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60 Cards in this Set
- Front
- Back
Skin Tumors can derive from
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Epidermal components
Dermal components Hypodermal components “Immigrant cells” (i.e.lymphocytes, histiocytes, metastases, etc,) |
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Epidermis 2 major cell types
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Keratinocytes
Melanocytes |
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Seborrheic Keratosis
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Hyperkeratotic pigmented papules and plaques
( especially on face and trunk) Occurs in middle aged/elderly Stuck on appearance |
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Papules similar to seborrheic keratosis in african americans known as
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Dermatosis Papulosa Nigra
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Sign of “Lesser Tralet
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is a sudden onset of numerous seborrheic keratosis due to a paraneoplastic syndrome
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Histology of Seborrheic Keratosis
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Sharply demarcated, exophytic, hyperplastic epithelium with pigmented basal cells
Keratin Horn Cyst formation and hyperkeratosis |
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Acanthosis Nigricans
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Thickened, hyperpigmented velvety zones in flexural areas (axilla, groin, anogenital)
Usually arises in childhood (autosomal dominant) Associated with obesity and endocrine disorders (i.e. diabetes) |
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Sudden onset of Acanthosis Nigricans may be associated with
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occult malignancy (i.e. adenocarcinoma releasing growth factors)
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Fibroepithelial Polyp(a.k.a. Skin tag, Acrochordon, Squamous papilloma)
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Commonly found on neck, trunk, face or intertriginous (skin folds)
Soft flesh colored polyps |
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Keratoacanthoma
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A self limited spontaneously healing, rapidly growing lesion in sun exposed Caucasians (usually > 50 y/o)
Flesh colored dome-like nodule with a central keratin filled crater often on hand or hand |
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Epithelial Inclusion Cyst
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Common, well circumscribed, firm dermal or subcutaneous nodules formed by downgrowth and cystic expansion of:
Epidermis (i.e. epidermal inclusion cyst) Clinicians sometimes refer to these as “sebaceous cyst” |
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A small Epithelial Inclusion Cyst known as
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milium
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Xanthelasma
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Not a tumor but a lipid deposition (i.e.xanthoma) that typically occurs around the eye
Appears as soft yellow plaques on eyelids (“chicken fat”) May or may not be associated with lipid abnormalities A patient with xanthoma(s) should have a lipid profile work up |
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Most common form of cancer in United States
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Almost 50% of people living to the age of 65 will have skin cancer at least once in their lifetime
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Epidermal transformation into skin cancer
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KeratinocytesNonmelanoma
Melanocytes Melanoma |
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3 Major types of skin cancer
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Squamous Cell Carcinoma (SCC)
Basal Cell Carcinoma (BCC) 3. Melanoma |
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The vast majority of skin cancers are of non
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melanoma type usually begin as Actinic Keratosis
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Actinic (Solar) Keratosis (premalignant) can develop into
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Squamous cell carcinoma (SCC)
Basal cell carcinoma (BCC) |
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Dysplastic nevus (premalignant)
can develop into |
Melanoma (can also occur de novo)
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Actinic Keratosis(Solar Elastosis)
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, dysplastic lesion associated with sun exposure, especially in light skinned individuals
Ionizing radiation, hydrocarbon, arsenicals may induce similar lesion |
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In actinic Keratosis, hyperkeratosis increases leading to
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Cutaneous Horn
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Actinic (Solar) Keratosis Histology
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Cytologic atypia in the lower epidermis frequently with
basal cell hyperplasia and dyskeratosis; usually have damaged collagen in the dermis (elastosis) demonstrated by blue-gray elastic fibers. |
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Squamous Cell Carcinoma (SCC) predisposing factors
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Sunlight (UV) irradiation include:
Other predisposing factors include: Industrial carcinogens Old burn scars Tobacco Immunosuppression Human Papilloma Virus (i.e. HPV36,18,16) Xeroderma pigmentosum (inherited defect in DNA repair) |
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Squamous Cell Carcinoma In Situ SCC ( Bowen’s Disease)
Appears as |
well demarcated red scaling plaques
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Squamous Cell Carcinoma In Situ SCC ( Bowen’s Disease) Histology shows
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full thickness epidermal atypia”
- lack of epidermal maturation - intact basement membrane at epidermal-dermal junction |
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Squamous Cell Carcinoma (SCC) Invasive SCC
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nodular, variably hyperkeratotic
Prone to ulceration -> “nonhealing ulcer” |
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Squamous Cell Carcinoma (SCC) Invasive SCC Histology shows
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atypical squamous cells breaking through D-E junction (basement membrane) into underlying dermis
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Mucosal involvement by SCC looks like
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white thickened plaques (i.e. leukoplakia)
can be seen in: Lips, oral cavity Esophagus Ano-genital area |
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Most common malignant skin tumor
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Basal Cell Carcinoma slow growing tumor, typically in
sun-exposed skin Appear as “pearly papules” or plaques that may ulcerate ->nonhealing ulcer May extensively invade local tissue (i.e. rodent ulcer) |
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Basal Cell Carcinoma Histology:
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Atypical basal cell proliferation with peripheral pallisading, multifocal (skip lesions), budding, superficial growths or nodular extensions from the basal cell layer of epidermis into dermis
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A nonhealing ulcer needs to be biopsied!
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MUST RULE OUT MALIGNANCY!
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benign Melanocytic Neoplasms can be
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a. Lentigo (simplex
b. Melanocytic Nevus (Mole): |
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. Lentigo (simplex)
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It is an increase in number of single basal melanocytes
Common, benign hyperpigmented macules (5-10mm on skin and mucous membrane that appear in infancy and childhood) In contrast to freckles, these do not darken due to sun exposure |
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Melanocytic Nevus (Mole):
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can be acquired or congenital - common variants:
i. Junctional nevus ii. Compound nevus iii. Intradermal nevus |
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Lentigo Simplex histology
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Linear basal pigmentation due to# melanocytes along basal cell layer with elongation of epidermal rete ridges (lentiginous growth)
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Melanocytic Nevus may appear as
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flat, papular or pedunculated black or brown pigmented lesions
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Junctional Nevus clinical manifestations
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flat, smooth bordered, uniformly pigmented (brown to black) pigmented lesions
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Junctional Nevus Histology
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well defined, symmetrical nests of melanocytes along the dermal-epidermal (DE) junction
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Blue Nevus Clinical manifestation
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common, well-circumscribed, small, bluish-black nodules
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Blue Nevus Histology
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common blue nevus has heavily pigmented dendritic melanocytes
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Dysplastic Nevus may occur as
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isolated sporadic lesions
- may be associated with an autosomal dominant inheritance (on chromosome 1) pt has hundreds of lesions (Dysplastic Nevus Syndrome) |
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Dysplastic Nevus Can occur on both
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sunexposed and nonexposed areas
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Dysplastic Nevus increases the risk for
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melanoma transformation (Heritable Melanoma Syndrome)
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Dysplastic Nevus Clinical
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Gross appearance warrants biopsy to rule out melanoma
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Dysplastic Nevus Histology
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Cytologic and architectural atypia
shows features of “pre-melanoma” |
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Malignant melanoma causes more than
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75% of all deaths from skin cancer
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Malignant melanoma Metastatic sites include:
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Local and regional sites in skin and lymph nodes
lung, liver, bone and intestines Tumor spreads both through blood and lymphatics |
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Risk of Malignant Melanoma
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Family history
Presence of red or blonde hair Presence of marked freckling History of >3 blistering sunburns before 20 y/o History of >3 outdoor jobs as a teenager Presence of actinic keratosis Dysplastic nevus syndrome UVA light therapy, tanning salons Increased socioeconomic status |
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Risk of Malignant Melanoma
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3.5x risk if you have 1 or 2 risk factors
20 x increase risk if you have 3 or more risk factors |
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Main risk factor Skin Cancer Risk
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UV (light exposure) Main risk factor
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Major types of Melanoma
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Superficial spreading melanoma
Nodular melanoma Lentigo maligna melanoma Acral lentiginous melanoma: Unclassified type |
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Acral lentiginous melanoma
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Pigmented lesions on soles, palms,subungual areas
Usually occurs in nonwhite individuals |
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Melanoma most commonly invovles skin, but can involve
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mucosa, conjunctiva, orbit, nailbeds, esophagus and leptomeninges
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5 Signs of Malignant Melanoma(the A,B,C,D,E’s)
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Asymmetry in shape
Border is irregular, fuzzy or scalloped Color is mottled, variegated Diameter is >5mm (greater than an eraser tip) Elevation (almost always present, except for acral sites) |
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The most important clinical sign of melanoma is
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change in color in a pigmented lesion
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Histology Of Melanoma
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Atypical melanocytes with:
Nuclear enlargement, hyperchromasia and nucleoli Cell necrosis Mitosis Lack of maturation Immunpositivity for S-100, HMB45 and MART (melanoma related antigen) |
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Melanoma Prognosis is mainly dependent upon:
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. Depth of invasion:
Breslow depth Clark’s level 2. Clinical stage: Nodal involvement Distant metastasis |
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Breslow Depth
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Measurement of vertical tumor depth
below the stratum granulosum Superficially invasive (<1.0mm) have better prognosis than deeper invading tumors |
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Clark’s Leveland Prognosis of 5 year survival
class 1-5 |
1)In Situ =100% survival
2) Superficial dermal invasion-->90% survival 3)Tumor filling papillary dermis->70% " 4) Reticular dermis involvement-> 40% " 5) Tumor extension into fat->25% |
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Malignant Melanoma Metastatic sites include
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Local and regional sites in skin and lymph nodes
Lung, liver,bone and intestines Tumor spreads both through blood and lymphatics |