2013 07 12 Plastic-Skin Tumor
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Transcript of 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