Dermatologic Board Review Lane Bower, MHSc, PA-C

Which is the SK?

Seborreic Keratosis Most common benign cutaneous neoplasm Origin unknown No malignant potential Easily and quickly removed Vary in size shape, most oval Most common on torso, lesser degree on face Increasing numbers with age Leser Tre’lat Sign

Nevus A benign, pigmented lesion that is not caused by any outside catalyst. There are many types of nevi; junctional, compound, dermal. Refer to text Main job is differentiating from dysplastic nevi which have malignant potential

What to do? When in doubt, remove it and send it to pathology. Do a conservative full excision If it just doesn’t look right, remove it That’s the thing with dysplastic nevi, if you can’t make up your mind as to whether it is benign or a possible melanoma, it is probably the middle ground of dyplastic

Actinic Keratosis Common, sun induced, pre-malignant, changes that increase with age Most common sites are forehead, shoulders, back, and dorsum of arms Start as an erythematous, rough, area, that forms a yellow crust. They are usually very symmetrical in distribution.

……actinic keratosis Basal cell and other skin cancers can develop in these transitional type lesions.

Treatment of AK 5-FU get incorporated in to rapidly reproducing cells and causes cell death Retin-A has been helpful Cryotherapy for early lesions is effective Laser is excellent! Avoidance of further sun damage is paramount Explain the Course using 5-FU

Who’s the Mole?

Zosteriform Lesions arranged along the cutaneous distribution of a spinal dermatome They are unilateral and denote herpes zoster metastatic carcinoma of the breast dermatomal hemangiomatous growths of Sturge- Weber syndrome

Impetigo Level of Infection Port of Entry Susceptibility Epidermal superficial infection Port of Entry Cuts, abrasions, bug bite Likes moist areas (mouth, nose) and hot moist climates Susceptibility Common in infants & children VERY Contagious!

Impetigo Symptoms Signs (Appearance) Itch Vesicular Toxins cause epidermal cleavaging of stratum corneum Some strains Strep. aureus cause thin-roofed bulla Evolves to pustules and become “honey-crusted” Satellite lesions on periphery (asymptomatic)

Impetigo Causative Agents Staphylococcus aureus (most usual) ? 2wk incubation Streptococcus pyrogenes (occ. alone OR together)

Impetigo Course of Disease Self-limiting !! But… may last weeks or months Post streptococcal glomerulonephritis may follow! Esp. 2 - 4 yo. Hematuria/proteinuria. Osteomyelitis, septic arthritis & pneumonia from otherwise seemingly innocuous impetigo Non-severe: controversial ?<1% body area

Impetigo Treatment (cover both Staph & Strep) Non Bullous Bullous All Wash with anti-bacterial soap 1-2/d to remove crusts. Wash entire body to prevent spread 1- 2/day Non Bullous Dicloxicillin 250-500 mg Qid X5-10 days Cloxicillin 500-1000 mg Q6h X 5-10 days Bactroban apply TID X 5-10 days Azithromycin 500mg QD for 1 day then 250 mg X 4days Erythromycin 250-500 mg TID X 5-10 days 2nd Generation Cephalosporin Bactroban Bullous Keflex 250-500 mg QID X 10 days Augmentin 875/125 mg BID x 10 days or 500/125 mg TID X 10 days Non-severe: controversial ?<1% body area

Erysipelas & Cellulitis Level of Infection Erysipelas  epidermis & dermis (defined border). Acute inflammatory version of Cellulitis with streaking. Cellulitis  dermis & subcutaneous tissue (diffuse) Symptoms Area is red, hot, swollen, tender, edema, ?malaise perhaps vesicles, bullae, petechiae/purpura Perhaps spread to lymphatics, “red streaks” lymph nodes may be swollen and tender chills and fever may be present Differences between Erysipelas & Cellulitis are unimportant and unclear Lymphangitis: Usually stretococci. Red warm irregular , tender streaks. Common fever, chills, headache, tachycardia. Leukocytosis usual (sometimes marked). Course: rarely suppuration, necrosis and ulceration. Lymphadenitis: Regional: usually streptococcal, TB or mycobactial (non-TB), tularemia, plague, cat-scratch dz, primary syphilis, herpes simplex. Generalized: mononucleosis, cytomegalovirus, toxoplasmosis, brucellosis, secondary syphillis, disseminated histoplamosis.

Erysipelas & Cellulitis A portals of entry Open lesion, trauma, surgical wound, athletes foot, IV drug use, insect bite, fissure Radiation therapy Arms usually in young adults Legs usually in children and older adults Puerperal sepsis common form before antibiotics Peripheral vascular disease is a common underlying factor ****** ***** Strep pyrogenes: enzymes bread down cellular components which would otherwise contain and localize the inflammation (streptokinase, Dnase, hyaluronidase) Groups B, C , D or G-beta hemolytic less common to cause infection Why extremities? (trauma prone)

Erysipelas & Cellulitis Diagnosis Largely Clinical: typical presentation and appearance Labs CBC gram stain and culture wounds poor yield needle aspiration (5% yield), biopsy (20% yield), blood cultures (5% yield) Films (?) Plain / CT / MRI: underlying fasciitis or osteomyelitis Referrals: (?) Ortho if over joint

Erysipelas & Cellulitis Differential Diagnosis Necrotizing Fasciitis: deeper and much more virulent. Consider if patient doesn’t respond to antibiotics within 48 hours. Deep vein thrombosis Course Antibiotics possible abscess (I&D), sepsis, fasciitis (rare) Erysipelas  Endocarditis Recurrent cellulitis  persistent lymphedema

Erysipelas & Cellulitis Differential Diagnosis Necrotizing Fasciitis: deeper and much more virulent. Consider if patient doesn’t respond to antibiotics within 48 hours. Deep vein thrombosis Course Antibiotics possible abscess (I&D), sepsis, fasciitis (rare) Erysipelas  Endocarditis Recurrent cellulitis  persistent lymphedema

Erysipelas & Cellulitis Inpatient IV methacillinase-resistant penicillin (nafcillin) or cephazolin Consider pseudomonas in immunocompromised patients--ticarcillin, piperacillin Others: Elevate limbs, treat sources Warning: May get worse first day or two of tx. Draw on pt. Out vs. Inpatient: Fever, Toxic Immuncompromised (Diabetic, HIV positive, CA pt.(neutropenic patient) Circumferential

Cellulitis Pitfalls Necrosis Devitalized tissue (tense, cyanotic, necrotic, bronzing of the skin, blanched) will not be perfused, so antibiotics will not get to the site. If not improvement on ABX, consider devitalized tissue & surgical debridement

Cellulitis Pitfalls (cont.) Facial Cellulitis in adults H. Flu in adult is rare and may be toxic with airway compromise. (usually >50yo) Admit & tx (cefuroxime IV) Facial Cellulitis in children Potentially serious !!!! If no obvious entry for, probably H. Flu ? Meningitis (8% infants) ?tap.

Cellulitis Pitfalls (cont.) Cellulitis around the eye Dangerous !!! Orbital vs. Peri-orbital cellulitis Periorbital (more common) Limited to eyelids in the preseptal region Treat aggressively with IV abx Orbital is EMERGENCY Infection spreads both by extension and retrograde H. Flu usual IV abx, admit, ? CT (globe displacement)

Cellulitis Pitfalls (cont.) Necrotizing Fasciitis Dangerous !!! S. pyrogenes or others Sx: painful, edema, necrosis, widespread Occlusion of small blood vessels to gangrene (growth of anaerobes - eg Bacteroides). Risk factor: DM Dx: x-rays show gas Mortality 30% ! Surgical treatment

Upper lid avulsion

Animal Bites Cats- Pasteurella multocida, S. aureus Primary Antibiotic Augmentin 875mg BID x 10 days Alternative- Cefuroxime 500 mg TID x 7dyas 80% of all cat bites become infected! DO NOT USE KEFLEX!!!!!!

Animal Bites Dogs- Pasteurella mutlicoda,S. aureus Primary- Augmentin 875 mg BID Alternative- Clindamycin 300 mg QID plus a flouroquinolone ONLY 5% become infected.

Tinea of the Foot Uncommon in women! Uncommon in prepubertal children Inevitable in immunocompromised patients Acquired from locker-room floors and communal baths Once infected, patient becomes a carrier and is at risk for recurrence Tight fitting shoes and work-boots

Tinea Pedis

Treatment Promote dryness Drysol 20% (aluminum chloride) H.S. Topical antifungal (Loprox, Lotrimin, Spectazole) Sometimes oral if refractory (Lamisil tablets) Shoes that “breathe” and socks that wick away moisture Lamb’s wool between the toes Treat secondary infection!!!!! (staph & pseudomonas)

Special Treatment Considerations Tinea Capitis is not responsive to topical agents. You must use an oral drug such as Giseofulvin 500 mg. po qd. Pediatric dosing: 10-20 mg/kg po qd X 4 – 6 weeks. Max 1 g/d. Absorption is better with a fatty meal.

Tinea Cruris Warm, moist, dark, environment most conducive to growth If any dermatitis is treated with topical steroids, it will initially look better and lead to what is called, “tinea incognito”

How Do We Know?

Melanoma A. One-half of the mole does not match the other half (i.e. it is asymmetric) B. The edge (border) of the mole is jagged or irregular C. More than one color is present in a mole D. It is larger than 5mm in diameter (the size of a pencil eraser

How Can I Determine My Personal Risk? It is estimated that 1 out of 7 people in the United States will develop some form of this cancer during their lifetime. One serious sunburn can increase the risk by as much as 50%. These early studies are coming into question. Risk determination is complex

Pathologic Staging Depth of invasion offers the greatest prognostic value in determining survival Depth of invasion determines need for therapy up and above surgical excision

Treatment Wide excision Regional lymph node dissection for higher stage disease Chemotherapy for higher stage disease

Psoriasis Extensor surfaces most common Palms and soles not commonly involved but can be. R/O Reiter Syndrome Localized plaques may be confused with eczema or seborrheic dermatitis Guttate form may be confused with secondary syphilis or pityriasis rosea

Principles of Treatment Control stress Stress reduction techniques are effective in controlling flares in certain patients Determine end of treatment Patients perceive discoloration after clearing plaques as continued disease

Principles of Treatment Calcipotriol (Dovonex) Discovered in 1985 by chance-Women taking Vitamin D for osteoporosis noted marked improvement in psoriasis Vitamin D3 analogue Inhibits cell proliferation and induces terminal differentiation Inhibits epidermal cell proliferation Safe and effective Applied BID in amounts up to 100 grams per week Rx for 6-8 weeks gives 60% improvement Does not effect ca++ or bone metabolism

Principles of Treatment Topical steroids Control itching Results very gratifying early Tachyphylaxis occurs Skin atrophy and tangelectasias limit extensive use Useful for treating intertriginous plaques and inflamed areas Plastic occlusion potentiates Diprolene, Temovate

Principles of Treatment Intralesional steroids Kenalog 5-10 mg.Ml (atrophy with 10 mg strength) Anthralin (Anthra-Derm) Used only for chronic plaques Messy stains long treatment times Best used in combination with UVB

Principles of Treatment PUVA Psoralens and UVA radiation in combination Methotrexate Cyclosporine Retinoids Etretinate (Tegison) Hydrea

Psoralin UVA Treatment

UVB Treatment – Before and After

Contact Dermatitis contact dermatitis, Skin rash resulting from exposure to either an irritating or allergic substance. In the first type, an irritant, as detergent or acid, causes a sore much like a burn. In the allergic type, the reaction is delayed. Symptoms are swelling, blisters, and large amounts of fluid in the body tissues. Poison ivy is a common example of this type.

Contact Dermatitis Rhus dermatitis – (allergic) poison ivy, poison oak and poison sumac account for more cases of allergic contact dermatitis than all other contactants combined Occurs from contact with the leaf,or internal parts of the stem or roots Occurs from direct contact with the oleo resin Can not be spread via the blister fluid of current lesions

Contact Dermatitis Metal dermatitis Nickel is the most common contact allergen Women >men Jewelry most often the source

Contact Dermatitis Diagnosis – History – persistent questioning may eventually uncover the offending antigen Date of onset Relationship to work Skin care products Jewelry Physical exam Distribution Types of lesions Patch testing – indicated in cases in which inflammation persists despite avoidance and appropriate topical therapy

Contact Dermatitis Fundamental principals of dermatological therapy : Avoid the offending agent Wet lesions dried Dry lesions hydrated Inflammation treated with corticosteroids

Contact Dermatitis Treatment – the aim of treatment is to decrease erythema, pruritis and edema Prevent secondary infection – keep clean Remove/avoid causative agents Topical steroids Oozing lesions should be dried with Burrow’s solution compresses 3 to 4 times daily Oral prednisone may be necessary for severe cases (tapering dose)

Contact Dermatitis Wide variation in potency Vehicle affects potency Topical corticosteroid precautions Wide variation in potency Vehicle affects potency Ointments more potent than creams Occlusive dressing increases potency (do not use ointments – folliculitis) Adverse effects – Atrophy Telangiectasia /tlan'je-ekta'zh/, permanent widening of groups of superficial capillaries and small vessels (venules). Common causes are damage due to excess sunlight, some skin diseases, as rosacea, too-high levels of female hormone, and collagen blood vessel diseases.

THE END