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60 Cards in this Set

  • Front
  • Back
Skin Tumors can derive from
Epidermal components
Dermal components
Hypodermal components
“Immigrant cells” (i.e.lymphocytes,
histiocytes, metastases, etc,)
Epidermis 2 major cell types
Keratinocytes
Melanocytes
Seborrheic Keratosis
Hyperkeratotic pigmented papules and plaques
( especially on face and trunk)
Occurs in middle aged/elderly
Stuck on appearance
Papules similar to seborrheic keratosis in african americans known as
Dermatosis Papulosa Nigra
Sign of “Lesser Tralet
is a sudden onset of numerous seborrheic keratosis due to a paraneoplastic syndrome
Histology of Seborrheic Keratosis
Sharply demarcated, exophytic, hyperplastic epithelium with pigmented basal cells

Keratin Horn Cyst formation and hyperkeratosis
Acanthosis Nigricans
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)
Sudden onset of Acanthosis Nigricans may be associated with
occult malignancy (i.e. adenocarcinoma releasing growth factors)
Fibroepithelial Polyp (a.k.a. Skin tag, Acrochordon, Squamous papilloma)
Commonly found on neck, trunk, face or intertriginous (skin folds)
Soft flesh colored polyps
Keratoacanthoma
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
Epithelial Inclusion Cyst
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”
A small Epithelial Inclusion Cyst known as
milium
Xanthelasma
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
Most common form of cancer in United States
Almost 50% of people living to the age of 65 will have skin cancer at least once in their lifetime
Epidermal transformation into skin cancer
KeratinocytesNonmelanoma
Melanocytes Melanoma
3 Major types of skin cancer
Squamous Cell Carcinoma (SCC)
Basal Cell Carcinoma (BCC)

3. Melanoma
The vast majority of skin cancers are of non
melanoma type usually begin as Actinic Keratosis
Actinic (Solar) Keratosis (premalignant) can develop into
Squamous cell carcinoma (SCC)
Basal cell carcinoma (BCC)
Dysplastic nevus (premalignant)
can develop into
Melanoma (can also occur de novo)
Actinic Keratosis (Solar Elastosis)
, dysplastic lesion associated with sun exposure, especially in light skinned individuals
Ionizing radiation, hydrocarbon, arsenicals may induce similar lesion
In actinic Keratosis, hyperkeratosis increases leading to
Cutaneous Horn
Actinic (Solar) Keratosis Histology
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.
Squamous Cell Carcinoma (SCC) predisposing factors
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)
Squamous Cell Carcinoma In Situ SCC ( Bowen’s Disease)
Appears as
well demarcated red scaling plaques
Squamous Cell Carcinoma In Situ SCC ( Bowen’s Disease) Histology shows
full thickness epidermal atypia”
- lack of epidermal maturation
- intact basement membrane at epidermal-dermal junction
Squamous Cell Carcinoma (SCC) Invasive SCC
nodular, variably hyperkeratotic
Prone to ulceration -> “nonhealing ulcer”
Squamous Cell Carcinoma (SCC) Invasive SCC Histology shows
atypical squamous cells breaking through D-E junction (basement membrane) into underlying dermis
Mucosal involvement by SCC looks like
white thickened plaques (i.e. leukoplakia)

can be seen in:
Lips, oral cavity
Esophagus
Ano-genital area
Most common malignant skin tumor
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)
Basal Cell Carcinoma Histology:
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
A nonhealing ulcer needs to be biopsied!
MUST RULE OUT MALIGNANCY!
benign Melanocytic Neoplasms can be
a. Lentigo (simplex

b. Melanocytic Nevus (Mole):
. Lentigo (simplex)
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
Melanocytic Nevus (Mole):
can be acquired or congenital - common variants:
i. Junctional nevus
ii. Compound nevus
iii. Intradermal nevus
Lentigo Simplex histology
Linear basal pigmentation due to# melanocytes along basal cell layer with elongation of epidermal rete ridges (lentiginous growth)
Melanocytic Nevus may appear as
flat, papular or pedunculated black or brown pigmented lesions
Junctional Nevus clinical manifestations
flat, smooth bordered, uniformly pigmented (brown to black) pigmented lesions
Junctional Nevus Histology
well defined, symmetrical nests of melanocytes along the dermal-epidermal (DE) junction
Blue Nevus Clinical manifestation
common, well-circumscribed, small, bluish-black nodules
Blue Nevus Histology
common blue nevus has heavily pigmented dendritic melanocytes
Dysplastic Nevus may occur as
isolated sporadic lesions
- may be associated with an autosomal dominant inheritance (on chromosome 1)  pt has hundreds
of lesions (Dysplastic Nevus Syndrome)
Dysplastic Nevus Can occur on both
sunexposed and nonexposed areas
Dysplastic Nevus increases the risk for
melanoma transformation (Heritable Melanoma Syndrome)
Dysplastic Nevus Clinical
Gross appearance warrants biopsy to rule out melanoma
Dysplastic Nevus Histology
Cytologic and architectural atypia
 shows features of “pre-melanoma”
Malignant melanoma causes more than
75% of all deaths from skin cancer
Malignant melanoma Metastatic sites include:
Local and regional sites in skin and lymph nodes
lung, liver, bone and intestines

Tumor spreads both through
blood and lymphatics
Risk of Malignant Melanoma
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
Risk of Malignant Melanoma
3.5x  risk if you have 1 or 2 risk factors
20 x increase risk if you have 3 or more risk factors
Main risk factor Skin Cancer Risk
UV (light exposure) Main risk factor
Major types of Melanoma
Superficial spreading melanoma
Nodular melanoma
Lentigo maligna melanoma
Acral lentiginous melanoma:
Unclassified type
Acral lentiginous melanoma
Pigmented lesions on soles, palms,subungual areas
Usually occurs in nonwhite individuals
Melanoma most commonly invovles skin, but can involve
mucosa, conjunctiva, orbit, nailbeds, esophagus and leptomeninges
5 Signs of Malignant Melanoma (the A,B,C,D,E’s)
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)
The most important clinical sign of melanoma is
change in color in a pigmented lesion
Histology Of Melanoma
Atypical melanocytes with:

Nuclear enlargement, hyperchromasia and nucleoli
Cell necrosis
Mitosis
Lack of maturation
Immunpositivity for S-100, HMB45 and MART (melanoma related antigen)
Melanoma Prognosis is mainly dependent upon:
. Depth of invasion:
Breslow depth
Clark’s level

2. Clinical stage:
Nodal involvement
Distant metastasis
Breslow Depth
Measurement of vertical tumor depth
below the stratum granulosum
Superficially invasive (<1.0mm) have better prognosis than deeper invading tumors
Clark’s Level and 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%
Malignant Melanoma Metastatic sites include
Local and regional sites in skin and lymph nodes
Lung, liver,bone and intestines

Tumor spreads both through blood and lymphatics