Audio-Digest Foundation: family-practice

Main Written Summaries Listing | Family-practice: 2005 Listings
Audio-Digest FoundationFamily Practice


Volume 53, Issue 40
October 28, 2005

The following is an abstracted summary, not a verbatim transcript, of the lectures/discussions on this audio program. If, after reviewing this written summary, you would like to hear the contents and/or earn CME/CE credit:

View Main Program Listing

Visit Audio-Digest Home Page

Family Practice Program InfoAccreditation InfoCultural & Linguistic Competency Resources





DERMATOLOGY UPDATE

From the Annual Spring Family Practice Review, sponsored by the Temple University School of Medicine, Philadelphia

COMMON SKIN PROBLEMS —Jennifer T. Clarke, MD, Assistant Professor of Dermatology, Pennsylvania State University, College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania

Acne
Physical examination of acne: look for comedones, papules, pustules, nodules, cysts, and scarring; acne affects face, upper trunk, shoulders, and chest
Comedones: closed—flesh-colored follicular-based papules; whiteheads; initiating lesions of acne; seen in patients with mild acne and in older children or early adolescents; open—dilated follicular papules with dark centers; blackheads
Inflammatory acne: red inflamed papules; pustules; patients who develop nodules, cysts, and have potential for scarring need more aggressive therapy; patients with history of scarring need strong therapy and referral
Pathogenesis of acne: 1) increased cohesion or hyperkeratosis of epidermal cells that line follicular ostia; epidermal cells lining hair follicle become more cohesive, plug follicular ostia, and prevent outflow of dead keratinocytes and sebum; 2) increased sebum production and follicular hyperkeratinization result in comedones; 3) influx of inflammatory cells often in response to overproliferation of Propionibacterium acnes; 4) development of red papules and pustules; can progress to cyst formation and rupture; patients develop deeper nodules, large cysts, and scarring
Treatment: choose agents that target pathogenic factors; topical retinoid for retention hyperkeratosis that causes comedonal acne; treat P acnes with oral or topical antibiotic and benzoyl peroxide; no antibiotic resistance shown with benzoyl peroxide; oral antibioticseg, tetracycline, for inflammatory acne; wait 6 to 8 wk for anti-inflammatory effect (give minimum 3-mo course); oral contraceptives, hormonal therapy, and isotretinoin (Accutane) decrease sebum production; combination of topical retinoid, benzoyl peroxide, and antibiotic works synergistically

Atopic Dermatitis
Major criteria for diagnosis: patient should meet 3; 1) pruritus; 2) typical morphology and distribution of rash; infants often present with first signs on face and extensor surfaces (areas where infant able to rub or scratch); later distribution on popliteal and antecubital fossa, neck, and wrists; 3) chronic or chronically relapsing course; 4) personal or family history of atopic disease (including allergic rhinitis, asthma, eczema)
Treatment: flares—bathing for maintenance and prevention; mid-potency steroid (eg, triamcinolone ointment); adequate moisturization and skin care recommended between flares; for earliest signs of erythema or pruritus, use topical immunomodulator (eg, tacrolimus, pimecrolimus); bathing once daily or once every other day; recommend mild soap (eg, Dove) and immediate moisturization; minimize bath time to 5 to 10 min in lukewarm water; no bubble baths; wash child’s hair at end of bath to avoid having child sit in soapy water; bar soaps recommended; moisturizing with ointments (eg, Vaseline petroleum jelly) and creams (eg, Eucerin, Cetaphil) important; avoid lotions; encourage patients to moisturize skin at least twice daily all over body in between flares; overmedication occurs when patients use moisturizer and combination product of medication and moisturizer; topical immunomodulators as efficacious as low-potency corticosteroids; for flares, use stronger mid-potency steroids (eg, triamcinolone, mometasone); prescribe ointments rather than creams

Dermatophyte Infections
Case presentation: Puerto Rican woman 61 yr of age presents with 2-mo history of itchy burning papules and purplish plaques around swollen eyelids; woman presents 1 day after arriving in United States from visiting Puerto Rico; no improvement with low- and ultra-high potency steroids, mupirocin ointment, oral ampicillin sulbactam, oral ciprofloxacin, and oral acyclovir; woman had annular patches on cheeks and forehead; diagnosis—KOH examination of scraping from patches on eyelids showed branching hyphae; dermatophyte infection; scraping scales allows for definitive diagnosis; pets common source of dermatophyte infections; scraping scales on scalp often unhelpful because fungus lives within hair shaft (obtain culture); untreated tinea capitis can result in inflammatory plaques with alopecia, widespread patches of alopecia, or permanent alopecia
Treatment of dermatophytosis: topical azoles or allylamines; if fungus affects hair or nails, use oral agent (eg, griseofulvin, azole, allylamine); griseofulvin 25 mg/kg daily for 8 wk; corticosteroids—allow fungus to thrive and penetrate deeper into hair follicles, resulting in deep plaques with patches of alopecia (Majocchi’s granuloma), and topical treatment ineffective (patients need oral antifungal agents); combination products (eg, clotrimazole, betamethasone, lotrisone) do not treat fungus adequately, and patients develop side effects from steroid (eg, atrophy and hypopigmentation from betamethasone)

Warts
Wart therapy: destructive or immunologic; requires repeated applications; 35% to 65% resolve spontaneously over 2 yr; duct tape—61 patients randomized to cryotherapy for 10-sec freezes every 2 to 3 wk or duct tape every 6 days for 2 mo; 51 patients completed study; 22 of 26 in duct tape group cleared; 15 of 25 in cryotherapy group cleared
Flat warts: flat-topped papules on back of hand; patients often misdiagnosed with seborrheic keratoses or actinic keratoses; can appear on face; spread by trauma (often seen in areas where patients shave); tretinoin liquid effective
Plantar warts: distinguish from corns—warts interrupt skin lines with black puncta (dilated blood vessels); corns occur over bony prominences (warts do not)

Psoriasis
Evaluation of psoriasis: look at morphology and distribution; determine whether psoriasis involves localized amounts of skin, small scaly plaques, facial skin, or scalp; identify large confluent plaques that involve most of body surface; determine whether disease more localized with potential to cause functional impairment
Topical therapy: best for patients with limited skin involvement, milder psoriasis, or widespread disease (but for whom systemic therapies too risky); refer patients when psoriasis spreads
UV light therapy: UV-A (add oral sensitizing agent [eg, psoralens]) and UV-B can produce excellent results in widespread psoriasis; tanning beds increase risk for skin cancer (screen patients periodically)
Systemic agents: immunosuppressive agents (eg, methotrexate, cyclosporin); retinoids (eg, acitretin [Soriatane]); biologic agents—best for patients with involvement of 10% of body surface or patients with less body surface involvement in whom psoriasis causes functional impairment; refer to specialist; etanercept (Enbrel), alefacept (Amevive), and efalizumab (Raptiva) approved by Food and Drug Administration (FDA) for psoriasis

Skin Cancer
Evaluation of melanoma: patients often have irregularly shaped, dark-colored macules and papules all over body, representing atypical nevi and melanoma; watch for “ugly duckling” sign (look for things that stand out on skin); ABCDs— asymmetry; border of growth; color; diameter
Treatment of benign growths: when uncertain, refer or perform biopsy; when concerned about melanoma, perform excisional biopsy or deep-shave biopsy
Basal cell carcinoma: scarlike morphology characteristic of morphea-form basal cell carcinoma (tends to infiltrate widely and deeply); can be locally aggressive when left alone for long time; surgical removal can be disfiguring; be aware of “red dot” (spot on skin that does not resolve)
Skin cancer therapy: preventive therapy includes education about looking for “ugly duckling” and “red dot,” using sunscreen, performing self-skin examinations; performing biopsy on suspicious lesions; referral to dermatologist for surgical treatment after diagnosis; radiation plays small role
MALIGNANT MELANOMA Robert J. Pariser, MD, Professor, Department of Dermatology, Eastern Virginia Medical School, Norfolk, Virginia
Introduction: 59,000 new cases annually estimated in United States (excluding in situ lesions); most common malignancy in 20- to 30-yr age range; slight male predominance; >100,000 new cases yearly worldwide
Risk predictors: positive history of melanoma highest predictor; increased nevi; positive family history; atypical nevi; fair complexion, blue eyes, and red or blonde hair; history of blistering childhood sunburns; immunosuppression; xeroderma pigmentosum
Prognosis: depth of invasion of melanoma related to likelihood of regional and distal metastases; penetration <0.75 mm implies nearly no risk for distant disease and small risk for regional adenopathy; most patients have regional and distant metastases with penetration >4.00 mm
Types of melanoma: superficial spreading—flat and broad; clearly violates ABCDs; ruler sign shows long diameter; hypopigmented or amelanotic melanomas difficult to diagnose or recognize; nodular—round; may or may not be dark or asymmetric; ABCD criteria may fail; lentigo maligna—broad, flat, spreading melanoma seen in sun-damaged skin; usually on face in elderly people; can be large with typical irregular border and variable pigmentation; presents in shades of brown rather than red, white, and blue as seen in more deeply situated melanomas; acral lentiginous—affects distal parts; subungual and periungual melanomas often diagnosed late because often treated as other condition (eg, fungal infections, psoriasis); small melanomas—ABCDs least useful; lesions 2 to 4 mm with some irregularity in color, shape, and border; some lesions round; diagnosis not obvious
Emerging criteria: newly noted lesion in at-risk patient; “ugly duckling” syndrome; melanomas can affect eyes and central nervous system (CNS)
Nevi: preexisting nevus—performing biopsy on thickest part of lesion may result in benign results and missed melanomas; dysplastic nevus syndrome—people with above-average number of pigmented nevi at risk; follow patients who have moles; congenital nevi—substantial risk for melanoma from large bathing-trunk nevi; less risk with smaller (eg, palm-sized) nevi; halo nevus—preexisting nevus suddenly surrounded by hypopigmented halo; usually benign; lymphocyte attack on melanocytes results in regressed nevus and vitiliginous circle
Pigmented nail streak (melanonychia striata): present and stable cases with involvement of multiple nails usually do not imply risk; recent involvement of one nail usually benign nevus (perform nail matrix biopsy to rule out melanoma)
Melanoma: public awareness increasing; uncertainty in clinical and pathologic diagnosis increasing; width of specimen becoming more important than depth
Diagnostic tools: 60% accurate; dermoscopy or epiluminiscent microscopy—magnification under oil; algorithm— look at dermatoscopic structures (eg, pigment network); score according to ABCDs (eg, 0 points for symmetry, 1 point for asymmetry in only 1 plane, 2 points for asymmetry in 2 planes); multiply by appropriate factor; score <4.76 implies benign lesion, >5.45 implies melanoma, 4.76 to 5.45 implies suspicious lesion; not standard of care
Conclusion: better prognosis with earlier diagnosis; less concern about width and surgical margins; lymph nodes “up in the air”; sentinel nodes becoming standard of care; suspicious mole—remove entire lesion if possible; request consultation when uncertain
SKIN MANIFESTATIONS OF SYSTEMIC DISEASE AND DRUGS O. Fred Miller III, MD, Director, Department of Dermatology, Geisinger Medical Center, Danville, Pennsylvania
Approach to cutaneous diagnosis: adequate lighting (no incandescent bulbs); magnification; use fingers to examine skin (eg, pinch or stretch skin to bring out morphology); location, distribution, color, and size of lesions; determine whether lesions primary or secondary; pruritus—itchy; look for primary lesions; impetigo—honeycomb-colored (ie, brown yellow) crust; seen more in pediatric population than adult population; look for systemic implications (eg, small ulcerations caused by group A β-hemolytic Streptococcus and associated glomerulonephritis); blisters frequently not seen because completely contained within epidermis and often become broken or rubbed off; may or not present with associated adenopathy; usually caused by Staphylococcus
Dermatomyositis: distinctive purple color with unusual reticulated pattern of hypopigmentation within pigmented area; more pruritus (especially on scalp) than lupus
Lupus: more erythematous color; sometimes subacutely ery-thematous; no lavender color; discoid lupus—coin-shaped lesions present in more discrete patches; little plugs of keratin (carpet-tack plugging) visible with good lighting and magnification in lupus plaque; severity of lesions varies; usually fade without scarring; butterfly rash of lupus—usually presents with systemic signs and symptoms; frequently occurs with lupus flare; patients often lose hair; hairs break and become unmanageable (hair returns after acute episode); scarring of scalp can be permanent; some patients develop rheumatoid nodules
Seborrheic dermatitis: waxy scales in nasolabial folds, glabella, and anterior chest can be misdiagnosed as systemic disease; responds well to ketoconazole cream
Medication reactions: itchiness variable; no rash specificity for particular drug (eg, cephalexin [Keflex] can result in maculopapular eruption or Stevens-Johnson eruption); adverse cutaneous reaction usually fades when drug discontinued; eosinophilia variable (not significant criterion); bilateral involvement; skin can react with identical rash to many stimuli and drugs; phototoxic reaction (ie, sunburn) seen with hydrochlorothiazide; pigmentary changes seen with amiodarone; pigmentation with minocycline (Minocin) common; fixed-drug eruption (involvement of same area every time drug taken) unusual; consider group A β-hemolytic streptococcal infection in children with urticaria; erythema nodosum—can be caused by medications but usually caused by β-hemolytic Streptococcus and ulcerative colitis or Crohn’s disease; also associated with sarcoidosis, hilar adenopathy, and deep fungal disease; can be caused by oral contraceptives; toxic epidermal necrolysis— patients shed skin in entirety; can be caused by sulfonamides

Educational Objectives

The goal of this program is to educate the listener about common skin disease and skin cancer. After hearing and assimilating this program, the clinician will be better able to:
1. Select appropriate therapy for acne and atopic dermatitis.
2. Choose effective therapy for dermatophyte infections and warts.
3. Assess risk for malignant melanoma.
4. Evaluate lesions for cutaneous diagnosis.
5. Recognize adverse skin reactions to medications.

Discussed on This Program

Acitretin [Soriatane]
Acyclovir (acycloguanosine) [Zovirax]
Alefacept [Amevive]
Ampicillin [Principen]
Benzoyl peroxide (several trade names)
Betamethasone [Celestone]
Cephalexin [Biocef, Keflex]
Cetaphil (soap-free therapeutic cleanser) Ciprofloxacin [Ciloxan, Cipro, Cipro I.V., Cipro XR]
Clotrimazole (several trade names)
Cyclosporine (cyclosporin A) [Neoral, Sandimmune, SangCya]
Efalizumab [Raptiva]
Etanercept [Enbrel]
Eucerin (petrolatum, mineral oil, mineral wax, woolwax alcohol) Griseofulvin microsize [Fulvicin U/F, Grifulvin V, Grisactin 250, Grisactin 500]
Griseofulvin ultramicrosize [Fulvicin P/G, Grisactin Ultra, Gris-PEG]
Isotretinoin (13-cis-retinoic acid) [Accutane]Ketoconazole [Nizoral, Nizoral A-D, Nizoral Cream Shampoo]
Lotrisone (combination of betamethasone [as dipropionate] and clotrimazole )
Methotrexate (amethopterin; MTX) [Methotrexate LPF, Rheumatrex Dose Pack, Trexall]
Minocycline HCl (minomycin) [Arestin, Dynacin, Minocin, Minocin IV, Vectrin]
Mometasone furoate [Elocon, Asmanex Twisthaler]
Mupirocin (pseudomonic acid A) [Bactroban, Bactroban Cream, Bactroban Nasal] Pimecrolimus [Elidel]
Tacrolimus (FK506) [Prograf, Protopic]
Tetracycline HCl (several trade names)
Tretinoin (trans-retinoic acid; vitamin A acid) [Altinac, Atragen (investigational), Avita, Renova, Retin-A, Retin-A Micro, Vesanoid]
Triamcinolone (oral) [Aristocort, Atolone, Kenacort]
Triamcinolone acetonide (several trade names)
White petrolatum [Vaseline]

Suggested Reading

Aloia TA et al: Management of early-stage cutaneous melanoma. Curr Probl Surg 42:460, 2005; Chapman MS et al: Tacrolimus ointment 0.03% shows efficacy and safety in pediatric and adult patients with mild to moderate atopic dermatitis. J Am Acad Dermatol 53:S177, 2005; Charles CA et al: Variation in the diagnosis, treatment, and management of melanoma in situ: a survey of US dermatologists. Arch Dermatol 141:723, 2005; Dyson SW et al: Impact of thorough block sampling in the histologic evaluation of melanomas. Arch Dermatol 141:734, 2005; Joseph WS: The oral antifungal patient. Clin Podiatr Med Surg 21:591, 2004; Khachemoune A et al: Assessing malignant melanoma: a case study. Dermatol Nurs 17:188, 2005; McKenna JK et al: Dermatologic drug reactions. Immunol Allergy Clin North Am 24:399, 2004; Micali G et al: Management of cutaneous warts: an evidence-based approach. Am J Clin Dermatol 5:311, 2004; Schattner A et al: The future of the treatment of systemic lupus erythematosus. Clin Exp Rheumatol 23:254, 2005; Simonart T et al: Treatment of acne with topical antibiotics: lessons from clinical studies. Br J Dermatol 153:395, 2005; Van de Kerkhof PC et al: Recommendations for the topical treatment of psoriasis. J Eur Acad Dermatol Venereol 19:495, 2005; Wong SL: The role of sentinel lymph node biopsy in the management of thin melanoma. Am J Surg 190:196, 2005; Zouboulis CC et al: What is the pathogenesis of acne? Exp Dermatol 14:143, 2005.

Faculty Disclosure

In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported nothing to disclose.


Drs. Clarke, Pariser, and Miller spoke in Lancaster, Pennsylvania at the annual Spring Family Practice Review, presented March 13-18, 2005, by Temple University School of Medicine and Lancaster General Hospital. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.


Reproduction of this summary in whole or in part in any form or medium without express written permission is prohibited.

If, after reviewing this written summary, you would like to hear the contents and/or earn CME/CE credit:

View Main Program Listing

Visit Audio-Digest Home Page