1. DERMATOLOGIC DISEASES AND DISORDERS
Suggestions for Lecturer
-1-hour lecture
-Use GRS slides alone or to supplement your own teaching materials.
-Refer to GRS and Geriatrics At Your Fingertips for further content.
-Supplement your lecture with handouts.
-See GRS7 questions 8, 13, 91, 209, 262, and 270 for case vignettes on dermatology.
Topic

2. OBJECTIVES Know and understand: Normal age-related changes in skin
How to recognize and treat photoaging
The diagnosis and treatment of skin conditions common in older adults

3. TOPICS COVERED Changes in Skin with Aging Photoaging Common Conditions
Seborrheic Dermatitis
Rosacea
Xerosis
Neurodermatitis
Intertrigo
Bullous Pemphigoid
Pruritus
Psoriasis
Stasis Dermatitis
Venous and Arterial Ulcers
Onychomycosis
Herpes Zoster
Candidiasis
Scabies
Louse Infections
Cherry Angiomas
Seborrheic Keratoses
Actinic Keratoses
Skin Cancers

4. DERMATOLOLOGIC CHANGES WITH AGING
Epidermal and dermal changes
Reduced lipids
Slower wound healing
Lower immune function
Reduced collagen
Hair changes

5. EPIDERMAL AGING In youth, epidermis interdigitates with dermis
With aging, the interdigitations flatten, resulting in:
Reduced contact between epidermis and dermis
Decreased nutrient transfer
Increased skin fragility

6. LIPIDS AND AGING
Aging is associated with decreased lipids in the top skin layer, which leads to:
Dryness and roughness
Decreased barrier function

7. IMPAIRED HEALING AND IMMUNE FUNCTION WITH AGING
Slower turnover of epidermal cells may account for slower rate of wound healing
Lower number of immune antigen-presenting cells (such as Langerhans) may cause reduced cutaneous immune surveillance

8. CHANGES IN THE AGING DERMIS
Decrease in ground substance leads to wrinkling, atrophy
Decreases in collagen and elastin cause haphazard, fragmented fiber orientation

9. AGING SKIN AND HAIR
Changes in follicular melanocytes cause graying hair
Shortened duration of anagen (growth phase of hair follicle) and increased duration of telogen (resting phase) results in decreased hair density

10. PHOTOAGING The Effects of UV Exposure on Skin
Shorter wavelengths are more biologically
active (UVA and UVB)
UV light causes:
DNA damage
Decreased DNA repair
Oxidative and lysosomal damage
Altered collagen structure

11. PHOTODAMAGED SKIN Appears wrinkled, coarse, or rough
Has mottled pigmentation, hypopigmentation, telangiectasias
Cutaneous malignancies more common

12. PREVENTING PHOTODAMAGE
Use broad-spectrum sunscreens
Avoid direct sunlight
Use protective clothing, including hats
Use sunglasses

13. TREATING PHOTODAMAGE: TOPICAL AGENTS
Only agent shown to be effective: topical tretinoin at high concentrations for long periods
Increases thickness of superficial skin layers
Reduces pigmentary changes and roughness
Increases collagen synthesis
Claims that other agents decrease photodamage are not well substantiated

14. TREATING PHOTODAMAGE: SURGERY
Procedures include chemical peeling, dermabrasion, laser resurfacing
Destroys surface populations of keratinocytes, followed by repopulation of keratinocytes from deep within sun-protected follicular structures
Controlled trials of effectiveness of surgical approaches are inconclusive and rare

15. SEBORRHEIC DERMATITIS
Common chronic dermatitis
Erythema and greasy-looking scales
Typical locations:
Hairline
Nasolabial fold
Midline chest
Dandruff is often a precursor
More common in Parkinson’s disease
Cause unclear; normal yeast flora may cause inflammation

16. TREATMENT OF SEBORRHEIC DERMATITIS
Can be suppressed but not cured
Mild topical corticosteroids useful for acute forms (1% to 2% hydrocortisone)
Once controlled, maintenance with medicated shampoos that act against yeast, eg, selenium sulfide, ketoconazole, tar shampoos

17. ROSACEA Common in fair-skinned people Affects all ages
Common symptom: Recurrent facial flushing from a variety of stimuli (sunlight, alcohol, hot beverages, drugs that cause vasodilation)
Chronic condition with frequent flares
Cause unknown

18. ROSACEA
ROSACEA
Diffuse erythema and erythematous papules and papulopustules are seen on the cheeks, forehead, and chin
The nose shows thickening of the skin and changes consistent with an early rhinophyma
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19. TREATMENT OF ROSACEA Avoid skin irritants, strong soaps
Reduce sun exposure; use sunscreens
For moderate to severe flares, use oral antibiotics (tetracyclines, eg, doxycycline, minocycline, or erythromycin)
For mild cases and maintenance, use topical antibiotics (erythromycin, benzoyl peroxide, metronidazole)

20. TREATMENT OF SEVERE ROSACEA
Severe or refractory rosacea: Oral isotretinoin
Erythema and telangiectasias:
Difficult to treat
Lasers provide option to reduce redness and improve cosmetic appearance
Rhinophyma:
Less common
Can be treated with surgical excision or electrosurgery

21. XEROSIS Dryness of the skin
Causes: reduced water content and reduced barrier function of aging epidermis
Exacerbated by environmental factors
Decreased humidity from cold weather/central heat
Irritation by hot water, harsh soaps
Skin findings often more on legs
Rough itchy skin or scales; if severe, may manifest as eczema craquelé (dry, cracked appearance)
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22. XEROSIS
Eczema craquelé. Dry, erythematous, fissured, and cracked skin was seen on the lower legs of this patient.

23. TREATMENT OF XEROSIS Avoid environmental triggers
Take tepid, not hot, showers
Use emollients immediately after bathing
Use moisturizing agents containing lactic acid or α-hydroxy acids to reduce roughness
Use mild topical corticosteroids episodically for irritation or inflammation

24. NEURODERMATITIS Chronic, pruritic conditions of unclear cause
Also known as lichen simplex chronicus
Lesions show signs of chronic scratching
Exclude irritant or allergic contact dermatitis
Treatment:
Potent topical corticosteroids (often under occlusion)
Emollients
Behavioral modification

25. INTERTRIGO
More common in older adults because of increased skin folds from decreased dermal elasticity
Often associated with secondary candidal or mixed bacterial colonization

26. INTERTRIGO AND CANDIDIASIS
Intertrigo and candidiasis are commonly found in the web space between the 4th and 5th toes
Moist erythema, maceration and superficial erosion is apparent
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27. TREATMENT OF INTERTRIGO
Keep area dry, open to air
Use topical antifungal powder or cream (eg, miconazole or nystatin)
Use mild topical corticosteroid occasionally to reduce inflammation

28. BULLOUS PEMPHIGOID An autoimmune blistering disorder
Occurs most often in adults in 60s and 70s
Blisters are usually large and tense, on normal or erythematous skin; may be filled with clear or hemorrhagic fluid
Diagnosis by biopsy and immunofluorescence
Condition may last from months to years, but often is self-limited
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29. BULLOUS PEMPHIGOID
Tense, fluid-filled, and hemorrhagic bullae on an erythematous base were seen on the trunk and extremities
Some of the bullae have ruptured and left a scab with crusting

30. BULLOUS PEMPHIGOID: PATHOPHYSIOLOGY IS UNCLEAR
Antibodies develop in the hemidesmosomes
Antibodies bind to bullous pemphigoid antigen, activating the complement cascade
Attracted leukocytes and degraded mast cells cause separation of epidermis from basement membrane

31. TREATMENT OF BULLOUS PEMPHIGOID
For localized disease, use topical corticosteroid, calcineurin inhibitors, and nicotinamide with tetracycline
For more extensive disease, use:
Systemic corticosteroid
Other immunosuppressant (azathioprine or cyclophosphamide)
Tetracycline and niacinamide combination therapy
IV immunoglobulin and rituximab (off-label)

32. PRURITUS
In older adults can be very severe and compromise quality of life
Extensive differential diagnosis: xerosis; scabies; allergic, irritant, or atopic dermatitis; bullous pemphigoid; renal disease; liver disease; thyroid disease; anemia; occult malignancies; drugs

33. TREATMENT OF PRURITUS Treat the underlying cause if possible
For symptom relief, use topical corticosteroids, emollients, menthol in calamine, capsaicin (off-label), pramoxine
Use oral antihistamines with caution
UVB phototherapy has been used for severe, refractory cases

34. PSORIASIS
Affects 2% of the population, with bimodal incidence (mid-20s, 50s and 60s)
Genetic predisposition; multigene mode of inheritance
Environmental factors may trigger
Other triggers include physical trauma, infections, stress, medications (oral corticosteroids, lithium, β-blockers, ACE inhibitors, NSAIDs)
5% to 8% also have psoriatic arthritis with pain, swelling, and stiffness in small joints

35. PSORIASIS
Characteristic well-demarcated beefy red plaques with overlying silvery-white scales are evident on the back of this patient
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36. TREATMENT OF PSORIASIS (1 of 2)
Topical treatment
May control mild disease but may be irritating or messy
Include corticosteroids, vitamin D derivatives (calcipotriene), topical retinoids (tazarotene), salicylic acid, tar compounds
Long-term use of topical corticosteroids is limited by cutaneous atrophy

37. TREATMENT OF PSORIASIS (2 of 2)
Systemic treatment
If no response to topicals
Phototherapy
Immunosuppressive agents (cyclosporine, methotrexate)
Oral retinoids, anti-TNF agents
UV therapy
Can be used with topical therapy
PUVA (psoralen with UVA light) and UVB
Evaluate risks, benefits of all therapies for older adults

38. STASIS DERMATITIS
An early sign of chronic venous insufficiency of legs triggered by chronic venous hypertension and incompetent valves
Typically seen in medial supramalleolar areas and associated with pruritus
Risk of ulceration
Treatment
Compression bandages or stockings
Emollients and cautious topical corticosteroids

39. VENOUS AND ARTERIAL ULCERS
Lower-extremity ulcers most often caused by vascular disease or neuropathy
72% venous disease
22% mixed arterial and venous cause
6% pure arterial disease

40. CHARACTERISTICS OF VENOUS AND ARTERIAL ULCERS (1 of 2)
Venous Disease
Arterial Disease
Signs and symptoms
Limb heaviness, aching and swelling that is associated with standing and is worse at end of day, brawny skin changes
Claudication (pain in leg with walking), ankle-brachial index <0.9, loss of hair, cool extremities

41. CHARACTERISTICS OF VENOUS AND ARTERIAL ULCERS (2 of 2)
Venous Disease
Arterial Disease
Risk factors
Advanced age, obesity, history of deep-vein thrombosis or phlebitis
Age >40 years, smoking, DM, hyperlipidemia, hypertension, male gender, sedentary lifestyle
Location of ulcers
Along the course of the long saphenous vein, between the lower medial calf to just below the medial malleolus
Over bony prominences
DM = diabetes mellitus

42. ONYCHOMYCOSIS Fungal infection of the nail plate
Causes thickening of the nail  can cause pain
Present in ~ one-third of older adults; increased incidence in those with obesity, immunodeficiency, diabetes, peripheral arterial disease, chronic tinea pedis, or psoriasis
~80% of infections caused by dermatophytes, the remainder caused by saprophytes or yeast

43. ONYCHOMYCOSIS
Nails infected by fungi are often yellow, thickened, and friable, with yellow-brown debris under the nail plate
Slide 43 43

44. TREATMENT OF ONYCHOMYCOSIS
For cosmetic concerns, comorbidities (diabetes), or pain
Topical antifungal agents not effective
Topical ciclopirox: <12% achieve clear or almost clear nails in clinical trials
Oral agents, such as terbinafine, fluconazole, itraconazole:
Potential for drug interactions
Treatment may take 3 to 4 months
Relapse rate is high

45. HERPES ZOSTER More than 2/3 of cases occur in people 50
Lifetime risk 20% in healthy adults and 50% in immunocompromised individuals
Most important reason for varicella zoster virus (VZV) reactivation is senescence of the cellular immune response to VZV with increasing age
Reactivation also associated with HIV, malignancy, use of immunosuppressive drugs
Usually self-limited if immunity is intact

46. HERPES ZOSTER
This patient had clusters of vesicles and pustules on an erythematous base involving a thoracic dermatome
Slide 46 46

47. COMPLICATIONS OF ZOSTER (1 of 2)
Involvement of ophthalmic branch of trigeminal nerve
Requires careful ophthalmic monitoring
Hutchinson’s sign: vesicles on the tip of the nose; represents involvement of nasociliary branch
Ramsay-Hunt syndrome (involvement of facial or auditory nerves)
Presents as herpes zoster of external ear or tympanic membrane
Leads to facial palsy with or without tinnitus, vertigo, and deafness

48. COMPLICATIONS OF ZOSTER (2 of 2)
Pain can precede, co-exist, or persist after rash
Post-herpetic neuralgia: pain that persists or appears after rash has healed, or 30 days after onset of rash
Occurs in 70% of those ≥70 years
Often difficult to treat

49. DIAGNOSIS OF HERPES ZOSTER
Characteristic physical exam findings (ie, dermatomal distribution)
Tzanck smear from base of vesicle shows multinucleated giant cells and epithelial cells containing intranuclear inclusion bodies
Smear can be sent for direct fluorescent antibody staining
Definitive diagnosis by viral culture

50. TREATMENT OF HERPES ZOSTER
Should start within 72 hours of rash
Acyclovir, valacyclovir, or famciclovir
Early treatment halts progression of disease, increases rate of clearance of virus from vesicles, decreases incidence of visceral and cutaneous dissemination, decreases ocular complications when eye is involved, may decrease pain and incidence of post-herpetic neuralgia
Wet compresses/topical antibiotics can treat secondary bacterial infection

51. TREATMENT OF POST-HERPETIC NEURALGIA
No definitive therapy
Tricyclic antidepressants (off-label), opioids, topical capsaicin, gabapentin, topical lidocaine, pregabalin, tramadol
Zoster vaccination recommended for adults >60 years

52. CANDIDIASIS (1 of 2)
At risk: older people with decreased mobility, increased skin moisture or friction, poor hygiene, diabetes mellitus
Rash may resemble intertrigo but have peripheral satellite pustules
Oral thrush may develop in those on corticosteroid inhalers, antibiotics, or immunosuppressants, and those with concomitant diabetes

53. CANDIDIASIS (2 of 2)
Diagnosis: KOH preparation reveals spores and pseudohyphae
Treatment:
Keep skin dry
Improve hygiene
Use topical or oral anticandidal agents (nystatin, ketoconazole)

54. SCABIES (1 of 2) Infestation of mite Sarcoptes scabiei
Common in institutionalized older people; epidemics occur in long-term care facilities
Spread by person-to-person contact
Eradication can be difficult
Signs and symptoms include severe pruritus (esp. of hands, axillae, genitalia, and peri-umbilical region), erythematous papules, and linear burrows

55. SCABIES (2 of 2)
Diagnosis: scraping of suspected lesion (mite excreta, eggs, or mite may be seen)
Treatment often initiated when clinical suspicion of infestation is strong
Treatment:
Topical permethrin 5%, or oral ivermectin 200 mcg/kg
Re-treat in 1 week if itching and lesions persist
Launder bed linens and clothing in hot water and dry in high heat or leave in closed bag for 10 days
Pruritus may persist for weeks to months
Treat caregivers

56. LOUSE INFESTATIONS
Lice can infest the body (pediculosis corporis), scalp (pediculosis capitis), or pubic hair (pediculosis pubis)
Treatment
Pyrethrin or derivatives (permethrin) topically
Treat caregivers and close contacts
Combs, brushes, hats, clothing, bedding, and towels must be washed in hot water

57. SEBORRHEIC KERATOSES Benign growths common in adults > 40 years
Present as waxy, warty, stuck-on papules in a variety of colors
Can be removed for cosmetic purposes
Occasionally confused with melanoma
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58. CHERRY ANGIOMAS Most common acquired cutaneous vascular proliferations
Round to oval, bright red, dome-shaped papules
Benign and made of dilated congested capillaries and postcapillary venules
Remove with excision, electrodessication, or laser ablation

59. ACTINIC KERATOSES
Considered premalignant, but majority resolve without treatment
Up to 20% progress to squamous cell cancer
Treatment:
Cryotherapy with liquid nitrogen
Photodynamic therapy
Topical acids
Topical 5-fluorouracil or imiquimod (off-label)
Excision

60. ACTINIC KERATOSES Rough, scaly, red-brown macules on sun-exposed skin
Also known as solar keratoses; results from chronic UV radiation exposure
Poorly circumscribed, occasionally scaly erythematous macules and papules in sun-exposed areas
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61. SQUAMOUS CELL CARCINOMA
Second most common form of skin cancer
Affects people in mid- to late life
Occurs most commonly in chronically sun-exposed areas
Propensity to occur in longstanding nonhealing wounds and in burn and radiation scars
Presentation: chronic erythematous papules, plaques, or nodules with scaling, crusting, or ulceration

62. TREATMENT OF SQUAMOUS CELL CARCINOMA
Surgical excision
Mohs’ micrographic surgery in cosmetically important areas
Cryotherapy or local radiation for patients unable to tolerate surgery

63. BASAL CELL CARCINOMA Most common cancer in United States
Risk factors: fair skin, chronic sun exposure
Treatment: surgical excision
Mohs’ micrographic surgery may be needed to ensure adequate excision and tissue sparing
When surgery is not feasible, can be treated with ablative methods such as cryosurgery, radiation, curettage with electrodesiccation and topical imiquimod

64. BASAL CELL CARCINOMA
This is also a pearly, fleshy papule but is ulcerated in the center and has a characteristic rolled border
Basal cell carcinoma, ulcerated
Slide 64 64

65. MAJOR CLINICAL PATTERNS OF BASAL CELL CARCINOMA
Description
Nodular
Most common variant; waxy, translucent papule with overlying telangiectasias
Morpheaform
Scar-like appearance; can look atrophic
Superficial
Erythematous macule or papule with fine scale or superficial erosion
Note: Some lesions appear as superficial ulcers with characteristic rolled borders; others are pigmented and confused with melanomas

66. MELANOMA Incidence is increasing; affects adults of all ages
Risk factors: fair skin, family history, dysplastic or numerous nevi, sunlight exposure
Regular skin examinations and early recognition are key for favorable prognosis
Treatment: surgical excision, possibly lymph node dissection or adjuvant therapy (immunotherapy, chemotherapy)

67. MELANOMA
Irregular variegation in pigment (shades of brown and blue-black) and irregular borders suggest melanoma
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68. TYPES OF MELANOMA Clinical Pattern Description Lentigo maligna
Seen most commonly on atrophic, sun-damaged skin; an irregularly shaped tan or brown macule that slowly enlarges
Superficial spreading
Irregularly shaped macule, papule, or plaque with varied color
Nodular
Rapidly growing papule or nodule, often black or gray
Acral lentiginous
Palms, soles, or nail beds; all skin types; dark brown or black patch; highest incidence in those 65 and older
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69. ACRAL LENTIGINOUS MELANOMA
Presents as a dark macular growth with irregular borders on volar surfaces of palms, soles (as in this case), or nails
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70. SUMMARY
The incidence of skin disease increases with aging and sun exposure
Dermatologic care of older people requires:
Knowledge of cutaneous changes of aging and effects of cumulative UV radiation exposure
Knowledge of common tumors, inflammatory diseases, and infections commonly seen in older adults

71. CASE 1 (1 of 4)
A 70-year-old Chinese-American man comes to the office because he has a widespread maculopapular eruption with formation of flaccid bullae and erosions.
For 2 days before the rash, he had fever, odynophagia, and eye pain. Over the next few days, the rash evolved to extensive sloughing and peeling of the skin.
His history includes hypertension, diabetes, and peripheral neuropathy.
Two weeks ago, he began carbamazepine at 200 mg q12h for peripheral neuropathy.

72. CASE 1 (2 of 4)
Other medications include glipizide, felodipine, simvastatin, and enteric-coated aspirin.
On examination, the sloughing and peeling involve 40% of the patient’s body surface.
His oral mucosa has erosions and exudates.
He also has bilateral conjunctivitis.
The patient is admitted to a burn unit.

73. CASE 1 (3 of 4) Which of the following is the most likely diagnosis?
Bullous pemphigoid
Staphylococcal scalded skin syndrome
Disseminated herpes zoster
Toxic epidermal necrolysis
Slide 73 73

74. CASE 1 (4 of 4) Which of the following is the most likely diagnosis?
Bullous pemphigoid
Staphylococcal scalded skin syndrome
Disseminated herpes zoster
Toxic epidermal necrolysis
ANSWER: D
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severity variants of the same disease, characterized by epidermal detachment. Skin detachment affects <10% of the body surface in SJS and >30% in TEN. When skin detachment is between 10% and 30%, the syndrome is considered overlap SJS/TEN. Often, fever and mucosal involvement develop days before the rash appears. Initial lesions are macular and can form target lesions with purpuric centers. The lesions can coalesce and progress to superficial flaccid bullae. Usually at least two mucous surfaces are involved. Epidermal necrosis is pathognomonic for SJS and TEN.
SJS and TEN are rare reactions to medications. More than 200 medications have been implicated; the most common are antibiotics, NSAIDs, and anticonvulsants. The risk of SJS or TEN from carbamazepine is significantly increased in patients who have the HLA-B*1502 allele, found in individuals with ancestry from across broad areas of Asia, including South Asian Indians.
Bullous pemphigoid is a bullous disorder mainly found in older adults. The bullae are tense, not flaccid, because they are subepidermal. Oral involvement is seen in about 20% of cases and is rare in drug-induced pemphigoid. Staphylococcal scalded skin syndrome is caused by exfoliative exotoxins released by group 2 staphylococci. It presents as a generalized, superficial exfoliative dermatitis without mucosal involvement. The lesions of herpes zoster are small vesicles, or blisters, on an erythematous base. They appear in clusters and in various stages of healing, and distributed along a single dermatome. New lesions appear every few days and heal with crusting over 1 to 2 weeks. Although there can be mucosal involvement, the lesions are clearly different from those of TEN on appearance.

75. CASE 2 (1 of 3)
A 65-year-old woman comes to the office because she has facial rash with stinging, burning, and tender pimples.
The rash began recently and is causing increasing redness.
On examination, there is erythema underlying central facial papules and pustules with telangiectasias.
The distribution is over the central region of her face and includes her cheeks and chin.

76. CASE 2 (2 of 3)
Which of the following is the most appropriate initial approach?
Ketoconazole
Tetracycline
Biopsy
Antinuclear antibody titer
Review of exposure to skin irritants
Slide 76 76

77. CASE 2 (3 of 3)
Which of the following is the most appropriate initial approach?
Ketoconazole
Tetracycline
Biopsy
Antinuclear antibody titer
Review of exposure to skin irritants
ANSWER: B
This patient has stage III papulopustular rosacea, a vascular disorder with distinct, predictable symptoms. Correct diagnosis and early treatment are important because, untreated, rosacea can progress to irreversible disfigurement and even vision loss. Rosacea usually involves the cheeks, nose, chin, and forehead, with a predilection for the nose in men. There is no specific test, but its characteristic appearance, distribution, discrete course, older age population, and response to various therapies allow accurate diagnosis. Although rosacea is incurable, its progress can be controlled and even halted through medical therapy and lifestyle modification. Besides avoiding triggers, management includes antibiotic therapy, such as tetracycline, especially for stage III lesions. Topical metronidazole can be used alone, or in combination with oral antibiotics, particularly for earlier stage disease.
The differential diagnosis of rosacea includes seborrheic dermatitis, which is treated with topical ketoconazole. Seborrheic dermatitis presents with a greasy scale and eczematous changes but no papules, pustules, or telangiectasias. Its pattern of distribution involves the paranasal area, the nasolabial grooves, and areas beyond the face, such as the scalp. It can coexist with rosacea.
Sarcoidosis can mimic rosacea clinically as well as histologically by producing red papules on the face, but biopsy will reveal sarcoidal granulomas. This patient does not have the pigmentary changes, atrophy, scarring, and adherent scaling that are characteristic of systemic lupus erythematosus. Conversely, the pustules found in rosacea are not characteristic of lupus. However, a low antinuclear antibody titer can be present in rosacea. Contact dermatitis can resemble rosacea, but it is usually pruritic and has a cutaneous linear pattern, which follows the size and shape of contact by the external causal agent.

78. CASE 3 (1 of 3)
A 72-year-old woman comes to the office for a routine physical examination.
Skin examination reveals multiple small (<5 mm) macules and papules scattered over her body.
They have smooth, well-defined borders and brown, homogeneous coloration.
A lesion on her right lower leg is a 7-mm papule with more irregular borders and tan-brown heterogeneous coloration.

79. CASE 3 (2 of 3)
Which of the following is the most appropriate next step?
Laser therapy
Cryosurgery
Observation
Excision
Electrodesiccation
Slide 79 79

80. CASE 3 (3 of 3)
Which of the following is the most appropriate next step?
Laser therapy
Cryosurgery
Observation
Excision
Electrodesiccation
ANSWER: D
Recognizing the clinical signs of early melanoma improves detection rates and decreases overall mortality. Melanomas that are detected early are highly curable; most are found by the patient. No single clinical feature determines or excludes a diagnosis of melanoma.
The mnemonic ABCDE is used to identify features that can indicate melanoma in pigmented lesions: Asymmetry, Border irregularity, Color variation, Diameter (>6 mm), and Evolving or changing. A definite change in a pigmented lesion, especially a change observed over a period of months, should arouse suspicion of an evolving melanoma. Most melanomas are varying shades of brown, but black, blue, gray, white, pink, or red can be seen, and some melanomas are not pigmented.
This patient’s lesion is symmetric but has irregular borders, color variation, and a diameter of 7 mm. It requires immediate biopsy with experienced pathology review, rather than observation.
Skin lesions that are suspicious for melanoma should not be treated with laser, cryosurgery, or electrodesiccation.

81. Copyright © 2010 American Geriatrics Society
ACKNOWLEDGMENTS
Editor: Annette Medina-Walpole, MD
GRS7 Chapter Authors: Sumaira Aasi, MD
Jaehyuk Choi, MD, PhD
GRS7 Question Writer: Angela Gentili, MD
Pharmacotherapy Editor: Judith L. Beizer, PharmD
Medical Writers: Beverly A. Caley
Faith Reidenbach
Managing Editor: Andrea N. Sherman, MS
Copyright © 2010 American Geriatrics Society