Dermatology

Justin Love, MPAS, PA-C Loma Linda University Department of Dermatology

Description
• Why is the description so important in dermatology? – Allows for proper communication between specialties – Will prioritize the patient placement into clinic or when to be seen as inpatients – Can sometimes make the Dx over the phone • Two phrases to avoid – Lesion, Mass, growth – can sometimes be confusing or misleading – “Macuolpapular” – implies drug eruption, typically all rashes have a macular component, and a papular component (active vs inactive)

Morphology - Primary
• • • • • • • • • Macule - flat, nonpalpable, <1.0cm Papule - raised, palpable, <1.0cm Patch - flat, nonpalpable, >1.0cm Plaque - raised, palpable, >1.0cm Vesicle – fluid filler blister, <1.0cm Bulla – fluid fill blister, >1.0cm Nodule – firm/solid, deeper than a papule Cyst – fluid filled nodule Pustule – pus filled papule/plaque

• Macule: non-palpable, < 1 cm

Patch: non-palpable, > 1 cm

Papule: palpable, < 1 cm

Plaque: palpable, > 1 cm

Nodule: A firm (indurated) lesion that is thicker or deeper than the average papule or plaque

Cyst: a firm filled nodule with an associated pore/ostia. >1cm .

Vesicle: Elevated with clear fluid. < 1 cm .

Bulla: elevated with clear fluid. > 1 cm .

Pustule: a follicular based pus filled papule .

Secondary • • • • • • • Erosion Ulcer Excoriation Fissure Scale Crust Scar .Morphology .

Erosion: superficial loss of tissue .

Ulceration: reaches at least the depth of the dermis .

similar to abrasion but self inflicted .Excoriation: Scratched.

groove.Fissure: cleft. cracked usually linear .

flaky rough to touch .Scale: shedding.

Crust: thick. rough to touch .

sore. surgery . burn.Scar: healed wound.

Arrangement • • • • • • • Linear Round/nummular – no central clearing Annular – central clearing Iris/targetoid Group/herpetiform Zosteriform/dermatomal Reticular .

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Atopic Dermatitis • EPIDEMIOLOGY 90% of patients with AD have disease onset before the age of 5 years AD is thought to arise from an interaction between environmental and genetic factors maternal history of atopy was found to be one of the strongest risk factors .

and increased IgE levels. reported a positive family history of atopy – AD related to defective filaggrin appears to be inherited in a semidominant fashion. 59% had respiratory allergies and 73% . predisposed to asthma(AD.Pathogensis • Genetics – study of 372 AD patients. asthma and allergic rhinitis) .

Pathogensis • Immunology – Respiratory allergy is commonly (70% of patients) associated with childhood and adult AD – most frequent allergens are dust mites. animal dander and molds – Food allergies occur primarily in infants and children with moderate to severe AD – Microbial agents. especially Staphylococcus aureus. colonize over 90% of AD skin lesions – predisposed to viral (herpes simplex virus. molluscum contagiosum and human papillomavirus) and superficial fungal (Trichophyton rubrum and Malassezia species) skin infections . pollen.

edematous papules and plaques. hyperkeratotic plaques with lichenification as well as prurigo nodularis. erythematous. . oozing and serous crusting can be seen. vesicles. often with secondary excoriations. childhood and adulthood • Acute predominates in infantile form. with scaling and excoriations as secondary changes. • Chronic AD is characterized by thickened. whereas chronic changes typify adult intensely pruritic. • Subacute skin lesions appear as erythematous papules and plaques.Clinical Features • AD skin is characterized by severe dryness with an impaired barrier function of the stratum corneum • higher transepidermal water loss and lower skin surface hydration levels • Three classical stages of AD–infantile.

scrotal. etc .Atopic Dermatitis • 3 stages – infantile 2mo – 2y • seborrheic dermatitis more likely if <2mo • clue: SD. nipple. pt comfortable – childhood 2y – 10y – adult • pruritus is hallmark – precedes rash – “the itch that rashes” itchscratch cycle • distribution – nummular = coin shaped – hand / foot dermatitis • eczematous. scaly • dy idrotic = “tapioca pudding-like” vessicles on lateral fingers – papular • usually in darker skinned pts – location specific = eyelid.

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wrists. subsequent repeated washing scalp.Infantile Atopic Dermatitis • facial involvement – erythema and scaling of cheeks – chin 2/2 drooling. neck. extensor extremeties • child’s capacity to scratch – spares diaper area – crawling extensor surfaces • exudative • development – normal growth if < 50% of BSA – impaired growth with more extensive disease . forehead.

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RAST is high IgE high s . pollens. relationship between high IgE levels to foods.Pathology & Diagnostic Test • The histologic features of AD vary according to stage of the lesion sampled • Peripheral blood eosinophilia is often seen in patients with ADneither sensitive nor specific enough to be of diagnostic utility • Total IgE levels-elevated. minor diagnostic criterion • radioallergosorbent testing (RAST)-elevated. dust mites & aggravation AD is controversial.

family h/o atopy – asthma.Diagnostic Criteria MAJOR (3+) • pruritus • typical morphology. AD . hay fever. extensor MINOR (3+) • • • • • • • • • • • • • • • • • • • • • • xerosis Dry skin ichthyosis/hyperlinear palms/keratosis pilaris formation IgE reactivity (RAST test serum IgE early age of onset cutaneous infxn tendency tendency to non-specific hand/foot dermatitis nipple eczema cheilitis recurrent conjunctivitis Dennie Morgan folds keratoconus anterior subcapsular cataracts orbital darkening facial pallor / erythema pityriasis alba itch when sweating intolerance to wool and lipid solvents perifollicular accentuation food hypersensitivity environmental &/or emotional factors infl course white dermatographism of dry. distribution – adults: flexural lichenification – infants: facial. f • chronically relapsing • personal.

and wheezing in early childhood in at risk infants • no clear evidence – supporting the use of soy-based infant formulas for the purpose of allergy prevention – after 4-6 mo. including highly allergenic foods. has a significant protective effect .Recent Literature • maternal dietary restrictions during pregnancy or lactation does not prevent atopic disease • exclusive breastfeeding for at least 4 mo.s. cow’ s milk allergy. delaying solid food introduction.s prevents or delays the occurrence of atopic dermatitis.

indurated plaques • growth retardation – > 50% BSA involvement – rebound growth with treatment . eyelids. flexor wrists. face common sites • lichenified.Childhood Atopic Dermatitis • less exudative • atecubital / popliteal fossae.

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Childhood Atopic Dermatitis • prognosis – 40% resolve by age 5 – 40% carry to adulthood • unfavorable prognostic factors – widespread dermatitis in childhood – family h/o AD – associated bronchial asthma – early age of onset – female sex – persistent dry / itchy skin in adult life .

and hypopigmentations – papular variants . prurigo-like nodules • darker skinned individuals – hyper. around neck. scaly.Adult / Adolescent AD • erythematous. papular. eyelids • lichenification. flexor wrists. exudative or lichenified plaques • classic sites = antecubital / popliteal fossae.

Adult / Adolescent AD • pruritus occurs in crises or paroxysms • flares triggered by heat or stress – decreased itch perception – difficulty delivering sweat to surface and in transepidermal water loss (TEWL) • improvement occurs with time. uncommon after middle life • new onset HIV may serve as trigger r/o if high risk .

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scales. upper arms. colorless patches of skin appear on the face. • Ichthyosis vulgaris • Dennie–Morgan lines • Palmoplantar hyperlinearity • Pityriasis alba Round or oval. • Lichenification • Infection • Edema • Complications of treatment . neck.Associated clinical findings and complications • • • Pruritus Xerosis Keratosis pilaris protein in the skin called keratin forms hard plugs within hair follicles. and upper middle of the body.

follicular erythematous lesions – outer aspects of upper arms legs.Associated clinical findings • pityriasis alba – poorly marginated. hypopigmented slightly scaly patches on cheeks – typically in young children • keratosis pilaris – horny. agminated. buttocks grouped together • hyperkeratosis. hyperpigmentation dirty neck . cheeks.

keratosis pilaris .

pityriasis alba .

Ophthalmologic Abnormalities Atopic Dermatitis • 10% develop cataracts – anterior most common – posterior subcapsular well-established complication of systemic steroids – more common in severe atopic dermatitis • 1% develop keratoconus – elongation and protrusion of the corneal surface secondary to – considered to be 2/2 continuous rubbing of eye or as a degenerative change – onset usually p/ adolescence .

Staphylococcus Colonization • staph colonization nearly universal – lesion superinfection common – antibiotic of benefit during flares • recovered in – 90+% lesions vs 76% uninvolved skin – 79% anterior nares in atopics vs 10% nonatopics • staph exacerbates atopic derm – organism superantigen production T-cell activation – organism superantigen production alternative glucocorticoid receptor expression topical steroid resistance .

electrosurgery.Superinfection Atopic dermatitis • flat warts / molluscum contagiosum – chemical treatments (salicylic acid. curretage for molluscum) often required to clear lesions • dermatophyte infections • widespread vaccinia infxn (eczema vaccinia) – vaccinations against smallpox contraindicated – even if atopic dermatitis in remission • coxsackie A16 virus (eczema cosackium) . cantharidin) poorly tolerated – destruction (cryosurgery.

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areas pt is scratching at – lichenification / pigmentation will take mo.s-yr. pat dry after shower antihistamines treat erythematous pruritic areas – truly active. fillagrin deficiency) – moisturize after TCS avoid hot showers. Vanacream) – wear white cotton. avoid wool .s to resolve avoid potential allergens – bathe with allergen free cleanser (Cetaphil.Management • • • • • • parental education key heavy emollients – barrier disruption (ceramide.

Management TCS • topical corticosteroids hypothalamic-pituitary-adrenal – AE: irreversible atrophy. They are a type of immunosuppressant . which is part of the body's immune response. days not using TCS – approved for children > 2y block the inflammation process. This can relieve itching and improve the rash of atopic dermatitis.controls reactions to stress and regulates processes • avoid mid-high potency on face/axillae/groin – interrupted therapy • AE • tachyphylaxisrapid decrease in the response to a drug due to previous (long term) exposure – ointments better absorption. more effective than creams – better to tx hi potency x short term than lo potency x long term – occlusion efficacy (but also risks (wet wraps)) • topical calcineurin inhibitors (Elidel. Protopic) – steroid sparing – great for facial involvement. striae. systemic absorption with HPA axis inhibition major part neuroendocrine syst.

recurrent sinopulmonary infxns susceptibility – Netherton's syndrome = atopic diathesis. thrombocytopenia. PUVA) • immunosuppresants (cyclosporine) • avoid sy stemic steroids…rebound flare . trichorrhexis invaginata • phototherapy (UVB. genodermatosis – Wiskott .Management SEVERE / RECALCITRANT CASES • work-up for associated immunodeficiency.Aldrich = eczema. pyogenic infxn – hyper IgE (Job) syndrome = eczema. icthyosiform erythroderma (icthyosis linearis circumflexa).

Contact Dermatitis Irritant and Allergic .

IL-6 and IL-1B .Contact dermatitis Irritant Contact • localized to contact site (hands. face) • direct cytotoxic effect inflammatory response. not immunologic • Pathogenesis – Penetration through permeability barrier – Mild damage to keratinocytes – Release of mediators of inflammation • TNF-a.

often an occupational accident • Must be a potent irritant. bullae and necrosis . most commonly acids and alkaline solutions resulting in chemical burns • Symptoms include burning. stinging and soreness • Physical signs: erythema.Irritant Contact dermatitis ICD Subtypes Acute ICD • Developes 2/2 potent irritant exposure. edema.

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pustules. caterers. benzalkonium chloride. ethylene oxide rxn not seen until 8-24h after exposure mimics ACD. redness. however burning > pruritus wet chemical environments hairdressers. metal workers scaling.ICD Subtypes • acute delayed ICD – – – – – – – – retarded inflammatory response anthralin. erosions begins under occlusive jewelry • irritant reaction ICD . vesicles.

superficially cracked intense pruritus . pain – Examples include soaps.ICD Subtypes • cumulative ICD – multiple subthreshold insults. • asteatotic dermatitis / eczema craquele – – – – dry winter months elderly. household products. frequently bathe without remoisturization dry icthyosiform scale. water... without sufficient time for barrier restoration – lichenification/hyperkeratosis – pruritus.

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philtrum and submental regions – lichenification. hyperkeratosis hyperpigmented. tars. cutting and metal fluids. naphthalenes – Chloracne – Consider when folliculitis or acneiform lesions develop in setting outside of typical acne – Developes in irritant exposed sensitive skin – Distinguish from photoallergic reactions by looking for involvement of upper eyelids. acanthosis. greases.ICD Subtypes • pustular acneiform ICD – metals. mineral oil. croton oil. velvety plaques • airborne ICD • frictional ICD thickening of the stratum corneum .

concurrent chromate ACD) • metal salts – cobalt – mercury bluish linear pigmentation tongue. gums – thimerosal • alcohols • detergents/cleansers • disinfectants – ethylene oxide – aldehydes.Irritants • acids – inorganic > organic • solvents – benzene petechial eruption (aplastic anemia) – turpentine • alkalis – more painful/destructive (with exception of HF) – wet cement (+/. iodines – quaternium ammonium salts • plastics .

incontinent pts – drool angular cheilitis (+/. feces diaper rash. Io (green.candida) • plants – spurges (poinsetta) milky sap – oxalate crystals (tulips. daffodils) bulb sorter’s disease • caterpillars = puss (wooly).candida) • bodily fluids – urine.Irritants • food • water = universal solvent – maceration intertrigo (+/. red stripe) .

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Allergic contact dermatitis ACD Pathogenesis • type IV delayed type hypersensitivity reaction • allergen specific rxn • requires prior sensitization – initial contact sensitization primed T-cell milieu – low concentration of allergen cytokine release eczematous dermatitis 8-96h after exposure • allergens – – – – > 3000 chemicals known to cause ACD low MW lipid soluble low concentration required .

ACD Clinical • rash initially localized to site of contact • may spread to other areas (in contrast to ICD) • Id/autoeczematization • activated epidermal T cells migrate locally or through the circulation dermatitis at remote sites (hypersensitivity) • most often seen in ACD assoc c/ stasis dermatitis • symmetric .

Id to Poison Ivy .

urticarial to milk toilet seat neosporin / mastisol / sutures / anesthetics .

acrylates essential oils. thiuram. fragrance. botanicals . cocamidopropyl betane thiuram (latex) gluteraldehyde (disinfectant.Occupations at risk for ACD Textile workers Cashiers Construction Shoemakers Hairdressers Medical Dentistry Masseuse disperse dyes. cold sterilizer). cobalt formaldehyde. formaldehyde nickel chromate. chromate PPD.

imidazolidinyl urea. quinolone mix • steroids = budesonide.Patch Test • True test – 2 panels = 23 allergens + 1 control – 3rd panel = expanded allergen series • preservatives = diazolidinyl urea. tixocortol-21-pivalate • North American Contact Dermatitis Group (NACDG) = 45 allergens • European Standard= 26 allergens .

neomycin – distinguish irritant from allergic • common mild irritant allergens = nickel. PPD. glutaraldehyde. formaldehyde. gold. corticosteroids. potassium dichromate.Patch Test • 1st read = 48h (remove patches) • 2nd read = 72h – 1wk – delayed response = bacitracin. carba. chlorhexidine. disperse blue dyes. cocamidopropyl betaine • many allergens near irritant threshold • irritant decrescendo response = in severity between reads .

contactderm.Management • Avoidance • Photoprotection for photodermatitis • Education • American Contact Dermatitis Society (www.org) allergen avoidance lists • Contact Allergen Replacement Database (CARD) safe shopping lists • topical/systemic steroids • antihistamines • wound care .

Top 10 Allergens METALS • gold • cobalt • nickel • (thimerosol) PRESERVATIVES • formaldehyde • quaternium-15 • thimerosal ANTIBIOTICS • neomycin • bacitracin FRAGRANCES • balsam of Peru • fragrance mix .

Nickel .

Nickel • most common allergen • role of ear piercing sensitization • classic locale – periumbilical dermatitis • replace buttons or sew fabric over divot • avoid nickel belt-buckles – earring dermatitis • bilateral pseudotumor of the earlobe – eyelid dermatitis (eyelash curlers) • In children may lead to widespread lichenoid papular eruption • Dimethylglyoxime test can identify objects that release nickel .

Neomycin .

bacitracin and neomycin • Neomycin is also found in: – Hemorrhoid creams. otic and ophthalmic preparations and in topical steroid preparations • co-reactivity with bacitracin • cross-reactivity with aminoglycosides .Neomycin • 2nd most common allergen • Neosporin aka “triple antibiotic ointment” polymyxin B.

Poison Ivy microvesicular .

spp. let it be” poison sumac contains 7-13 leaflets per stalk poison ivy has pointed tips. Toxicodendron • distinct genus from Rhus . poison oak has round tip • family Anacardiaceae.Poison Ivy/Oak/Sumac • plant ACD • structure – – – – poison oak/ivy contain 3-5 leaflets per stalk “leaves of 3.

- . but alows pt to sleep. • potent topical corticosteroids only help if applied during the earliest stages of the outbreak-no vesicles or blisters • Systemic corticosteroids-very effective dose of 1–2 mg/kg/day.Treatment • Wash body should be thoroughly washed with copious amounts of water. but early use of soap may expand the area of resin on the body. Soap may be used afterwards. slowly tapered over 2-3 weeks • Antihistamine doesn't take care of pruritus.

SEBORRHEIC DERMATITIS • confined to skin regions with high sebum production &large body folds • link to sebum overproduction and the commensal yeast Malassezia .

Parkinson‟s.SEBORRHEIC DERMATITIS • Epidemiology – Infantile-self-limited and confined to the first 3 months of life – Adult-chronic with a peak in the fourth to sixth decades – no indication of a genetic predisposition • Associated with? • HIV. mood disorders .

overenthusiastic treatment) • a predilection for areas rich in sebaceous glands. less often. inguinal and inframammary folds. e. vesiculation and crusting may occur but are rare and mostly due to irritation (e. the intertriginous areas (e.Clinical Features • sharply demarcated patches or thin plaques that vary from pink– yellow to dull red to red–brown in color with bran-like to flaky "greasy" scales. presternal region and. face. and umbilicus) • a mild course with little or moderate discomfort • Immunocompromised? . the scalp. the axillae. ears.g.g.g.

Infantile seborrheic dermatitis • • • 1 week after birth and may persist for several months mild greasy scales adherent to the vertex and anterior fontanelle regions coherent scaly and crusty mass covering most of the scalp („cradle cap‟) • • axillae and inguinal folds Superimposed infection with Candida species may occur .

Adult seborrheic dermatitis

less often on central upper chest and the intertriginous areas slight to moderate fine white or greasy scaling of the scalp and terminal hair-bearing areas of the face, without significant erythema or irritation symmetric: forehead, medial portions of the eyebrows, upper eyelids, nasolabial folds and lateral aspects of the nose, retroauricular areas, and occasionally the occiput and neck

SEBORRHEIC DERMATITIS
• DDX
– AD, Irritant diaper dermatitis, Infantile psoriasis, Langerhans cell histiocytosis, Wiskott–Aldrich syndrome, tinea capitis, psoriasis,
systemic lupus erythematosus, rosacea

SEBORRHEIC DERMATITIS
• Infantile seborrheic dermatitis – bathing and the application of emollients – Ketoconazole cream (2%)if persistent – Short courses of lowpotency topical corticosteroids may be used initially to suppress inflammation – Avoidance-strong keratolytic shampoos, or mechanical measures • Adult seborrheic dermatitis – topical azoles ketoconazoleshampoo/cream – initial stages- low-potency topical corticosteroids & emollients – Second-line-zinc pyrithione & tar shampoos

NUMMULAR DERMATITIS
• coin-shaped lesions • Men are affected slightly more often and at a later age than women (>50 vs <30 years, respectively). • pathogenesis has not been fully clarified? Microbial vs contact sensitization • defined as an eruption of round (discoid) eczematous patches almost exclusively of the extremities- well demarcated, may be acutely inflamed with vesicles and weeping • excoriations are often prominent, usually takes a very chronic course

NUMMULAR DERMATITIS
• DDX – atopic dermatitis & dissemination secondary to contact dermatitis, stasis dermatitis. Psoriasis, Bowen's disease, mycosis fungoides and tinea corporis. • Treatment – Medium- to high-potency topical corticosteroid ointments, topical tacrolimus or pimecrolimus macrolide lactones or calcineurin inhibitors – phototherapy

Perioral and Periocular (Periorificial) Dermatitis
• • • • common acneiform condition juvenile form of acne rosacea etiology-unknown use of mid- to high-potency topical corticosteroids related to the pathogenesis


Blepharitis and conjunctivitis can occasionally occur generally self-limited, although resolution may take months to years Can heal with scarring

Perioral and Periocular (Periorificial) Dermatitis
• DDX
– Seborrheic Dermatitis, Acne Vulgaris, Erythromelanosis Faciei and Keratosis Pilaris Rubra, Lupus Erythematosus, Demodex Folliculitis

500 mg (30–50 mg/kg/daily) [bid to qid. foam. 333. 90. 40. 40 mg qd • Minocycline 50. 20 mg bid. suspension or wash](with sulfur) • Azelaic acid 15% and 20% bid [cream or gel] • Bp/clindamycin 5% / 1% qd [gel] • Tretinoin 0.Perioral and Periocular (Periorificial) Dermatitis • Tx – Topical • Metronidazole 0. lotion. 250. 400. 75.1 % qd [cream or gel] • Tx – Oral • Tetracycline 250 –500 mg qd to bid • Doxycycline50–100 mg qd to bid. 100 mg qd to bid. gel or lotion] • Sodium sulfacetamide (with or without sulfur and/or urea)10% qd to bid [cream.01% to 0. depending on dose] • – – Azithromycin250 500 mg (5 mg/kg)3times/week • Isotretinoin10 to 40 mg qd Please be aware of S/E peds pt!! Not for pregnant women • 2 form of contraceptive . 135 mg (1 mg/kg) qd • Erythromycin 200.75% and 1% qd to bid [cream.

distends capillaries & damages capillary permeability barrier. and women are affected more often than men • venous ulcers are almost invariably accompanied by this form of dermatitis • Venous hypertension slows blood flow in microvasculature.STASIS DERMATITIS • Clinical spectrum of chronic venous insufficiency of the lower extremities • Prevalence rates rise with age. . allowing passage fluid & plasma proteins into the tissue (edema) & extravasation of erythrocytes (stasis purpura and hemosiderin deposition) • Release of inflammatory mediators lipodermatosclerosis tissue remodeling.

Dermatitis occurs dilated varicose veins. and stasis dermatitis displays features of asteatotic eczema. inflammation is known to induce epidermal dysfunction (hyperproliferation.oozing and crusting Contact sensitization to components of topical therapies found in 58-86% of patients • • • CVI Chronic venous insufficiency . Dry skin very common finding w/ CVI. barrier impairment. severely pruritic.STASIS DERMATITIS • • Occurs-medial supramalleolar regions where microangiopathy is most intense. desquamation).

STASIS DERMATITIS • DDX– straightforward diagnosis – asteatotic eczema – irritant or allergic contact dermatitis – psoriasis – mycosis fungoides • Tx– management of venous hypertension adequate compression bandages or stockings(if ulcer present must r/o arterial) – lifestyle changes – exercise calf muscles – removal of insufficient saphenous veins – topical corticosteroids and emollients .

secondary infection with bacteria or Candida albicans • three most common types of diaper dermatitis are chafing dermatitis. skin maceration. and. irritant contact dermatitis. in many cases.Diaper Dermatitis • most common cutaneous disorder of infancy & early childhood • being prolonged contact with urine and feces. and diaper candidiasis .

and the abdomen) – presents as mild redness and scaling and tends to wax and wane quickly. buttocks. the genitalia. frequent diaper changes and good diaper hygiene. .Diaper Dermatitis • Chafing Dermatitis – most prevalent form – friction is the most pronounced (the inner surfaces of the thighs.

and proximal thighs. perineal area.Diaper Dermatitis • Irritant Contact Dermatitis – buttocks. lower abdomen. and bacterial products and urine pH – petrolatum-based formulations as a barrier • Diaper Candidiasis – suspected whenever a diaper rash fails to respond to usual therapy. bacteria. – Candidiasis possible 2/2 systemic antibiotic therapy and should be considered in any diaper dermatitis . the vulva. with sparing of the intertriginous creases – etiology-potential roles for ammonia.

Diaper Dermatitis • widespread. and inner aspects of the thighs • raised edge. lower abdomen. beefy red erythema on the buttocks. sharp marginization w/ white scales at border.pinpoint pustulovesicular satellite lesions (diagnostic hallmark) .

biotin deficiency – Allergic contact dermatitis. cystic fibrosis. – Atopic dermatitis • DDX– – – – – – – – – Atopic dermatitis Granuloma gluteale infantum Langerhans cell histiocytosis Burns Child abuse Epidermolysis bullosa Congenital syphilis Varicella/herpes Tinea cruris Chronic bullous dermatosis of childhood – Bullous mastocytosis .Diaper Dermatitis • DDX– Seb derm – Psoriasis – Intertrigo – Jacquet's dermatitis – Perianal pseudoverrucous papules and nodules – Miliaria – Folliculitis – Impetigo – Scabies – acrodermatitis enteropathica.

e.e.Diaper Dermatitis • Tx – – – – – – appropriate etiology Educating keeping the skin dry. azoles) .C. nystatin.) Stronger steroids and combination antifungal-corticosteroid preparations should be avoided – appropriate systemic antibiotic – Candidal infection requires the use of a topical antifungal agent (i. and infection-free Zinc oxide and petrolatum-based formulation low-potency. nonfluorinated topical corticosteroid (i.. 1% H.. protected.

can occur in children Emotional stress and hot weather may exacerbate the condition • DDX – inflammatory tinea pedis/manuum – photoinduced pompholyxlike hand dermatitis – dyshidrosiform pemphigoid cutaneous – T-cell lymphoma – scabies(children) – infantile acropustulosis .Dyshidrosis • • • • Dyshidrotic eczema not a disorder of the sweat gland most common in adults.

palms and soles and parts of palmar and plantar surfaces .Dyshidrosis • extremely pruritic vesicles (filled with clear fluid) • „tapioca pudding‟-like appearance • lateral and medial aspects of the fingers.

broadband or narrowband UVB.g. UVA1. methotrexate and mycophenolate mofetil (although mycophenolate mofetil-induced dyshidrosis has been described) – Botulinum toxin injection – Psychotherapy .Dyshidrosis • Tx – identification and treatment of underlying causes – High-potency topical corticosteroids – Topical calcineurin inhibitors and phototherapy (e. PUVA) – Short courses-systemic corticosteroids severe outbreaks • Tx – Severe recalicitrantazathioprine.

Lichen Simplex Chronicus • • • • excessive scratching Predisposing factors include xerosis and atopy characterized as hyperpigmented. leathery plaques well circumscribed -occipital and nuchal areas in women &perineum and scrotum in men wrists and extensor surfaces of the forearms and lower legs QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. • . lichenified.

Lichen Simplex Chronicus • Tx – – – – – – breaking the itch-scratch cycle Antipruritics Moisturizers Topical corticosteroids under occlusion Intralesional corticosteroids situational stressors-psychological .

S.Tinea Corporis • Fungi that invade keratinized tissue via keratinases – Hair. Microsporum. Nails. except tinea capitis .cornuem • Dermatophytes – Trichophyton. Epidermophyton – Trichophyton rubrum-most common dermatophyte worldwide – occur most frequently in postpubertal.

Tinea Corporis • Transmission of dermatophytes to humans occurs via three sources – Geophilic-soil-human – Zoophilic-animal-human – Anthropophilic-human-fomite-human – Inhibited by sebum QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture. .

Tinea Corporis • Incubation-1 to 3 weeks • Spreads centrifugally w/ central clearing annular lesions of varying sizes • Scaly. granulomatous or verrucous in appearance. can be vesicular. although scale may be lessened or absent if topical corticosteroids have been used (tinea incognito) • Pustules within the active border. • Symptoms include pruritus and burning • Dx made via KOH. occasional fungal cx & PAS stain via bx .

.QuickTime™ and a TIFF (Uncompressed) decompressor are needed to see this picture.

Granuloma annulare. Erythema annulare centrifugum. Parapsoriasis. Pityriasis rosea.Impetigo • Tx – Topical antifungals-first line – Systemic antifungal therapy-higher incidence and increased severity of side effects-Fluconazole. Subacute lupus. Stasis. Itraconazole. Pityriasis versicolor. Griseofulvin. Terbinafine . Annular psoriasis. Contact. Atopic. Seborrheic.Tinea Corporis • DDX– Nummular eczema.

Interdigital. affecting both sexes • most believe acquried going barefoot (locker rooms. T. Inflammatory (vesicular). gyms. tonsurans (in children)-typical dermatophytes • Four types-Moccasin. Ulcerative . mentagrophytes. floccosum and T. E. public facilities).Tinea Pedis • • • • Epidemiology and pathogensis similar to corporis soles of feet interdigital web spaces most common location for dermatophyte infections more common in adults and is found around the world. rubrum. no specific susceptibility has been determined • T.

Moccasin Interdigital/maceration QuickTime™ and a TIFF (Uncompr essed) decompressor ar e needed to see this pic ture. Inflammatroy .

onychomycosis and tinea manus Erythrasma chronic superficial infection of the intertriginous areas of the skin . and those with moccasin type • other dermatophyte infections often associated with tinea pedistinea cruris. empiric treatment with topical erythromycin • oral antifungals should be considered in diabetics. immunocompromised patients. DDX and Tx-similar to tinea corporis • Erythrasma can be diagnosed with Wood's light examination because of its coral-red fluorescence.Tinea Pedis • Dx.

also in temperate climates • Malassezia has an oil requirement for growth. pregnancy and corticosteroid use . has been implicated in seborrheic dermatitis and atopic dermatitis • potassium hydroxide (KOH) examination-‟ziti and meatballs‟ • Other factors have been implicated-oily skin. excessive sweating. immunodeficiency. increased incidence in adolescents and sebum-rich areas of the skin.Tinea Versicolor • Caused by Malassezia furfur • occurs in tropical climates w/ high ambient temperatures & high humidity. poor nutrition.

less frequently. submammary region and groin • most common colors are brown (hyperpigmented) and tan(hypopigmented) occasionally there is mild inflammation leading to a pink color • asymptomatic and the major concern is its appearance.. lesions are seen on the face (more so in children). antecubital fossae. scalp. are the favored sites of involvement.Tinea Versicolor • multiple oval to round patches or thin plaques with mild scale • upper trunk and shoulders. .

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seborrheic dermatitis. pityriasis rosea. postinflammatory hypopigmentation. fluconazole or itraconazole may provide simple and effective . tinea corporis and secondary syphilis may mimic the disease • Tx – Ketoconazole (1% or 2%) or 2. salicylic acid and a variety of over-thecounter dandruff shampoos – Systemic tx-ketoconazole.Tinea Versicolor • DDX – vitiligo. pityriasis alba.5% selenium sulfide shampoo is quite effective – azole/allylamine creams and lotions – nystatin.

Drug Eruptions • • • • • • Exanthematous or morbilliform eruptions are the most common Urticaria. Angioedema and Anaphylaxis Photosensitivity Vasculitis Neutrophilic Drug Eruptions Drug Reaction with Eosinophilia and Systemic Symptoms: Hypersensitivity Syndrome • Bullous Eruptions • Drug-induced bullous pemphigoid .

1% of users). fluoroquinolones (1.6%) and penicillins (1. • Common eruptive cutaneous drug eruptions are hypersensitivity reactions with an underlying immunologic mechanism .Drug Eruptions • skin is one of the most common targets for adverse drug reactions • women are more susceptible than men • increases with the age of the patient. the most frequently reported skin reactions to antimicrobials were due to trimethoprim/sulfamethoxazole (2.1%). as well as the number of drugs taken by the patient • In a retrospective cohort study from the Netherlands of 13 679 patients from general practices.

cell-mediated drug reactions (formerly type IV) versus undefined: exanthematous. as well as Stevens-Johnson syndrome (SJS) and TEN. Gell-Coombs classification): urticaria. formerly type II): petechiae secondary to drug-induced thrombocytopenia – Immune complex-dependent drug reactions (formerly type III): vasculitis. angioedema and anaphylaxis. fixed and lichenoid drug eruptions. .Drug Eruptions • Immunologically Mediated Drug Reactions – IgE-dependent drug reactions (formerly type I. serum sickness and certain types of urticaria – Possible delayed-type. – Cytotoxic drug-induced reactions (antibody against a fixed antigen.

and complementary or alternative treatments • time between initiation of drug & onset of eruption is a key element in identifying offending drug-most immunologically mediated drug reactions occur within 8 to 21 days after initiation of a new medication • usual practice is to discontinue all drugs that are non-essential .Drug Eruptions • Non-immunologic Mechanisms – Overdose. non-prescription/over-the-counter. Exacerbation of disease • complete list of current (as well as past) medications. Drug-drug interactions. Delayed toxicity. including prescription. Alterations in metabolism. Pharmacologic side effects. Cumulative toxicity.

confluent areas on the thorax and purpuric lesions on the ankles and feet – possibility of a more severe drug-induced eruption-edema of face or a marked peripheral blood hypereosinophilia( hypersensitivity syndrome/DRESS) and mucous membrane lesions or painful or dusky skin. the distribution is usually symmetric. begins on the trunk and upper extremities and progressively becomes confluent – polymorphous with morbilliform or sometimes urticarial lesions on the limbs.Drug Eruptions • Exanthematous Drug Eruptions – most common adverse drug reactions affecting the skin – maculopapular drug eruptions – erythematous macules that sometimes become slightly palpable. – A biopsy of morbilliform-not particularly helpful . which may announce TEN or SJS.

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Drug Eruptions
• DDX-viral exanthems (e.g. Epstein-Barr virus, enteroviruses, adenovirus, early HIV, human herpesvirus type 6 [HHV-6], parvovirus B19), which are often indistinguishable • drug etiology is favored in adults, whereas a viral cause is favored in the pediatric population • Tx-largely supportive, Topical corticosteroids may help to alleviate pruritus,discontinuing the offending agent is the first therapeutic measure • drugs have a significantly higher incidence (>3% of patients): aminopenicillins, sulfonamides, cephalosporins and anticonvulsants • ACEI, NASIDS

Lichen Planus
• idiopathic inflammatory disease of the skin and mucous membranes • pruritic, violaceous papules that favor the extremities • has been associated with multiple disease processes and agents, including viral infections, autoimmune diseases, medications, vaccinations and dental restorative materials • fifth or sixth decade, with 2/3 patients developing the disease between the ages of 30 and 60 years • Variants- Bullous, atrophic, hypertrophic, Ulcerative/Erosive, Inverse, Linear, Annular, Lichen planopilaris • Assoc w/hep c more with oral LP • VirusesHSV,Varicella, HHV6, Hep C • VaccineHep B • Drugs • Contact allergensnickel(ID), amalgem • Neoplasms

Lichen Planus
• Flexor surfaces • Wickham striae • small, polygonal-shaped, violaceous, flat-topped papule; some papules are umbilicated • slightly shiny • Pruritic • Koebner phenomenon

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Lichen Planus

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Lichen Planus
• Dx made via clinical features and bx • DDX – lupus erythematosus (LE), lichen nitidus, lichen striatus, lichen sclerosus, pityriasis rosea, erythema dyschromicum perstans (ashy dermatosis), psoriasis, annular lichenoid eruption, lichenoid GVHD and secondary syphilis • Tx – TSC(superpotent), Topical calcineurin inhibitors, Intralesional corticosteroids, Intramuscular triamcinolone acetonide [0.5-1 mg/kg/month X 3-6 months], Phototherapy, Oral metronidazole, Antimalarials, Systemic retinoids

PITYRIASIS ROSEA

• • • • •

healthy adolescents and young adults absence of significant systemic manifestations & spontaneous resolution provides great consolation to the patient ages of 10 and 35 years no racial predilection eruption lasts 6 to 8 weeks cause of pityriasis rosea remains elusive-(HHV-7) herald patch is a skin- to pink- to salmon-colored patch or plaque with a slightly raised advancing margin

PITYRIASIS ROSEA
• Couple days after herald patch increase number of smaller usually round to oval in shape long axis following Langer's lines of cleavage. On the posterior trunk-„fir tree‟ or „Christmas tree‟ pattern approximately 25% of patients, pruritus is noted that is mild to severe darkly pigmented skin, the lesions tend to be more papular and hyperpigmented

PITYRIASIS ROSEA .

to medium-strength topical corticosteroids. low. nummular eczema. UVB light treatments or natural sunlight exposure and oral antihistamines 73% of patients had complete resolution after receiving 14 days of erythromycin . guttate psoriasis • Tx.PITYRIASIS ROSEA • clinical picture is quite characteristic and the histopathology relatively non-specific. • DDX-secondary syphilis. drug eruptions. tinea corporis.patient education and reassurance.

7% • Psoriatic arthritis probably occurs in 5-30% of the patients • skin lesions appear well before the psoriatic arthritis • peaks in age of onset-one at 20-30 years of age and at 50-60 years. In approximately 75% of patients-before the age of 40 years • positive family history has been reported by 35% to 90% • Obesity. Norwegian Lapps. African-Americans. increased alcohol consumption.4% and 0. and Asians of between 0. prevalences as high as 4. and an increased incidence of smoking have all been associated with psoriasis .6% • Africans.Psoriasis • The impact of psoriasis on quality of life is significant given its chronicity and prevalence (up to 2% worlds population) • US and Canada.

2-6wk lag – psychogenic stress – HIV (greater dz severity) – strep pharyngitis guttate (1-2wk lag) – hypocalcemia pustular psoriasis • Triggers – – – – – – – – – – – Drugs steroid withdrawal -blockers Lithium IFN Terbinafine ACE-I Antimalarials NSAIDs GCSF Rapid tapers of corticosteroid • . sunburn. HLA-B37 and HLABw16 Triggers – cutaneous injury-Koebner phenomenon. viral exanthems. HLA-B17.Psoriasis • associated with several: HLA-B13.

Plaques may persist for months to years at the same locations . elbows. genitalia are involved in up to 30%. knees and presacrum predilection. as are the hands and feet.Psoriasis • symmetric distribution of sharply defined erythematous scaly plaques • scalp.

Psoriasis .

. common form of the disease in children.Psoriasis • Guttate psoriasis-2% of the patients. preceding severe upper respiratory infection.

diagnosis of psoriatic erythroderma include previous plaques in classic locations. characteristic nail changes. .Psoriasis • Erythrodermic Psoriasisgeneralized erythema and scaling. and facial sparing.

in case of localized disease. rapid tapering of corticosteroids (or other systemic therapies).Psoriasis • pustular psoriasis-erythema and the appearance of sterile pustules dominate clinical picture. triggering factors-pregnancy. topical irritants • . infections. hypocalcemia.

Psoriasis • Pustulosis of the palms and solessterile‟ pustules of the palmoplantar surfaces admixed with yellow–brown macules scaly erythematous plaques may also be seen commonly associated with sterile inflammatory bone lesions • .

nail bed shedding of nail plates .Psoriasis • Acrodermatitis continua of Hallopeau. pustules are seen on the distal portions of the fingers.rare manifestation.

Psoriasis .

CI-Abnormality in bone or calcium metabolism. max app 100g/week. (Dovonex. Renal insufficiency. lactation . Allergy Pregnancy. tinea incognito Clinical picture and bx to confirm dx • Tx- • – Vitamin D3 Analoguesinhibits epidermal proliferation. Vectical). cutaneous candidiasis.Psoriasis • DDX-mycosis fungoides variant of cutaneous T-cell lymphoma (CTCL) keratotic eczema of the palms and soles pityriasis rubra pilaris drug reactions intertrigo seborrheic dermatitis.

viral and mycotic infection – Atrophy of the skin – Allergic contact dermatitis due to corticosteroids or constituents of the formulation – Pregnancy or lactation 80% of patients treated with high-potency topical corticosteroids experience clearance Combination topical therapy • • • . topical retinoid. anthralin or tar – Monotherapy for flexural and facial psoriasis (usually mild strength – Recalcitrant plaques often require occlusion (plastic.Psoriasis • TCS. hydrocolloid CI– Bacterial.first-line therapy in mild to moderate psoriasis • Indications– Mild to moderate psoriasis: first-line treatment as monotherapy or in combination – Severe psoriasis: often in combination with a vitamin D3 analogue.

Psoriasis
• Anthralin – inhibits mitogen-induced Tlymphocyte proliferation and neutrophil chemotaxis – treatment in an inpatient setting or day-care center – Indications-second-line treatment as monotherapy or in combination – CI-Unstable plaque psoriasis in a phase of progression, pustular and erythrodermic psr
• Topical Retinoids: tazarotene (Tazorac) – second-line treatment as monotherapy – Selectively binds RAR-beta and RAR-gamma – epidermal proliferation, inhibits transglutaminase and K16 expression – max BSA = 10-20% – CI-Unstable plaque psoriasis, Erythrodermic psoriasis, Allergic contact dermatitis, Pregnancy and lactation

Psoriasis
• Photo(chemo)therapy – BB or NB UVB(311nm), UVA oral or topical psoralen – Mod-Severe: first line – CI-Insufficient efficacy of UVB and PUVA • Pustular psoriasis (UVB and PUVA) • Erythrodermic psoriasis (UVB and PUVA) • Light-sensitive dermatoses (UVB and PUVA) • Photodermatoses (UVB and PUVA) • Phototoxic systemic or topical medications (UVB and PUVA) • Vitiligo (UVB and PUVA) • Previous history of arsenic exposure, excessive irradiation or excessive photo(chemo)therapy (UVB and PUVA) • Excessive exposure to UV light • Previous cumulative PUVA therapy >2000 J/cm2 • Immunosuppressive medication • Previous history of skin cancer (UVB and PUVA) • Men and women in reproductive years without contraception (PUVA) • Pregnancy and lactation (PUVA) • Liver and kidney impairment (PUVA) • Cataracts (PUVA)
I-

Psoriasis
SYSTEMICS • Methotrexate – Severe chronic(>20 BSA), pustular, erythrodermic, psoriatic arthritis, Severe nail psr – lymphocyte effect – max effect = 8-12wk – CI-kidney function (creat cl <60 ml/min), Concomitant medications, pregnancy and lactation, planning to have children liver function abnormalities, hepatitis, severe anemia, leukopenia, thrombocytopenia, active infections Peptic ulcer (active) unreliable patient – AE: liver tox, pancytopenia
• Cyclosporine – Severe, failed conv tx – rapid clearance – blocks IL2 upregulation – CI-Impaired renal function, Uncontrolled hypertension,Past or present malignancy, Concomitant immunosuppressive therapy, drugs affecting cyclosporine pharmacokinetics, history of arsenic exposure, history of excessive photo(chemo)therapy, Concurrent photo(chemo)therapy, Active infections, Pregnancy or lactation, immunodeficiency, Severe chronic organ dysfunction Non-compliance, Alcohol and drug abuse – AE: HTN, renal tox

Psoriasis
• Acitretin – Severe monotherapy – pustular, erythrodermic – CI-liver/kidney dysfxn, Pregnancy and lactation Women of childbearing potential who cannot guarantee adequate contraception during and up to 3 years following discontinuation of acitretin, hyperlipidemia, especially hypertriglyceridemia, concomitant medications and hepatotoxic meds,diabetes mellitus, alcohol abuse – AE: hyperlipidemia, liver tox

Psoriasis
BIOLOGICS • T-cell activation inhibitors(Alefacept) • TNF- inhibitors(Etanercept, Infliximab, Adalimumab) • CI-Significant viral, bacterial or fungal infections, Increased risk for developing sepsis, Active tuberculosis Immunocompromised or immunosuppressed, Pregnancy* (anti-TNF agents are category B, efalizumab is category C, alefacept is category B), Allergic reaction to the biologic agent, Excessive chronic exposure to UVR or photo(chemo)therapy • AE: immunosuppresion – Etanercept AE: demyelinating dz, lupus-like syndrome – Adalimumab AE: thrombocytopenia – Infiximab CI in CHF

EM/SJS/TEN
• Erythema Multiforme (rarely caused by drugs) is a distinct disease from Stevens-Johnsons Syndrome / Toxic Epidermal Necrolysis (caused by drug) • EM does not commonly progress to SJS/TEN • SJS and TEN same fatal disease spectrum • Skin is major target organ for many drug reactions • Drug reactions usually 7-21 days after drug exposure, not next day typically • It is often very difficult to identify the exact drug causing the reaction

Erythema Multiforme
• • • • • • acute, self-limited, abrupt onset of symmetrical fixed red papules, typical and/or occasionally „atypical‟ papular target lesions precipitated by an infection, particularly HSV Minor-ext, face, mild to no mucosal, no systemic sx Major-ext, face, severe mucosal, systemic sx – fever and asthenia(weakness) of varying degrees, arthralgias w/ joint swelling, pulmonary. Renal, hepatic and hematologic abnormalities-rare • Pathogensis – Infection(90%) • HSV 1,2 • Mycoplasma Pneumoniae • Histoplasma Capsulatum • Drugs <10% • Exposures (poison ivy) • Systemic disease (rare)(IBD, LE/Rowell‟s syndrome,Bechets)

.

Erythema Multiforme • • • Painful mucosal erosions – usually absent in EM minor Natural History – Abrupt 24-72 hours – 50% preceded by herpes labalis 3-14 days – Last up to 2 weeks Recurrences quite common when? – Each spring .

Erythema Multiforme .

Erythema Multiforme .

mycophenolate mofetil and PUVA(no controlled trials • • . prednisone [0.g. erythema annulare centrifugum. and several forms of vasculitis Dx-skin bx. thalidomide. good H&P. fixed drug eruptions subacute cutaneous LE. cyclosporine. despite the absence of controlled studies – azathioprine (100 mg/day for several months). dapsone.5 mg/kg/day for several months).5–1 mg/kg/day]) or pulse methylprednisolone [1 mg/kg/day for 3 days]) should be considered. prednisone (0.Erythema Multiforme • DDX-Urticaria. Tx-topical antiseptics for eroded skin lesions and antiseptic/antihistamine rinses and local anesthetic solutions for oral lesions – Tx underlying cause-bacterial vs viral – HSV-associated EM.acyclovir (10 mg/kg/day in divided doses) valacyclovir (500-1000 mg/day) famciclovir (250 mg twice daily) systemic corticosteroids (e.

Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) • Rare.2 per million persons • TEN affects women more frequently than men.5:1. lymphoma) – Brain tumor patients undergoing radiotherapy and concomitantly receiving antiepileptics . and the incidence increases with age • Patient groups particularly at risk – AIDS (1000x greater risk!) – Slow acetylator genotypes – Immunocompromised (HIV.2-6 and 0.4-1. acute and life-threatening mucocutaneous diseases that are almost always drug-related • unpredictable course • annual incidence of 1. with a ratio of 1.

Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) • mortality rates – 25% to 50%-TEN – 5% for patients-SJS Pathogensis – Massive Keratinocyte Apoptosis – Overwhelms phagocytes‟ ability to eliminate apoptotic cells • Drugs associated – Allopurinol – Aminopenicillins – Amithiozone (thioacetazone) – Antiretroviral drugs – Barbiturates – Carbamazepine – Chlormezanone – Phenytoin antiepileptics – Lamotrigine – Phenylbutazone – Piroxicam – Sulfadiazine – Sulfadoxine – Sulfasalazine – Trimethoprim–sulfamethoxazole • .

ocular and genital mucosae are present in more than 90% of patients • • • .Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) • • • SJS <10% TEN >30% Typical interval between the onset of drug therapy and SJS/TEN is between 1 and 3 weeks (2 months for aromatic anticonvulsants) Epidermal detachment Initial sx-fever. and pain upon swallowing can precede cutaneous 1-3 days Erythema and erosions of the buccal. stinging eyes.

Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) • • • • • respiratory tract is involved in 25% of patients with TEN lesions are usually tender. dusky red or purpuric macules of irregular size and shape. lesions appear as erythematous. hepatitis and cytopenias First. LAD. and have a tendency to coalesce Nikolsky sign-Tangential pressure on erythematous lesion to induce cleavage . and mucosal erosions are very painful Additional systemic manifestations include fever.

Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) .

Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) • epidermal involvement progresses toward full-thickness necrosis. the dusky red macular lesions-hours to days epidermis then detaches -fluid fills the space between the dermis (flaccid) and can be extended sideways by slight pressure of the thumb as more necrotic epidermis is displaced laterally (Asboe-Hansen sign) • • .

58.8% – 4 .2% – 2 .3% – >5 .3.12.Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) • • SCORTEN 1 point for ? – Age >40 – Heart rate >120 – Malignancy – BSA above 10% – Serum Urea >10 mmol/l – Serum Bicarbonate <20 mmol/l – Serum glucose > 14mmol/l • Mortality rate – 0-1 .35.90% .1% – 3 .

renal insufficiency and sepsis – Burn care/ ICU – Careful manipulation – Vaseline gauze on denuded areas – Regular eye exam by optho – Periodic cultures of eyes. SSSS.4 days . – Discontinue all meds – Protect against hypovolemia. LE. sputum. AGEP and generalized fixed drug eruption. Paraneoplastic pemphigus. druginduced linear IgA bullous dermatosis (LABD). and severe acute GVHD • Tx – early diagnosis. drainage – Steroid efficacy controversial – IVIg 1g/kg/day x 3 . electrolyte imbalance.Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) • DDX-EM. Kawasaki disease.

Stevens-Johnson Syndrome (SJS) Toxic epidermal necrolysis (TEN) .

BPAG2 or type XVII collagen) and the BP antigen 230 (BP230 or BPAG1) • Manifestations extremely polymorphic(bullous vs nonbullous) . and it predominantly affects the elderly • after 60 years of age • patients over 90 years of age appears to be about 300-fold higher • higher predominance in men • immune-mediated disease-self-antigens: the BP antigen 180 (BP180.BULLOUS PEMPHIGOID • most common autoimmune subepidermal blistering disease.

including the abdomen. annular or figurate pattern blisters are tense. Within intertriginous zones. • Symmetrical distribution pattern. vegetating plaques can be observed. and they predominate on the flexural aspects of the limbs and the lower trunk. burns. up to 1–4 cm leaving eroded and crusted areas. papular and/or urticarial lesions that may persist for several weeks or months • Bullous-vesicles and bullae on apparently normal or erythematous. eczematous. • increased risk of malignancy in patients with BP appeared to be marginal-ca screening correlate w/ sx • Triggers-trauma.BULLOUS PEMPHIGOID • Nonbullous-non-specific mild to severe pruritus w/o excoriated. radiotherapy or UV irradiation • Assoc w/ psr & LP .

BULLOUS PEMPHIGOID .

BULLOUS PEMPHIGOID .

BULLOUS PEMPHIGOID .

bumetanide) – Analgesics (e. IIF.drug reactions.g. amoxicillin. scabies . CP. furosemide. ciprofloxacin) – Potassium iodide – Gold – Captopril • Dx & DDx – Clinical – Histo. arthropod.g. vasculitis. linear. phenacetin) – D-penicillamine – Antibiotics (e. prurigo nodularis. continuous deposits of IgG and/or C3 along the epidermal basement membrane – EBA.g.BULLOUS PEMPHIGOID • Drug Induced BP – Diuretics (e. LABD. DIF – DIF-fine. contact dermatitis. urticarial dermatitis.

g.BULLOUS PEMPHIGOID • Tx-Mild and/or localized disease – Superpotent TCS – Nicotinamide in association w/ minocycline or tetracycline – Erythromycin. penicillins – Dapsone. tacrolimus) • Tx-extensive/persistent disease – Superpotent TCS – Oral corticosteroids – Azathioprine – Mycophenolate mofetil – MTX – Chlorambucil – Cyclophosphamide – IVIg – Plasma exchange – Rituximab . sulfonamides – Topical immunomodulators (e.

Gram-positive.Acne Vulgaris • disorder of the pilosebaceous unit • primarily a disorder of adolescence(85% btw between 12 & 24 y/o) • sebaceous gland is controlled primarily by hormonal stimulation – High in 1st 6 mos – Decreases at 1yr + stabilizes – Dramatically increases at adrenarche. correlating w/androgen production and acne – Stable in adulthood – Decreases in women at menopause and men in 6th and 7th decade • Propionibacterium acnes contributes significantly to the production of acne. non-motile rods .

Acne Vulgaris • Sticky corneocytes proliferate in infrainfundibulum • Comedone expands. comedo ruptures. sebaceous lobule regresses • Pressure increases. keratin and sebum are extruded • Inflammation ensues .

Acne Vulgaris Comedonal acne .

Acne Vulgaris Closed comedones .

Acne Vulgaris Papules. pustules. small cysts Severe cystic acne .

these lesions frequently coalesce to form massively inflamed complex plaques that can include sinus tracts.Acne Vulgaris • papules. nodules form and become markedly inflamed. nodules and cysts of varying severity • lesions progresses. • DDX– – – – – – – – – – Milia Sebaceous hyperplasia Eruptive vellus hair cysts Steatocystoma multiplex Corticosteroids and anabolic steroid induced Contact acne Follicular mucinosis Rosacea Folliculitis Keratosis Pilaris • Not an exhaustive list . indurated and tender • severe nodulocystic acne. pustules.

tretinoin. intralesional corticosteroid – 2nd line-oral dapsone • • . tazarotene) – 2nd line-azelaic acid. tazarotene) and topical antibiotic – 2nd line-add azelaic or salicyclic acid Tx-Mod papular pustular nodules – 1st line-oral antibiotic. tretinoin. salicyclic acid Tx-Mild papular/pustular – 1st line-Topical retinoid(adaplene. isotretinoin(only if multi nodules/recalcitrant) – 2nd line-alt oral anitbiotic. BPO. topical retinoid.Acne Vulgaris • • Tx-Mild comdonal – 1st line-Topical retinoid(adaplene. azelaic or sal acid Tx-Severe – 1st line-isotretinoin w/wo oral prednisone.

bloody nose. acnes unable to thrive. lab Abnormalities (lipids. headaches. compliance is an issue with multi product! • Isotretinoin / Accutane ( 5 .6 months) Last Resort – Sebaceous gland atrophy. leukopenia) psych (Mood swings. laser. exuberant granulation tissue**Teratogenicity ( 2 Forms of BC) • other tx – Extraction. alopecia. P. LFTs.Acne Vulgaris • Tx-multi tx modalities. blurred vision) cutaneous Infections (S. but no increase in suicidality). dry eyes + lips. poor wound healing. blue light. myalgias pseudotumor cerebri (N/V. aureus). skeletal hyperostoses. – Normalization of follicular keratinization – 1 mg/kg/d for total of 120-150 mg/kg to prevent relapse – S/E-Xerosis. etc .

Rosacea • • • • • • • common in fair-skinned individuals Incidence third and fourth decades of life vascular hyperreactivity Blushing. but the evidence is largely circumstantial • Propionibacterium acnes probably plays a role • oral niacin worsens • Topical steroids . gradual reddening Foods/liquids induce facial vasodilation increased incidence Parkinson's Demodex folliculorum-mite w/in sebaceous follicles of the head that has been implicated as a cause of rosacea for decades.

phymatous and ocular • Erythematotelangiectatic(vascular)-Flushing and persistent central facial erythema with or without telangiectasia. chin. ocular photosensitivity. blurred vision. burning or stinging. irregular surface nodularities and enlargement(nose.Foreign body sensation in the eye. • Papulopustular-Persistent central facial erythema with transient papules and/or pustules • Phymatous-Thickening skin. telangiectasia of the sclera or other parts of the eye. papulopustular (inflammatory). itching. or periorbital edema . cheeks or ears) • Ocular.Rosacea • Four types-erythematotelangiectatic (vascular). forehead. dryness.

Rosacea Vascular type .

Rosacea Inflammatory rosacea .

Rosacea Rhinophyma Phymatous & inflammatory .

Rosacea Occular .

Demodex • Tx-topical – Metronidazole-topical therapy daily to BID – Azelaic acid cream – BPO if not too irritating. Acne. pyoderma faciale. Erythromelanosis Faciei and Keratosis Pilaris Rubra. Lupus Miliaris Disseminatus Faciei. granulomatous rosacea. steroid rosacea. bx only severe persistent cases • DDX-perioral derm. topical anitbiotics not very effictive. Seb derm. Lupus Erythematosus.Rosacea • Dx-clinical. – topical tretinoin – Sulfa based face washes Tx-oral – Tetracyclines-anti-inflammatory – Isotretionoin-severe cases Tx-surgical – IPL or PDL – electrosurgery – CO2 laser • • .

pruritic • Neck.axillae and groin • Areas of terminal hair .scalp.painful. upper trunk. buttocks and thighs.Folliculitis • very common disorder • Culture contents often fails to identify a bacterial pathogen • Staphylococcus aureus is the most common • Perifollicular pustules. arising on an erythematous base • pierced by a hair • Tender. beard area.

HSV. drug induced always culture • . culture • DDX-acne.Dermatophyte. rosacea. pseudofolliculitis barbae. Candida. gram negative. demodex. neutrophils and macrophages • Late stage-granulomatous • DX-clinical.g.Folliculitis • shaving (e. irritant. pubic hair) and occlusion can exacerbate folliculitis • intense follicular infiltrate of lymphocytes. Pityrosporum.

g.4–1.5% permethrin cream • • • . Valacyclovir 500 mg po tid for 5– 10 days Demodex.aeruginosa)-self-limited. quinolones (e.2–7.Folliculitis • • • Tx-cx dependent. topical clinda. pH 7.4) and changed every 6–8 weeks) Dermatophyte/PityrosporumCandida-topical or oral antifungals HSV-Acyclovir 200 mg po 5 times per day for 5–10 days. oral tetracycline Irritant-d/c agent.0 ppm. severe or immunocompromised host: ciprofloxacin. Famciclovir 500 mg po tid for 5–10 days. ciprofloxacin) – Hot tub(p. tcs-midpotency Gram neg(klebsiella/enterbacter)-topical gent/BPO. 500 mg po bid for 7–14 days Water(chlorine (0. for cx negative/acne-BPO.

velvety or verrucous. more common in Caucasian populations and to affect men and women with equal incidence begin to appear during the fourth decade of life sun exposure implicated solitary or multiple. macular. papular or verrucous lesions waxy . „stuck -on‟ appearance occur anywhere except mucous membranes.SEBORRHEIC KERATOSIS waxy • common benign. palms and soles very rare sign of Leser–Trélat-abrupt increase size and number(internal malignancygastric or colonic adenocarcinoma. breast ca. lymphoma) stuck-on • • • • • • . tan to black.

SCC. eccrine poroma. acrochordon. Sx-destruction(LN2.SEBORRHEIC KERATOSIS • SCC. KA. condyloma acuminatum. melanocytic nevus and melanoma • Tx-asx(cosm only). cutaneous melanoma. BCC. solar lentigo. verruca vulgaris. possible bx • DDx-dermatosis papulosa nigra. acrokeratosis verruciformis. tumor of the follicular infundibulum. stucco keratoses. and SCC in situ have been associated w/SKs-represents a coincidental neoplasm developing in adjacent skin • Dx-clinial appearance.inverted follicular keratoses. curettage) asymptomatic biopsy it . Bowen's disease.

neck and upper extremities (dorsal hands and forearms). men. AKs are also markers for an increased risk for developing invasive NMSC(SCC)/(BCC) • resistance to UV-induced keratinocyte apoptosis-contributes to pathogenisis(much more extensive…carcinogensis.Actinic Keratosis • AKs are most often found in fair-skinned individuals • accounted for 3 million annual visits to dermatologists in the US during the early 1990s • 80% of AKs occur on the head. DNA repair and apoptosis. cell cy s. tumor suppersor genes) p53 protein is a key factor for integrating pathways regulating DNA synthesis. • Prolonged UV exposure/intense UV expousre holiday . oncogenes.more often in individuals w/ prior history. increasing age.

PUVA. human papillomavirus. cigarette smoking .Ionizing radiation. Intermittent/recreational sun exposure.Cumulative/occupational sun exposure. tanning beds.chemicals (arsenic).Actinic Keratosis • number of mutations in a cell increases with time and partially explains the increasing risk for acquiring cancer as we age • inactivation of p53 facilitates angiogenesis-essential for tumor mass expansion • „precancerous‟ or „premalignant‟ because the aty pical keratinocy within these lesions are confined to the epidermis • Environmental risk factors.

light eye color – Genetic syndromes-rare Lupus on skin only – Chronic non-healing wounds. longstanding DLE. freckling. red hair. chronic lymphocytic leukemia treated with fludarabine. always burn. nevus sebaceous – Organ TPLT.Actinic Keratosis • Risk factors– Fair skin. AIDS patients with HPV infection . LP. never tan.

scalp in bald individuals) . malar eminences. dorsal hands. nasal bridge.096% per lesion per year • sun-damaged skin of the head. neck. extensor forearms.in areas of highest sun exposure(ears. upper trunk and extremities may report tenderness • rough erythematous papule with white to yellow scale • Advanced lesions thicker and well defined w/hyperkeratosis and erythema.075-0.forehead.Actinic Keratosis • likelihood of an invasive SCC evolving from a given AK has been estimated to occur at a rate of 0.

pale. papule Actinic Keratosis flaky .

Actinic Keratosis .

lip. nose so take biopsy tell about scars • Dx-clinical and histo in situ • DDX-SCCis. maybe sk It will make them red and ugly for 2 wks • Tx-Cyrotherapy. imiqiumod 5%. SCC. Photodynamic therapy cutting blood supply w laser .Actinic Keratosis ear. 5-FU. topical diclofenac.

SCC • • • • • • UV solar radiation is also a major etiologic factor UV radiation received over time „classic cancer‟. tumor progression and the potential to develop metastatic disease metastases is infrequent (less than 5%) mucocutaneous interfaces(lips. higher risk of metastases The precise genetic events and number of mutations required for malignant transformation are unknown • • • actinic keratoses and Bowen's disease-precursor-slight to severe dysplasia Alterations in the p53 gene are the most common genetic abnormalities Lip-30% risk of developing metastasis regional lymph nodes. genitalia and perianal area) more aggressive. but distant hematogenous spread can also be observed . as it has precursor lesions.

SCC • incidence of SCC has been rising worldwide in all age groups over the last several decades at an estimated 3-10% per year • Same risk factors apply to AK‟s • Men have a 3:1 greater SCC mortality rate compared to women • described as keratotic. pink. erythematous patch/plaque/nodule/papule biopsy .

superficial squamos cells SCCis (aka Bowen‟s Disease) .

Bowenoid Papulosis(SCCis in genital warts) .

SCC(Marjolin‟s Ulcer (scars) Verrucous Carcinoma .

SCC High-risk sites include the lip and ear .

type of squamos cell rapid growth 1 month Keratoacanthoma Volcanic in appearance .

atypical fibroxanthoma. neuroendocrine carcinoma. verruca and irritated seborrheic keratosis. • Tx-Standard exc – 6mm margins for SCC(high risk lesions) – 10% recurrence rate curette ED&C electrodissecation & – Cure rate 97-98% (smaller the better) Curettage alone – 96% cure rate (avoids hypertrophic scar) • • . adnexal tumors. prurigo nodularis. amelanotic melanoma.SCC • Dx-clinical and histo • DDX-BCC.

SCC • Mohs Micrographic Surgery – 1% recurrence rate over 5 years – 5.6% recurrence in prior recurrent BCCs – Preferred treatment in: • Recurrent type • Poorly delineated • High-risk • Incompletely removed BCC • Sites of tissue conservation • Need for reliable clear margins .

SCC • Radiation – Use if surgery is contraindicated – Disadvantages: • Lack of margin control • Poor cosmesis in some patients (scars worsen with time. unlike surgery) • Prolonged course of therapy • Increased risk for future skin cancers • High recurrence rates .

suggests that anatomic site • BCC appears to have a capacity for infinite growth and spontaneous regression is not a feature • virtually never develop metastases • no known precursors (with the possible exception of p53 clones) • BCC is the most common skin cancer in humans • Men generally have higher rates of BCC than do women . and in particular on the nose.BCC • Sun exposure and anatomic site appear to be of etiologic importance • development of BCCs is restricted to skin containing pilosebaceous units • commonly develop on the face.

SCC .BCC • Women have a greater frequency of BCC on the lower extremities while men have more ear lesions • incidence of BCC is increasing • increase with age and the median age at diagnosis is 68 years • Mortality from BCC is quite rare and can occur in immunocompromised patients • metastatic BCC are more likely from tumors with aggressive histologic patterns (morpheaform. basosquamous) • Perineural space invasion an indicator of aggressive disease • Metastases often involve regional lymph nodes. bone and skin • Risk factors similar to AK. metatypical. lungs. infiltrating.

morpheaform. and fibroepithelioma of Pinkus • 60% of all primary BCCs are nodular type presents as a raised. slightly atrophic lesion. translucent papule or nodule with telangiectasias. or as a plaque without well-demarcated borders. or a benign inflammatory lesion appears on trunk and extremities. cystic. the head and neck also may be affected • Morpheaform BCC derives its name from an appearance similar to a plaque of morphea/sclerosing presents as a flat. often difficult to differentiate from a scar . SCC in situ.BCC pink pairly papule • Variants of BCC include nodular. basosquamous. superficial. and it may be difficult to differentiate clinically from AK. micronodular. and has a propensity for the face • Superficial BCC commonly presents as an erythematous macule or thin plaque.

papules.BCC • con‟t morpheaform-actual size of the cancer is often much greater than the clinical extent of the tumor • Cystic BCCs have a clear or blue–gray appearance and exude a clear fluid if punctured or cut. it may be confused with a hidrocystoma • Basosquamous carcinoma (metatypical BCC) is a tumor that has basaloid histologic features as well as eosinophilic squamoid features of SCC. If the lesion is in the periorbital area. behave more like SCC more aggressive and destructive likely to metz(9-10%) and reoccur after tx • Micronodular basal cell carcinoma-very destructive. or slightly elevated plaques and may be difficult to differentiate from nodular BCC . high reoccurence ratespresent as macules. subclinial spread.

BCC • Fibroepithelioma of Pinkus rare variant presents as a pink plaque or nodule smooth. may be pedunculated on the lower back difficult to distinguish clinically from amelanotic melanoma .

BCC Nodular BCC Pigmented BCC .

BCC Superficial bcc .

BCC morpheaform .

medical management. Curettge alone.BCC • Dx-clinical and histo • DDX-AK. photodynamic aldera . SCC(is). XRT. AMM. hidrocystoma • TX. inflammed SK.Standard excision – 4mm margins for BCC radiation – ED&C. Mohs for high risk types and sites.

which usually is associated with death • Germline genetic mutations and polymorphisms can predispose individuals to melanoma • CDKN2A(gene locus) • Immunogenic tumor(provokes immune response).up to one-fifth of patients develop metastatic disease.Vitiligolike depigmentation.Halo nevi.Melanoma • Melanoma is a malignancy arising from melanocytes-incidence and overall mortality rates have been rising in recent decades • most common forms of cancer in young adults.Higher rate of melanoma in immunosuppressed pts • melanoma incidence rate in Australia is the highest world-wide .

Melanoma .

Melanoma .

Melanoma • Risk factors – Genetic(Family history of atypical (dysplastic) nevi or melanoma. xeroderma pigmentosum)) – Environmental factors(Intense intermittent sun exposure. red hair color.g. tendency to burn. lightly pigmented skin. ephelides. personal history of melanoma . inability to tan. sunburn. residence in equatorial latitudes) – Phenotypic expressions of gene/environment interactions(Melanocytic nevi: – Increased total number. Multiple atypical (dysplastic). congenital (particularly large axial lesions with multiple satellites). dNA repair defects (e.

Melanoma .

preference for trunk. trunk (men and women)-radial growth-More pagetoid spread. head. preference for lower extremities (women). especially nose and cheeks-radial growth-Slower growth over years within sundamaged skin – Acral lentiginous melanoma-5-10%-Palms. less solar elastosis – Nodular – 15-30%-Any site.Melanoma men in their back • Types – Superficial spreading – 70%-Any site. nail unit-radial growth-Most common melanoma type in patients with darker skin types . neck-no radial growth-Nodule with more rapid vertical growth – Lentigo maligna melanoma-5-15%-Face. soles.

Melanoma Superficial spreading melanoma .

Melanoma c Superficial spreading arising w/ in compund melanocytic nevus .

no cystic look Nodular melanoma .Melanoma no waxy appearance.

Melanoma Acral lentiginous melanoma more common in AA Melanoma in situ of the nail .

Melanoma • Hutchinson sign-pigmentation of the periungual tissues--is a valuable clue to the diagnosis of subungual melanoma .

1st 3 months) – Increased pigmentation – Not a risk factor though – Transplacental metastases can arise .Melanoma • Pregnancy – Melanocyte-stimulating hormones elevated – Darkening of nevi(more than 10% of women.

Melanoma stagging system how much to cut .

shape or size of a pigmented skin lesion over the course of months is the most sensitive clinical sign – Public awareness campaign-ABCD's of melanoma: Asymmetry.Melanoma • Dx-Early detection is a key factor – history of change in the color. and Diameter greater than 5 mm. Border irregularity. These have recently been joined by for „evolving‟ to E' ‟ connote the importance of change as mentioned above – BX!!!! exsitional Bx • DDX-Nevi. Color variegation. non-melanocytic stimulators .

Melanoma • DDX-melanocytic – – – – – – – – – – – – – – – – – – – – – – – – Acral nevi Ancient nevi Black (hypermelanotic) nevi Blue nevi and variants Clonal nevi Combined nevi Congenital nevi biopsied shortly after birth Deep penetrating nevi Atypical (dysplastic. lichen planus-like keratosis.g.broma Seborrheic keratosis Pigmented poroma and pigmented porocarcinoma Pigmented pilomatricoma Subungual hematoma Black heel (hemorrhage in stratum corneum caused by trauma) Pyogenic granuloma Tinea nigra Thrombosed hemangioma. Clark's) nevi Halo nevi Hyperplasia of melanocytes in sun-damaged skin Melanocytic proliferation overlying a benign neoplasm Longitudinal melanonychia Melanosis of mucosal regions Nevi arising within areas of lichen sclerosus Nevi exposed to UV radiation Nevi in genital regions (including milk-line nevi and flexural nevi) Nevi in patients with epidermolysis bullosa Nevi on or around the ear Pigmented streaks in melanoma scars Proliferating nodules in giant congenital nevi in neonates Recurrent (persistent) nevi Reticulated (ink-spot) lentigo Spitz nevi and variants • DDX-non-melanocytic – – – – – – – – – – – – – – – – – – – Paget's disease Extramammary Paget's disease Pigmented epidermotropic metastasis of breast carcinoma Epidermotropic neuroendocrine carcinoma Bowen's disease (pagetoid or pigmented) Pagetoid reticulosis „Clear-cell‟ artefacts around keratinocy tes Complete regression of skin tumors other than malignant melanoma (e. halo nevi) Pigmented basal cell carcinoma Pigmented actinic keratosis Dermato. angiokeratoma .

CT chest/abd/pelvis. PET scan or PET-CT Melanoma . LDH & CXR • Limited value for melanomas <4mm -surgery is going to want most of these anyway for pre-op – New marker not routinely used S100beta and MIA – StageIII/IV – MRI head. CMP.the deeper the worse • Management – Bring pt back for a total body skin exam – Studies – usually a CBC.

evidence of regression.99 mm – 2. male sex.Exceptions – For those patients with a lesion < 1mm a selective SLN biopsy will be performed.0mm • Provides info on subclinical nodes with minimal morbidity • Identifies metastatic nodes for early therapeutic dissection • Identifies candidates for IFN alpha NOT theraputic however Sentinel lymph node biopsy • SLNB. no nationwide guidelines) – 1.Melanoma • SLNB – Primary melanomas >1. Those with some “soft” poor prognostic criteria: head and neck or trunk melanomas. Those patients who we would consider (Controversial.75-0. Ulceration – 4. vascular or neural invasion We have had 2 young women with positive lymph nodes with thin melanomas • . Clark level IV or higher – 3. Those with a depth between 0.

the elderly. and transplant patients) as well as those with decreased sensory functions (e. or indirectly via fomite transmission • Prevalence is higher in children and in people who are sexually active • Spread of the infestation between family members and close contacts is common • Crusted scabies-compromised immune systems (e. people infected with HIV. sexual or otherwise. and lack of public awareness of the condition • Transmitted directly by close personal contact.g. patients with leprosy or paraplegia) . races and socioeconomic groups are susceptible • Environmental factors-overcrowding.SCABIES • Worldwide problem and all ages.g. delayed treatment of primary cases.

which require 10 days to mature incubation period before symptoms-days to months first-time infestations.SCABIES • • • • • • Sarcoptes scabiei var. resulting in pruritus and cutaneous lesions Asymptomatic scabies-infested individuals are not uncommon. hominis causes human scabies entire 30-day life cycle of mites is completed within the epidermis female mite will lay 60-90 eggs.2-6 weeks before the host's immune system becomes sensitized to the mite or its byproducts. and these individuals can be considered „carriers • .

including the scalp and face . buttocks and belt area • men-penile and scrotal lesions are common • women-areolae. feet.SCABIES • history distribution. flexural aspect of the wrists. elderly and immunocompromised-all skin surfaces are susceptible. waist. nipples and genital area are often affected • infants.types of lesions. axillae. ankles. behind the ears. and pruritus form the basis of the clinical diagnosis • intense pruritus at night exacerbated by a hot bath or shower • Symmetrical-interdigital/web spaces.

excoriations vesicles. grayish-white and 1-10 mm in length .SCABIES • • • small erythematous papules are present. eczematous dermatitis and secondary bacterial infection are common pathognomonic sign is the burrowwavy. thread-like. indurated nodules.

SCABIES .

areas of eroded skin. eggs and/or fecal pellets • DDx. overnight treatment. Good.SCABIES • Dx-mineral oil examination in which skin scrapings from infested areas are inspected under light microscopy for adult mites. contact or nummular dermatitis. Poor. current recommendation is to repeat on day 8.RF-for CNS toxicity. on days 1 and 8. autosensitization („id‟ reaction).atopic. bullous pemphigoid. RF-Allergy to formaldehyde. resistance very common(not used anymore) . – Lindane lotion (1%)Topically overnight. dermatitis herpetiformis. pregnancy. but some signs of tolerance developing. breastfeeding. age <2 years. pyoderma. and other insect bites should be considered • Tx-Topical – Permethrin cream (5%)Originally a single.

breastfeeding. RFfor irritant contact dermatitis. Excellent • Pruritus and lesions can persist for 2-4 weeks after successful treatment . commercially available as 3 and 6 mg tablets. <15 kg. RF-for potential CNS toxicity. pregnancy. Very poor. denuded skin. has antipruritic properties and may be used for post-scabetic pruritus • Tx-oral – Ivermectin (200–400 mg/kg). on days 1.SCABIES • Tx-topical – Crotamiton (10%)Topically overnight. 2. Orally on day 1 and 14. 3 and 8.

Pediculus capitis . race or socioeconomic class • children 3-11 years of age have the highest incidence • more frequently observed in girls • head louse. wingless insects belonging to the order Anoplura • worldwide with no strict limitations based upon age.Lice(head) • Lice are bloodsucking. sex.

helmets and other head gear • head lice do transmit coagulase-positive Staphylococcus aureus and group A Streptococcus pyogenes by carrying these organisms on their external surfaces. excoriations. pyoderma. blow-dryers. irritability. • scalp. and scaliness of the scalp and posterior neck are common • diagnosis is made by id of nits and/or adult lice on the scalp hair. bedding. viable eggs are tan to brown in color • occ pt will present with a low-grade fever. erythema. lymphadenopathy and a secondary bacterial infection • . brushes. behind the ears and the nape of the neck-pruritus. hair accessories.Lice(head) • Transmission occurs via direct head-to-head contact or by fomites such as combs.

Lice(head) .

Lice(head) • DDX-seb derm. psoriasis • Tx-similar to that of scabies. are advisable in order to: • (1) kill any nits that survived treatment • (2) better defend against the seemingly growing resistance to most pediculicides • (3) reduce the risk of reinfestation by means of fomites . 1 week apart. two applications. – With all topical preparations (regardless of package instructions).

the crab louse may coexist with other sexually transmitted slightly higher in men highest prevalence in msm. • . Indeed. in scalp. moustache. Infestation is most frequently observed in those 15 to 40 years of age infestation in pubic hair. eyebrows. 60% of patients with pubic lice are infested in two different hair-bearing sites. beard.Crab lice(pubic) • • • • Pthirus pubis. axillae and perianal area. eyelashes.

Crab lice(pubic) • skin-colored or simply appear as hemorrhagic crusts. tx similar to scabies . excoriations. may be erythema around the hair follicles. other other ds w/pruritus • Tx-all tx should be given 1 week apart. and lymphadenopathy • DDX-ID diagnostic. secondary bacterial infection. all infestation and bites.

poverty. poor hygiene. and trench fever and bacillary angiomatosis or endocarditis (caused by Bartonella quintana) • Transmission not by louse bites but contaminated fecal pellets being scratched into excoriated skin or inhalation of dry. Borrelia recurrentis). relapsing fever (caused by a spirochete. wars and natural disasters • primary vectors for several diseases caused by Rickettsia. Borrelia and Bartonella species • Pediculosis corporis is caused by an infestation of humans and their clothing by Pediculus humanus var. corporis.Body Lice • associated with overcrowding. infestation requires an inability to wash and change clothes • transmitted by the body louse-epidemic typhus (caused by Rickettsia prowazekii). . powdery louse feces from infected bedding or clothing.

neck. crusts and excoriations. Clinical findings include small pinpoint red macules. papules.Body Lice • nits and lice are rarely found on the patients' skin they reside primarily on the clothing of their host • back. occasionally complicated by impetigo and lymphadenopathy . shoulders and waist areas are commonly involved.

the clothing and bedding of infested individuals are discarded in tightly sealed.Body Lice • DDX-any condition causing pruritus • Preferably. plastic biohazard bags and incinerated • involves fumigating the clothing and heating it to a temperature of 65°C for 15-30 minutes .

Spider Bites • • • • • Black widows are large. alphalactrotoxin. bites are painful. an hourglass design is seen on the abdomen most common in North America Lactrodectus mactans. shiny black spiders with a large round abdomen Found in woodpiles. in shoes and under outhouse seats In Latrodectus mactans. releases Neurotoxin: Ach is irreversibly releasedsevere pain in local muscles crampy abd pain. mimicks acute abdomen. chills. paralysis. vomiting. rhabdomyolysis Benzodiazepines and intravenous calcium gluconate can be helpful for the associated tetany .

Spider Bites • Loxosceles spiders are found throughout the world. Coombs'-positive hemolytic anemia . In the US. sys rxn-DIC. laeta. L. L. L. L. arizonica cause skin necrosis • Brown recluse spiders are commonly found in south central US. necrotic eschars or ulceration. rufescens. from Tennessee and Missouri to Oklahoma and Texas. often found in woodpiles. reclusa. • Brown spiders are non-aggressive • diagnosis can now be confirmed either by an enzyme immunoassay to detect Loxosceles venom in a skin biopsy • Sphingomyelinase D interacts with serum amyloid protein gravity dependent state • majority of bites do not cause serious reactions • Dermonecrotic reactions can present as dry. attics and under radiators. deserta and L.

ice and elevation • more widely available agents such as dapsone. triamcinolone and prednisone have been inconsistent and often disappointing • Antivenin • Avoid heat and immediate surgery as they can spread venom • Augmentin 2/2 infection . colchicine.Spider Bites • Most bites can be treated with rest.

Spider Bites • Tegenaria agrestis. moist areas.Large. aggressive spiders found in dark. hemolysis and thrombocytopenia Funnel shapped web • • • • . Canada and Europe Hobo spider toxins may cause local necrosis and directly affect the CNS Systemic symptoms include headache. especially basements found in the northwest US. nausea and weakness. hairy.

Spider Bites • • • • Tarantulas are large hairy spiders common in the southwestern US tarantulas possess urticating hairs on the dorsal abdomen Itching at the site of urticating hair penetration may persist for several weeks after exposure-Hairs that penetrate the cornea can result in ophthalmia nodosa. a chronic granulomatous reaction that can result in loss of vision do not produce severe systemic toxicity .

Androgenetic Alopecia • • 80% of Caucasian men by age 70 Genes and hormones are implicated. inheritance is polygenic Hormones in AGA – Testosterone-Increased muscle mass – Growth of the phallus & scrotrum – Voice change – Sex drive – Terminal pubic and axillary hair fibers • .

external ears. acne. growth of terminal hairs in the beard region. nostrils & limbs . growth of the prostate.AGA • Hormones in AGA – Testosterone • Increased muscle mass • Growth of the phallus & scrotrum • Voice change • Sex drive • Terminal pubic and axillary hair fibers – Testosterone is converted to DHT by 5 alpha reductase which leads to temporal scalp hair recession.

AGA • The genetic absence of type II 5areductace prevents male androgenetic alpecia • 5a-reductase activity and DHT levels are increased in affected skin .

AGA • Classification systems – Ludwig – Hamilton Norwood .

and appropriate screening laboratory tests (total and free testosterone. and 17-hydroxyprogesterone) should be performed . • Dx-clinical in men bx to confirm. hair loss in women should suggest the possibility of pathologic hyperandrogenism.AGA • DDX-other non scarring alopecias. dehydroepiandrosterone sulfate.

AGA • Tx – Hair transplant – Minoxidil 2% and 5%. spironolactone or even finasteride(off-label use. birth defects) . 1ml applied to scalp bid – Finasteride 1mg po daily • Stops hair loss in 90% of men for at least 5 years • Can regrow hair in 65% of men – hyperandrogenemia in women-Oral contraceptives.

particularly at the margins of areas of alopecia • Other presentations include alopecia totalis (loss of all scalp hair).e.Alopecia Areata localized hair loss • 0.1% to 0. alopecia universalis (loss of all scalp and body hair and an ophiasis pattern (band-like pattern of hair loss along the periphery of the temporal and occipital scalp) .2% of the population • Normal follicle keratinocytes lack MHC class I and II giving them immunologic privilege • In AA human leukocyte antigens become expressed by the hair follicle • T lymphocytes then interact with hair matrix cells causing destruction • presents as round or oval patches of non-scarring hair loss • Short „exclamation mark‟ hairs (i. distal end broader than the proximal end) can often be seen.

AA .

up to 30% of patients have alopecia areata) – Type 1 diabetes increased in relatives of patients with alopecia areata . vitiligo. asthma). atopic dermatitis.g. inflammatory bowel disease – Autoimmune polyendocrinopathy syndrome type 1 (autosomal recessive. >40% in some studies – Autoimmune thyroid disease (e. due to mutations in the autoimmune regulator gene [AIRE].AA • Assoc Disease – Atopy (allergic rhinitis. Hashimoto's thyroiditis).

but a scalp biopsy may be needed. trichotillomania. aplasia cutis and „burnt-out‟ cicatricial alopecia. secondary syphilis and loose anagen syndrome. The diffuse variant may initially be confused with telogen effluvium and androgenetic alopecia • DX-history and clinical examination is sufficient to distinguish between these conditions. traction alopecia. pressure-related alopecia. . temporal triangular alopecia.AA scaring or no scaring • DDx – Tinea capitis.

into the mid dermis. anthralin. q 4-8 wks (1) – – Minoxidil (2) – Immunotherapy: Squaric Acid.3-5mg/ml . diphenylcyclopropenone (2) – Systemic steroids (2) – PUVA (2) – Excimer laser (3) – Photodynamic therapy (3) – Systemic cyclosporine (3) .AA • Tx – May improve on its own – Topical steroids – clobetasol (1) intralesionalIL steroids .

and the frequent recurrence • dermatophytes as well as non-dermatophytes-3 main pattern types – distal/lateral subungual with invasion via the hyponychium (most common) – white superficial with direct invasion into the superficial nail plate (often due to T. long treatment periods. mentagrophytes) – proximal subungual with direct invasion under the proximal nail fold (immunocompromised hosts) • discomfort and pain associated with trimming the nails. potential side effects of systemic medications. running .Onychomycosis • affects men more than • challenging to manage due to difficulty in diagnosis.

mentagrophytes and E.Onychomycosis • frequently associated with chronic tinea pedis • most common causative pathogens are T. floccosum • Toenail more common than fingernail. 80% reoccur • Clinical and Histologic examination of formalin-fixed. rubrum. lower reoccurrence rates than iatraconazole. other antifungals avalible many med interactions – Topical cicloprox 8% nail lacquer-expensive . T. check LFT‟s prior to tx and mid-way. PAS-stained nail plates is a quick and reliable method for diagnosing onychomycosis • Tx-preferred terbinafine 250mg daily x3months.

Onychomycosis .

red and painful • Compression of the nail fold may produce pus drainage • most commonly due to bacteria. systemic antibiotics according to culture results. direct fluorescent antibody assay. Viral cultures.Paronychia • affected digit becomes swollen. • Tx-drainage of the abscess. systemic antivirals when due to HSV . in particular Staphylococcus aureus or Streptococcus pyogenes. and follows minor trauma to the nail • Recurrent episodes of acute paronychia should raise the suspicion of an HSV infection. and/or PCR should be obtained to identify the responsible agent.

Paronychia .

-11 • childhood vertical trans.. gym) – aerosolized • laser.Condyloma Acuminatum • • Caused by human Paillomavirus transmission – direct skin : skin – indirect contaminated surfaces (swimming pool.may have been caused by sexual abuse should always be carefully considered one of the most common sexually transmitted infections (STI) among adolescents and adults • • . ED&C • absence of viral envelope resistance to dessication – recurrent respiratory papillomatosis = HPV -6. adult genital : oral – cellular target = basal keratinocytes – maceration promotes Genital warts are uncommon in prepubertal children and are of special concern to healthcare providers.

or adult-onset form and is caused by HPV-6 and -11. -18. It occurs in a juvenile. and more often progress to intraepithelial neoplasias • Recurrent respiratory papillomatosis (RRP)-exophytic lesions of airways and not seen by dermatologists. tend to persist.Condyloma Acuminatum • Most genital papillomavirus infections resolve spontaneously • median duration of high-risk HPV infections in women is reported to be 8 months and persistence is observed in 30% after 1 year and in 9% after 2 years of observation • HPV-16. -31 and -45 are found in approximately 80% of cervical cancers worldwide • Immune suppression in HIV-infected patients or organ transplantinfections are more frequent. low incidence RRP is the most common benign tumor of the larynx and the second most common cause of hoarseness in children .

31. or in adjacent areas such as the inguinal fold and the mons pubis . upper aerodigestive malignancies.Condyloma Acuminatum • non-enveloped dsDNA virus • cellular target = basal keratinocytes(enter through break in skin) • oncogenicity – HPV-16. -8 SCCs in EDV • Most will resolve w/in 2 years • external genitalia and the perineum. -33. -45 – cervical cancer. perianally. SCC – HPV -5. -18. . bowenoid papulosis.

but rarely beyond the dentate line . sessile. the urethra. brown or whitish (especially when macerated in moist areas) pedunculated or broad-based papillomas up to several centimeters in diameter large confluent plaques and may extend into the vagina.Condyloma Acuminatum • • • • • Condylomata-one to several millimeters in diameter discrete. or the anal canal. smooth-surfaced exophytic papillomas skin-colored.

mumps antigens. curettage.Condyloma Acuminatum • • • DDX-diagnosis of skin and genital warts is uncomplicated if typical clinical features are present Dx-hx. laser – Salicylic acid – Cantharadin (occlusion) – Imiquimod • 3x per wk x 16wks – 5-fluorouracil – Podofilox (Condylox) – cytotoxic • BID x 3 days in weekly cycles – Cimetidine – activates Th1 cells to make IL-2 and interferon – Cidofovir (topical. clinical. TCA. trychophyton. bleomycin . histo Tx – Cryotherapy. systemic) – Intralesional candida. excision.

Verruca Vulgaris • • • • • • • • person-to-person transmission Cutaneous warts are caused by a small group of specific HPV types prevalence of 20% in schoolchildren and a decline One of the three most common dermatoses in children and occur with equal frequency in both sexes. exophytic and dome-shaped papules or nodules associated typically with HPV-1. -2 or – 4 . suggesting that protective type-specific immunity may develop Pathogensis similar for all HPV hyperkeratotic. Patients living in larger households often report an infected cohabitant The majority of warts will regress spontaneously within 1-2 years Reinfection with the same HPV type appears uncommon after clearance.

with gently sloping sides and a central depression • painful to pressure when walking . and lateral aspects of the hands and feet. the dorsal surfaces of hands. endophytic papules on palms. but may occur at any anatomic location • Palmar and plantar appear as thick. soles. and other sites prone to trauma such as knees or elbows.Verruca Vulgaris • commonly located on fingers.

lesions of acrokeratosis verruciformis. curettage. mumps antigens. excision. keratoacanthoma. TCA.Verruca Vulgaris • DDX-Seborrheic keratoses. trychophyton. systemic) Intralesional candida. bleomycin . LP Dx-clinical and histo • • • • • • • • • Cryotherapy. cornu cutaneum. laser Salicylic acid Cantharadin (occlusion) Imiquimod – 3x per wk x 16wks • 5-fluorouracil Podofilox (Condylox) – cytotoxic – BID x 3 days in weekly cycles Cimetidine – activates Th1 cells to make IL-2 and interferon Cidofovir (topical. actinic keratoses. angiokeratoma and amelanotic melanoma may resemble common warts.

Viral Exanthems • Varicella-Zoster Virus (HHV-3) – Etiologic agent of chicken pox and herpes zoster (shingles) – High morbidity and mortality in immunocompromised hosts – Transmission via airborne droplets or direct contact with vesicle fluid – Incubation 11-20 days – Extremely contagious(8090%) – Zoster = reactivation of latent VZV .

pruritic macules and papules – Start on scalp and facetrunk and extremities – Dew drops on a rose petal – Hallmark: Lesions in all stages of development .Viral Exanthems • Primary Varicella (Chickenpox) – Fever. myalgia – Erythematous. malaise.

Viral Exanthems • • Herpes Zoster (Shingles) Complication: Ramsay-Hunt Syndrome – VZV infection of the geniculate ganglion of the facial nerve – Zoster involves external ear – Facial paralysis – ipsilateral – Tinnitus or other auditory symptoms .

ocular and CNS abnormalities • 5 days before and 2 days after delivery – Neonatal varicella – Neonate develops at 5-10 days of age – Treat with VZIG + IV Acyclovir .Viral Exanthems • Varicella in Pregnancy • First 20 weeks of gestation: – Congenial varicella syndrome: – hypoplastic limbs.

previous history of varicella or receipt of the varicella vaccine) & the physical examination. occasionally.Viral Exanthems • DDX-HSV. a drug eruption. vesicular viral exanthems (Coxsackie.g. contact dermatitis. based upon both the history (e. and. insect bites or even scabies • Dx-clinical diagnosis. ECHO). pityriasis lichenoides et varioliformis acuta (PLEVA). initial episode versus multiple recurrences. rickettsialpox. is very important because a decision regarding instituting antiviral therapy is critical • Tzanck smear(cannot differentiate HSV types) and/or a DFA(allows distinction) are initially performed • Histo not too helpful b/w VZV and HSV(need staining) • PCR is a highly sensitive molecular technique and its use as a diagnostic test of choice is increasing .

but initiation of antiviral therapy after 72 hours but within 7 days also appears to be beneficial Acyclovir. calamine lotion and tepid baths acyclovir has been shown to decrease the duration and severity of varicella infection(24 to 72 hours from start) Acyclovir is clearly recommended for varicella in the adult population Varicella zoster immunoglobulin (VIG)-prophylaxis for all susceptible immunocompromised individuals VZV vaccine (Oka strain. Varivax®)-ages 12 months and 4-6 years herpes zoster-early tx within 72 hours of the onset of the first vesicle. is optimal.Viral Exanthems • • • • • • • • Varicella in children-symptomatically with antipyretics. famciclovir and valacyclovir are all FDA-approved for the treatment of zoster in immunocompetent individuals and result in decreased disease duration and pain. Intravenous acyclovir is indicated for the treatment of zoster in immunocompromised patients as well as those with serious complications . antihistamines.

Viral Exanthems • Epstein-Barr Virus (HHV-4)-causes – Infectious mononucleosis – Endemic Burkitt‟s lymphoma – Oral hairy leukoplakia – Nasopharyngeal carcinoma – Post-transplant lymphoproliferative disorders – Gianotti-Crosti Syndrome .

primary infection with EBV results in the infectious mononucleosis syndrome in 50% of individuals. . – adolescents and young adults. non-specific.2 cases per 100 000 – EBV is transmitted primarily through infectious saliva. In the US. although its presence in genital secretions and breast milk has been reported – Cell-mediated immunity to EBV infection is persistent and protects against developing infectious mononucleosis syndrome with virus superinfection later in life. the annual incidence of infectious mononucleosis is 45. similar rates are reached during adolescence in the US – Most children with primary EBV infection will have either no symptoms or a mild.Viral Exanthems • EPSTEIN–BARR VIRUS (HHV-4) – seropositivity approaches 60-80% in children of developing countries. febrile illness.

headache. pharyngitis.Viral Exanthems • Infectious mononucleosis – Fever. lymphadenopathy – Malaise. myalgias – Hepatosplenomegaly – Commonly morbilliform eruption 7-10 days after treatment with ampicillin • Cross-reaction between anti-EBV antibodies and penicillin-like drug • Desquamation 1 week later – Affects teens and young adults .

Viral Exanthems • Oral Hairy Leukoplakia – Slightly raised white plaque on lateral tongue – Corrugated appearance – HIV and immunocompromised .

and primary CMV. mild thrombocytopenia and an absolute and relative lymphocytosis • Diagnosis is usually made by a positive monospot test (a simple slide test that detects IgM heterophile antibodies) or increased titers of heterophile antibodies. acute viral hepatitis. lymphoma. drug reaction with eosinophilia and systemic symptoms (DRESS). toxoplasmosis. HHV-6 and HIV • Dx-mild to moderately elevated hepatic transaminase levels.Viral Exanthems • DDx-group A streptococcal infection. the latter are >1:40 in approximately 90% of young adults infected with EBV • EBV-specific serologies are often needed .

Viral Exanthems • Tx-self-limited and treatment is supportive .

breast milk and cervical and vaginal secretions. – spread indirectly by contaminated fomites.5% of all newborn infants – Transmission. transplanted organs and hematopoietic stem cells. – Transplacental transmission of CMV to the fetus is more likely in the setting of a primary infection in the mother. including saliva. with 40% of fetuses becoming infected.5-1. congenital CMV infection occurs in approximately 0.Viral Exanthems • Congenital CMV(HHV-5) – In immunocompetent hosts. urine. blood.is via body fluids. such as toys. compared to less than 1% in recurrent cases – incubation period of 4 to 8 weeks – „mononucleosis-like syndrome‟ similar to that seen with EBV is the most common clinical presentation in immunocompetent persons . semen. 95% of infections are asymptomatic or subclinical – inversely proportional to socioeconomic status – in the US.

interstitial pneumonia.Viral Exanthems • morbilliform. myocarditis. petechial or purpuric. arthritis. thrombocytopenia. meningoencephalitis. Guillain– Barré syndrome. rare complications include hemolytic anemia. . urticarial. develops in a small percentage of patients • administration of ampicillin during this symptomatic period leads to a cutaneous eruption in 80-100% of individuals • clinical course is benign and self-limited.g. granulomatous hepatitis. and gastrointestinal and genitourinary symptoms (e. gastroenteritis).

intracranial calcifications – #1 infectious cause of deafness and mental retardation in the U. retinitis. – Most common congenital viral infection – TORCH syndrome – Blueberry muffin baby . colobomas. microcephaly.Viral Exanthems • Congenital CMV – Infection during 1st and 2nd trimester – SGA.S.

Nowadays.Culture of CMV (from infected tissues) in human fibroblasts is „gold standard‟ for definitive diagnosis. • more rapid detection of CMV in tissue cultures (within 24-48 hours) is possible with the shell vial assay in which monoclonal antibodies are used to detect antigens associated with early CMV replication • most commonly employed laboratory tests analyze peripheral blood for the presence of CMV antigenemia or CMV DNA (the latter PCRbased test is necessary in the setting of neutropenia) .Viral Exanthems • DDX-EBV-induced infectious mononucleosis. viral hepatitis and lymphoma • Dx. toxoplasmosis. takes a few days to several weeks for confirmation.

Valganciclovir – If no reponse  Foscarnet and Cidofovir .Viral Exanthems • Tx – prevention plus prophylaxis or pre-emptive antiviral treatment in susceptible individuals – First line: Ganciclovir.

Viral Exanthems • HHV-6(Roseola) – most common in young children. occurring between the ages of 6 months and 3 years in 95% of cases – Transmission is through infected saliva – clinical manifestations of exanthem subitum occur in about 30% of those with primary HHV-6 infections .

Viral Exanthems • HHV-6 – Roseola Infantum/6th disease – Rapid onset high fever – Cutaneous eruption as fever subsides – Discrete. rose-red macules or maculopapules 2-5mm – Surrounded by white halo – Nagayama‟s spots  soft palate – HHV-6 usually requires no treatment . circular.

and Kawasaki disease • Dx-hx and clinical. and parvovirus infections) as well as scarlet fever. and enterovirus. rubella. Rocky Mountain spotted fever. PCR detection of cell-free HHV-6 DNA in serum or plasma has diagnostic value • Tx-benign and requires no treatment .Viral Exanthems • DDx-(rubeola. adenovirus. EBV.

Viral Exanthems • HHV-7 – Can also cause roseola – Possible role in pityriasis rosea – epidemiology appears to be similar to that of HHV-6 – HHV-7 has not been clearly associated with any clinical disease .

is a latent virus found in the vast majority of all types of Kaposi's sarcoma (KS) – classic form of KS peaks after the sixth decade of life and typically occurs in men of Mediterranean and Ashkenazi Jewish descent.Viral Exanthems • HHV-8 – transmission are not well understood – Kaposi's sarcoma-associated herpesvirus (KSHV). developing KS at a rate 20 000 times greater than that of the general population – KS is a vascular endothelial malignancy . HIV-positive men who have sex with men are at extreme risk.

Viral Exanthems • Associated with 2 neoplasms: – Kaposi‟s sarcoma – Castleman‟s disease • Lymphoproliferative disorder defined as "a localized hyperplasia of lymphoid follicles with and without a germinal center formation and marked capillary proliferation with endothelial hyperplasia 4 types of KS: – Classic KS – AIDS-related KS – Immunosuppression-KS – African endemic KS • .

ecchymosis. Of note. hemangioma. radiotherapy. intralesional interferon-α and systemic chemotherapy. the latter has markedly reduced the incidence of AIDS-related KS. for AIDS-related KS. angiosarcoma. topical alitretinoin. pyogenic granuloma and pseudolymphoma/lymphoma • Dx-confirmed by a skin biopsy • Tx-cryotherapy. and. highly active antiretroviral therapy (HAART). Surgery is usually not effective. .Viral Exanthems • DDx-acroangiodermatitis (pseudo-KS). bacillary angiomatosis.

It also occurs in adults. molluscum contagiosum (MC) became the only remaining poxvirus infection to specifically afflict humans. This disorder is caused by the MC virus (MCV). usually as a sexually transmitted disease. . self-limited process in children. most notably HIV-infected individuals. benign. fomites.Molluscum Contagiosum • With the eradication of smallpox. Transmission is via skin-to-skin contact and. less commonly. and more recently has been observed with increasing frequency in immunocompromised hosts. a member of the Molluscipox genus of Poxviridae • Most common infections in humans • Poxviridae • MC is a common.

pyogenic granuloma or pyoderma • Dx-clinicial and histo if necc . juvenile xanthogranuloma. verrucae. basal cell carcinoma. particularly AIDS • An associated molluscum dermatitis is common.Molluscum Contagiosum • MC lesions are firm. papular granuloma annulare. umbilicated pearly papules with a waxy surface • occur anywhere. condylomata acuminata. especially in children with atopic dermatitis. large and occasionally deforming lesions may be seen in the setting of immunosuppression. melanocytic nevi (especially Spitz nevi). Inflammation of MC lesions is sometimes seen • DDx-appendageal tumors. most common in skin folds and the genital region • Widespread.

tape stripping and laser – In children. topical cidofovir.Molluscum Contagiosum • Tx – Most papules of MC resolve spontaneously – curettage. liquid nitrogen. topical keratolytics. which has the added benefits of being painless and non-traumatic. application of cantharidin is a safe and effective therapy. more visits than curettage . chemovesicants. manual expression.

aureus-in adults • in childhood is caused by S. intravenous drug abuse. and less commonly by H. diabetes mellitus. saphenous vein harvest or prior episode of acute cellulitis) . aureus.Cellulitis • infection of the deep dermis and subcutaneous tissue caused most commonly by Str.g. alcoholism. Recurrent bouts of cellulitis may be caused by damage to the lymphatic system (e. previous lymph node dissection. pyogenes and S. influenzae • mixture of Gram-positive cocci and Gram-negative aerobes and anaerobes is associated with cellulitis surrounding diabetic ulcers and decubitus ulcers • Lymphedema. and peripheral vascular disease all predispose to cellulitis.

such as fever. vesicles. • Children usually have cellulitis of the head and neck region. bullae. non-palpable borders • In severe infections. chills and malaise • cardinal signs of inflammation: rubor (erythema). whereas in adults the extremities are most often affected . calor (warmth). pustules or necrotic tissue may be present. dolor (pain).Cellulitis • often preceded by systemic symptoms. and tumor (swelling) • ill-defined. Ascending lymphangitis and regional lymph node involvement may occur.

such as stasis dermatitis. and panniculitis (especially lipodermatosclerosis) . superficial thrombophlebitis.Cellulitis • DDX-lower extremity cellulitis includes deep vein thrombosis and other inflammatory diseases.

in penicillin-allergic patients. metronidazole plus ciprofloxacin) Immobilization and elevation. cultures and sensitivities should be obtained and antibiotics adjusted accordingly. Diabetic or decubitus ulcers complicated by cellulitis require broad-spectrum coverage (e. are recommended. needle aspiration and skin biopsy leukocyte count is usually normal or only slightly elevated Blood cultures are almost always negative in immunocompetent hosts 10-day course of an oral antibiotic that has good Gram-positive coverage Hospitalization and parenteral antibiotics should be reserved for patients who are seriously ill and those who have facial cellulitis. NSAIDs may mask the signs and symptoms of deeper necrotizing infections and should be avoided when treating cellulitis • .g.Cellulitis • Dx – – – Tx – – – – – – usually clinical. piperacillin/tazobactam or. as well as the application of wet dressings to areas with bullae or exudate. If signs and symptoms do not improve after 24-36 hours of treatment.

except for very young patients. the aged.Erysipelas • primarily an infection of the dermis with significant lymphatic involvement. S. and Haemophilus influenzae type b have been known to cause an erysipelas-like infection. the debilitated. • increased frequency during the summer months • less often caused by group G. where boys are more commonly affected. It has a distinctive clinical presentation and is most often caused by Str. aureus. • . C or D. Pneumococcus species. and those with lymphedema or chronic cutaneous ulcers • Women outnumber men. pyogene s (group A streptococci) • disease of the very young. Klebsiella pneumoniae. B. Yersinia enterocolitica.

A few hours to a day later. malaise and nausea. hot. bullae and small areas of hemorrhagic necrosis may also form • • • . Pustules. clearly demarcated from uninvolved tissue. vesicles.Erysipelas • • • well-defined margins. a small plaque of erythema develops that progressively spreads. tense and indurated with non-pitting edema. chills. painful to palpation and may burn LAD w/o lymphatic streaking. involves the face or the lower extremity is the most common location incubation period of 2 to 5 days. there is an abrupt onset of fever.

g.g. especially in immunocompetent hosts • Anti-DNase B and ASO titers are good indicators of streptococcal infections • Tx-10-14-day course of penicillin is the treatment of choice for erysipelas caused by streptococci. Routine laboratory evaluation will show an elevated leukocyte count with a left shift. Swabs from local ports of entry. Sweet's syndrome. erysipeloid.Erysipelas • DDx-cellulitis and other soft tissue infections (e. and the nares • Culture of skin biopsy specimens-yield poor results. the throat. necrotizing fasciitis) as well as inflammatory causes of „pseudocellulitis‟ (e. contact dermatitis) • Dx-Clinical. pustules or bullae. Although macrolides such as erythromycin may be used in penicillin-allergic patients(increase in macrolide resistance among certain strains of Str. Pyogenes) • Hospital admission and intravenous or intramuscular antibiotics should be reserved for children and debilitated patients .

superficial skin infection that primarily affects children • Two most common responsible organisms: – Staphylococcus aureus – Streptococcus pyogenes • Mode of spread: – Person-to-person contact – Contact with fomites • Two types of impetigo: – Non-bullous impetigo • Honey-colored crusts at sites of minor trauma – Bullous impetigo • Caused by S. aureus • Localized form of SSSS • Blister formation • Mediated by exfoliative toxin binding to Dsg1 • Acantholysis in granular layer • Lesions can occur on intact skin . highly contagious.Impetigo • common.

varicella tinea corporis scabies. pediculosis. bullous erythema multiforme. candidiasis. HSV. pemphigus foliaceus – Bullous impetigo • Bullous insect bite. bullous pemphigoid).g.Stevens–Johnson syndrome . Autoimmune bullous dermatoses (e. Eczematous dermatoses.Impetigo • DDx– Non-bullous impetigo• Insect bites. thermal burns. Herpes simplex viral infection. linear IgA bullous dermatosis.

or .or .first.or second-generation cephalosporin . including cleansing. removal of crusts.macrolide . and application of wet dressings – mupirocin 2% ointment or fusidic acid cream or ointment can be prescribed – β-lactamase-resistant penicillin .Impetigo • Tx– local wound care.

Vasculitis • Pathogensis – Immune complex deposition in vascular wall – Complement fixation – Increased neutrophil/lymphocyte adhesion to endothelial cells – Endothelial cell damage – Complement also causes mast cell degranulation  increased vascular permeability .

g. Caliber of affected vessel Small Classification Cutaneous small vessel vasculitis Subclassification Henoch–Schönlein purpura Acute hemorrhagic edema of infancy Urticarial vasculitis Erythema elevatum diutinum Infections Inflammatory disorders (e. autoimmune connective tissue diseases) Drug exposure Neoplasms Microscopic polyangiitis Wegener's granulomatosis Churg–Strauss syndrome Classic (systemic) PAN Cutaneous PAN Small and medium-sized Secondary Cryoglobulinemic ANCA-associated Medium-sized Large[*] Polyarteritis nodosa (PAN) Temporal arteritis[†] .AUTHORS' PROPOSED CUTANEOUS VASCULITIS CLASSIFICATION SCHEME.

• the lesions are asymptomatic. but urticarial papules. but they can be associated with burning. subcutaneous nodules and/or digital necrosis. pustules. • In contrast to small vessel disease. retiform purpura. vesicles.Vasculitis • Cutaneous findings of vasculitis depend upon which vessels are primarily involved • palpable or macular purpura. ulcers. petechiae or erythema multiforme-like lesions • favor dependent sites. reflecting the influence of hydrostatic pressure and stasis on the pathophysiology. . medium-sized vessel vasculitis typically presents with livedo reticularis. areas under tight-fitting clothing. pain and pruritus.

vesicles or urticarial lesions Initial lesion is often a purpuric macule or partially blanching urticarial papule – Favors dependent areas. erythematous papules. pain or pruritus – – Post-inflammatory hyperpigmentation . as well as areas affected by trauma (pathergy) or under tight-fitting clothing Usually asymptomatic but can be associated with burning.Vasculitis • Small Vessel Vasculitis – 7 to 10 days after exposure to inciting agent – – Palpable purpura.

Vasculitis .

associated with a preceding respiratory infection – – Acute onset of purpura. arthralgias and colicky abdominal pain Macular erythema or urticarial papules – – – Progress to inflammatory purpuric macules and papules Predilection for lower extremities and buttocks Lesions regress in 10 to 14 days. with resolution of skin involvement over a period of several weeks to months Recurrences in 5-10% of patients – .Vasculitis(scvv) • Henoch-Schonlein Purpura (HSP) – Most common in children < 10 yo.

Chronic renal failure. Continue to follow UA and serum Cr .Vasculitis(scvv) • HSP – GI complication-Intussusception/GI bleeding/Acute surgical abdomen – rare potential chronic problem after cutaneous lesions of HSP resolve.

edematous. ears and extremities Painful. . Immunizations Presents abruptly with large rosette-shaped purpuric and petechial plaques Favors face. Drugs (Antibiotics and NSAIDS). Bacteria. coin-shaped or targetoid Can involve the trunk and genital region: scrotum Facial edema – – – Fever but non-toxic appearing Mucosa/visceral involvement RARE Resolution in 1 to 3 weeks.Vasculitis(scvv) • Acute Hemorrhagic Edema of Infancy – – – – – – – Children 4 to 24 months of age Antigenic trigger: Viruses.

indurated wheals – Trunk and proximal extremities – Distinguish from urticaria: • Lesions persist beyond 24 hours • Associated with burning and pain rather than pruritus • Resolve with postinflammatory hyperpigmentation .Vasculitis(scvv) • Urticarial Vasculitis – Erythematous.

mucosal ulcerations. cough. gingival hyperplasia. and saddle nose deformity – Dyspnea.Vasculitis(small/med) Wegener‟s Granulomatosis Necrotizing granulomatous inflammation of the upper and lower respiratory tracts – Recurrent epistaxis. hemoptysis or pleuritis • Glomerulonephritis • Palpable purpura. nasal septal perforation. nodules. and livedo reticularis • immune factor is positive c-ANCA • treatment of choiceCyclophosphamide . oral ulcers.

subcutaneous nodules (typically on the scalp or extremities) • Less often. livedo reticularis. urticaria. nasal polyps and asthma. may persist for years – Second: peripheral eosinophilia. respiratory tract infections and gastrointestinal symptoms – Third: full-blown systemic vasculitis with granulomatous inflammation. retiform purpura and papulonecrotic lesions – Majority have p-ANCA against myeloperoxidase – Leading cause of death-Granulomatous inflammation of myocardium .Vasculitis(small/med) • Churg-Strauss – First: symptoms of allergic rhinitis. which can occur several years to decades after the initial symptoms – Cutaneous findings in 55% of patients – Palpable purpura.

Vasculitis(small/med) Subtype Molecular composition Associations Pathophysiology Clinical manifestations Raynaud's phenomenon. retiform purpura. gangrene. glomerulonephritis III Polyclonal IgM[*] against IgG Cryoglobulinemia . autoimmune connective tissue diseases. acrocyanosis I Monoclonal IgM or IgG Plasma cell dyscrasias. lymphoproliferative disorders Vasculitis Palpable purpura. HIV. arthralgias. lymphoproliferative disorders Vascular occlusion II Monoclonal IgM[*] (>IgG[*]) against polyclonal IgG HCV. peripheral neuropathy.

Vasculitis(med) • Polyarteritis Nodosa – Multisystem segmental necrotizing vasculitis affecting medium. painful subcutaneous nodules. digital infarcts – p-ANCA positive – Associated with: • Hepatitis B • Hepatitis C • HIV • Strep • IBD .and small-sized arteries – 50% have skin findings: livedo reticularis and punchedout ulcers.

ASLO/anti-DNase B. cryoglobulins Gastrointestinal Renal Liver function tests. platelets.BASIC LABORATORY EVALUATION FOR PATIENTS WITH CONFIRMED CUTANEOUS VASCULITIS. serum and urine protein electrophoresis. hepatitis B surface antigen. urinalysis. creatinine. C-reactive protein. HIV antibody Immunologic Rheumatoid factor. CH50. serum immunofixation electrophoresis. Organ system Hematologic Laboratory tests Complete blood count with differential. ESR. electrolytes Infectious Anti-hepatitis C antibody. stool guaiac Blood urea nitrogen. C3. ANA. C4. ANCAs[*] .

inflammatory disease. NSAIDs) may be all that is necessary. but there are no data to support this practice.Vasculitis • Tx – determine whether the disease is either primary or secondary to an underlying condition (e. rest) or symptomatic therapy (e.g. antihistamines. drug exposure or neoplasm) that can be treated (or.g. calcineurin inhibitors and antihistamines are sometimes used. avoiding tight clothing. in the case of medications. • mild skin-limited disease. • Topical corticosteroids. . infection. leg elevation.g. discontinued) – next step is to evaluate the patient for systemic involvement – based on the extent and severity of systemic involvement – CSVV frequently resolves without any treatment avoidance inciting trigger. supportive measures (e.

Colchicine (0. chronic lesions. ulcerating or progressive cutaneous disease. Dapsone (50-200 mg/day orally) can lead to improvement of mild to moderate.g.short course of high-dose oral corticosteroids (e.g. ANCA-associated vasculitides).Vasculitis • Tx – Chronic (>4 weeks) or more severe cutaneous disease may require more aggressive systemic. but it can take several weeks to induce a response – severe. Immunosuppressive agents such as azathioprine (2 mg/kg/day) and methotrexate (<25 mg weekly) – significant systemic vasculitis (e.high-dose corticosteroids in combination with cyclophosphamide.6 mg orally two to three times daily). up to 1 mg/kg/day of prednisone). More recent data suggest that mycophenolate mofetil and azathioprine may help .

• • . epidermal nevus. The sign of Leser–Trélat may also appear with acanthosis nigricans. DDx-as SK. other endocrinopathies. as a side effect of certain drugs. diabetes mellitus. or as a manifestation of an underlying visceral malignancy. or other papillomatous epithelial proliferation Acanthosis nigricans has overlapping clinical features with confluent and reticulated papillomatosis.Acanthosis Nigricans • • clinical presentation-hyperpigmented velvety plaques on the neck and in the axillae association with obesity. acrochordon. especially when it is a harbinger of an internal malignancy.

erythema. including deep follicular structures. hypertrophic scars and marked wound contracture . no blistering. More extensive epidermal necrosis with vertical elongation of keratinocytes. erosion and exudation Heals in 10–21 days with mild but variable scarring. Intense pain but reduced sensation. deep red to pale and speckled in color. tenderness. Severe pain. deep rubor. serous or hemorrhagic bullae. pain. fibrin and cellular debris.Burns(thermal) • 1st-Epidermis only. serosanguineous bullae and erosions. Heals without scar • 2nd-(superficial)-Epidermis and superficial dermis. tenderness. may appear devitalized initially. subepidermal bullae possible • 2nd-(deep)-Epidermis and most of dermis destroyed. prolonged healing time. Necrotic areas may have serous crust w/neutrophils.

hard. coagulation necrosis. most require surgical correction superficial second-degree burn .Burns(thermal) • 3rd-Full-thickness epidermal and dermal destruction. charred. Dry. non-blanching. insensitive areas.small lesions heal with significant scarring.

Burns(thermal) Second degree .

Burns(thermal) 3rd degree .

Burns(thermal) • definitive diagnosis of wound depth may not be possible for the first 24 to 72 hours because of vascular occlusive changes severity of burn injuries is based upon depth and BSA involvement. BSA is estimated in adults by the „rule of nines‟ • .

including prostaglandins.Burns(thermal) • Necrosis of the epidermis occurs in about 45 minutes at 47°C (117°F). • Interstitial edema develops from altered osmotic pressure and capillary permeability • chemical mediators with vasoactive and tissue-destructive properties are released. but only 1 second at 70°C (158°F) • Denaturation and coagulation of cellular proteins occur in thermal injury. lipid peroxides and oxygen radicals • Heat-related illness accounted for more than 8000 deaths in the US between 1979 and 1999. histamine. serotonin. and is responsible for 7% of wilderness deaths . bradykinin.

rehydration. heat stroke • most important diagnostic issue with thermal burns is the depth of the injury • important distinction is the degree of neurologic compromise • Tx – removal from the hot environment. heat edema. rest. cleaned gently to remove any foreign material. heat exhausation. infection prevention. and evaluation of involved systems – assessment of cardiopulmonary status as well as the extent and depth – cool compresses.Burns(thermal) • DDx-Heat cramps. heat syncope. restoration of electrolyte balance. – proper healing environment .

Silver sulfadiazine has gained wide acceptance for both pediatric and adult burn tx-absorption can lead to leukopenia. – silver sulfadiazine produces a pseudoeschar that may interfere with burn depth assessment. Superficial wounds may require little additional therapy – Deeper burn wounds need more aggressive therapy.Burns(thermal) • Con‟t Tx – Topical antimicrobial effective in burn wound care include silver sulfadiazine. the most popular approach being serial excision – 3rd degree excised early – Newer skin substitutes such as acellular dermal matrix (AlloDerm®). mafenide acetate and silver nitrate. bilaminar collagen-chondroitin sulfate and silicone (Integra®) and cultured epithelial autografts are gaining popularity .

PMNs ____________________________ PROLIFERATION within hrs cells detach from BM migrate MØs phagocytize. cytokines activate inflammatory cells. thickness PATHOGENESIS • pressure – > 32mmHg at risk – > 70mmHg rapid ulcer formation – 150mmHg lying on hospital mattress – bone : muscle interface • shearing forces – HOB > 30 shearing forces in sacral/coccygeal area • friction – dragging across bed sheets – damage to stratum corneum • moisture . release VEGF granulation tissue formation ____________________________ REMODELING fibrobalsts remold collagen matirx strength. permeability. damaged parenchymal cells growth factors. fibroblasts vasodilation.Decubitus Ulcers • An ulcer is a wound with loss of epidermal and dermal layers • INFLAMMATION platelets.

Decubitus Ulcers .

Decubitus Ulcers STAGE I • erythema • induration • warmth STAGE II • shallow ulcer • loss of epi +/.dermis STAGE III • deep ulceration • necrotic base STAGE IV • deep ulceration to bone .

and poor nutrition . most of which develop during the first few weeks of hospitalization • approximately 20%-at home • 70% occur in patients over 70 years of age • 95% on lower body. sensory deficit. legs • Risk factors that predispose to the development of pressure ulcers include prolonged immobility. circulatory disturbance.Decubitus Ulcers • The US Department of Health and Human Services reports that approximately 10% of all hospitalized patients and 25% of nursing home patients have pressure ulcers. pelvic.

anticardiolipin. CRP – nutritional satus • albumin/pre-albumin. transferrin/ferritin. mycobacterial. infection • CBC • ESR. hep B/C biopsy – r/o malignancy (Marjolin ulcer). vasculitis. zinc – throbogenic state. RF. panniculitis – r/o unusual ulcer causes – tissue culture (bacterial. antithrombin III. lupus anticoagulant. vasculitis • protein C/S. vit A/C. fungal) patch testing • • . factor V Leiden • cryoglobulins/cryofibrinogens.Decubitus Ulcers • labs – anemia/polycythemia. ANA.

zinc. manganese. E – selenium.Decubitus Ulcers • Tx• nutrition – sound nutrition essential to wound healing – carbohydrates. anaerobes (Pseudomonas. fungal lack signs of intense inflammation . pathotenic acid – bariatric surgery risk • infection – polymicrobial – staph. thiamine. enterobacter) – mycobacterial. C. fats cellular energy – protein anabolic repair – vitamins A. copper.

Accuzyme) – mechanical • wet-moist saline • surgical antiseptics – chlorhexidine.01% gel • diabetic ulcers • black box = risk of cancer mortality with 3+ tubes • • . booties stage IV surgical debridement debridement – enzymatic • controversial • collagenase (Santyl) • papain (Panafil.Decubitus Ulcers • • • • rotation q 2h appropirate mattress. providone-iodine cytotoxic to open wounds growth factors – topical becaplermin (Regranex) 0. pillows. acetic acid. foam wedges.

Decubitus Ulcers • • • Fonder M. J Am Acad Dermatol 2008.58:185-206. et al. macerated tissue semi-occlusive dressings – semipermeable to gass. films . foams. . A. alginates. moisture – Impermeable to liquids – hydrogels. moist environment – wounds heal best in moist environment – dry wounds further tissue death – occlussive dressings infection rate – caution in wounds with heavy exudate. Treating the chronic wound.

Alginate. Foam. III.Decubitus Ulcers Pressure / Decubitus Stage I. thin Hydrocolloid Stage II.Film ( friction).Hydrocolloid. Debriding agent Stage IV.Buerger‟s Disease. Cryofibrinogenemia . Debriding agent DDX. Hydrofiber. Hydrogel.

deep venous thrombosis and/or phlebitisIn addition. the factor V Leiden mutation is more prevalent in patients with venous ulcers than in the general population – incidence of venous ulcers is equal in men and women – recurrence rate can be over 70% .Leg Ulcers • Venous Ulcer – Prevalence increases with age. as demonstrated by one study which found that >85% of those affected were over 64 years of age – Risk factors for the development of leg ulcers include obesity and a history of significant leg injury.

factor V Leiden – neuromuscular dyfunction pathogenesis – tissue ischemia theories • distension of capillary bed fibrinogen leakage capillary fibrin cuffs O2 depriv • fibrin traps growth factors inavailablity • white cell trapping release collagenase.Leg Ulcers • ulcer subtypes – venous – arterial – neuropathic (diabetic) – pressure/decubitus – vasculitic – other: infectious. malignancy. PG. drug induced (hydroxyurea). NLD. vasculitic. panniculitis. vaso-occlusive. genetic (Klinfelter) • venous insufficiency risk factors – obesity – phlebitis – DVT. TNF – inappropriate wound healing • . free radicals.

Leg Ulcers .

Leg Ulcers • Venous Stasis • edema – limb heaviness. aching • stasis changes – hemosiderin in macs. arabesque bodies . extravasated RBCs • red-brown dusky disoloration • petechiae – stasis dermatitis = eczematous • lipodermatosclerosis – aka sclerosing panniculitis membranous lipodystrophy – woody induration – inverted champagne bottle – fibrosed sub q.

warmth. induration. may involve entire circumference – irregularly shaped – superficial – yellow fibrinous base w. unilateral.Leg Ulcers • • DDx-cellulitis(acute. systemic sx) Venous Ulcer – – – – medial large along sup saphenous v. erythema. beefy red tissue beneath .

Leg Ulcers Venus Ulcer ATROPHIE BLANCHE • aka livedoid vasculopathy • smooth ivory white atrophic sclerotic plaques • peripheral trelengectasias • ulcerations of various sizes .

Leg Ulcers • DDx • elephantiasis nostra – chronic lymphedema – hyperkeratotic. verrucous – massive enlargement • infestation aka lymphatic filariasis parasitic filarial worms Wuchereria bancrofti Brugia malayi Africa .

vasculitis • protein C/S. lupus anticoagulant. factor V Leiden • cryoglobulins/cryofibrinogens. hep B/C biopsy – r/o malignancy (Marjolin ulcer). zinc – throbogenic state. antithrombin III. RF.Leg Ulcers • • Venous labs – anemia/polycythemia. vasculitis. fungal) patch testing • • . mycobacterial. vit A/C. anticardiolipin. panniculitis – r/o unusual ulcer causes – tissue culture (bacterial. infection • CBC • ESR. transferrin/ferritin. CRP – nutritional satus • albumin/pre-albumin. ANA.

wound care and dressing • Tx underlying cause .Leg Ulcers • venous – compression ~40mmHg (cautionn in PAD). infection control. leg elevation – debridement of necrotic fibrinous debris • All other tx methods similar to that of decubitus-nutrition.

Leg Ulcers • Arterial – PAD 10% in the general population over the age of 45 years – risk factors are age >40 years. hyperlipidemia. hypertension. cigarette smoking and diabetes mellitus. – Peripheral arterial disease increases the risk of death from cardiovascular causes even in the absence of a history of a myocardial infarction or ischemic stroke . and sedentary lifestyle. hyperhomocysteinemia. male gender.

Leg Ulcers • pathogenesis – progressive luminal narrowing • PVD – embolic • thromboembolic/cholesterol emboli • infectious – vasospastic • Raynaud‟s .

Leg Ulcers • atherosclerosis > cholesterol emboli. AVM • clinical clues – claudication – poor pulses – acute palor rubor – severe pain • ulcer – over bony prominence – round – sharply demarcated borders – little granulation tissue – exposure of deep tendons. may be shiny/atrophic . bone – surrounding skin often normal.

Leg Ulcers • labs – anemia/polycythemia. antithrombin III. CRP – nutritional satus • albumin/pre-albumin. vit A/C. anticardiolipin. factor V Leiden • cryoglobulins/cryofibrinogens. fungal) patch testing • • . vasculitis • protein C/S. zinc – throbogenic state. vasculitis. lupus anticoagulant. hep B/C biopsy – r/o malignancy (Marjolin ulcer). RF. panniculitis – r/o unusual ulcer causes – tissue culture (bacterial. ANA. mycobacterial. infection • CBC • ESR. transferrin/ferritin.

nutrition issues similar to prev wounds .Leg Ulcers • Tx• arterial – angioplasty +/. dressings.bypass • Wound care .

spina bifida. which are responsible for 85% of all amputations – Risk factors include male gender. medications and leprosy. 15-25% will require an amputation – major cause of non-traumatic lower-extremity amputations in the US is in fact non-healing diabetic foot ulcers.Leg Ulcers • Neuropathic and Diabetic Ulcers – The most common cause of neuropathic foot ulcers in the US is diabetes mellitus. poor glucose control. . 20% of the 16 million people in the US known to have diabetes will develop an ulcerated foot at some time during their lifetime – Of these. retinal or renal complications. diabetes for >10 years. and associated cardiovascular. alcohol abuse. – Other causes of peripheral neuropathy that are associated with neuropathic ulcers include spinal cord lesions.

Leg Ulcers .

hair loss. atrophic skin. onychodystrophy – impaired wound healing HbA1C – > 9% risk – > 12% WBC fxn altered • chemotaxis. intracellular bacterocidal activity • . brittle skin – macrovascular dz • calcification of arteries pulse exam less reliable • pallor on limb elevation. adherence • phagocytosis. rubor with dependency • shiny.Leg Ulcers • combination – peripheral neuropathy • sensation loss trauma • motor dysfxn foot deformities • autonomic dysfxn dry.

Leg Ulcers .

fungal) • patch testing . transferrin/ferritin. zinc – throbogenic state. hep B/C • biopsy – r/o malignancy (Marjolin ulcer). factor V Leiden • cryoglobulins/cryofibrinogens. lupus anticoagulant.Leg Ulcers • labs – anemia/polycythemia. vit A/C. mycobacterial. vasculitis. vasculitis • protein C/S. RF. anticardiolipin. ANA. infection • CBC • ESR. antithrombin III. panniculitis – r/o unusual ulcer causes – tissue culture (bacterial. CRP – nutritional satus • albumin/pre-albumin.

enzymatc) – pressure off loading – address vascular dz – Wound care . infection control – aggressive debridement (surgical.Leg Ulcers • DDx-arterial. venous. ACD • Tx-nutirtion. other causes of peripheral neuropathy. dressings similar to prev .

EIC • present to clinicians because of medical or cosmetic concerns. or due to discomfort from mechanical irritation or inflammation of the cyst • histologic features determine the definitive diagnosis • Can occur any where on body • most common cutaneous cysts • most common on the face and upper trunk • range from a few millimeters to several centimeters in diameter • derive from the follicular infundibulum • multiple epidermoid cysts may occur in individuals with a history of significant acne vulgaris .

EIC • Multiple cysts may also occur in the setting of Gardner syndrome (familial adenomatous polyposis) and in nevoid basal cell carcinoma syndrome Non-inflamed epidermoid cysts are usually asymptomatic. with pressure. and this is a common reason for presentation to a physician's office • • . but. cysts contents may be expressed that may have an objectionable odor Rupture of the cyst wall can result in an intensely painful inflammatory reaction.

the cyst may recur. . • Inflamed epidermoid cysts may require incision and drainage.occasionally. antibiotic therapy • Intralesional triamcinolone may be helpful in speeding the resolution of the inflammation.EIC • Tx-excision is curative • incision and expression of the cyst contents and wall through the surgical defect • If the entire cyst wall is not removed.

including keratin and bacteria.Hidradenitis Suppurativa • • • • • targets apocrine gland-bearing skin sites axillae and anogenital region starts at or soon after puberty women are affected three times as often as men thought to represent an inflammatory disorder originating from the hair follicle • Rupture of the follicle allows introduction of its contents. possibly from ruptured follicular epithelia. Epithelial strands are generated. and form sinus tracts . into the surrounding dermis This excites a vigorous chemotactic response and abscess formation.

leading to a marked degree of frustration. sometimes with metastasis. peritoneum and rectum • Other complications include hypoproteinemia. perianal and/or inframammary areas • tender and extremely painful • sinus tracts and hypertrophic scars form • chronic drainage. nephrotic syndrome and arthropathy.Hidradenitis Suppurativa • inflammatory nodules and sterile abscesses develop in the axillae. groin. self-consciousness and depression. embarrassment. . lymphedema. in varying proportions • Complications include. blood and pus. and fistulae to the urethra. secondary amyloidosis. may be an occasional complication of chronic scarring disease. bladder. • Squamous cell carcinoma.anemia. especially when the discharge is malodorous • discharged fluid is often a mixture of serous exudate.

Hidradenitis Suppurativa .

granuloma inguinale. – Incision and drainage should be minimized because it may result in scarring and chronic sinus tract formation. Crohn's disease. but none are successful all of the time – weight reduction – measures to reduce friction and moisture – ILK 5mg – topical clindamycin-Staphylococcus aureus – 5-day courses of intranasal mupirocin are used in nasal carriers of S. mycetoma and tuberculosis • Dx.clinical. infection control • Tx-Many are successful some of the time.Hidradenitis Suppurativa • DDx-staphylococcal furunculosis. histo. aureus. .

Hidradenitis Suppurativa • Systemic corticosteroids (prednisone 60-80 mg/day)-improves initially then flare once d/c‟d • Isotretinoin has not been particularly effective • Specific systemic antibiotics are chosen on the basis of the results of bacterial cultures • cyclosporine and TNF-α inhibitors • Surg/exc-often not helpful .

and patients with elevated serum cholesterol • predilection are the neck. diabetics. proximal lower extremities. arms.Lipomas • • • • • • benign tumors composed of mature lipocytes among the most common neoplasms in humans often solitary most commonly-beyond the fourth decade of life incidence in men to be higher than in women incidence of lipomas is increased in overweight individuals. and buttocks • round to oval. unless they encroach upon and compress nerves. trunk. in which case they may be painful . soft. mobile subcutaneous nodules with a normal overlying epidermis • asymptomatic.

Lipomas • DDx-epidermoid cysts • Dx-clinial and histo • Tx-easily excised .

phenytoin-related anticonvulsants.g. Asian or of African or Middle Eastern descent • Exacerbating factors include pregnancy. of course. characterized by symmetric. hyperfunctional melanocytes within involved skin produce increased amounts of melanin as compared to uninvolved skin • Potential aggravating factors include other medications (e. It is most prevalent among young to middleaged women who are Hispanic. oral contraceptives and. acquired disorder.Melasma • common. hyperpigmented patches with an irregular outline that occur most commonly on the face. sun exposure • following exposure to UV irradiation (or another inducer). phototoxic drugs) and autoimmune thyroid disease .

malar and mandibular • Additional sites of involvement include the extensor forearms and the mid upper chest • fade during the winter months and they frequently either first appear or are accentuated following exposure to UV irradiation or during pregnancy .Melasma • Light to dark brown or brown–gray patches with irregular borders appear primarily on the face • three classic patterns–centrofacial.

Melasma .

Lichen planus pigmentosus. Q-switched ruby) . clinical. Erythema dyschromicum perstans Dx-hx. also an inhibitor of tyrosinase) Salicylic acid and glycolic acid peels can be used as adjunctive therapy Deeper chemical peels.g. Lichen planus pigmentosus. dermal pigmentation is notoriously difficult to treat.Melasma • DDx-Drug-induced hyperpigmentation or discoloration. Actinic lichen planus. broad-spectrum sunscreens w/o all tx will fail While epidermal pigmentation is somewhat amenable to topical therapies and chemical peels. Pigmented contact dermatitis. tretinoin (0. possible bx • • • • • • • Tx-sun protection.050.1%) and a corticosteroid (class V– VII) topical lightening include glycolic acid. Postinflammatory hyperpigmentation. laser therapy (e. kojic acid (a tyrosinase inhibitor). hydroquinone (2-4%). Acquired bilateral nevus of Otalike macules (Hori's nevus). and azelaic acid (15-20%. Exogenous ochronosis.

oval or linear in shape • Lesions enlarge centrifugally over time.5-2% of the general population worldwide • age of onset is approximately 20 years • absence of functional melanocytes • autoimmune theory proposes that alterations in humoral or cellular immunity result in the destruction of melanocytes • most common form of vitiligo is a totally amelanotic macule (or patch) surrounded by normal skin • fairly discrete margins.Vitiligo • acquired. but the rate may be slow or rapid . and they are round. idiopathic disorder characterized by circumscribed depigmented macules and patches • 0.

digits. periorificial). sacrum. flexor wrists. nipples. dorsal aspect of the hands. dorsal ankles and shins • .e. knees. axillae. facial vitiligo occurs around the eyes and mouth (i. and on the extremities it favors the elbows. umbilicus.Vitiligo • face. Typically. and inguinal and anogenital regions.

but not clearly in a segmental distribution – Unilateral (segmental): one or more macules involving a unilateral segment of the body lesions stop abruptly at the midline – Mucosal: mucous membranes alone • Generalized – Vulgaris: scattered patches that are widely distributed – Acrofacial: distal extremities and faceMixed: various combinations of segmental. acrofacial and/or vulgaris • Universal – Complete or nearly complete depigmentation .Vitiligo • Localized – Focal: one or more macules in one area.

Vitiligo .

. postinflammatory depigmentation.g. leprosy). Prior treatment with potent topical corticosteroids can also lead to hypomelanosis. and the late stages of treponematosis or onchocerciasis. or other cutaneous infections (e. the leukodermas associated with melanoma or scleroderma. pityriasis (tinea) versicolor.Vitiligo • case-by-case basis is unpredictable • Associations: – IDDM – Pernicious Anemia – Grave‟s Disease – Hashimoto‟s Thyroiditis – Addison‟s Disease – Alopecia areata • DDx-chemical leukoderma. postinflammatory hypopigmentation.

0. Minigrafting is the simplest method. 20% monobenzyl ether of hydroquinone (MBEH). PUVA. TCS-for small localized.1% tacrolimus ointment. applied once to twice daily to the affected areas for 9-12 months or longer – MBEH is a potent irritant and/or allergen.Vitiligo • Tx – NB-UVB. and an open use test should be performed before more widespread application(only for small area of normal pigment) .

• Hallmark-individual lesions come and go w/in 24 hours • as high as 30% in the general population • Urticaria is a worldwide disease and may present at any age. the most important of which is histamine . • The peak incidence depends on etiology • female:male ratio of approximately 2:1 for chronic urticaria • mast cell is the primary effector cell of urticaria • Mast cell granules contain preformed mediators of inflammation. pink or pale swellings of the superficial dermis that may have an initial flare around them • Lesions may be a few millimeters in diameter or as large as a hand.Urticaria • recurrent whealing of the skin • pruritic. and numerous or single.

g.and kinin-dependent (C1 esterase inhibitor def) • Non-immunologic – Direct mast cell-releasing agents (e. opiates) – Vasoactive stimuli (e.g. other non-steroidal anti-inflammatory drugs. nettle stings) – Aspirin.Urticaria • Immunologic – Autoimmune (autoantibodies against FceRI or IgE) – IgE-dependent (allergic) – Immune complex (vasculitic) – Complement. dietary pseudoallergens – Angiotensin-converting enzyme inhibitors .

Urticaria • important to distinguish urticaria from urticarial dermatoses. single or multiple • Classification – Ordinary urticaria (all urticaria not classified below) – Physical urticarias – Urticarial vasculitis (defined by vasculitis on skin biopsy) – Contact urticaria (induced by percutaneous or mucosal penetration) – Angioedema without wheals – Distinctive urticarial syndromes . such as urticarial drug eruptions.e. they last less than 24 hours) • Wheals may be small or large. eosinophilic cellulitis and bullous pemphigoid • „here today and gone tomorrow‟ (i.

Urticaria

Urticaria

Urticaria
• Acute urticaria is common in young children with atopic dermatitis, but chronic urticaria peaks in the fourth decade

Urticaria
• Chronic
– Autoimmune
• • • • • • • • • • Thyroid ds Vitiligo Insulin-dependent diabetes RA Pernicious anemia H. Pylori Parasitic infection Gastric anisakiasis simplex Dental infection G.I. Candidasis

– Infectious

Urticaria
Cold urticaira

Urticaria

dermatographism

Urticaria

Pressure urticaria

Urticaria
• Urticarial vasculitis – >24 hours – Histo will show LCV – Choose newest lesion when performing bx – Causes-hep b,c, SLE, sjorgrens, lyme ds, infectious mononucleosis, Drugs(cimetidine, diltiazem)

pre-bullous pemphigoid (i. urticarial drug reactions (e. acute febrile neutrophilic dermatosis (Sweet's syndrome). bx. . antibiotics) • Dx – comprehensive history and phys exam is essential – CBC.g. ANA. acute facial contact dermatitis. urticarial bullous pemphigoid).e. ESR.Urticaria • DDx – insect bite reactions (papular urticaria).

.

. Results of both have to be interpreted in the clinical context.Urticaria • IgE-mediated reactions to environmental allergens as a cause of acute urticaria and contact urticaria can be confirmed by skin prick testing and radioallergosorbent tests (RAST) of blood.

Urticaria • Tx-1st line antihistamine • Classic (sedating) – Chlorpheniramine -4 mg tid (up to 12 mg at night) – Hydroxyzine-10–25 mg tid (up to 75 mg at night) – Diphenhydramine-10-25 mg at night) – Doxepin-10-mg at night • 2nd gen – Acrivastine-8 mg tid – Cetirizine-10 mg once daily – Loratadine-10 mg once daily – Mizolastine-10 mg once daily .

Urticaria • Newer 2nd gen – Desloratadine-5 mg once daily – Fexofenadine-180 mg once daily – Levocetirizine.5 mg once daily • H2 antagonist – Cimetidine-400 mg bid – Ranitidine-150 mg bid .

submammary area or groin. submammary are or groin Avoid use in infants and children under 12 Best for thick. – for short term use only(2-3 weeks at a time). – avoid use in infants and children under 12. – avoid extensive app(>50g weekly). – best for thick lichenified or hypertrophic skin – – – – – – Severe Avoid ext use(>50g weekly) Short term use(2-3 weeks at a time) Do not use on the face axillae. lichenified or hypertrophic skin • High(2&3) . – Do not use on the face.Topical Corticosteroids • Superpotent(1) – dermatoses resistent to intermediate or high potency TCS. axillae.

and other occluded Infants and children Best for thin skin • Low(6&7) . axilla. groin.Topical Corticosteroids • Intermediate(4&5) – Moderate – Best for short term tx of extensive dermatoses – Avoid extended use(>1-2 weeks in infants and children – Best on trunk and ext – Safer for short term use on thin skin – – – – – – Steroid sensitive Preferred for large areas Best if long term tx required Best choic for face.

Topical Corticosteroids .

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