3 Seborreic KeratosisMost common benign cutaneous neoplasmOrigin unknownNo malignant potentialEasily and quickly removedVary in size shape, most ovalMost common on torso, lesser degree on faceIncreasing numbers with ageLeser Tre’lat Sign
4 NevusA benign, pigmented lesion that is not caused by any outside catalyst.There are many types of nevi; junctional, compound, dermal. Refer to textMain job is differentiating from dysplastic nevi which have malignant potential
6 What to do? When in doubt, remove it and send it to pathology. Do a conservative full excisionIf it just doesn’t look right, remove itThat’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
7 Actinic KeratosisCommon, sun induced, pre-malignant, changes that increase with ageMost common sites are forehead, shoulders, back, and dorsum of armsStart as an erythematous, rough, area, that forms a yellow crust.They are usually very symmetrical in distribution.
8 ……actinic keratosisBasal cell and other skin cancers can develop in these transitional type lesions.
10 Treatment of AK5-FU get incorporated in to rapidly reproducing cells and causes cell deathRetin-A has been helpfulCryotherapy for early lesions is effectiveLaser is excellent!Avoidance of further sun damage is paramountExplain the Course using 5-FU
12 ZosteriformLesions arranged along the cutaneous distribution of a spinal dermatomeThey are unilateral and denoteherpes zostermetastatic carcinoma of the breastdermatomal hemangiomatous growths of Sturge- Weber syndrome
14 Impetigo Level of Infection Port of Entry Susceptibility Epidermal superficial infectionPort of EntryCuts, abrasions, bug biteLikes moist areas (mouth, nose) and hot moist climatesSusceptibilityCommon in infants & childrenVERY Contagious!
15 Impetigo Symptoms Signs (Appearance) Itch Vesicular Toxins cause epidermal cleavaging of stratum corneumSome strains Strep. aureus cause thin-roofed bullaEvolves to pustules and become “honey-crusted”Satellite lesions on periphery (asymptomatic)
17 Impetigo Course of Disease Self-limiting !! But… may last weeks or monthsPost streptococcal glomerulonephritis may follow! Esp yo. Hematuria/proteinuria.Osteomyelitis, septic arthritis & pneumonia from otherwise seemingly innocuous impetigoNon-severe: controversial ?<1% body area
18 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/dayNon BullousDicloxicillin mg Qid X5-10 daysCloxicillin mgQ6h X 5-10 daysBactroban apply TID X 5-10 daysAzithromycin 500mg QD for 1 day then 250 mg X 4daysErythromycin mg TID X 5-10 days2nd Generation CephalosporinBactrobanBullousKeflex mg QID X 10 daysAugmentin 875/125 mg BID x 10 days or 500/125 mg TID X 10 daysNon-severe: controversial ?<1% body area
19 Erysipelas & Cellulitis Level of InfectionErysipelas epidermis & dermis (defined border).Acute inflammatory version of Cellulitis with streaking.Cellulitis dermis & subcutaneous tissue (diffuse)SymptomsArea is red, hot, swollen, tender, edema, ?malaiseperhaps vesicles, bullae, petechiae/purpuraPerhaps spread to lymphatics, “red streaks”lymph nodes may be swollen and tenderchills and fever may be presentDifferences between Erysipelas & Cellulitis are unimportant and unclearLymphangitis: 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.
20 Erysipelas & Cellulitis A portals of entryOpen lesion, trauma, surgical wound, athletes foot, IV drug use, insect bite, fissureRadiation therapyArms usually in young adults Legs usually in children and older adultsPuerperal sepsis common form before antibioticsPeripheral 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 infectionWhy extremities? (trauma prone)
21 Erysipelas & Cellulitis DiagnosisLargely Clinical:typical presentation and appearanceLabsCBCgram stain and culture wounds poor yieldneedle aspiration (5% yield), biopsy (20% yield), blood cultures (5% yield)Films (?)Plain / CT / MRI: underlying fasciitis or osteomyelitisReferrals: (?) Ortho if over joint
22 Erysipelas & Cellulitis Differential DiagnosisNecrotizing Fasciitis: deeper and much more virulent. Consider if patient doesn’t respond to antibiotics within 48 hours.Deep vein thrombosisCourseAntibioticspossible abscess (I&D), sepsis, fasciitis (rare)Erysipelas EndocarditisRecurrent cellulitis persistent lymphedema
23 Erysipelas & Cellulitis Differential DiagnosisNecrotizing Fasciitis: deeper and much more virulent. Consider if patient doesn’t respond to antibiotics within 48 hours.Deep vein thrombosisCourseAntibioticspossible abscess (I&D), sepsis, fasciitis (rare)Erysipelas EndocarditisRecurrent cellulitis persistent lymphedema
24 Erysipelas & Cellulitis InpatientIV methacillinase-resistant penicillin (nafcillin) or cephazolinConsider pseudomonas in immunocompromised patients--ticarcillin, piperacillinOthers: Elevate limbs, treat sourcesWarning: May get worse first day or two of tx. Draw on pt.Out vs. Inpatient:Fever, ToxicImmuncompromised (Diabetic, HIV positive, CA pt.(neutropenic patient)Circumferential
25 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
26 Cellulitis Pitfalls (cont.) Facial Cellulitis in adultsH. Flu in adult is rare and may be toxic with airway compromise. (usually >50yo) Admit & tx (cefuroxime IV)Facial Cellulitis in childrenPotentially serious !!!!If no obvious entry for, probably H. Flu? Meningitis (8% infants) ?tap.
27 Cellulitis Pitfalls (cont.) Cellulitis around the eyeDangerous !!!Orbital vs. Peri-orbital cellulitisPeriorbital (more common)Limited to eyelids in the preseptal regionTreat aggressively with IV abxOrbital is EMERGENCYInfection spreads both by extension and retrogradeH. Flu usualIV abx, admit, ? CT (globe displacement)
28 Cellulitis Pitfalls (cont.) Necrotizing FasciitisDangerous !!!S. pyrogenes or othersSx: painful, edema, necrosis, widespreadOcclusion of small blood vessels to gangrene (growth of anaerobes - eg Bacteroides).Risk factor: DMDx: x-rays show gasMortality 30% ! Surgical treatment
30 Animal Bites Cats- Pasteurella multocida, S. aureus Primary Antibiotic Augmentin 875mg BID x 10 daysAlternative- Cefuroxime 500 mg TID x 7dyas80% of all cat bites become infected!DO NOT USE KEFLEX!!!!!!
31 Animal Bites Dogs- Pasteurella mutlicoda,S. aureus Primary- Augmentin 875 mg BIDAlternative- Clindamycin 300 mg QID plus a flouroquinoloneONLY 5% become infected.
32 Tinea of the Foot Uncommon in women! Uncommon in prepubertal children Inevitable in immunocompromised patientsAcquired from locker-room floors and communal bathsOnce infected, patient becomes a carrier and is at risk for recurrenceTight fitting shoes and work-boots
34 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 moistureLamb’s wool between the toesTreat secondary infection!!!!! (staph & pseudomonas)
35 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: mg/kg po qd X 4 – 6 weeks. Max 1 g/d. Absorption is better with a fatty meal.
36 Tinea Cruris Warm, moist, dark, environment most conducive to growth If any dermatitis is treated withtopical steroids, it will initiallylook better and lead to what iscalled, “tinea incognito”
38 MelanomaA. 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 irregularC. More than one color is present in a moleD. It is larger than 5mm in diameter (the size of a pencil eraser
39 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
40 Pathologic StagingDepth of invasion offers the greatest prognostic value in determining survivalDepth of invasion determines need for therapy up and above surgical excision
41 Treatment Wide excision Regional lymph node dissection for higher stage diseaseChemotherapy for higher stage disease
43 Psoriasis Extensor surfaces most common Palms and soles not commonly involved but can be. R/O Reiter SyndromeLocalized plaques may be confused with eczema or seborrheic dermatitisGuttate form may be confused with secondary syphilis or pityriasis rosea
44 Principles of Treatment Control stressStress reduction techniques are effective in controlling flares in certain patientsDetermine end of treatmentPatients perceive discoloration after clearing plaques as continued disease
45 Principles of Treatment Calcipotriol (Dovonex)Discovered in 1985 by chance-Women taking Vitamin D for osteoporosis noted marked improvement in psoriasisVitamin D3 analogueInhibits cell proliferation and induces terminal differentiationInhibits epidermal cell proliferationSafe and effectiveApplied BID in amounts up to 100 grams per weekRx for 6-8 weeks gives 60% improvementDoes not effect ca++ or bone metabolism
46 Principles of Treatment Topical steroidsControl itchingResults very gratifying earlyTachyphylaxis occursSkin atrophy and tangelectasias limit extensive useUseful for treating intertriginous plaques and inflamed areasPlastic occlusion potentiatesDiprolene, Temovate
47 Principles of Treatment Intralesional steroidsKenalog 5-10 mg.Ml (atrophy with 10 mg strength)Anthralin (Anthra-Derm)Used only for chronic plaquesMessy stains long treatment timesBest used in combination with UVB
48 Principles of Treatment PUVAPsoralens and UVA radiation in combinationMethotrexateCyclosporineRetinoidsEtretinate (Tegison)Hydrea
51 Contact Dermatitiscontact 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.
52 Contact Dermatitis Rhus dermatitis – (allergic) poison ivy, poison oak and poison sumac account for more cases of allergic contact dermatitis than all other contactants combinedOccurs from contact with the leaf,or internal parts of the stem or rootsOccurs from direct contact with the oleo resinCan not be spread via the blister fluid of current lesions
53 Contact Dermatitis Metal dermatitis Nickel is the most common contact allergenWomen >menJewelry most often the source
54 Contact Dermatitis Diagnosis – History – persistent questioning may eventually uncover the offending antigenDate of onsetRelationship to workSkin care productsJewelryPhysical examDistributionTypes of lesionsPatch testing – indicated in cases in which inflammation persists despite avoidance and appropriate topical therapy
55 Contact Dermatitis Fundamental principals of dermatological therapy : Avoid the offending agentWet lesions driedDry lesions hydratedInflammation treated with corticosteroids
56 Contact Dermatitis Treatment – the aim of treatment is to decrease erythema, pruritis and edemaPrevent secondary infection – keep cleanRemove/avoid causative agentsTopical steroidsOozing lesions should be dried with Burrow’s solution compresses 3 to 4 times dailyOral prednisone may be necessary for severe cases (tapering dose)
57 Contact Dermatitis Wide variation in potency Vehicle affects potency Topical corticosteroid precautionsWide variation in potencyVehicle affects potencyOintments more potent than creamsOcclusive dressing increases potency (do not use ointments – folliculitis)Adverse effects –AtrophyTelangiectasia /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.