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Primary Care Update: A Practical Approach to Common Problems

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Skin Cancers

Robert A. Baldor, M.D. FAAFPProfessor, Family Medicine and Community Health

University of Massachusetts Medical School

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Learning Objectives

• by the end of the session you will be able to recognize the precursor lesions and common features for skin cancers and understand primary care diagnosis and treatment modalities for these common skin cancers.

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Predisposing Factors

• Fair skin• Poor tanning ability• Predilection to burn• Excessive solar radiation exposure

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Classification of Sun-Reactive Skin Types

Blue eyes Red hair

Gray eyes Blond hair

Brown eyes & hair

Brown/Black eyes & hair

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Basal Cell Cancer (BCC)

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Epidermis

Junction

Dermis

Stratum corneum

Keratinocytes

Basal cells

Melanocytes

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Basal cell carcinoma (BCC)

• Most common form of skin cancer• The most common of all cancers!• 1 million Americans diagnosed annually• Associated with childhood sunburns• Sunscreens in later adulthood do not appear

to prevent

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Location

• Areas of chronic sun exposure• Predilection for head (ears) and neck (90%)

• A persistent, non-healing sore• But….

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A Reddish Patch or irritated area

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A Shiny, pearly bump or nodule

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A white, yellow or waxy scar-like area

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Rodent ulcer

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Squamous Cell Cancer (SCC)Second most common skin cancer > 250,000 new cases annuallyElderly (mean age 70 years)

Common in sun exposed areasrim of ear, lower lip, face, bald scalp, neck, hands

Occurs on all areas (mucous membranes, genitals)Skin with signs of sun damage

pigmentation change, wrinkling,,loss of elasticity

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Sun Damage and….

• Environmental exposure – arsenic, radiation, petroleum products

• Smoking• Inflammatory dermatosis

• Sunscreens are preventive

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Epidermal Keratinocytic Atypia

• Actinic keratosis• Bowen’s disease• Squamous cell cancer

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Epidermis

Junction

Dermis

Stratum corneum

Keratinocytes

Basal cells

Melanocytes

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Actinic Keratosis

• UV light induced• Circumscribed rough lesions• Pinpoint to plaque (most 3-6 mms) • Variety of colors• May form horns• Blend to background skin

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Actinic Keratosis

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Actinic Keratosis

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Precancerous

• Although < 20% transformed to SCC• Slow process, very rare mets

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Bowen’s Disease

• Erythematous plaque• Sharp, irregular border• Hyperkeratosis• Erosions, ulcerations• Not just sun exposed

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Bowen’s Disease

• Suspect in any persistent chronic plaque• Confused with psoriasis or eczema• May transform to SCC• Treat like actinic keratosis

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Squamous Cell Ca

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Actinic keratosis

Squamous Cell

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Basal Cell

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Metastatic Potential

• 2-3% rate to regional nodes• Local destruction

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BC/SC Treatment Goals

• Remove cancerous tissues• Preserve normal tissue• Preserve optimal cosmetic result

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Punch Biopsy

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Shave biopsy

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Office Treatment Modalities

• Electrodesiccation and curettage• Cryotherapy• Excision• Topical agents

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Curettage & Electrodesiccation

• Cure rates approaching surgical excision• Not useful if in high-risk or difficult sites.• No biopsy

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Cryosurgery

• Freezing with liquid nitrogen x 2• Lesion scabs over; falls off within weeks• Cure rates 85-90%• No biopsy• Not recommended for SCC

– deeper portions of the tumor may be missed– scarring might obscure a recurrence.

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Excision biopsy

• Remove the entire growth along with a thin margin of normal skin

• Cure rates around 90%• Biopsy available

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Topical treatment modalities

• 5-Fluorouracil 5% cream• Imiquimod 5% cream• Diclofenac 3% gel

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5-Fluorouracil (5-FU)

• FDA-approved for superficial BCC & AK• Used to treat Bowen’s disease• Cure rates 80-90 %• BID for 3-6 weeks• Normal skin minimally effected• Significant Inflammatory response…

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Imiquimod

• FDA-approved for superficial BCC & AK • Used for treatment of Bowen’s disease• 5X a week for 6+ weeks • Stimulates the immune system

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Diclofenac 3% gel

• FDA-approved for superficial BCC & AK • BID x 2-3 months• Less effective than 5-FU/Imiquimod

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Referrals

• Radiation– Difficult surgical locations– Elderly in poor health

• Laser (Not FDA approved for BCC or SCC)

• Photodynamic therapy– for multiple BCC (not FDA approved)

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Mohs Micrographic Surgery

• Saves the greatest amount of healthy tissue• Highest overall cure rate — up to 99% • For poorly demarcated & hard-to-treat tumors

around the eyes, nose, lips, and ears. • May require reconstructive closure

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QUESTIONS ABOUT NON-MELANOTIC SKIN CANCERS???

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Melanoma• The incidence has increased 690% since 1950 • 69,000 new cases of melanoma annually• 8,700 deaths

– 99% 5-year survival for localized disease– 15% 5-year survival for metastatic disease

• Genetic predisposition

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Sites

• 83% arise de novo• 80% trunk and extremities• Most common site in men is the upper back• Most common sites in women are the lower

legs and upper back

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A Moles Life cycle…

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Simple Lentigo

Junctional Nevus Compound Nevus Intradermal Nevus

epidermis

dermis

Epidermal/dermal junction

melanocytes

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•Junctional Nevi change in adolescent years< 6 mms macules; sun exposed skin

•Simple Lentigo arise in childhood< 5 mms, round macule

epidermis

dermis

Epidermal/dermal junction

melanocytes

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• Seen in early adulthood• < 6 mms; macular, gradually elevate• Smooth or rough surface (excess hair)

Compound Nevi

epidermis

dermis

Epidermal/dermal junction

melanocytes

Intradermal Nevi

• Frequently disappear later in life • A new mole that develops after the age of 40

is abnormal!

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Halo Nevus

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Solar Lentigo

• Uniformed tan to brown macules• Sun damaged skin• ‘Liver spots’

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Seborrheic Keratosis

• Verrucal, warty, raised surface• Brown to black• Stuck on appearance, sharply demarcated• Few mm to several cms• Face, neck, trunk

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“I have a suspicious looking mole on my shoulder.”

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Dysplastic Nevi

• Markers of MM prone individuals• Precursor lesions

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Dysplastic Nevus Syndrome

• Multiple heterogenous lesions

• Familial

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Management

• Examine entire skin - watch scalp• Biopsy worst looking lesion• Patient education/sunscreens• Follow up 3-12 months

– Excise suspicious lesions

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Melanoma Evaluation

AsymmetryBorderColorDiameter

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Asymmetry

• A line drawn through the middle will not create matching halves

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Border

• Uneven scalloped or notched edges

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Color

• Variable shades of brown or black hues of blue, grey, white, pink or red

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Diameter

• > 6 mm (pencil eraser)

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Malignant Melanoma

• Superficial spreading melanoma (70%)• Nodular melanoma (15%)• Acrolentiginous melanoma (10%)• Lentigo maligna melanoma (5%)

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Superficial Spreading Melanoma • 70% of all melanomas

– most common type in light-skinned people

• Peak incidence 40-60 yrs • Usually a mole changing slowly (1-5 years)• Commonly affects areas with the greatest

nevus density - upper backs & lower legs

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Characteristics

• SSM subtype usually has the classic early signs of melanoma (ABCDs)

• Borders are often very irregular• Absence of pigmentation often represents

regression of the melanoma

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Nodular Melanoma

• 2nd most common subtype of melanoma (15% )• Median age at onset is 53 years• A uniform blue-black, blue-red, nodule (E)• Most common sites are trunk, head, and neck• Usually begin in normal skin rather than in a

preexisting lesion• Rapid growth is a hallmark of nodular melanoma

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Acral lentiginous melanoma

• 10% of melanomas overall• Most common types among Japanese, African,

Latin, and Native Americans• Median age 65 years; equal gender distribution.• Palms or soles; beneath the nail plate

– sole is the most common site in all races– not associated with sun exposure

• Average size at diagnosis is 3 cm (? delayed Dx)

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Lentigo maligna (melanoma in situ)

• Least common subtype (5% of all melanomas)• Occurs on sun-damaged atrophic skin

– Head & neck (nose and cheek most common)

• Median age at diagnosis is 65 years• Usually quite large (3 to 6 cm or greater)• A tan irregular macule that extends peripherally• 1/3rd progress to lentigo maligna melanoma • Grow slowly for 5 -15 years before invading

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Treatment – Excision

< 0.5 mm thick: 1 cm margin0.5-1 mm thick: 1-2 cm margin1 mm thick: 3 cm margin w/underlying fat/fascia

< .76 mm thick: no mets - 99.5% 10 yr survival> 3 mm thick: 48% 10 yr survival

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DNA Damage

• UV light damages epidermal DNA• Age related decline in ability to repair DNA• 20-30 years of exposure for tumor

development

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Ultraviolet Radiation

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Epidermis

Junction

Dermis

Stratum corneum

Keratinocytes

Basal cells

Melanocytes

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Ultraviolet Light

• UVB causes sunburn and skin cancer• UVA penetrates deeply, causing photo-aging

(wrinkling, leathering, sagging)• UVA exacerbate UVB carcinogenic effects

and likely plays a role on it’s own• Tanning Booths…….

– Why pay for skin cancer, when you can get it for free!

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Photo aging treatment options

• Retin A – best evidence for improvement• Sunscreens…

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Sun Protection Factor (SPF)

• It takes 10 minutes for unprotected skin to start turning red, SPF 15 sunscreen prevents reddening 15 times longer — about 2 1/2hrs– SPF 15 blocks 93 % of incoming UVB rays– SPF 30 blocks 97 %– SPF 50 blocks 98 %

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And for how long?

• no sunscreen is effective longer than 2 hours without reapplication

• So SPF-15 is good for 2.5 hours…..

• I recommend SPF-30 – every 2 hours

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Sunscreens

• Vary in their ability to protect against UVA and UVB• Usually 3 active ingredients…• UVB absorption (eg PABA derivatives)

• UVA short-waves (benzophenones )

• Remaining UVA spectrum (Parsol, zinc oxide)

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New FDA labeling

• Change to UVB sunburn protection factor– Low protection (SPF 2-15)– Medium protection (SPF 15-29)– High protection (SPF 30-50)– Highest protection (SPF >50)

• Added 4-star rating for UVA protection– 1 star lowest to 4 stars highest protection

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