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SHARMIN BANU ANAM, MD PGY-3 Feb 27, 2014. Common Dermatological Conditions in Primary Care 2.

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Presentation on theme: "SHARMIN BANU ANAM, MD PGY-3 Feb 27, 2014. Common Dermatological Conditions in Primary Care 2."— Presentation transcript:

1 SHARMIN BANU ANAM, MD PGY-3 Feb 27, 2014

2 Common Dermatological Conditions in Primary Care 2

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5  Macules: Macules are nonpalpable lesions that vary in pigmentation from the surrounding skin. Macules are not raised or atrophic  Papules: Papules are palpable, discrete lesions measuring ≤5 mm diameter  Nodules: Nodules are palpable, discrete lesions measuring ≥6 mm diameter  Plaques: Plaques are large (>5 mm) superficial flat lesions, often formed by a confluence of papules  Pustules: Pustules are small, circumscribed skin papules containing purulent material  Vesicles:Vesicles are small (<5 mm diameter), circumscribed skin papules containing serous material  Whales: Irregularly elevated edematous skin, erythematous  Scales: Superficial epidermal cells that are dead and cast off from the skin  Crusts: Dried exudate 5

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9 9 Skin dryness, erythema, oozing and crusting, and lichenification - Itching is hallmark Treatment: Avoid trigger factors - heat, perspiration, low humidity Treat skin infections - staphylococcus aureus, herpes Antihistamines – sedation, control of itching Treat stress and anxiety Immunomodulator (protopic) UVA, UVB, nbUVB,PUVA

10 10 Causes: Infections Allergic reactions to medications, foods, or insect stings and bites Mast cell activation- narcotics NSAIDs Treatment: Antihistamine( 1 st and 2 nd generation) H2 blocker( ranitidine) Short course of steroid ( prednisone/ prednisolone)

11 11 – Poison ivy – Poison oak – Poison sumac – Cashew – Mango – Ginkgo – Japanese lacquer tree Linear lesions Vesicles – Fluid does not contain resin and won’t spread rash Erythema May occur within 8 hrs or up to a week after exposure

12 12 Treatment: Decontamination within 10 min after exposure– Not helpful after 1 hr Wet compresses Topical corticosteroids Systemic corticosteroids – Prednisone 20 mg BID x 1 week – Prednisone 40-60 mg single dose IM steroids – Triamcinalone acetonide (Kenalog) 40 mg IM

13 13 Autoimmune blistering diseases in adults IgG antibodies against bullous pemphigoid antigen Treatment: Clobetasol, immunomodulators, antibiotics, immunosuppressant

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15 15 Herpes Zoster (Shingles) Varicella-zoster virus Reactivation of latent infection 10-20% lifetime incidence Generally involves skin of a single dermatome Pre-eruptive pain, itching, burning (4-5 days) Fever, headache, malaise

16 16 Herpes Zoster (Shingles) Vesicles, of varying size, on erythematous base Successive crops over 7 days Crust lasts 2-3 weeks Postherpetic neuralgia – Increases with age of patient – Increases with pain during eruptive phase – Incidence = 20% at 1 month Herpes Zoster – Treatment Analgesics Wet compresses (Burrow’s Solution) Antiviral therapy – Acyclovir (Zovirax) 800 mg QID x 7 days – Famciclovir (Famvir) 500 mg q 8 hrs x 7 days – Valacyclovir (Valtrex) 1 g TID x 7 days

17 17 Herpes Zoster – Treatment Oral corticosteroids (Prednisone) – May decrease pain initially during acute phase – Does not reduce subsequent postherpetic neuralgia Sympathetic nerve blocks – Bupivacaine – Must be given within 2 months of onset to be effective Postherpetic Neuralgia – Treatment Narcotic analgesics Anticonvulsants – Pregabalin (Lyrica) – Gabapentin (Neurontin) Tricyclics Capsaicin

18 18 Herpes Zoster Vaccine (Zostavax) Contains the same live attenuated varicella virus as Varivax but at a much higher titer of vaccine virus Approved by FDA for persons 50 years of age and older Recommended by CDC for > 60 y/o Regardless of past hx of zoster Do not use if immunosuppressed,immunodeficient, pregnant, TB, or allergic to neomycin/gelatin Administered by the subcutaneous route

19 19 Psoriasis Oval, erythematous, plaque-like lesions Can develop at sites of trauma Often involves extensor surfaces – Elbows, knees & scalp Pitting fingernails Associated with asymmetric polyarthritis

20 20 Types Chronic plaque psoriasis Guttate psoriasis Pustular psoriasis Erythrodermic psoriasis Treatment < 20% of body involved – Topical corticosteroids – Calcipotriene (Dovonex) Vitamin D3 analog – Tazarotene (Tazorac) – Anthralin (Anthra-derm) – Tar – UVB – Intralesional steroids Treatment Contd > 20% of body involved (phototherapy) – UVB Broad band, narrow band +/- topical, systemic, biologic agents( protopic) – PUVA Ultraviolet + psoralen +/- topical, systemic, UVB – Excimer laser

21 21 Treatment Contd Severe recalcitrant disabling (FDA approved) – Methotrexate (Rheumatrex) Gold standard – Acitretin (Soriatane) Plaque type – Cyclosporine (Sandimmune) Anti-TNF agents – Infliximab, Etanercept, Adalimumab

22 22 Squamous cell ca in situ: Head and neck (55 %) Dorsum of the hands and forearms (18 %) Legs (13%) Arms (3%) Shoulder or back (4%) Chest or abdomen (4%) Diagnosis: Shave, punch, or excision biopsies Treatment: Mohs surgery

23 23 Keratinization or disorders of cornification Inherited/acquired( malignancy, autoimmune or infectious disease, and nutritional deficiency) Treatment: topical steroid moderate to high potency- Triamcinolone Betamethasone Intralesional steroid -Tacrolimus -Antimalarial

24 24 ? virus/ herpes 50 to 90 percent -"herald" or "mother" patch, ( single round or oval, sharply delimited, pink or salmon-colored lesion on the chest, neck, or back) Spreads centrifugally KOH to r/u dermatophytosis Treatment: If pruritus- medium potency topical steroid/ oral antihistamine -Erythromycin/ acyclovir -UVB

25 25 Scabies Hypersensitivity reaction to Sarcoptes scabiei – Eggs, fecal pellets (scybala) Nocturnal pruritis – Scratching spreads mites to other areas Curved or linear burrows Vesicles or small papules Pustules indicate secondary infection Location of lesions – Finger webs – Wrists – Elbows – Knees – Buttocks – Axilla – Waist – Breasts – Genitals

26 26 Scabies – Diagnosis Locate burrow with felt tip pen ink Scrape with #15 curved scalpel blade View under mineral oil or KOH Look for mites, eggs, feces (scybala) Norwegian (Crusted) Scabies Overwhelming infestation Crusted lesions Not particularly pruritic Seen mostly in immunocompromised patients

27 27 Treatment Launder all bedding and clothes worn within 48 hrs in hot water or dry clean Treat patient, intimate contacts, and family members in same household 5% Permethrin cream (Elimite) – Drug of choice – Apply below the neck, may repeat in 1 week Lindane (Kwell) – More toxic, especially in children/pregnancy Ivermectin (Stromectol) – Effective for Norwegian scabies Crotamiton (Eurax) Benzyl benzoate 25% lotion 6% precipitated sulfur in petrolatum

28 28 Acne Vulgaris Androgen mediated disorder of pilosebaceous units Androgens stimulate sebum production and proliferation of keratinocytes Keratin plug obstructs follicle os Proprionibacterium acnes proliferates in plugged follicle P. acnes growth produces inflammation

29 29 Acne Vulgaris – Treatment Comedonal acne – Keratinolytic agent Mild inflammatory acne – Keratinolytic agent +/ topical antibiotic Moderate inflammatory acne – Topical antibiotic +/- systemic antibiotic Severe (nodulocystic) acne – Isotretinoin Topical keratinolytics – Tretinoin (Retin-A) start with lowest concentration of cream and advance as tolerated apply qhs after washing may cause an initial flare of lesions side effects include erythema, dryness, scaling – Adapalene (Differin) apply hrs after washing better tolerated than tretinoin and equally effective

30 30 Treatment: Topical keratinolytic: Tretinoin( retin A), Adapalene, Tezarotine, Azeleic acid Topical antibacterial: Benzoyl peroxide with or without antibiotic Topical antibiotic: erythromycin,clindamycin,tetracycline,metronidazole,dapsone Systemic antibiotic: Tetra / mino/ doxycycline, erythro/ azithromycin, Bactrim OCP Spironolactone Isotretinoin, Acutane(2 form of birthcontrol) need to register to iPLEDGE program

31 31 Chronic, relapsing Asymptomatic (dandruff) to more widespread involvement Associated with: HIV, Parkinson disease, neuroleptic medications Scalp, the external ear, the center of the face, the upper part of the trunk, and the intertriginous areas Clinical diagnosis Treatment: antifungal shampoo with or without a topical high-potency corticosteroid -selenium sulfide 2.5%, ketoconazole 2%, or ciclopirox 1% shampoo - fluocinolone acetonide 0.01% shampoo/lotion -pimecrolimus cream, tacrolimus ointment

32 32 Rosacea Prevalence = 15 million in US Most common in Celtic ethnicity Most common after age 30 More common in women Unknown etiology Chronic, intermittent Involves forehead, cheeks, nose, ocular area

33 33 Primary features – Erythema Transient symmetric flushing – Accentuated by hot liquids and alcohol Non-transient – Papules and pustules – Telangiectasia Secondary features – Burning or stinging – Plaque – Dry appearance – Edema – Nasal hypertrophy/scarring (rhinophyma) – Ocular manifestations Triggers for flushing Extremes of temperature Sunlight Spicy foods Alcohol Exercise Acute psychological stressors Medications Menopausal hot flashes

34 34 Rosacea – Treatment Topical antibiotics 0.75% Metronidazole (Metrogel) – BID 1% Metronidazole (Noritate) – daily Azelaic acid 15% (Azelex) – BID Benzoyl peroxide 5% - BID +/- erythromycin or clindamycin Clindamycin cream – less effective Other topical agents Pimecrolimus (Elidel) 1% cream Adapalene 0.1% gel, Tretinoin 0.025% cream Permethrin

35 35 Rosacea – Treatment Oral antibiotics Doxycycline (Vibramycin) 100-200 mg/day Tetracycline 1 gram/day Erythromycin 1 gram/day Minocycline (Minocin) 100-200 mg/day Metronidazole (Flagyl) 250 mg BID Azithromycin (Zithromax) 500 mg, then 250 mg x 4 days Retinoids Isotretinoin (Accutane) 0.5 mg/kg/day x 20 weeks for severe resistant cases

36 36 Rosacea – Treatment Vascular laser – Useful for resistant telangectasia & persistent erythema Rhinophyma Rx – Mechanical dermabrasion – CO2 laser peel – Surgical excision – Electrocautery

37 37 Face, neck, upper trunk, and proximal extremities Usually asymptomatic Cause: Atopy, sun exposure, bathing Treatment: protect from sun exposure Topical steroid/ calcinurin inhibitor May take months to year to get better

38 38 1% population Antibody to melanocyte Associated with: Other autoimmune disorders, thyroid disease, pernicious anemia, SLE, Addison disease Treatment: Corticosteroids( 10% of body) – medium potency >6 mo Calcineurin inhibitors( elidel, protopic) UVA/ UVB Surgery

39 39 Tinea Versicolor Caused by Malassezia (Pityrosporum)species Lesions result from conversion from budding to mycelial form Occurs with heat, humidity, pregnancy, steroids, immunosupression More common at ages associated with high sebaceous activity

40 40 Tinea Versicolor – Treatment Topical – for limited disease – Ketoconizole 2% shampoo (Nizoral) x 3 days – Selenium sulfide 2.5% x 7 days or q week x 4 – Terbinafine 1% solution (Lamisil) BID x 1 week Oral – for extensive disease or nonresponders – Itraconazole (Sporanox) 200 mg daily x 5-7 days – Fluconazole (Diflucan) 300 mg single dose,repeat in 1 week – Avoid oral ketoconizole-Concern about hepatotoxicity Prophylaxis – Ketoconizole 2% shampoo (Nizoral) q week – Itraconazole (Sporanox) 200 mg PO BID q month x 6 months

41 41 Pruritic, circular or oval, erythematous, scaling patch or plaque that spreads centrifugally. Central clearing Outbreaks among athletes who have skin-to-skin contact, wrestlers (tinea corporis gladiatorum) Diagnosis: KOH preparation, segmented hyphae and arthrospores Treatment: Topical antifungals (nystatin is ineffective) Oral terbinafine, fluconazole, and itraconazole

42 42 Mostly in small children Three forms, "gray patch," "black dot" and favus Diagnosis: KOH examination of manually epilated hair Treatment: Grieseofulvin Terbinafine

43 43 Tinea corporis has been altered by the use of topical corticosteroids

44 44 HPV type 1 -plantar warts 6 and 11 -anogenital Spread by: Skin-to-skin contact,sites of trauma (Koebner phenomenon Spontenious remission in 2/3 patients Cellular immunity impaired Diagnosis: clinical, may see thrombosed vein on scraping by 15 scalpel Treatment: Trichloroacetic acid, imiquimod, canthraridin Cryotherapy, snip or shave excision Planter wart – consult dermatologist ( painful)

45 45 Genital Wart – Treatment Patient administered – Podofilox -0.5% BID x 3 days, off 4 days, repeat cycle x 4 – Imiquimod -5% cream (Aldara) HS, 3x/week, x 16 wks – Sinecatechins 15% ointment (Veregen) TID for maximum of 16 wks Provider administered – Cryotherapy – TCA – Podophylin resin 10-25% – Surgical or laser removal – Interferon alfa-2B (Intron-A)

46 46 Genital Herpes – Treatment Acyclovir (Zovirax) – Primary = 400 mg TID x 7 days, 200 mg 5x/day x 7 days – Recurrent = 400 mg TID x 5 days, 800 mg TID x 2 days – Suppression = 400 mg BID Famciclovir (Famvir) – Primary = 250 mg TID x 7 days – Recurrent = 125 mg BID x 5 days, 1 g BID x 1 day – Suppression = 250 mg BID Valacyclovir (Valtrex) – Primary = 1 g BID x 7 days – Recurrent = 1 g daily x 5 days, 500 mg BID x 3 days – Suppression = 500 mg or 1 g daily

47 47 Molluscum Contagiosum Caused by double-stranded DNA Poxvirus Spread by skin to skin contact and autoinoculation Umbilicated, firm, flesh-colored, domeshaped papules Children -Lesions anywhere except palms & soles Adults – Lesions mostly in genital area

48 48 Molluscum Contagiosum –Treatment Curettage– May cause scarring Cryosurgery Imiquimod 5% cream (Aldara)– TID x 5 days/wk x 1 month Cantharidin Cimetidine (Tagamet) 40 mg/kg/day x 2 months(children) Laser TCA peel q 2 weeks KOH 5%

49 49 Basal Cell Carcinoma Most common skin cancer Male > female Mostly in age > 40 85% occur in head/neck Clinical course is unpredictable – Can remain small for years or develop in growth spurts Subtypes Nodular-Most common,less aggressive Superficial– Plaque like Sclerosing– Rare Pigmented

50 50 Diagnosis by biopsy Excisional biopsy– Often adequate for small lesions Electrodesiccation/curettage, cryotherapy– Nodular & superficial < 6 mm in size, < 3 mm in depth

51 51 Moh’s micrographic surgery – Sclerosing, poorly defined margins – High-recurrence areas - Nose, eyelid – Large (> 2 cm) primary or recurrent BCCs – Lesions where conservation of tissue is important Radiation Chemotherapy Imiquimod 5% cream(Aldera) 5FU 5% ( Efudex)

52 52 Hypertrophy of sebaceous glands Diagnosis is clinical No treatment necessary May do electrosurgery or shave biopsy

53 53 Dome-shaped nodule,keratin-filled crater Resemble cutaneous squamous cell carcinoma Hair-bearing, sun-exposed skin Middle-aged, elderly adults, fair complexions Diagnosis: clinical, Excisional Biopsy Spontanious resolution

54 54 De Morgan spots Capillary proliferation in middle age Confused with amelanotic melanomas Treatment:Small – electrocauterization Large - shave excision - laser

55 55 Benign acquired melanocytic neoplasm -Asymmetric, irregular borders, multiple colors, and diameter >5 mm -Increases risk of melanoma Diagnosis: Clinical Management: Total body skin exam Life long follow up

56 56 ABCDE’s of Melanoma A – Asymmetry B – Border irregularity C – Color variegation D – Diameter greater than 6 mm E – Evolving (changing) Malignant Melanoma Thickness determines prognosis – Breslow microstage (mm) Measured depth of tumor invasion Most accurate – Clark level Histologic layer of dermis involvement

57 57 Malignant Melanoma Mostly found in non-Hispanic Caucasians Median age = 53 Men 1.5x > women Metastasize widely Risk Factors Large number of atypical nevi Other skin cancers Congenital giant nevus Family history of melanoma Immunosuppression UV radiation exposure Subtypes Superficial spreading – Most common – Upper back & legs in 40-50 y/o Nodular – Mostly men in 50-60 y/o Lentigo maligna – Facial location in 60-70 y/o Acral lentiginous – Digits & mucous membranes

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59 59 Stuck on appearance Benign Treatment: Not necessary Curettage +/- electrodesiccation Cryosurgery

60 60 Squamous cell carcinoma: papules, plaques, or nodules, and smooth, hyperkeratotic, or ulcerative lesions develop in sites of chronic wounds, chronic inflammation, or scarring Biopsy is necessary for diagnosis: Shave, punch, or excisional biopsies Treatment: Mohs surgery Actinic keratosis Squamous cell carcinoma

61 61 Photo Quiz

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70 70 References: AAFP Family Medicine Board Review Express, 2014 Phillips, Charles M. MD, Dept. of Medicine, Brody School of Medicine Usatine, Richard P MD, Dept. of Family Medicine, UTHSCSA Habif, Thomas Clinical Dermatology 5th Edition, 2009 Centers for Disease Control & Prevention,Sexually Transmitted Diseases Division Daniel BS, Borradori L, Hall RP 3rd, Murrell DF. Evidence-based management of bullous pemphigoid. Dermatol Clin 2011; 29:613. Joly P, Roujeau JC, Benichou J, et al. A comparison of oral and topical corticosteroids in patients with bullous pemphigoid. N Engl J Med 2002; 346:321. Joly P, Roujeau JC, Benichou J, et al. A comparison of two regimens of topical corticosteroids in the treatment of patients with bullous pemphigoid: a multicenter randomized study. J Invest Dermatol 2009; 129:1681. Murrell DF, Daniel BS, Joly P, et al. Definitions and outcome measures for bullous pemphigoid: recommendations by an international panel of experts. J Am Acad Dermatol 2012; 66:479. English DR, Armstrong BK, Kricker A, et al. Demographic characteristics, pigmentary and cutaneous risk factors for squamous cell carcinoma of the skin: a case-control study. Int J Cancer 1998; 76:628. Gloster HM Jr, Neal K. Skin cancer in skin of color. J Am Acad Dermatol 2006; 55:741. Asuquo ME, Ngim O, Ugare G, et al. Major dermatologic malignancies encountered in a teaching hospital surgical department in South Nigeria. Am J Clin Dermatol 2008; 9:383. Mora RG, Perniciaro C. Cancer of the skin in blacks. I. A review of 163 black patients with cutaneous squamous cell carcinoma. J Am Acad Dermatol 1981; 5:535. Fleischer AB Jr, Feldman SR, McConnell RC. The most common dermatologic problems identified by family physicians, 1990-1994. Fam Med 1997; 29:648. García-Hidalgo L, Orozco-Topete R, Gonzalez-Barranco J, et al. Dermatoses in 156 obese adults. Obes Res 1999; 7:299. Romano G, Moretti G, Di Benedetto A, et al. Skin lesions in diabetes mellitus: prevalence and clinical correlations. Diabetes Res Clin Pract 1998; 39:101. Nahass GT, Meyer AJ, Campbell SF, Heaney RM. Prevalence of cutaneous findings in hospitalized medical patients. J Am Acad Dermatol 1995; 33:207. Krowchuk DP, Bradham DD, Fleischer AB Jr. Dermatologic services provided to children and adolescents by primary care and other physicians in the United States. Pediatr Dermatol 1994; 11:199. Ernst E. The usage of complementary therapies by dermatological patients: a systematic review. Br J Dermatol 2000; 142:857. Gerbert B, Maurer T, Berger T, et al. Primary care physicians as gatekeepers in managed care. Primary care physicians' and dermatologists' skills at secondary prevention of skin cancer. Arch Dermatol 1996; 132:1030. Federman DG, Reid M, Feldman SR, et al. The primary care provider and the care of skin disease: the patient's perspective. Arch Dermatol 2001; 137:25. Gropper CA. An approach to clinical dermatologic diagnosis based on morphologic reaction patterns. Clin Cornerstone 2001; 4:1. Federman DG, Kirsner RS. The patient with skin disease: an approach for nondermatologists. Ostomy Wound Manage 2002; 48:22.

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