welcome! primary care update: a practical approach to common problems 1
Post on 27-Dec-2015
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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 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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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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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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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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BC/SC Treatment Goals
• Remove cancerous tissues• Preserve normal tissue• Preserve optimal cosmetic result
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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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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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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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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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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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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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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 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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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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