Leonard C. Sperling, M.D.,
COL, MC, USA
Department of Dermatology
Uniformed Services University of the Health Sciences
Please note: this handout is a supplement to the most valuable part
of the lecture – the
clinical photographs and histologic photomicrographs. Hope you enjoy
the show!
MALIGNANT NEOPLASMS (Tumors)
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Basal Cell Carcinoma: clinical
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most common human cancer: more than 400,000 new patients annually
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found most commonly on sun-exposed areas of fair-skinned, sun-damaged individuals
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translucent, "pearly" or "waxy" papule; associated telangiectasia, sometimes
central ulceration
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locally destructive, very rarely metastasizes; can cause death
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sun-exposure, ionizing radiation, immunosuppression are all predisposing
factors
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several clinical and histologic subtypes

Basal Cell Carcinoma: histology
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proliferation of atypical basal cells (large, oval, deep-blue staining,
but with little anaplasia and infrequent mitoses)
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"peripheral palisading" – outermost layer of cells "line up"
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often clefts between tumor and dermis
Squamous Cell Carcinoma
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malignant tumor of epithelial keratinocytes – skin and mucous membranes
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induced by various carcinogens, but in the skin SUN EXPOSURE is
the most common
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ionizing radiation, oncogenic viruses such as certain wart viruses, arsenic
ingestion, chronic wounds also induced cutaneous SCC
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usually arises as solitary, keratotic or eroded, pink papule or nodule
– persists and grows
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may arise from a precancerous actinic keratosis
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SCC arising in sun-damaged skin less prone to metastasis than mucosal
SCC
Squamous Cell Carcinoma: histology
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irregular masses of tumor cells proliferate from the epidermis down into
the dermis
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composed in varying proportions of normal-appearing squamous cells and
atypical squamous cells
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differentiation is in the direction of keratinization
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ranges from well to poorly differentiated
Malignant Melanoma
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a proliferation of markedly atypical melanocytes with the potential for
dermal invasion and widespread metastasis
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several clinical subtypes have been described, but the prognosis for all
subtypes depends on the histologic thickness (Breslow level) of the tumor
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sun exposure is an important predisposing factor, but not as clearly causative
as in the base for BCC and SCC.
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most lesions arise de novo, but some arise from "precursor lesions"
such as large congenital nevi or "dysplastic" nevi

A, B, Cs of Melanoma:
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Asymmetry of shape: one half does not look
like the other
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Border is irregular: scalloped, notched, discontinuous
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Color is uneven: multiple shades ranging from
white to tan to brown to black occasionally some red as well
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Diameter is larger than 6mm in most cases
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Enlargement: gradual increase in size and elevation
Lentigo maligna and lentigo maligna melanoma
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a clinical and histologic subtype of melanoma that occurs in sun-exposed
areas (usually face) of elderly persons. Lentigo maligna is the "in situ"
lesion, after dermal invasion, it is a lentigo maligna melanoma
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lentigo maligna is macular (flat), and shows all the A, B, C, Ds of melanoma;
grows slowly for years before invasion; prognosis excellent before invasion
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the invasive lesions (lentigo maligna melanoma) develops a papular (palpable)
component
Superficial spreading malignant melanoma
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found almost exclusively in white-skinned persons

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most common form of melanoma
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incidence rapidly increasing, especially in young urban professionals (intense,
intermittent SUN EXPOSURE)
Nodular melanoma
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less common in whites than superficial spreading type but more common
in Japanese
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tends to grow "up" rather than spread outward, so has a worse prognosis
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A,B,Cs less helpful here: may be symmetrical and may have uniform black
color

Acral lentinginous melanoma

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arises on sole, palm, fingernail or toenail bed, or the mucocutaneous skin
of mouth, genitalia or anus
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most common form of melanoma in African-Americans and Japanese, groups
that are not as prone to other forms of melanoma as Caucasians
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tends to invade dermis fairly quickly, so has a worse prognosis overall
Malignant melanoma: histologic features
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increased number of atypical melanoctyes along the dermoepidermal junction
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cells are not evenly dispersed, but crowd together, form variable sized
nests, extend down follicles and sweat glands
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atypical melanocytes are pleomorphic (differ from one another), are larger
than normal, and have nuclei of differing size, shape and staining intensity
– cellular atypia
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atypical melanocytes may migrate upward within the epidermis – "buckshot
spread"
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margins of lesion are not sharply defined, but seem to "peter out"
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the overall appearance is asymmetric – one half does not look like the
other
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the pigmentation of atypical melanocytes is highly variable from one cell
to another
Kaposi’s sarcoma: clinical
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classic form = "Old World" Kaposi’s: elderly men of Mediterranean ancestry.
Very slowly growing dark purple nodules on lower extremities

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epidemic form – AIDS patients/HIV: young men with widespread lesions, affecting
any part of the cutaneous surface and mucous membranes

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endemic African form: similar to epidemic form, very aggressive
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association with Herpesvirus 8 (probably causative agent)
BENIGN NEOPLASMS (Tumors)
Seborrheic Keratoses
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often called "moles" or "warts" by patients – but aren’t
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average size is 1cm; can be up to 3cm
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flesh-colored, tan, brown, or black
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oval-shaped, elevated, "greasy" feel
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appear "stuck-on" the skin


Seborrheic Keratoses: histology
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hyperkeratosis (thickening of stratum corneum)
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acanthosis (thickening or non-keratinized layer)
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"straight line" can be drawn along bottom of tumor
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horn cysts are common
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no cellular atypia
Skin Tags
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also called: acrochordons, soft fibromas, pedunculated fibromas
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neck and axillae of middle-aged, often obese adults
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flesh-colored, pinhead to grape-sized



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may become inflamed or necrotic (painful)
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histology: bag or sack-shaped specimen; some hyperkeratosis and acanthosis;
collagen and sometime fat centrally
Dermatofibroma
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very common
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can be found at any age
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legs most common site; also thighs, arms, trunk
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possibly a scar-like reaction to insect bite
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characteristic histology
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slow growing, round to oval, firm nodules
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deep component is attached to overlying skin
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a few millimeters to several centimeters
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pink to brown, darker in the center

Dermatofibroma: histology
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overlying epidermis is thickened (acanthosis) and hyperpigmented
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proliferation of bland-appearing spindle-shaped cells, randomly oriented,
in upper and mid dermis
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variable number of small capillaries among the spindle cells
Melanocytic Nevi (Common Moles)
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first appear after 6-12 months, enlarge with body growth, regress in later
life
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more numerous in light skinned persons
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maximal number in third decade; 24 (average) in women, 16 in men
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less than 5 remain after sixth decade
Classification of Acquired Melanocytic Nevi
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junctional nevus – cells at dermoepidermal junction
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intradermal nevus – cells found only in dermis, not at junction
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compound nevus – combined features of junctional and intradermal nevi
Junctional Nevi
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flat and uniform tan, brown, or dark brown
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less than 10mm – usually less than 6mm

Intradermal Nevi
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round, dome-shaped, evenly pigmented

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color lighter than junctional nevi
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often on face and neck
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often associated with coarse terminal hair
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may resemble basal cell carcinoma
Compound Nevi
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features of both junctional and intradermal nevi

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usually a histologic diagnosis
Reasons to Remove Acquired Nevi
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change in size, shape, or pigmentation, especially is there is asymmetry
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located in area difficult to monitor: anogenital, scalp, soles
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persistent itching, or pain or bleeding
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have a low threshold for biopsying pigmented lesions
Halo Nevus
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children and young adults
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may be multiple
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hypopigmented oval halo around pre-existing nevus

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nevus eventually involutes and halo repigments (months to years)
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biopsy if central nevus appears atypical
Common Blue Nevus
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acquired, benign, firm, usually less than 10mm
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blue, blue-gray or blue-black
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most common on dorsa of hands or feet, but may occur anywhere

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small, stable, long-standing lesions do not require removal
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new onset or recent change: remove
Melanocytic nevi: histology
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composed of benign melanocytes: little pleomorphism or cellular
atypia
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overall distribution of melanocytes is symmetrical
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melanocytes tend to form nests (clustered groups) of cells
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cells become smaller with less cytoplasm as they descend deeper into the
dermis
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in junctional nevi, the melanocytes or nests are all in contact with the
dermoepidermal junction
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in intradermal nevi, all the cells have lost contact with the overlying
epidermis; compound nevi have features of both junctional and intradermal
nevi
Nevus Flammeus (Port-Wine Stain)
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vascular malformation (not neoplasm) of dermal blood vessels
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always present at birth
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never spontaneously disappears
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macular in infancy; become papular and darker with age
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histology: increased number of blood vessels, with larger lumens, in upper
dermis
Nevus Flammeus: Variants
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nuchal lesions (stork bite, salmon patch) occur in 1/3 of infants and do
not fade; eyelids and glabella also
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Sturge-Weber syndrome: large facial lesions with cranial involvement and
seizures

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Klippel-Trenaunay-Weber: limb lesions with soft tissue and bone hypertrophy
Capillary Hemangioma of Infancy
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"Strawberry mark"
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appears within the first months of life and grows rapidly
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reaches a certain size (1-8cm), then begins to regress
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usually complete involution by age 6
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face, trunk, legs, oral and vaginal mucosa

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histology: tightly packed, very small blood vessels; lumens not always
present among the plump endothelial cells
Cherry Angioma
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Senile angioma, lobular capillary hemangioma
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Almost universal with aging
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Trunk and proximal extremities
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Barely perceptible to 8mm, bright red to purple

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Histology: clusters (lobules) of tightly packed, small blood vessels in
upper dermis
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Pyogenic Granuloma
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usually persons younger than 30
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fingers, lips, mouth, trunk, toes
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positive "band-aid sign"
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moist, friable, bloody surface

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lesions do not spontaneously disappear
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histology: same as for cherry angioma, but often there is edema and epidermal
erosion
Hypertrophic Scars and Keloids
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hypertrophic scars remain confined to site of original injury
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keloids extend beyond wound with clawlike extensions

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keloids may arise without history of injury, often in presternal site
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more common in blacks than whites
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earlobes, shoulders, upper back, chest
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hypertrophic scars tend to regress in time
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keloids may expand for decades
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histology: densely packed, bright pink collagen bundles in a haphazard
array; increased number of fibroblasts and blood vessels in early
lesions
Epidermal Inclusion Cyst
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epidermoid cyst, wen, sebaceous cyst, infundibular cyst
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globular, dermal-to-subcutaneous nodule

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often an overlying pore or punctum
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face, neck, upper trunk, scrotum
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filled with "cheesy", rancid material (keratin)
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treatment of EIC: complete removal of cyst sac
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ruptured cysts can mimic a severe, localized infection – but are rarely
infected
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histology: oval cyst has an epithelial wall resembling the surface epidermis,
but the stratum corneum cells are "shed" into the center of the cyst
Trichilemmal Cyst (Pilar Cyst)
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90% on scalp, more common in women
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often multiple lesions

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can be inherited trait
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no central punctum
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cyst often "pops out" on excision
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histology: similar to an epidermal inclusion cyst, but epithelial cells
do not produce a stratum corneum, but rather a solid, pink, central ball
of keratin
Digital Mucous Cyst
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myxoid cyst
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middle-aged to elderly
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dorsal aspect of distal phalanx of finger

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often just proximal to nail
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filled with clear, gelatinous substance
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histology: empty "spaces" in dermis, which were filled with mucin (hyaluronic
acid) before processing
Neurofibroma
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soft, dome-shaped, skin colored, asymptomatic
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very common as a single or few scattered lesions
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multiple lesions may be associated with neurofibromatosis


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closely resembles intradermal nevus clinically
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histology: haphazard dermal collection of small, spindle-shaped cells with
comma-shaped nuclei and wavy, pink cytoplasm
Venous Lake
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older individuals
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lips, ears, face
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dark blue to purple, soft, fully compressible

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do not spontaneously resolve, but harmless
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histology: massively dilated vascular lumen in dermis