I.
Introduction
A. Skin layers and structure: epidermis vs dermis
B. Terms: macule vs papule, plaque, pustule, vesicle, scale vs crust
C. Examination techniques
i. Optometrist: palpation, magnification, lighting, blanching
ii. Dermatologist: biopsy (shave, punch, incisional, excisional)
II.
Epidermal or inclusion cyst (“sebaceous cyst”)
A. Common tumor, varying sizes, face/scalp/axillary areas
B. Lid: along margin, at canthi; milia are tiny/pearly spots
C. Yellow, solid, rubbery, movable, central communicating channel
D. Result from invagination epidermis into dermis
E. Evacuation, incision and drainage, surgical excision of sac and contents
III.
Senile sebaceous hyperplasia
A. Related to epidermal cysts
B. Occurring on the face (forehead), often with multiple lesions
C. Usually doughnut-shaped, mimicking a basal cell carcinoma
IV.
Sudoriferous cyst (“eccrine hidrocystoma”)
A. Blockage of sudoriferous gland duct, on lid margin or periorbital area
B. Soft or “tense” and fluid-filled; easily transilluminated with slit lamp beam
C. Syringoma = small, multiple cysts, typically in younger females
D. Simple incision and drainage, but must remove sac for definitive treatment
V.
Viral papilloma
A. Keratinocytes infected by human papilloma virus (HPV)
B. Common wart (verruca vulgaris)
i. Dome-shaped, mosaic surface, variable degrees of keratin
ii. Thrombosed capillaries are classic (textbook) black dots
iii. Most often on hands or soles of feet (“plantar warts”)
C. Flat wart (verruca planar)
i. Slightly elevated, round or flat-topped papule
ii. Typically on the face, forehead, beard line; smooth, flesh-colored
D. Filiform wart (digitate wart)
i. Finger-like projections, with a narrow to broad base
ii. Frequently around eyelids, nose, and mouth
E. Warts lose their fine skin lines as they develop (like basal cell carcinoma)
F. Treatment: scissors excision vs surgical excision, chemical cautery, or
potential resolution without treatment
VI.
Non-viral papilloma
A. Skin tags of polyps (nomenclature depends on size)
B. Axillary areas (groin, underarms), neck, eyelids; eyelid margin may have a
unique form, at mucocutaneous junction (relatively sessile)
C. Skin tags are tiny excrescences vs polyps which are larger tags with broad tips
and variably thick stalks or bases
D. Scissors excision if the stalk is sufficiently narrow
VII.
Molluscum contagiosum
A. Viral etiology, infection by a poxvirus unique to humans
B. Appearance: domed papule, central umbilication, with gray-white color and a
cheesy central core
C. Single, but usually multiple, since auto-inoculation is common due to ready
spread of the shedding virus
D. Conjunctiva: toxic follicular conjunctivitis due to draining core material
E. Cornea: toxic keratitis, even pseudo-trachoma
F. Treatment: incision and drainage (multiple times) or liquid nitrogen
VIII.
Basal cell carcinoma (BCC)
A. Background
i. Most common skin cancer
ii. Grows slowly, never resolves, in areas of chronic exposure
iii. 90% appear on head/neck, with primary location = nose
iv. Heavy cumulative UV-B, red or blonde hair, tans poorly, family history
v. UV causes p53 tumor suppressor gene mutation, plus suppression of
Langerhans cells and cytotoxic T cells (CD8 cells)
vi. Grows by direct extension with “stromal dependence” and rare
metastasis
B. Characteristics
i. There is no precursor lesion to a basal cell carcinoma
ii. Nodular: translucent, waxy papule, pink/flesh colored, telangiectasias
haphazard on surface, loss of fine skin lines, hard/rolled/pearly
borders
iii. Initially smooth surface umbilicates and ulcerates, leading to noduloulcerative type (poor surface protection, inherent structural weakness)
iv. Superficial type resembles eczema, usually on trunk/back, rare on face
v. Sclerosing (morpheaform) type is flat, hard, waxy, yellow/ivory,
resembling scar tissue, with vague borders; infiltrates into collagen,
periosteum, cartilage – much more dangerous than nodular types
vi. Greatest risk of recurrence is BCC located on eyelids (lower lids), nose,
and ears (thin skin, closer to underlying structures); less risk on trunk
or neck
IX.
Squamous cell carcinoma (SCC)
A. Background
i. Second most common after BCC; non-ocular frequency is 5:1 for
BCC:SCC for facial cancers; many other types of SCC (lung, throat)
ii. Occurs on sun-damaged skin and scar tissue, burns, areas of chemical
exposure, chronically infected sinuses, and stasis ulcers
iii. Frequently seen on scalp, tops of ears, and backs of hands
iv. Fair-skinned patients most vulnerable (see the BCC at-risk patient)
v. Precursors to SCC can be an actinic keratosis (up to 60% of SCC
derive from actinic keratosis) or cutaneous horn
vi. Etiology: see BCC (p53 gene, Langerhans cells, CD8 cells suppressed)
vii. Quite uncommon on eyelids vs BCC (SCC is 5-10% of lid cancers)
B. Characteristics
i. Down-growth of abnormal keratinocytes into the dermis
ii. Begins as a small, firm, erythematous nodule or as a flat, red, scaly
patch – neither of which are specific
iii. Early SCC in epidermis only is Bowen’s disease (SCC-in-situ)
iv. Enlarges, with variable surface scale (heavy when SCC arises from an
actinic keratosis)
v. SCC grows faster than BCC, ulcerates, bleeds, crusts sooner than BCC
vi. SCC has no standard appearance, being readily confused with actinic
keratosis, keratoacanthoma, seborrheic keratosis, scabbed BCC, and
sebaceous gland carcinoma
vii. Risks of metastasis vary widely: Low (< 6%) if associated with actinic
keratosis, up to 40+% if arising from scar tissue or genital areas
X.
Conditions related to or confused with squamous cell carcinoma
A. Actinic keratosis: common, pre-malignant, sun-induced
i. Seen often in older patients, indicative of cumulative UV-B exposure
ii. Pink macule with sandpaper surface, “seen before it’s felt” and located
on the face, neck, scalp, and arms
iii. Thin keratin scale which thickens and darkens
iv. Malignant change indicated by induration, inflammation, red base
v.
Treatment: sunscreens, Retin-A, liquid nitrogen, topical fluorouracil
(0.5%, 1%, 2%, 5%), topical imiquimod (Aldara), topical diclofenac
(Solaraze)
B. Cutaneous horn: secondary lesion, occurring on a primary lesion (actinic
keratosis, viral wart, seborrheic keratosis, SCC, anything producing keratin)
i. Located on face, ears, hands, which are typical for primary locations
ii. Conical projection of lamellar layers of keratin
C. Keratoacanthoma: benign lesion with alarming growth and bad behavior
i. Domed papule which grows exuberantly in 2-3 months, opens to
display a keratin plug, which then stabilizes for up to 1 year
ii. Keratin plug is discharged, leaving a shallow scar
D. Seborrheic keratosis: common, slowly growing, no malignant potential
i. Derives from epidermis, as a “floating plaque” stuck on the epidermis
ii. Tan, brown, even black; variably elevated, granular/crumbly surface
XI.
Pigmented lesions and color changes
A. Guidelines for recognition of normal nevi
i. Size: less than 6 mm in diameter (old-fashioned pencil eraser)
ii. Color: uniform within the lesion; varies from tan to black
iii. Shape: symmetric, round/oval; halves should “match” if folded
iv. Borders: regular and usually distinct
v. Nevi remain stable in size, shape, color; should fade very slowly (over
decades) as they involute
B. Dysplastic nevi (DN)
i. May be < 5 mm, but “classic” DN are often large (> 10 mm), with
haphazard colors, 2 shades of brown, and asymmetric shape
ii. Flat plus elevated elements (“tan macular shoulder”) – fried egg
iii. Variable risks of malignant melanoma following DN
C. Mnemonic for malignant changes in nevi
i. A = asymmetry (non-matching halves)
ii. B = border irregularity (notching or regression)
iii. C = color changes or irregularities (variable or multiple colors, or
mixes of colors)
iv. D = diameter (greater than 6 mm in size)
v. E = evolving (changes in border, size, color, symmetry)
XII.
Malignant melanoma (MM)
A. Background and epidemiology
i. Malignancy of epidermal melanocytes, with epidermal spread
ii. Much lower incidence than BCC or SCC, but greater mortality
iii. Younger patients and increasing mortality = public health risk
iv. Australia (1 in 17 females, 1 in 14 males will have MM in their life)
v. Risks: fair skin, fair hair, poorly tanning skin, family history of MM,
blistering sunburns in teen years, equatorial residence (especially
during puberty), congenital nevi, thinning ozone layer
vi. Proposed #1 cause for the increasing incidence of malignant
melanoma: increased recreational exposure to high intensity UV,
intermittent; changes in fashions, avocation, exercise, vacations
vii. Most common locations: legs (females), torso (males)
viii. ~ 70% occur on normal skin (de novo), ~30% arise from nevi
B. Superficial spreading melanoma (SSM)
i. Most common type in US; typical age of onset is 40-5 years
ii. Irregular borders (notching), odd shape, mix of colors (red, white and
blue)
iii. Nodule formation is very dangerous, signaling deep invasion; SSM is
“safest” when remaining thin
C. Nodular melanoma (NM)
i. About 15% of MM in the US; typical age of onset is 50-60 years
ii. Dome-shaped; dark brown, black, gray, red-brown, amelanotic
iii.
iv.
D. Lentigo
i.
ii.
iii.
iv.
E.
F.
Misdiagnosed as blood blister, dermal nevus, or polyp
Very dangerous due to vertical growth
maligna melanoma (LMM)
Precursor is Hutchinson’s freckle; most related to UV of the MM’s
Perhaps the most common malignant melanoma on the face
Irregular borders, bizarre shape, varying mixes of brown
Nodule development within Hutchinson’s freckle = malignant
transformation into LMM
v. Generally the “safest” MM, due to an obvious precursor for decades
Acral lentiginous melanoma (ALM)
i. Rare in US, < 5% of total cases
ii. Occurs on palms, soles of feet, nail beds
iii. About a 4:1 ratio for lower to upper extremities
iv. Extremely lethal
Treatment of malignant melanoma
i. Excision; margins = 1 cm if tumor is < 1 mm in thickness, but margins
are 2-3 cm wide if tumor is > 1 mm in thickness
ii. Rigorous follow-up depending on tumor thickness
iii. Best prevention is early diagnosis and self-monitoring
XIII.
Sebaceous carcinoma
A. Meibomian glands, glands of Zeis, eyebrows, caruncle, follicle-associated
structures
B. Characteristics: uncommon compared to BCC (7% or less of lid malignancies),
older patients more affected, 70% in women, upper lid > lower lid per
involvement, and very risky (due to misdiagnosis and risk of metastasis)
C. May mimic chalazion, blepharitis, meibomitis, chronic conjunctivitis, SLK,
ocular pemphigoid, other malignancies (BCC, SCC)
D. Most often appears as firm, painless nodule; yellow color; pagetoid spread into
conjunctiva; diffuse pseudoinflammatory appearance of lid, caruncle, brow
E. Must biopsy any lesion that is suspicious or unresponsive to therapy
F. Surgical excision, Mohs surgery, and lymph node evaluation
XIV.
Merkel cell cancer
A. Very rare tumor, involving cells that act as “slow-acting mechanoreceptors”
B. Head/neck 43%, eyelids 9%, elsewhere 48%, most common in elderly
C. Variably sized cutaneous nodule; red, purple, violaceous color; painless, often
with superficial telangiectasias; over 50% of cases have regional metastasis
D. Preferred treatment is Mohs excision with local lymph node dissection
XV.
Guidelines for suspecting malignancy
A. Odd behavior, out of synch for patient’s age, wrong for the demographics
B. Other malignancy (self, family, NMSC, immunosuppression)
C. Older patient, heavy UV exposure regardless of age, occupation, hair/skin
D. Lesion characteristics
i. Unresponsive to therapy, or previously stable and now changing
ii. Change in lesion (breaks the ABCDE rule, odd growth pattern)
iii. Eroded/bleeding surface, inflamed, odd size, irregular tissue
iv. Localized telangiectasias (vs diffuse telangiectasis in sun damage)
v. Lid changes: madarosis, chronic hyperemia
E. “The Usual Suspects” = scabbing, bleeding, infection
XVI.
Prevention strategies
A. Sunscreens or avoidance to reduce aging changes, actinic keratoses, NMSC,
and possibly malignant melanoma
B. Sunscreen use – start early in childhood, apply enough and frequently
TEXT recommendation: Habif TP. Clinical dermatology: a color guide to diagnosis and
therapy, 4th edition; 2003. Mosby.