous Tumors

Sebaceous nevus of Jadassohn


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Keratoacanthoma

! Rapidly developing neoplasm that clinically and histologically may

mimic well-differentiated squamous cell carcinoma.! Often it will heal spontaneously, without treatment!! Lesions most frequently affect sun-exposed skin of whites older than

age 50 years.! Clinical features: Flesh-colored, dome-shaped nodules with a central,

keratin-filled plug, imparting a crater-like topography


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Dome-shaped nodule

with central keratin

plug; 1-5 cm. diameter

Cup-shaped lesion with central

crater of keratin; downward

pushing rounded border

Large keratinocytes;

mildly atypical nuclei

& glassy cytoplasm

Clinical features: rapidly growing mass (enlarges over a few weeks) on sun-exposed skin

of face, ears, dorsum of hands; age >50; on histologic exam, it may resemble a

squamous carcinoma, butfast growth historyfavors keratoacanthoma; may

spontaneously regress without excision over time, but most are excised to rule out

carcinoma

Keratoacanthoma


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Keratoacanthoma: treatment

! surgical excision! Electrodesiccation and curettage


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Premalignant and malignant

epidermal tumors

! Actinic keratosis! Squamous cell Carcinoma! Basal cell Carcinoma! Merkel cell Carcinoma


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Actinic keratosis

! Dysplasia change commonly on sites expose to sun; face, arms,dorsum of hands

! Usually the results of chronic exposure to sunlight and is associatedwith build-up of excess keratin. exposure to ionizing radiation,hydrocarbons, and arsenicals may also induce lesion.

! highly incidence in lightly pigmented individuals! Clinical features: Usually less than 1cm in diameter, tan-brown,red or

skin-colored; rough, sandpaper-like concistency.

! Some lesions may produce so much keratin that a cutaneous

horndevelops.


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Actinic keratosisActinic keratosis

Scaly, tan-red lesions on sun-

exposed skin, usually < 1cm

Nuclear abnormalities in basal keratinocytes;

dysplasia does notinvolve full thickness of epidermis.

Clinical: extremely common lesions on sun-exposed skin of older persons, especially

those with fair skin color (estimated 50% of Caucasian Australians over age 40 have

these); risk is proportional to intensity/duration of UV exposure; estimated 10-20%

will ultimately transform into a squamous carcinoma if left untreated.


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Cutaneous horn

Cutaneous horn:

clinical term for a mound of

excessive hyperkeratosis

developing on top of an

underlying epidermal lesion

with dysplasia.

Differential diagnosis of the

underlying epidermal lesion

includes: actinic keratosis,

squamous carcinoma-in-situ,

and invasive squamous

carcinoma.

Therefore, one must excisethe cutaneous horn to know

its definitive diagnosis (tissue

is always the issue !)


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Actinic Keratosis: treatment

! Avoidance of sun exposure! Cryosurgery with liquid nitrogen! Topical 5-fluorouracil BID for 3 to 6 wks! Carbon dioxide laser! Excision


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Squamous cell carcinoma

! Second most common tumor arising on sun-exposure sites in older

people! Male>female! Exposure to sunlight(subsequent DNA damage) is the major

predisposing factor; other include industrial carcinogens(tars andoils), Chronic ulcers and draining osteomyelitis, old burn scars,ingestion of arsenicals, ionizing radiation, and (in oral cavity) tobaccoand betal nut chewing.


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Squamous cell carcinoma

Nodule with irregular

edges, variable crusting,

and often a central ulcer

Irregular tongues of dysplastic squamous epithelium

invading the dermis; tumor is graded by degree of

cytoplasmic keratinization & nuclear pleomorphism


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Basal cell carcinoma

! Most common skin carcinoma; arise mainly in sun-damagedepidermis

! Clinical features: Pearly papules often containing prominent, dilatedsubepidermal blood vessels(telangiectasias), some containmelanin(appear similar to melanocytic nevi or melanomas).Advanced lesions may ulcerate(rodent ulcers).

! Slow-growing , circumscribed, Less than 0.5% of BCCs metastases! Larger tumors can be deforming and aggressive requireing wide

excision


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Basal cell carcinoma

Pearly raised gray-pink nodule, some with

telangiectasias; large ones may ulcerate. Variant:

superficial BCC is red/tan plaque (ddx melanoma)

Solid or cystic islands of

crowded basaloid keratinocytes

invading dermis


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Merkel cell carcinoma

!

Derived from merkel call of the epidermis; a neural crest-derived cellputatively important for tactile sensation in lower animals.! Lesion may clinically present as ulcerated nodules and thus resemble

eroded basal cell carcinoma or relatively nonpigmented(amelanotic)

forms of malignant melanoma.

! capable of metastasis and are potentially lethal


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Neuroendocrine neoplasm;potentially lethal after metastasis; pathologist must

differentiate this neoplasm from malignant lymphoma & metastatic carcinoma

Electron Microscopy: membrane-bound dense coreneurosecretory granules (blue arrows) and stacks of

perinuclear cytokeratin filaments (black arrows)Nests of small blue cells,

with minimal cytoplasm

Merkel call carcinoma


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Disorders and Neoplasms ofMelanocytes

! Non-neoplastic! Frecle(called ephelis )! Melasma! lentigo

! Neoplastic! Melanocytic nevus! Dysplastic Nevus! Melanoma


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1-5 mm diametercircumscribed

tan-red macule withincreased melanin

pigmentin basal

keratinocytes, butnohyperplasia of

melanocytes

Clinical: almost universally present to some degree in fair-skinned persons,

with predilection for face, arms, shoulders. Appear during childhood, darken

and lighten with sun exposure, may increase in number after a sunburn.

Freckle(ephilis)

Melasma(cholasma)


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pregnancy mask: asymmetrical macular

zone of

hyperpigmentation

involving forehead,

temples, and cheeks in

pregnant women

Histopathology: two types

1) Epidermal: melanin deposition in basal keratinocytes; pigment can bereduced with topical hydroquinone.

2) Dermal: macrophages in superficial dermis with phagocytosed melanin.(doesnt respond to hydroquinone as well as epidermal type)

Clinical: more common in Latinos and Asians; develops during pregnancy, less

often with oral contraceptives; usually resolves spontaneously after pregnancy

pregnancy post-pregnancy

Melasma(cholasma)


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Lentigo5-10 mm oval tan-brown

macules, with evenly

distributed pigment and fairlywell-demarcated edges; these

have no predilection for sun-

exposed skin.

Lentigo Freckle

Darker color Lighter color

Larger size Smaller size

Dont darken

with sun

exposure

Skin and mucous

membranes

Darken with sun

exposure

Skin only

L i


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Lentigo

Histopathology: a non-neoplastic hyperplasia of melanocytes;increased numbers of melanocytes in basal layer with associatedhyperpigmentation, plus elongation & thinning of rete ridges


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Melanocytic nevus (mole)

Normal: one

melanocyte

per 10

keratinocytes

Junctional

nevus: basal

nests

Compound nevus:

nests epidermis &

dermis

Intradermal nevus: deeper

melanocytes are smaller (D) or

grow in cords/spindle cells (E)


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Melanocytic nevus (mole)

Junctional nevus: usually flat

Clinical appearances of

melanocytic nevi

Compound nevus: usually elevated

Intradermal nevus: elevated early"flat later

Melanocytic nevus : Junctional


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Melanocytic nevus : Junctionalnevus

Small, flat, symmetric, uniform

(edges sharp; mostly evenly pigmented)

Nests (not single) ovoid melanocytes in

basal layer only, at tips of rete ridges

Melanocytic nevus:compound


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Melanocytic nevus:compoundnevus

Dome-shaped papule (compare to macular junctional

nevus); sharp edges and evenly distributed pigmentsuggest its benign

Junctional andintradermalnests of melanocytes;

minimal nuclear atypia and no mitotic activity

Melanocytic nevus: Intradermal


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Melanocytic nevus: Intradermalnevus

Macular-papular, sharp edges,

evenly distributed pigmentNests and cords of melanocytes confined to dermis;

cells decrease in size in deeper dermis (rectangle);

such maturation deep cells implies benign


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Dysplastic nevus

Management: pathologic diagnosis of dysplastic nevus: need for long-term

surveillance of the patient to identify/excise melanocytic lesions suspicious for

melanoma (goal: excision before malignant melanoma develops)

Reactive linear

fibrosis dermis

Fused nests of

atypical melanocytes

between rete pegs

Evolution of Dysplastic nevus into


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Evolution of Dysplastic nevus intomalignant melanoma over time

LentigoJunctionalNevus

Dysplastic

compoundnevus

Early MM:radial growth inepidermis, superficial dermis

Advanced MM:

vertical growth

into dermis


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Malignant melanoma! Common neoplasm

! >60,000 estimated U.S. cases/yr. (American

Cancer Society)! highest incidence : Queensland, Australia! Lifetime risk in U.S.

! 1 in 58 men! 1 in 82 women

! Most lesions cured by complete surgical excision! Deadly if metastatic

! 5,000 male / 3,000 female deaths expected in

2008.

! Skin most common; but also primary in eye,

oral mucosa, anogenital mucosa, esophagus


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Malignant melanoma! Inherited genes and sun exposure strongly implicated in (history of severe sunburns in early years + chronic long

exposure)! Risk factors

! Sun-exposed surfaces: upper back, face, legs in women>men! Lightly pigmented skin (blonde or redhead)!

Dysplastic nevi (either DN syndrome or solitary DN)! Molecular genetics

! Most knowledge based on 10-15% of melanomas that arise in context of heritable syndromes(Most melanomas

do notappear in the context of a heritable syndrome)! 1) Mutations CDKN2a gene "loss tumor suppressor proteins p16/INK4a (#RB suppressor activity) and p14/

ARF (#p53 suppressor activity)

! 2) increased RAS and PI-3 Kinase signaling (70% melanomas have activating mutation BRAF) "proliferation! Most melanomas have mutations in both pathways, but additional mutations needed for malignant melanoma,

because many dysplastic nevi have both, yet do not become melanomas


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Malignant melanoma! ABCDof lesions suspicious for melanoma

! Asymmetry (not the same appearance in all 4 quadrants of lesion)! Border irregularity! Color variegation! Diameter greater than 6 mm (most > 1cm.)

! Clinical warning signs! CHANGE IN COLORof pigmented lesion! ENLARGEMENT of pigmented lesion! Itching, pain, ulceration, or bleeding in a previously stable pigmented

lesion


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Malignant melanoma

Malignant melanoma, lentigo

maligna type (10%): slow growth

Malignant melanoma, superficial

spreading type (60%): sun-exposed skin


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Malignant melanoma

MM, acral lentiginous

type (5-10%) involving

palmar, plantar, or

subungual skin of

fingers & toes)

MM, nodular

type (20%)


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Superficial spreading melanoma Lentigo maligna melanoma

Acral lentiginous melanomaNodular melanoma


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Melanoma VS Malignant

Melanoma in-situ: abnormal, dysplastic

melanocytes within epidermis, esp.

migrating up into stratum spinosum

MM: Dysplastic melanocytes involve

epidermis and invade the dermis


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Malignant melanoma

Gross: both nodular and macular areas

Radial growth: note brisk host immune

lymphocytic response in dermis

Vertical downward growth into dermis pleomorphic melanocytes in dermis


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Malignant melanoma:prognosis Risk of metastasis strongly correlated

with vertical growth phase thickness

(depth of invasion into dermis) Lymph node metastasis: strongest

adverse prognostic factor Other useful factors:

Number of mitoses (more is worse) Presence and number of tumor infiltrating

lymphocytes (more is better, vigorous immuneresponse)

Evidence of tumor regression: zones whereinvasive tumor replaced by fibrosis/depigmentation (worse prognosis)

Female gender (better) Location on extremities better than central

MM invading

dermis


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R f


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Reference

! Robbins Basic Pathology: 9thEdition

!

NCCN guideline application

! Grabb and Smith"s PlasticSurgery (6th edition)

!

Ferri's Fast Facts inDermatology, 1st Edition

2013 07 12 Plastic-Skin Tumor

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