a eal ms — om a a a a y y - , , , STACY, LUCITO,MO "pal OOH PCaNC EAST AVET TORY AND PAHYSICAL EXAM ‘DERMATOLOGIC Buretion When the condition was first noted and fone Periodicity = constant, waxing and waning, worst at night, worst In winter evolution = How the condition has spread or developed over time Location = Where lesions were frst noted and ift spread ‘Symptoms = pruritus, pain, bleeding, non-healing Severity = Especially for painful or pruritic conditions ‘Ameliorating and Exacerbating Factors ~ Relation to sun exposure, heat, cold, wind, trauma, ond ‘exposure to chemicals, topleal praducts, plants, perfumes or metals Past Medical History ~ history of chronicillness and those that are associated with skin disease (asthma, allergles) Medication History ~ A detalled history with those medications started recently Allergies = to medications, foods, environmental antigens, and contactants Social History ~ Occupation, hobbies and lelsure activites, alcohol and tobacco use, ilict drug use, sexual history Family History = of skin dlsease, atopy (atopic dermatitis, asthma, hay fever) or skin cancer. PRIMARY LESIONS | SECONDARY LESIONS = Macule = Seales = Patch © Crust © Papule * Erosion © Plaque © Ulcer © Nodule © Fissure © Vesicle Atrophy * Bullae = Scar © Pustule * Excoriation *_Wheal + _Lichenification PRIMARY LESIONS © Macule- A circumscribed area of change in color, flat, rron-palpable, on skin or mucous membrane, < 1.em * Patch: Flat but larger than macules with 2 circumscribed area of change In color, flat, non- palpable on skin or mucous membranes, ‘measuring >1 cm +" Papule- are solid, raised lesions <1 cm caused by 3 proliferation of cells in epidermis or superficial dermis, Maybe sessile, pedunculated, flat topped, rough, smooth and umbiticated + Plaque- Solid, plateaustke elevation >1em caused by a proliferation of cells in epidermis. or superficial erm + Nodute- Palpable, solid, ound or elipsoidal lesion > or equal to 1 cm. itis caused by a proliferation of cells into the mid-deep dermis from inflammatory infiltrates, neoplasm or metabolic deposits EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY [NUE MEDICAL CENTER DEPARTMENT OF 0! |ERMATOLOGY elevated, «Vesicle: Vesicles are circumscribed, el superficial and fluid-filled cavity <2 cm Bulla. At tem) blister which arises from cleavage at inteaepidermal or subepidermal ‘ circumscribed, superficial cavity of the skin which contains purulent discharge made of leukocytes © Wheal- Round or flat topped that is evanescent in 24- {48 hours due to edema In the papillary body of dermis = Pustul SECONDARY LESIONS ‘scales- Build-up of dead skin cells that flakes off the Surface arising from the outer most layer of the steatum corneum CCrusts- A dried collection of blood, serum or pus. Also called a scab + Erosion: A moist, circumscribed, dep e thot results from a loss of a portion ar all of the viable ‘al or mucosal trauma, There Is detachment of sceratlon, rupture of vesicles essed lesion epiderm ‘epidermal layers with ma cor bullae ‘+ Ulcer- Lesion that Invalves loss of the epidermis and part of the dermis Fissure Linear loss of continuity of skin surface or ‘mucosa results from excessive tension and decreased elasticity ‘+ Atrophy: Diminution of some or all layer of the skin ‘Sear. Fibrous tissue replacement of the tissue defect ‘due to previous wound or ulcer ‘+ Excorlation- Punctate or linear abrasion produced by mechanical means caused by scratching usually Involving only the epidermis, © Uchenification- Repeated rubbing of skin results in ‘thickening and hyperpigmentation of skin BACTERIAL INFECTIONS. FURUNCLE (BOIL) ‘© deep-seated inflammatory nodule ‘+ usually from a preceding, more superficial folliculitis * evolving into an abscess iologic agent: Staphylococcus aureus * Lesion: hard, tender, red nodule that enlarges and becomes painful and fluctuant after several days. Rupture then occurs with discharge of pus. CARBUNCLE ‘+ more extensive, deeper, communicating, and infiltrated lesion. ‘* Closely set furuncles coalesce * Etiologic agent: Staphylococcus aureus ‘+ Lesion; initially red and indurated -> Multiple pustules on the surface, draining externally around multiple hair follicles yellow-gray irregular crater > heals slowly by ‘ranulating -> dense and readily evident permanent scar Furuncle and Carbuncle * SOP: halr-bearing sites (regions subject to friction, cecclusion and perspiration) ’ * Predisposing factors: Pre-existing lesions dermatitis, scabies, pediculosis) (nopSNS EEE EERE ® EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY * Systeinic host factors (obesity, blood dyscrasias treatment with: glucoeorteoids and cytotoxlc agents, immunoglobulin deficiency states, OM) + Diognosis: Grams Stain = clusters of Gram-positive cocel, of isolation of 5. aureus on culture + Management: ~ Simple furunculsis- local application of moist heat = With surrounding cellulitis - systemic antibiotic ~ Large, painful, and fluctuantlestons Incsion and drainage Systemic antibiotics Cloxaciin or Cephatexin ‘Adults: 250-500 mg QD x10 For peniciin allergic Erythromycin ‘Adults: 250-500 mg QID x 10, days days. Children: 30-50 MKO QID x | Children: 30-50 MKO QID x 0days 20days Co-amoxiciav (Ctindamycin ‘Adults: 375 mg TID/ 625 mg | Adults: 150-300 mg QIO x10 BID x 10 days days. Children: 25-50 MKD TID x | Children: 15 MKO QID x 10 odays days. SCAMRSA -> Vancomycin FOLLICULITIS © pyoderma that begins within the hair follicle * Etiologic agents: Staphylococcus aureus, Pseudomonas, ‘aeruginosa and Gram negative bacterias such as: Proteus, Klebsiela, E.coli ‘© Predisposing factors: Shaving, plucking or waxing hairy ‘areas, occlusion with clothing, adhesive plasters & prosthesis,natural occlusion in intertriginous sites and, warm climate ‘© Diagnosis: Clinical signs, Gram stain and culture ‘Superficial Folliculltis/ Follicular or Bockhart Impetigo ‘© Lesion: small fragile, dome-shaped pustule occurs at the infundibulum (ostium or opening) ofa hat follicle Children: Scalp ‘Adult: Beard area, axllae, extremities, and buttocks of adults © Treatment: = Topical Therapy: Warm saline compress, topical ‘Mupirocin or Clindamycin B10 x 10 days Systemic antibiotics Hot tub folicultls © Caused by Pseudomonas aureginosa «+ Usually follows bathing Ina communal "hot tub" ‘© follicular papules and pustules on the trunk + May resolve spontaneously ‘reatment if symptomatic: Ciprofloxacin S00 mg BID x 10 © days ‘© Prevention: pools cleaned regularly Gram negative follcults «Acne patients treated with ora antibiotics «= Ervthematous follicular papules & pustules 4 Management: Discontinue curren antibiotics, Ampllin 250 mg GIO x 10 dys, topal benzoyl peronide For severe unresponsive cases: Oral Isotretinoin EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY Deep follicultis/Sycosis barbae = Deep folliculitis with perifolcutar inflammation ‘occurring inthe bearded areas of the face andl upper lip ‘© Same treatment with Superficial Folliculitis IMPETIGO. ‘+ Predisposing factors: crowding, poor hygiene, neglected ‘minor skin trauma . # Diagnosis: Clinical signs, Gram stain and culture + Treatment = Topical: Mupirocin, Retapumulin, Fusidie acid ointment BID x 10 days = systemic: Dicloxacilin 250-500mg PO GID 5-7daysi ‘Amoxicilin-clavulanic acid 250-500m¢ QD 5-7 days; = Penicilin allergy: Azithromycin, Clindamycin or Erythromycin = CA-MRSA suspected: TMP-SMX, Clindamycin, Tetracycline, Doxyeyline or Minocycline Bapnnene nose Bullous impetigo ‘+ Newborns & young children ‘¢ caused by coagulase(+) S. aureus ‘+ SOP: face, trunk, extremities, buttocks, perineum ‘+ Lesion: vesicles turn to flaccid bullae that rupture & form light brown crusts ‘© Ritter disease/Pemphigus neonatorum — extensive bullous impetigo Nonbullous impetigo © More common : «In industrialized nations: most commonly caused by S. aureus, less often by group A Streptococcus ‘¢ Indeveloping countries: group A Streptococcus ‘¢ Impetigo in the newborn: Group 8 © SOP: nose, mouth, extremities after trauma ‘= Nasal carriers: very localized type of Impetigo {anterior nares and adjacent lip areas © Lesion: transient vesicle or pustule > honey-colored crusted plaque CELLULITIS extends deeper into the dermis and subcutaneous tissue ‘Predisposing factors: Liposuction and “skin popping” ‘© Etiologic agent :S. aureus and GAS © Group B streptococci in the newborn © pneumococci, Gram-negative Immunocompromised individuals '* Escherichia coll and other Enterobacteriaceae and anaerobes ~>extremes of age, prolonged hospitalization, percutaneous intravascular lines, diabetes, immunocompromised states, and glucocorticoids baci = inSSO ie ee | ‘© Lesion: erythema, tenderness, pain, lack of distinct ‘margins between affected and normal skin, deeper, firmer form of tender induration, fuctuance; occasionally (+) crepitus on palpation ERYSIPELAS ‘+ Type of superficial cutaneous cellulitis with marked sroup Cor G streptococcus) >S. aureus ‘+ Newborn: group 8 streptococci * Lesion: begins on the face or 9 lower extremities, heralded by pain, superficial erythema, and plaque-ike ‘edema, sharply defined margin to normal tissue, “peau orange appearance” Cellulitis and Erysipelas ‘Diagnosis: elevated WBC & ESR, Gram stain of aspirates, Bacterial Culture, Skin blopsy and X-ray and imaging Antinlerobil Treatment of Non Nerang infections Ceui, Eine DISEASE DRUGOF FIST CHOKE yeas Pein terme peenn rosen acon mpavasbacon Peesatnanobean Inpenervsttn eprom ‘Simple cutpaten: ‘cots Sever owpatond pater ‘Sipe curgatent Anosevataci Ppercinrabecar, FeacsintJendene Ingen Fetacon,highiathoed vaacomcn Sfsaltetn Une NECROTIZING FASCIITIS ‘© Diagnosis: Open Surgical Exploration ~ GOLD STANDARD © Others: Blopsy, Culture, MRI or CT scan Type | Necrotizing Fasciitis + Polyinerobial infection (mix of facultative and anaerobic organisms) Predisposing factors: Surgery, bowel perforation secondary to: neoplasm or dverticults, trauma, or Parenteral drug abuse via skin-popping, diabetes or malnutrition ‘=. SOP: extremity, abdominal wall, perineum, or about operative wounds ‘+ MOST COMMON FORM OF NECROTIZING Ff + Lesion: (+) painful > swelling, erythema, warmth, and tenderness" skin color becomes purple, bullae develop, and frank cutaneous gangrene-> anesthetic as a result of ‘occlusion of small blood vessels and destruction of superficial nerves In the subcutaneous. tissues, (+) crepitus Sea hipaa ae) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY a tthe process is not limited to the fascia > Streptococcal gangrene ‘SOP! extremity Lesion: indistinguishable from type |, But necrosis of the overlying skin can be rapid and dramatic, revealing deeper structures, including tendon sheaths and muscle ‘AotinicfbialHeatment for Infection of tn, Fascia and Muse: (oan neipewm — immonnenae = Scateiecrancyne nce measles) enGeracin twa Wrenn omen cowossunentrninan Samy csemante maa aren ems ‘Seareomet ECTHYMA ‘A cutaneous pyoderma characterized by thickly crusted erosions or ulcerations Causes = Usually a consequence of neglected impetigo classeally occluded by footwear and clothing = Staphylococcus aureus . = Group A Streptococcus = Poor hygiene = Neglect * Glnical Manifestations = Uleer has “punched out” appearance when the dirty grayish-yellow crust and purulent material are debrided = Margin of the ulcer isindurated, raised and violaceous ~ The granulating base extends deeply into the dermis = Lesions typically occur in the homeless and soldiers in ‘combat in a hot and humid climate = Most commonly occurs on lower extremities + Diagnosis = Clinicat Gram stain and culture of S, aureus or GAS ‘+ Treatment = Lesions are slow to heal = Requiting several weeks of antibiotic treatment for resolution > Management Is the same as what Is used for staphylococcal impetigo PARONYCHIA Inflammation of the proximal nail fold © Causes Acute Paronychia Is usually caused by infection = Individuals exposed to hand trauma or chronic moisture are predisposed to staphylococcal paronychia, as well as to other causes of paronychia Type it Necrotizing Fasciitis and Streptococcal Gangrene (eg, Condida, Pseudomonas, Streptococcus, ‘+ Monomicrobial (GAS) Setrnateniyyias) ‘© Usually healthy individuals “= Scares is thas malt Uoheieesitate oh, Boi paronychia FAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 3: : Z Clinical Manifestations ~ Site s usually around the finger nails = often originating from a break in the skin, such a8 a hhangail = skin and soft tissue of the proximal and laterat nail {old are red, hot, and tender ~ not treated, can progress to abscess formation + Diagnosis = Mainly Ctiniea! © History © Physical examination ‘+ Treatment = oral and topical antibiotics ‘© Mupirocin 81D, Fusidic Acid BID ©. Dictoxacilin 250-500 mg PO QIO for S~7 days © Amoxicilin plus clavulanic acid 25 me/ke TID; 250-500 mg gid © Cephalexin 25 mg/kg TIO; 250-500 mg aio Incision and drainage of abscesses ERYTHRASMA Erythrasma fs a common superficial bacterial infection of the skin characterized by well-defined but irregular reddish-brown ‘patches, occurring In the Intertriginous areas, or by fissuring, White maceration in the toe clefts * Causes = Etlologle agent: Corynebacterium mutissimum = more common in tropical climate = more common in men = may occur in asymptomatic form in the genitocrural area Clinical Manifestations, = completely asymptomatic = genitocrural form with considerable pruritus = generalized form with scaly lameliated plaques on the ‘trunk, inguinal area, and web spaces of the feet ~ When pruritic, irritation of lesions may couse secondary changes of excoriations and lichenification ‘© Diagnosis ~ Wood's lamp exam: cora-red fluorescence = Pigment may persist after eradication of the Corynebacterium asthe pigment is within the stratum corneum = Gram stain and culture of Corynebactrlum In the lesions (© Rod-like, gram positive organisms ‘© Treatment = For localized disease especially between the web spaces of the feet © Benzoyl peroxide wash and 5% gel ‘9 Clindamycin or erythromycin 2% cream = For widespread involvement: © Oral erythromycin (01 gram single dose of clarithromycin = For secondary prophylaxis ‘© Benzoyl peroxide bar when showering ‘STAPHYLOCOCCAL SCALDED SKIN SYNDROME The syndrome is a generalized exanthematous disease consisting of cutaneous tenderness and widespread superficial blistering and denudation i) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY (Wag? causes = Exfoiatn A and B (ETA and €T8) proteins produced by S.aureus ~ the epidermolysis takes place usually between the stratum spinesum and granulosum ~ This results in avery thin-walled, flaccid biter that is easily dlsrupted, exhibiting a postive Nikolsky sien {linical Manifestations = Faint, orange-red macular exanthem or uniform ‘erythema sparing mucosal surfaces = in association with a purulent conjunctivitis, otitis media, nasopharyngeal infection, or, occasionally, pyogenic skin infection such as bullous impetigo ~ These serve as the staphylococcal foci from which the toxinisreleased = Perioriicial and flexural accentuation of the exanthema ~ Severe tenderness = Within 1-2 days the rash progresses from an cexanthematous scarlainiform toa bilstering eruption = Very superficial tissue paper-wrinkling of the epidermis, which Is characteristic, progresses to large flaceid bullae in flexural and periorificial surfaces = A positive Niklsky sign ~ Large sheets of the epidermal surface are typically shed, revealing @ moist underlying erythematous, base resembling a generalized scalding burn. Diagnosis ~ Cultures from bilsters are usually sterile = Teanck smear shows acantholytic cells = Histopathology © Acantholysis in the granular layer and subcorneal cleft formation in early lesions ‘© Intact, viable epidermis with shedding of the stratum corneum in the desquamative stage © Dermis with few inflammatory cells Treatment = Intravenous anti-staphylocaccal antibiotics = Muplrocin ointment to clearly Impetignized areas ~ Managing flu and electrolyte abnormalities = Non-adherent dressings © Use of petrolatum-impregnated gauze SE rrr VIRAL INFECTIONS VARICELLA Varicella Zoster Virus (VZV) Herpesvirus family = Entry > MUCOSA of upper respiratory tract & ‘otopharynx “> tonsillar T cells -> reticuloendothelial system (major site of virus replication) and skin Prodrome (2-3 days) ~ fever, chills, mataise, headache, anorexia, severe backache, sore throat, dry cough Rash ~ FACE > scalp > trunk (relative sparing of the extremities) ~ scattered rather than clustered ~ rose-colored macules -> papules > vesicies > ustutes - crusts > depressed scars EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY. «: : Lap MEN NWWNASN AAA = Slasions in ail stages are usually present on the body atthe same time = "DEWOROPS ON ROSEPETALS” > Eythematous _papules.vesicles, ‘erosions at sites of excorlations ‘© Tzanck Smear: (+) multinucleated giant cells & epithelial ells w/ acidophille intranuclear Inclusion bodies ~ Same findings in Herpes Zoster Infection, Complications: > Child > staph/Strep skin infections Adult > Primary Varicella Preumonia ~ Pregnant > Congenital V2V infection crusts, and ‘Rye Syndrome ~ Aspirin use during Infection > acute encephalopathy with faty liver degeneration ~ occurs 2-7 days after the appearance of the rash + Treatment: = Neonate * Acyclovir 10mg/ke oF SOOme/m3 a8 x 10d = chia * Symptomatic alone * Valacyclovir 20 mg/kg a8 x Sd * Acyclovir 20 marks GID x5d = Adolescent * Valacyclovir 2g PO g8 x74 = Adult * Acyclovir 800 mg Sx/d x 74 ~ Pregnancy peyote = Immunocompromised mala 4. Valocycovir 1g PO @8 74 b. Famciclovir Soom PO g@ x 7-104 © Acyclovir 800 mg PO S/d «7-304 = Severe Acyclovir 10ma/kg V 9B x 7-104 = Acyclovir resistant (advanced AIDS) €, Foscarnet 40 mg/kg IV g8 until healed HERPES ZOSTER © Varicella Zoster Virus (VZV) Herpesvirus family = Enuy > MUCOSA of upper respiratory tract & oropharynx > tonsillar T cells > reticuloendothelial ‘system (major site of virus replication) and skin > sensory nerves > centripetal to sensory ganglia > Utent vzv + Prodrome - PAIN (>60 yo) and paresthesia = Rash ~ neary lways unilateral = Dermatomal: limited tothe area of skininnervated by a single sensory gangtion = Most common: trigeminal nerve (ophthalmic division), andthe teunk fom T3 to L2 most severe and lasts longest in older people ~ least severe and of shortest duration in children FAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY a) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY * closely grouped vesicles on an erythematous base ‘erythematous macules and papules > Vesicles (within 12-24 hs) > pustules (day 3) > crust (day 7-10, persist for 2-3 weeks) ‘+ ‘new lesions continue to appear for 1-4 days {occasionally for as tong as 7 days} ‘+ Tranck Smear: (¢) multinucleated glant cells & epithelial cells w/ acidophilic intranuclear inclusion bodies = Same findings in Varicella ‘= Complications: = Postherpetic neuralgia = Bacterial superinfection = Skin necrosis, scarring, cutaneous. dissemination {(immunocompromised) = Symptomatic alone = Acyclovir 800 mg Sx/d x74 = Famelclovir $00 mg PO q8x 7d ~ Valacyclovir ig PO q8 x 7d '* Immunacompromised 1 same as fr Varicella HPV (WARTS) ‘© Human Papillomavirus (HPV) = DNA virus * €1 and £2: replication and transcription * €5-7: transforming genes ‘G4: encodes a protein (release of virus from keratin framework) = La and 12: vical capsid TSE I a a Deep plantar/patmar warts 2,4,27,29 Common warts 3,10,28, 49 Fit wares 7 Butcher's wars 13,32 (ral focal epithelial hyperplasia 5,8,9, 12,14, 25,17, Eplderrodyspasia veruciformis 19.26,36,47,50 | Inimmunocompromised en ‘Anogerital warts, cervical condylomata 16, 18, 31, 38-35, 39, _Anogenital wars, cervical condylomata 40, 31-60 Bowencid papulosis, ‘Common warts (verruca vulgaris) ‘+ scaly, rough, spiny papules or nodules © single or grouped + hands and fingers ‘Flat warts (verruca plana) + 14 mm, slightly elevated, flattopoed papules with minimal rete © face, hands, and lower legs Treatment fr warts ~ Electrodessiction with curettage ~ Salicylic acid lactic acid, tricholoroacetic acid = Cryotherapy (Niquid nitrogen) MOLLUSCUM CONTAGIOSUM. © MC Virus (MCV) ~ powvirus ~ replicates within the cytoplasm = Mev.a: Children ~~ MCV-2: adults, immunocompromised © 2-7 weeks °+ small pink, pearly, or ‘esh-colored dome-shaped apules with centeal deil/ ymbliation '* Spontaneous clearance (months to years) *+ to adults, usualy indleatve of a more advanced stte of {, with higher viral load and lower CDé+ T-cell count * Curettoge, Canthardin, retinoid creams, imiquimod eam, sallcyic acid, trichloroacetic acl, cdofovlr, and silver nitrate paste and tape stripping Patient presented with grouped vesicles and crusting over the outer 2/3 of the lower lip ossociated with pain, burning ‘Sensation and occasional pruritus. OROLABIAL HERPES + caused by Hsva ‘+ acquired in childhood ‘+ mostly associated with orofacial disease ‘* most common site: Outer 1/3 of the lower lip assactated with paln, burning sensation, pruritus Patient presented with painful grouped vesicles with early ‘central crusting on a red base arising an the shaft ofthe penis. GENITAL HERPES © Hsv.2 ‘+ most prevalent sexually transmitted disease worldwide ‘+ the most common cause of uicerative genital disense * correlates with sexual behavior A patient presented with painful, grouped, confivent vesicles on ‘an erythematous base on the distal finger. Teamck smear was done which revealed muttinucleoted giant cells. HERPETIC WHITLOW > caused by: = HSV2 (<20y0) ~~ HSV2 (>20y0) HERPES SIMPLEX + HSV both can infect oral and genital areas and cause ‘acute and recurrent infections + Most recurrences are not symptomatic (asymptomatic shedding) ‘© Diagnosis: = Ismade by polymerase chaln reaction, viral culture, or serology, depending on the clinical presentation = Taanck Smear: Mutinucleated glant cells + Treatment: = Aeyelovir: 200mg Sx/day or 200mg 10 Valacyclovir tg 810 Famacylovir 250mg TID Regimens and dosages vary with the clinical setting (MEASLES (RUBEOLA) ‘A.3 yeor old child presented with erythematous, non-prurtc, ‘macules and papules beginning on the forehead gradvally ‘progressing to the neck, trunk, and extremities, History ‘evealed URTI (high grade fever, cough, coryzo, & conjuctvitis) 4 doys prior ta the eruption of the lesions, PE revealed tiny white lesions surrounded by erythematous halo described a: “arains of sonds” over the buccal mucaso. EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY Ge) EAST AVENUE MEOICAL CENTER DEPARTMENT OF DERMATOLOGY + Clues n diagnosing Measles: > sprenis centefugally hint grade fever precedes rash (~a days) (+) Kopitk Spots * smal, whitish leslons over the buccal mvcoss ‘= Pathognomonic for Measles HAND-FOOT-MOUTH DISEASE 1.5 year old child came In with chief complaint of loss of ‘oppetite. Mother also reported incessant crying of the child ‘upon feeding. PE showed few ulcerative oral Jesions. Cutaneous exam reveoted vesicies over the palms and soles. ‘= Cluos in diagnosing HEMD: = Painful oral ulcers-> difficulty feeding child = near papulovesicular lesions over the sides of fingers, toes, and (sometimes) on buttocks 7 Etiologie agent: Coxsackie Views GERMAN MEASLES Few doys prior to consult, mother of 0 3y0 patient noted petechlae on the soft palate and palpable cervical lymph nodes. These were accompanied by low grade fever. 1 day PTC, the patient was noted to hove pink macules and popules over the forehead spreading Inferlrly to the neck, trunk and extremities. What Is your diagnosis? + "3-day measles” ‘© caused by Rubella Virus (RNA Togavirus) + Transmission: Inhalation of aerosolized respiratory droplets + Period of infecthity: end of Incubation period unt disappearance of rash ‘links! Manifestation = exanthems & Lymphadenopathy + Forchhalmer Sign- petechiae on soft pal: in Infectious Mananucleoss) SUPERFIGIAL FUNGAL INFECTIONS, DERMATOPHYTOSIS. Classified further according to their natural habitats Humans, Animals, Soll ‘Attach to and Invade keratinized tissue of animals and humans © Skin, Hair, Nails Predisposing Factors © Host factors ~ Atopy = lethyosts ~ Immunosuppression xathloprine) = systemic diseases Syndrome} + Local Factors ~ Sweating = Occlusion Hot, humid weather ~ Occupational exposure ~ Geographic location (intake of glucocorticoids, (Diabetes mellitus, CushingGenera Patterns af integumentery tnfections by Superficial Mycoses ‘Genera ‘Skin | Hale Nails Trichophyton x | * ‘Microsporum x [x Epidermophyton x x Tineo Nigro x Block Piedra x white Piedra x Transmission ‘© Anthropophilic: Person to person + Zoophilic: Animal to human ‘© Geophilc: Soll or environment to human Pathogenesis Broad armamentarium of enzymes act as virulence factors to allow adherence and invasion of skin, hait, and nails, and also ‘tovutilize keratin asa source of nutrients for survival ‘+ Secretion of specific keratinolytic proteases, lipases and Cceramidases, the digestive products of which also serve as fungal nutrients 1. adherence to keratin 2. Invasion and growth 3. Host inflammatory response # Inflammatory host response against 2 spreading dermatophyte followed by 3 reduction or clearance of fungal elements from within the plaque ‘+ Result: dlassle “ringworm,” or annular morphology of tinea corporis Diagnostic Procedures Clinical diagnosis confirmed by ‘s Microscopie detection of fungal elements (10-20% KOH) = Active border, scaly lesion, depilate hair, crumbling debris (onychomycosis) © Culture # Histologic evidence of the presence of hyphae in the stratum corneum. ‘Supportive ‘= Wood's lamp examination = Coral red= Erythrasma, C. minutissimum = Greenish ~ Pseudomonas = Pale white yellow ~ Tinea versicolor = Bright Green ~M. oudouintl, M. canis Classification © Tinea corporis (body) 1 Tinea facials (face) Tinea cruris (groin) ‘¢ Tinea manuum (hands) # Tinea pedis (feet) ‘© Tinea capitis (scalp) ‘Tinea barbae (beard) ‘# Tinea unguium (nails) TINEA CAPITIS ‘¢ Trichophyton and Microsporum species, with exception ‘of Trichophyton concentricum = M. Canis (most common in Europe) or) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY Prepubertal children Spores in the air Possible transmission through contaminated inanimate objects Several round patches of scale or alopecia. with OF without inflammation Non-inflammatory = Noscarring “Gray Patch" ~ short stubs of broken hair — "Black Dot” ~ hairs broken off at surface laflammatory = with scarring = Kerion = swotten, bogey, pus exuding mass, (+) Pain = Favus~scutula, fetid odor Treatment wpfections involving. altcbearing skin Usually Mecesstate oral antifungal treatment since “Jermatophytes penetrating the follicle are usually Out of reach for topicals * Griseofulvin. Terbinafine + Fluconazole * itraconazole « adjuvant: Selenium sulfide (1% and 2.5%), zine pytthione (1% and 2%), povidone iodine (2.5%), End ketoconazole (2%) are shampoo preparations ‘contact with ‘TINEA BARBAE Rarest of dermatophyte infection ‘Adult males exposed to farm animals Lesions: discrete follicular papules and pustules to kerion Hike lesions. Hairs are easily plucked off May be easily mistaken for Staphylococcus aureus folliculitis Treatment = Oral antifungal Is usually necessary = Ulteamicronized Griseofulvin 500 mg twice dally for 6 weeks = Terbinafine 250 mg daily for 24 weeks = Itraconazole 200 mg daly for 2-4 weeks = Fluconazole 200 mg daily for 4-6 weeks = systemic glucocorticoids used for the first week-> helpful in cases with severe inflammation TINEA CORPORIS Refers to any dermatophytosis of glabrous skin except palms soles, and the groin Classic “rng worm’ lesion Starts as eythematous macule or papule spreading ‘outward to form ring shaped scaly plaques with sharply morginated raised red borders with central clearing ‘Most common: T. ubrum Other organisms: = Epidermophyton floccosum = Teinterdigitale = M.canis = Tetonsurans EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 7+ Treatment = Topical allylamines, —Imildazoles, __tolnaftate, butenafine, or ciclopirox twice a day for 2-4 weeks = Oral antifungal agents are reserved for widespread oF ‘more inflammatory eruptions Terbinafine 250 mg daily for 2-4 weeks. Itraconazole 200 mg daly for 1 week = Fluconazole 150-300 mg weekly for 4-6 weeks TINEA FACIALE ‘+ With or without central clearing + Proritus TINEA CRURIS ‘© “Jock itch” or *hadhad" In Tagalog ‘© Usually bilateral ‘+ Scaly reddish to brownish plaques with advancing border 1 Lesion starts onthe crural fold asa single inflamed scaly lesion with active margin extending downward on to the thighs, occasionally migrating to the pubic regions, to the buttocks, and gluteal cleft area ‘In contrast to candidal infection, it very rarely involves the scrotal area ‘+ Prurtusis always present and severe + Most common cause: 7. tubrum and, loccosum + Treatment = Topical alliomines, butenafine, or ccloprox = 2cadoy for2-4 weeks = Oratantifungal agents ae reserved for widespread or ‘more Inflammatory eruptions ~ Terbinafine 250 mg dally for 2-4 weeks = traconazole 200 mg dally for 1 week ~ Fluconazole 150-300 mg weekly fr 4-6 weeks imidazoles, tolnaftate, ‘TINEA MANUUM AND TINEA PEDIS = Organisms = T-rubrum (most common) = Toimterdigitale = & floccosum. TINEA PEDIS = Four types © Interdightat "= Most common presentation of tinea pedis = Begins as scaling, erythema and maceration of the interdigital and subdigital skin of the feet, an particular between the lateral third and fourth and fourth and fifth toes. » Rarely involves the dorsum * Occlusion and bacterial coinfection > produce erosions with pruritus -> malodor ~> “athlete's foot.” © Chronic Hyperkeratotle (MoceasinyType «= Patchy or diffuse scaling on the soles and the lateral and medial aspects of the feet, in a distribution similar to a moccasin on a foot = Most common: T. rubrum followed by £. floccosum and anthropophilic strains of T. Interdigitole EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ‘= Vesiculobutlous ‘Typically caused by z00phiic strains of 7. Interdigitale (former T. mentagrophytes var ‘mentagrophytes) Tense vesicles larger than 3 mm in diameter vesiculopustules, or bullae on the soles and periplantar areas + Acute Ulcerative Type ‘= Tinea pedis with zoophilic 7. Interdigitale along with rampant bacterial superinfection with Gram- negative organisms ‘Vesicles, pustules and purulent ulcers on the plantar surface = Cellulitis, Iymphangitis, lymphadenopathy and fever are frequently associated Treatment ‘Mild interdigital tinea pedis involvement = Topical alylamine, imidezole, cclopirax, benzylamine, tolnaftate, or undecenoic acid based creams ‘+ Terbinafine cream applied twice dally for 1 week ‘= Oral terbinafine is 250 mg dally for 2 weeks. + itraconazole in adults is given 400 mg dally for 1 week, 200 mg dally for 2-4 weeks, or 100 me dally for 4 weeks ‘= Itraconazole in children is administered at 5 mg/kg/day {or 2weeks ‘+ Fluconazole 150 mg weekly for 3-4 weeks ‘= Topical or systemic corticosteroids may be helpful for “symptomatic rellef during the intial period of antifungat ‘treatment of vesiculobutlous tinea pedis ‘= Patients suspected of having Gram-negative co- Infections without bacterial ‘TINEA UNGUIUM (ONYCHOMYCOSIS) ‘© Most prevalent nall disease 1 Risk factors = Nalltrauma = Immunosuppression (HIV infection, dlabetes mellitus) = Peripheral vascular insufficiency ‘© Begins astinea pedls before extending to-the nall bed ‘© Infected nail then becomes a reservoir for local recurrence ‘* ‘Most common cause: 7, rubrum and T. interdigitale Types ‘Distolateral subungual type = Most common form = Begins with invasion of the stratum corneum of the bhyponychium and distal nail bed, forming a whitish to brownish yellow opacification at the distal edge of the mall ‘= The infection then spreads proximally up the nail bed tothe ventral nail plate = Hyperproliferation or altered differentiation of the nail bed In response ‘to the infection results in subungual hyperkeratosis = Progressive Invasion of the nail plate results in an Increasingly dystrophic nail EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY aa = ao a ‘© Proximal Subungual Type = Infection of the proximal nail fold primarily with T. ‘rubrum and T. megninii = White to belge opacity on the proximal nal plate = Opactty gradually enfarges to affect the entirénail and ‘eventuates in subungual hyperkeratosis, leukonychia, proximal onycholysis, and/or destruction of the entire rail = Patients should be screened for HIV, as PSO has been considered a marker for this disease ‘© White Superficial Tne Results from direct invasion of the dorsal nal plate ~~ White to dull yellow sharply bordered patches anywhere on the surface of the toenail ~ Usually caused by 7: interdigitale Treatment ‘© Topical = Clelopirox 8% lacquer applied daly for 48 weeks = Amorolfine 5% applied twice weekly Systemic = Required for onychomycosis involving the matrix area, ‘or when a shorter treatment regimen or higher chance for clearance or cure is desived = Terbinafine, Fluconazole ‘CUTANEOUS CANDIDIASIS Candidal tntertrigo ‘© Intertriginous area (Inframammary, webspaces, axle, ‘roins intergluteal), ‘= Erythematous areas surrounded by satelite pustules '= Ory and scaly to moist and oozing © (+/+) pruritus, burning pain © Treatment: = Topical antifungals (e.g, clotrimazole, econazale, cloplrox, miconazole, ketoconazole, and nystatin) = Powder preparations = Systemic antifungals for extensive cutaneous infections, follicular Involvement, or infections in Immunocompromised patients Paronychia © Redness, swelling of nll folds pain, tenderness * Treatment: = Topical imidazole in solution form initially = Four percent thymot in ethyl alcohol is'drying to -scandida (alternative) = Oral azoles (refractory cases) ‘TINEA {PITYRIASIS) VERSICOLOR ‘¢ The infection occurs more frequently in regions with higher temperatures and relative humidity No sex predominance ‘Most common among adolescents and young adults = Iipid-producing sebaceous glands are more active ‘= Organisms: M. furfur, M. globose EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY = Oral contraceptive and systemic corticosteroid use = Cushing's disease = Immunosuppression = Malnourished state = Azelalé acid inhibits the action of the tyrosinase in the: melanin production pathway, which results in persistent hypopigmentation «= Scaly oval to round macules scattered over characteristic areas of the body, including the upper trunk, neck, and upper arms. ‘= The macules often coalesce forming irregular shaped patches of pigmentary alteration ‘= The color of patches varies from almost white to pink to reddish brown or fawn colored and may have a wrinkled surface appearance ‘= The scale is characteristically described as dust-ike or furfuraceous Diagnostics = Wood's Lamp examination: + Yellow-orange fluorescence thought to be due to the presence of pteridine = Potassium hydroxide (KOH) preparation * Confirmatory » Demonstrates the characteristic fungal spores and short cigar-butt hyphae ("spaghetti and meatballs”) “Visualization is enhanced through PAS stain = Treatment = Topical * Selenium sulfide * Zine pyrithione «Sodium sulfacetamide + Ciclopiroxolar * Azole and allylamine antifungal preparations, = Systemic * Ketoconazole, Fluconazole, and Itraconazole are the preferred oral agents "ACNE VULGARIS, "RENE VULGARIS + 2 selftimited disorder if the pilosebaceous unit that Is seen primarily in adolescents. ‘Epidemiology = Acne 1s common that Is often has been termed physiologic. = Acne prevalence hits its peak during the middle to late teenage period with more than 85% of adolescents affected and then steadily decreases, = In some cases, acne may persist through the third decade or even later particularly in women. © Etiology = Key elements for pathogene: * Follicular epidermal hyperproliteration, ‘Excess sebum production * Inflammation sence of Propionibacterium acnes cae History . peda 4 . = Onset of lesions usually around puberty however it = Warm, humid environment ‘ean also be seen In the neonatal or infantil ered nile age EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ° = an A an a =.WAAR SSSSSNSS RSET SA = Hyperandrogenism should be considered In fetnale patient on the ff * Severe acne * Hirsutism * Irregular menses ~ Drug-induced acne may be caused by the ft: mnabolic steroids /corticasteroids * corticotropin, phenytoin, lithium, isoniazid, vitamin B complexes, halogenated compounds, ‘and certain chemotherapy medications, like epidermal growth factor receptor (EGFR) Inhibitors, # Cutaneous Lesions ~The primary site of acne is the face and to a lesser degree the back, chest, and shoulders. On ~ The trunk, lesions tend to be concentrated near the midline. ~ Several types of lesions * Noninflammatory lesions are comedos ° wedones - appears as a flat or Slightly ralsed lesioh with 2 ventral dark colored follicular Impaction of keratin and Hii © Closed comedones appear as pale slightly ‘elevated, small papules, and do not have a Clinically visible orifice * Inflammatory lesions vary from ‘@ Papules © Pustules © Nodules = Laboratory Test = In general, laboratory workup is not indicated for patients with acne unless hyperandrogenism is suspected. + Treatment = The mechanism of action: of the most common treatments for acne can be categorized in the following categories 9s they relate to the pathophysiology: "Correct the altered pattern of folicular keratinization * Decrease sebaceous gland activity * Decrease the follicular bacterial population, particularly P. acres + Bxert an anthinflammatory effect ‘Treatment Algorth Vulgaris (see appends) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY Local Therapy = Cleansing ~ Twice dally washing with a gentle cleanser followed by the application of acne treatments may encourage ’ routine and therefore better compliance ‘© Topical Medications = Sulfur/Sodium Sulfacetamide/Resorcinol = Salley Acid = -Aaelaic Acid = Benzoyl Peroxide = Antibiotics ‘= Topical Clindamycin and Erythromycin. most common = Retinolds = both comedalytic and anti- properties, Inflammatory Systemic Therapy © Antiblotics = Tetracycines: Donyeyeline and Minocycline = Mactolides: Erythromycin and Azithromycin + Hormonal Therapy: goal isto counteract the effects of androgens on the sebaceous gland. = Oral Contraceptives ~ Glucocorticoids = Gonadotropin-Releasing Hormone Agonists * Leuprolide = Antiandrogens * Spironolactone += lsotretinoin (oral etinoid) ~ Teratogenic * Effect on organogenesis + Until month after stopping = Recommended dally dosage 0.5-1 mg/ka/day = Baseline complete blood count and liver function tests needed, but the greatest attention ison serum Ariglceride tevels ‘Acne Surgery ‘+ Mainstay of therapy inthe past used forthe removal of comedones and superficial pustules Intralesional Glucocorticolds + Can dramaticaly decrease the size of deep nodular lesions 4 Injection of a trlameinolone acetate suspension is recommended asthe ant-inflammatory agent Phototherapy ‘+ Athough utraviotet B (UVB) can also kill P.acnes in vitro, UVB penetrates poorly to the dermal fllide and only high doses causing sunburn have shown to improve acne Lasers ‘+ work by causing thermal damage tothe sebaceous glands ECZEMA ‘ATOPIC DERMATITIS. '* Chronic, relapsing skin disease occurring more frequently during Infancy and childhood; associated with Intense pruritus ‘Frequently with elevated IgE levels 3s| ” NNN NSS SSSA + Personal or family history of Atoph thinitis and/or bronchial asthe; ‘+ 35% of patients will develop asthma later in life ‘+ Typical distribution and morphology: = Facial and extensor surfaces in Infants and yOUNB childern = Flexural lichenicationin older children and adults ie Dermatitis, aller DYSHIDROTIC ECZEMA ‘© Aspecial vesicular type of hand and foot dermatitis ‘+ Dermatoses ofthe fingers, palms and soles, characterized by deep-seated, pruritl, clear “tapioca-like” vesicles oF ‘maybe described as “sago-erains” ‘= Later, there can be scaling, fssuring or lchenifiction SEBORRHEIC DERMATITIS '* Chronic, pruritic, recurrent, characterized by redness and scaling ‘= Can range from white fakes to yellow greasy thick scales ‘+ Predilection sites: scalp, eyebrows, nasolabial folds, retroauricular area, sternum, shoulder blades & V areas of chest and back |+ Molassezia furfur plays a role in its pathogenesis IRRITANT CONTACT DERMATITIS. ‘+ Exposure to a chemical capable of irritating the skin; reaction usvally ensues with single exposure ‘+ Hands are the most frequently affected area ‘+ Severe cases may even lead to necrosis ‘= Reaction depends on concentration of offending agent, penetrability and thickness ofthe stratum corneum ALLERGIC CONTACT DERMATITIS ‘= An ecrematous pruritic dermatitis due to re-exposure to a previously sensitized substance = Aclassic delayed-type cell-mediated hypersensitivity reaction = Exposure to a strong allergen may take a week or 50, while exposure to a weak allergen may take months toyears NUMMULAR DERMATITIS '« Chronic, pruritic, inflammatory dermatitis occurring In the form of coln-shaped plaques on an erythematous base «Site of predilection: lower legs, upper extremities ‘+ Often seen in atopic individuals ASTEATOTIC ECZEMA + *fexema craquele” © pve to excessive bathing with harsh soaps; common among elderly «= Ory crackled superficially fissured skin with sight scalng assoclated with pruritus «sites: legs, arms and hands but more severe on the shins and extensor arms STASIS DERMATITIS «+ Ina setting of Chronic venous insufficency/ Varicosties ‘+ Starts > medial malleolus - inflammatory papules, ‘scaling, crusting and erosions © Hyperpigmentation ~ stippled with recent and old hemorshages EAST AVENUE MEDICAL CENTER DEPAI \RTMENT OF DERMATOLOGY «Edema and infection may complicate the situation = Fibrosis of the skin and subcutaneous tissue (lipadermatoscierosis) = Uleoration LICHEN SIMPLEX CHRONICUS S Chvonic dermatitis characterized by circumscribed plaques with ichenificotion «s Results from repetitive scratching and rubbing + cccurs more frequently in older individuals (°20 years old) Legs, back and sides of the neck, wrists ankles Stepped. Jh to Treatment of Eczema ‘= Conservative Therapy ~ Education - prevention = Use of emollients/moisturizers = Antihistamines = Low to mid potency st ‘+ High potency steroid ereams + Phototherapy «+ Immunomodulators, First Line Therapy, ‘= Identify and eliminate/avoid exacerbating factors ‘+ Keep skin hydrated «Treat pruritus and prevent flares 1+ Treat exacerbations (flares) ‘s Treat secondary skin infections early 41) Identify ond Eliminate/Avold Exacerbating Foctors Avoid: = Extremes in temperature = Coarse wool or synthetic fibers in clothing, = Strong soaps and detergents = Anything known to increase disease severity 2) Keep Skin Hydrated "= Hydrate with warm soaking bath for at least 10 minutes, followed by application of moisturizers and emollients, ‘© Soap Free Cleansers = To cleanse, reduce irritation (if sensitive to soaps), ‘and reduce dryness (thereby increase absorption of ‘other topical). ‘= Emoltients / Molsturizers = To soften and soothe rough, dry skin and increase absorbabllty of topical medications id creams 4) Treat Prunus and Fores + Antihistamines 1 GENERATION HE-TPE hirpheniramine male Dimethindene maleate Camas fumarate Diphenhydramine hydrochloride |_Hdconpine yérocnorie _ | and 3" GENERATION HI-TVPE Catraine Loratadine Ferofenadine Desloratadine | _evastne OMAINATION Steroid» Avtar) etarethasone + Lortadine Betamethasone »Derclorpheniramine malate Betamethasone + Chlorphentramine maleate Drednisione + Chorpheniraminie maleate EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 1= Se tee SS ae a eee ae eee eel eee le ee eS = 3 = * Low to high potency topical corticosteroids (see appendix for potency table) = One of the ten definitive moments of modern medicine = Potent antiinflammatory and immunosuppressive ‘effects ‘© Immunomodulatory agents (e.g. topical tacrolimus or pimercrolimus used on the face, eyelids, and skin folds) 4) Treat Secondary Skin Infections Early ‘* Skin Infections with Stopylococcus aureus can be 2 recurrent problem ‘+ Treat with a short course of oral or topical antibiotics, ‘+ Fungat infections may complicate eczema and contribute to exacerbations, ‘+ Diagnosis and appropriate antifungal * treatments recommended '5) Follow-up Therapy ‘+ Education of patient and family members: about the chronic nature of eczema, exacerbating foctors, and ‘appropriate therapy to achieve effective contro oftheir condition ‘s THIS IS IMPORTANT AS IT ENSURES COOPERATION AND ‘COMPLIANCE WHICH LEADS TO BETTER OUTCOMES 6) Treatment of Refractory Eexemo ‘© Wet dressings ‘= Phototherapy ~ Itinvolves the use of light to treat a medical condition. = Ultraviolet light therapy improves eczema symptoms Insome people. = PUVAor UVB ~ ADR: erythema, blistering, nausea, lethargy, pruritus * Systemic Immunomodulators (Methotrexate, ‘mycophenolate mofetil, systemic corticosteroids) ‘+ Hospitalization ‘© Allergen immunotherapy Remninder in the Treatment for Ecrema ‘+ Patient Education ‘+ Treat the patient, not just the rash —_— PSORIASIS PSORIASIS + No gender predilection «Peak age of onset 15-30 years + 2types - Typet += Early disease onset (onset before the age of 40) «= (s) family history and an association with HLA Cw6, and HLA DRT = Type? * Later disease onset (onset after the age of 40) = (family history + Lack of any prominent HLA association ETIOLOGY AND PATHOGENESIS ‘© Disease of dysregulated inflammation ‘+ Mechanism of inheritance has not been completely clear (re) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ‘+ HLA-Cws allele (PSORS1) : major susceptibility gene Associated with an earlier age of onset = Associated with a positive family history ‘© Environmental factors = Drugs = Skin trauma (Koebner’s phenomenon) = Infection = Stress ‘+ Result of complex cutaneous immune reaction with 2 ‘major inflammatory component involving elements of the innate and adaptive immune systems and abnormal keratinocyte proliferation and differentiation Mediators that orchestrate changes in psoriasis: = 112,123, TNFa, IFNy CLINICAL FINDINGS © Well demarcated, raised, erythematous plaque with white-sivery scales + Lesions vary in size from pinpoint papules to plaques that ‘cover large areas of the body # Usually symmetric CLINICAL PATTERNS OF SKIN PRESENTATION ‘A. Plaque Type Psoriasis. = Most common form = Symmetrical, well-defined erythematous plaques ‘varying in size from one to several centimeters with 2 dry, thin, silvery-white or micaceous scale = AOP: scalp, trunk, buttocks, limbs (extensor surfaces ‘such as elbows and knees) 8. Guttate-Type Psoriasis = Dewdrop like imm-10mm, salmon-pink papules, usualy with a fine scale = Common in younger individuals (<30yo) = OP: trunk and proximal extremities . Erythrodermic Psoriasis ~ Can develop gradually from chronic plaque disease or acutely with ite preceding psoriasis. Generalized form of the disease that-affects all body sites (290% of BSA) ~ Erythema: most common feature Only superficial scaling, Pustular Psoriasis ‘Sheets of small, monomorphic pustules developing within erythrodermic skin or along the edges of ‘expanding inflammatory plaques May develop from established plaque psoriasis or ‘may present de novo 2types += Pustulosis palmaris et plantaris * Acrodermatitis continua Hallopeau RELATED PHYSICAL FINDINGS 4. Nail Changes In Psoriasis = Can affect the mall bed and nail matrix = Leads to thickening, pitting, discoloration and splintering ofthe nail plate, and separation of the nal plate from the nail bed [EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 2= a a oe 2. Psoriatic Arthritis = Seronegative inflammatory arthritis with, various clinical presentations = Develops at an average of 12 years after the onset of skin lesions. = Strong ganetic component (HLA 827) DIAGNosTic WORK UP 1, Histopathologic findings > Early lesion of pustular psoriasis: sight acanthosis of the epidermis ~ Older lesion: psoriasform hyperplasia * Spongiform pustules of Kogoj ' Hyperkeratosis and parakeratosis * Munro's microabscesses MANAGEMENT ‘A. TOPICAL THERAPY 4. CORTICOSTEROIDS ~ DOSING: Can be used as monotherapy 1-2x/day ~ Can be combined with other topical agents, UV and systernicagents = Duration of use: * Class |: avalable data for 2-4 weeks of treatment * Less potent agents: optimal endpoint unknown Gradual reduction in usage recommended following clinical response 2, CALCINEURIN INHIBITORS = Dosing: apply 2x/day on affected areas, no: duration of course is specified = More effective for intertriginous and facial psoriasis 3. TAZAROTENE = Dosing: apply once at night to affected areas = Best used in combination with topical corticdsterolds = Contraindication = Most common: skin Irritation in lesional and perilesional skin * Photosensitizing 4. VITAMIN D ANALOGS = Dosing: apply 2x/day on affected areas, = Use in combination with topieal corticosteroids gives ‘added benefit = Contraindication ‘= Translentiritation in lesional and perilesional skin 5, EMOLLIENTS = Dosing: apply 1-3x/day = Standard adjunctive therapeutic approach to the treatment of psoriasis, 6. SALICYLIC ACID = Dosing: apply ix/day = May reduce keratinocyte-to-keratinocyte binding as ‘well as reduce the pH of the stratum conrneum-> reduced scaling and softening of psoriatic plaques B, SYSTEMIC THERAPY 1, METHOTREXATE EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ~ Blocks inydrofotte reductase > inhibition of purine and pyrimidine synthesis inhibition of nucleic cid synthesis in activated tells and in keratinocytes > antiproiferae and immunomodulatory effets ~ Given once weekly, orally or parenteraty = Maximum dose should not exceed 30me/week ~ Monitoring: CBC, FT weekly 2. ACITRETIN = MOA: binds retinole acid receptors -> normalizing keratinization and proliferation ofthe epidermis = Dosing: 25-SOme/day = Monitoring: CBC, LFTs, lipid profile, pregnancy test 3. FUMARIC ACID ESTERS = MOA: interferes with intercellular redox regulation, Inhibiting NF aB translocation = Dosing: initiate at low dose, escalate dose weekly = Monitoring: CBC, comprehensive metabolic panel, urinalysis repeat test monthly for 6 months 4, CYCLOSPORIN A = MOA: Binds cyclophilin > blocks calcineurin > reduce the effect on NF-AT in T cells > inhibition of 2 and other cytokines 5. HYDROXYUREA ~ MOA: inhibits ribonucleotide diphosphate reductase ~ Monitoring: C&C, CMP, LFTs 6. MYCOPHENOLATE MOFETIL = MOA: noncompetitive inhibitor of inosine monophosphate dehydrogenase, blocking de novo purine biosynthesis = Monitoring: CBC, CMP 7. 6-THIOGUANINE = MOA: purine analog that interferes with purine biosynthesis cell cycle arrest and apoptosis, = Monitoring: CBC, CMP, LFTS PROGNOSIS Guttate psoriasis: selfsimited * 12-16 weeks without treatment = 1/3-2/3 of the patients develop chronic plaque * ‘ype psoriasis ~~ Chrontc plaque type * Ufelong disease ~ Erythrodermic and generalized pustular psoriasis * Poor prognosis, * Gan be severe and persistent HANSEN'S DISEASE ETIOLOGY # Leprosy is caused by acid fast bacilli called ‘Mycobacterium leprae (M, leprae}, It is an obligate Intracellular bacterium, ‘+ Itmainly affects the skin, peripheral nerves, eyes, mucosa of the upper respiratory tract &oe) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY a ‘+ Bacterium invades elther dermal (cutatieous) nerves of Getteaton| Shindesloas | 07? | Promin main peripheral nerve trunks situated superficially, in smear | Test regions that are relatively cooler. ‘waererminate | SHWGLE. TH . defined, . PATHOGENESIS OF HANSEN'S DISEASE 3 ee spect emerebody sty twenrnexpraanynen | & brnacaaa PSs + Migrate towards the neuraltissueandentertheSchwann | & J (7) Asyreetial cells z Well-defined - He «acl start multiplying slowly (about 12-18 day for one ae bacterium to divide into two) within the cells, get Seciaine | ar liberated from the destroyed cells and enter other Tuberauoid | Asyrmetteal ‘unaffected cells (en Wel-demarcated ‘+ As the bacili multiply, bacterial load increases in the body ony + + and infection is recognized by the immunological system ama a only sis Wenincgteal si leary defined ‘+ Lymphocytes and histiocytes (macrophages) invade the oe hatte infected tissue Torderine | Asymmerieal Borderine | Well demarcated ‘© At this stage clinical manifestation may appear a5 (68) inner border with Involvement of nerves with impairment of sensation and/ aston orskin patch Meetmetiones | ae | fe ‘IF it is not diagnosed and treated in the early stages, (characteristic further progress of the diseases is determined by the | & punched out strength of the patient's immune respon: j appearance) CLINICAL PRESENTATION OF HANSEN’S DISEASE & | Boniertne Many RIDLEY CLASSIFICATION OF CLINICAL PRESENTATION & | lexromeroes: | novel Flaw symmetrical ‘+ Based om high resistance to low resistance Shiny papules, 1. Tuberculoid (17) nodules, plaques | *** . 2, Borderline Tuberculoid (BT) ‘With sloping sees Tapromatous | NUMEROUS 5. Lepromatous Leprosy (LL) Leprosy (tt) | Symmetrical Exrthematous PERIPHERAL NERVE CHANGES shinymacules, | ga | Peripheral Nerve involvement is much more serious and causes papeles, nodules, permanent and progressive dlsabilty and crippling deformities, SSeidennet because neurons if destroyed do not regenerate and are seemnty replaced by fibrous tissue. The common nerves involved are: ‘¢ Factal Nerve Reactlonal States > BicseePeTNGR Sr Terve Feature | Reversal Reaction Relapse ee ubsiroene ‘Onset Sudden within afew | Slow and insidious hours) {weeks or months) «+ Radial nerve Time of onset Cceurs during ‘OccursTong after ++ Lateral popliteal nerve (Common peroneal nerve) treatment orwthin | treatment i + Posterior Tibial nerve siemonths of discontinued, after an stopping treatment _| interval of atleast mo WHO CLASSIFICATION: ‘CidTesions | Some orallexsting | The margins of ome PAUTERCLARY | MOLTRAGLLART tea bacone | arse become TAREE Syeas [Upto yrs feperta tny | eqteratue AFB SMEAR, : 2 ew esos | Several new lesions Se oA] Sone Weak ‘woe | imvcretpteseme | IMMUNE RESPONSE cases LESIONS. a. >s Uiezration | Sometimes Tusval FORM, Tuberc Tepromatous ‘Sealing Tesions desquamate | Absent CYTOKINE PROFICE | TFN-Gamma andilz | 4 and 20 as they subside Neve ‘Common; many | Asingle nerve PHYSICAL FINDINGS involvernent | nerves may rapidly | becomes involved; Cardinal signs become palnfuland | Disturbances develop «+ Hypopigmented or reddish skin lesions} with definite ee |e loss of sensation Generat Fever and malaise | Nat afected ‘© Enlargement plus tenderness of peripheral nerves condition __| are usual «+ Sit skin smear positive for acid fast boci Responseto | Excellent Tesionssubiide bot conticosterolds reappear, GASIFICATION: corticosteroids are not indicated in relapse EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 10SSS TTT ISIS aaa aa (a) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY TREVERSAUREACTION | ERYTHEMA (rvee a) NoposuM LEPROSUM. (ryee2) Tyee? Paucbacilary and ‘Mulilbaelory only lassteation | ruldbactary Tiolony Change delayed type | lreune complex hypersensitivity toh. | disease (when M. leprae Leprae ae led There also an and are atsociatedIncreate Inthe. | decomposed; the specific cellmediated | proteins rom Irmmunity In those ‘dead bal cause patients undergolnga | an allergic shift in cassifeation reaction whether sight or marked, Tanifestations | Leprosy lesions gradually | Crope of palnfal become swollen and | papules, nodules erythematous (e/-new | developingina lesions, nerve ow hours and enlargement, acute lasting afew days neurtis) Successive crops Lasts for weeks or months | may occur over any months years ‘Fever, general malaise and pain Complications | Skin ulceration, paralyls, | Neuris, ints, anesthesia ovens, lymphadenopathy, antrits, protaurla, tuleratng lesions Diagnostles '* Blood Examination = CBCPC, FBS, SGOT SGPT, Alkaline phosphatase, BUN, Creatinine = G6PO (should be normal to avoid hemolytic anemia ‘caused by Dapsone) slit skin Smear Skin Punch Biopsy = Stains: H&E (Hematoxylin and Eosin, Fite Faraco- Others = Urinalysis = Chest Xray LEPROMIN TEST = The lepromin or Mitsuda test consists of an intradermal injection of 0.1 mi of a suspension of be alled M, eproe = The response is positive when a nodule forms at the * site of injection 3 to 4 weeks iater, indicating that the patient is able to response to the bac! = The test provides information. MANAGEMENT A. Medical Management of Leprosy ‘Multi Orug Therapy (MOT) = Accepted standard treatment far leprosy ‘mount a specific cellsmediated prognostic, but not diagnostic, Itis positive in TT and 8T leprosy e = Renders patient non-infectious within 1. month after starting treatment 4)_Singte Lesion Pavel {ROM Regimen). ‘Adult Child (50-70kg)_| (3-14v/0) Rifampin | 600mg [ 300mg _| Single ‘Ofloxacin ‘400me | 200mg _| Single Minocycline [100mg | SOmg [Single “ofloxacin and Minocycline ~ not recommended for pregnant women and children < Sy/0 Dose 2) Pauci-bacllary Regimen Frequency adutt | child | Child a (60-70Kg) | 10-2490 | <19¥0 | uration Rifampicin | 600mg | 450mg | 300mg | Once a ‘month for 69 months Dapsone | T00me | 50mg | 25mg | Once a day for 69 months 3) Muk-Bocillary Regimen ‘adult | Chiid | Child | Frequency (50-70kg) | 10-14 yo | <10y0 | and Duration Rifampin | Oayi: | Daya: | Day: | Oncea 600mg | 450m_g | 300mg | month for 1218 months Clofaimine | Dayi: | Davi: | Oayl: | Oncea 300mg | 150mg | 100mg } month for then [then [then | 32-18 somgoD | 50mg | SOmg_ | months every | 2xa other — | week day Dapsone | 100me | Some | 25mg | Once a day for 12-18 months "MEDICATION | NOTABLE SIDE EFFECTS Rifampicin | Hepatotoxicity. ‘Clofazimine | Red orange skin discotoration Dapsone Hemolysis, anemia, agranulocytosis Second-tine Drugs = Offoxacin ‘© minocycline Points to Remember in Medical Management ‘+ Contact tracing of detected Hansen's Disease patients is essential ‘= Most effective way of preventing disabilities in leprosy and to prevent further transmission lies in early diagnosis and treatment with MOT ‘*Apatient on PB regimen should take 6 blister packs within ‘9 months while 2 patient on MB regimen should take 12 blister packs within 18 months = Proven safe and effective ‘+ If PB Is reclassified to MB after 6 blister packs, start Started as soon as diagnosis is made treatment with MB regimen to complete 12 bister packs = Combination of >? ant-leprosy drugs within 18 months EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY asBE EEE ES SA SNS SSS Se ST SSS SSS REE RE ER Ree ee ‘© Monitoring progress includes noting changes in character ‘of lesion, pain in eyes, changes in color of sclera and cconjunctivae, new disabilities or progression of previous slsablities, nerve damage. B. Medical Management of Reactional States “Type of wey Features Management WA Reversal |e ewoten | = Give ory anaes o lesion i = Do Nerve Function a tow-arde fever | Assessment (NFA) every 2weake ~ Advise bed est = Continye MOT Severe Nerve damage of [= Give presibed_ WHO Reversal | ess than 12 | Prednisone treatment ron. mace | conte MOT weakness ss of | poy arom eee DoNFA every two weeks sryer meme | Refer patients with pala) fesse eur an eto rectors tenderness = Swollen estos thetoce Severe ENC |—high fever | = Give_prescibed WHO "| reddish nodules | Prednisone treatment =Paintulneurtis. | ~ Comtinve MoT =Sont pain = DONTA every 2 weeks ~Stin eration |= Refer patient with oreniti, ies, | Perens, recurrent and costs, nephritis, | ROr~espanding swollen ands, | _eastons feet and face I Predrisone is conranccated or aufero contol recurence, give: Clfazimine or Thaomide ‘COMPLICATIONS ‘+ Common complications arise from perisheral nerve injury, venous insufficiency or searring '* One-quarter to one-third of newly diagnosed patients fave or will eventually have chronic disability secondary to Irreversible nerve Injury of the hands or feet or from ‘eye involvement ‘+ Exposure keratitis from dry eye, corneal insensitivity, and lagaophthalmos, Internal eye disease may resuit to blindness © Venous insufficiency, secondary to endothelial involvement of deep vein valves, leads to stasis. dermatitis and leg ulcers ‘= Destruction of joints (Charcot joints) may occur due to. Joss of protective pain sensation ‘+ Sympathete nerve Involvement results in decreased hidrosis, leading to dry palms and soles 1 Collapse of the nose in lepromatous leprosy is from the. contracture of the scar tissue PROGNOSIS AND CLINICAL COURSE ‘© Can be cured without therapy: TT or BT who upgrade to, 1 «Disease is progressive with morbidity due to nerve injury and/or superimposed reactlonal states +» Treatment arrests much of disease activity '» Stocking-glove pattern of sensory Impairment may progress. Peripheral neuritis of recent onset may improve with corticosteroid treatment ote) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY CONNECTIVE TISSUE DISEASES TUPUS ERYTHEMATOSUS © Agroup of heterogeneous ilnesses that have in common the development of immunity to self-nuclelc acids and their associated proteins, with skin-only disease at one ‘end of the spectrum and severe visceral involvenent at the other, + James N. Gilliam divides the cutaneous manifestations of LE into: = LEspecific skin disease:’ lesions that show characteristic histologic changes of t€ = Lenonspedfc akin disease: lesions that are_not histopathologicaly stint for LE and/or may be seen as, feature of another disease pec Skin Drs umneOog LECCE TRaieatneos (ACS ‘toate ACL (ata ashbuterty ah) 2. Gann’ ACLE Dp copa opus a, LE a8, 8h heres ups cera) ESuimcte cutineoos ECL ‘mer SCE tom. Tops marglnass sate, etme ervfagum, atcmne snl soem, taps eyterstons rasan) 7 Papulosquamous SCLE (s/n. disseminated DLE, subacute dsiominted UE apercal Garemnated LE, psoistorm UE piyreafom (and maclopapuarptorensve if) Coweniceutoneoste co.8 Vee dead EOL ‘ techest Ue i cenetaed 4 2.toporrophitecos LE 3 pur rtndusapas panicle Micon oe soaiDle 2 conjnctat ous 5. Lust rca aque of) {chin ein ape) 1 herd OLE Rho pons ove pus ans LeNonpedc shin Odeae 7 Ganeoen ana dase wncutes ‘leskogtoassc Chpapeble pupae G3) te cates etre don he itaneoslesons ascupathy 2. Degos dseasethelesons Secondary auophle blanche (syn, Wvedold vazcults, vedo vasa 3-Perungual telangiectasia ‘A Uvedo etculans 5 Trrombophiabits {6 Raynaud phenomencn 7. Ethomelaiga erythermalga) A. Nonscaring lope 1 Mapas? | 2 Telogen evi, 3, Alopecia areata CSdlerodaetyiy D. Rheumatoid nodules E.calonosiscuts F Lemonspectc bullous lesions G.Urteara H.Papulonodularruclnoss ‘Cuts tnavanetoderma 4. Aconthess nlglans ype nwalin resltance) K Erythema mltforme LLegucers MLchen planus 2 Etiology and Pathogenesis ‘+ The interplay between host factors (suscentiblity genes, hormonal miliey, etc.) and environmental factors [ultraviolet (UV) radiation, viruses, and drugs) leads to loss of self-tolerance, and induction of autoimmunity EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 16* This ts followed by activation and expansion of the immune system, and eventuates in immunologic injury to tend organs and clinical expression of the disease EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ‘= LE Profundus/Le Panniculltis: = LE ponniculltis: firm nodules, 1-3 em in diameter, overlying skin Is attached to subcutaneous nodules ‘and is drawn inward to produce deep, saucerized Clinical Findings depressions ‘Acute CLE = Located on the head, proximal upper arms, chest, back, breast, buttocks, thighs * confluent, symmetric erythema and edema are centered = LE profundus: Lé pannicul cover the malar eminences and bridges over the nose {casi buttery rash or malar rash) '¢ Head, chin and V area of the neck can be involved; severe '* Chilblain LE; purple-red patches, papules and plaques on facial swelling ‘the toes, fingers, face > scarred atrophic plaques with Generalized ACLE: widespread motiform or associate telanlectases eranthematous eruption often fused over the extensor = Precipitated by cold, damp climates aspects ofthe arms and hands, sparing the knucles Classic DLE + LE Tumidus: succulent, edematous, urticaria-lke plaques Subacute ‘with ttle surface change ‘+ Exythematous macules and/or papules thot evolve into ‘hyperkeratotic papulosquamous or annular/polycyclic Diagnostics ploques "ANA with profile (ant?- | ANA: positive in >95% of SLE patients, develop within 1 year of ‘© Photosensitive lesions, occur predominantly in sun- | 4SDNA,-Sm) ‘exposed areas (upper back, shoulders, extensor aspects | Complementievels | onset 1s, V ar ie neck, lateral face — less 4 ‘Anti-dsDNA specific for SLE, ear nnr YM Of eck earl fat a) a eras fae nephnt ° is), especially when * Aatve edge of lsons: undergoes » vecslobulus ‘soit with detain evel of change that subsequently produce a crusted appearance ace * Less transient and heal with more pigmentary change; | Gaowa LE nephritis less edematous and more hyperkeratotic ANP (CNSLE ssDNA Risk of SLE in OLE Chronic Histones Drug-induced SLE ‘ Discold LE: red-purple macules, papules or smal plaques | UIANP Mixed CTD | ‘that rapidly develop a hyperkeratotic surface; sharply RO/SS-A ‘SCLE, neonatal LE demarcated, coin-shaped erythematous plaques covered La/SS-B SCLE by prominent, adherent scale that extends into the Chest xtay To check for pleural effusion ottces of elated hair folicles T2LECG/2Decho | To checkfor pericardial effusion ~ Expand with erytherna and hyperpigmentation atthe ‘or pericarditis Urinalysis 724 hrurine | To check for proteinuria periphery, leaving hallmark atrophic central scarring, (0.Sg/day or 34) and cellular telangiectasia and hypopigmentation > large, confluent, disfiguring plaques — ae : = Hair-bearing skin > reversible scarring alopecia; eothine. fo check for other renal disorders keratotic plugs in dated folcies Electroiytes, ESR Tocheckforelecobre = Carpet tack sign - when adherent scale is Ifted from milan more advanced lesions, keratotle spikes can be seen | “/mlalCT Scan ea rep erengements in the to project from the undersurface of the scale beckcroond of esrclogea = Seen on the face, scalp, ears, V area of the neck, | CBC parpheralbload | To check for hemohnic anemia extensor aspect of the arms smear leukopenia, lymphopenia, thrombocytopenia ‘+ Hypertrophic DLE: exaggerated hyperkeratosis in classic [Stn punch biopsy | (se below) DLE lesions immunchistology | IgG > igM> igh and Complement = Extensor aspects of arms, upper beck, face components deposited in a i i = Lupus planus: overlap of hypertrophic DLE and lichen | Lupus bandtest continuous granular or linear planus band-like array at the dermal- - = Lupus erythematosus bypertrophicus et profundus: epidermal junction - hypertrophic DLE plus violacous/dull red, indurated, SLE: (4) lesional and non lesional rolled borders and striking central, crateriform skin ' atroohy DLE: (+) lesional skin only 7 © Mucosal DLE: painless, erythematous patches that evolve ene into sharply marginated, with irregularly sealloped, white ‘+ Evaluation torule out underlying SLE disease activity , borders with radiating white striae and telangiectasia; ‘Protection from sunlight and artificial sources of UVR honeycomb appearance * Avoid the use of potentially photosensitzing agents ; (hydrochlorothiazide, tetracycline, griseofulvin, = More common: buccal mucoss; others; palate, alveolar process, tongue, vermilion border ofthe lis, nasal, conjunctival, anogenital mucosa piroxicam) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ®EES SSSI ISAS IIIA aa - am a Local Therapy i) EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ‘Sun Protection ‘Avoid direct sun exposure, wear tightly woven clothing and broad-brimmed hats Regularly use broad-spectrurm, water resistant sunscreens (SPF 2 30 with an efficient UVA blocking agent). Apply UV blocking films. Toeal Glucocorticoids Totermediate strength preparations (Triamcinoione acetonide 0.1%) for sensitive reas Superpotent topical class | agents (Clobetaso propionate 0.05% or Betamethasone dipropionate 0.05%) ~ Produce the greatest benefit in CLE ‘Class 1oF I topical solutions and gels ~ best for treating the scalp Topical Caleineurin Inhibitors Pimecrolimus 1% cream and Tacrolimus 0.1% ointment Intralesional Glucocorticoids Triamelnolone acetonide suspension 25- 5.0mg/ml for the face; higher ‘concentration for other areas, every 4-6 weeks More useful for DLE; hyperkeratotic, lesions unresponsive to topical slucocorticoids ‘Active borders should be thoroughly infiltrated Others Topical Retinoids: Tazarotene 0.05% gel, ‘Tretinoin 0.025% gel 8% imiquimod cream ‘Systemic Theray ‘Antimalarials Pretreatment ophthalmologic ‘examination. Antimalarial retinopathy Is extremely rare especially in the First 10, years of therapy. Follow-up ‘ophthalmologic examination every 6-12 ‘months. Hydronychloroquine sulfate, 6-6.5 ‘me/kg, dally. 2-3 month delayed onset of therapeutic benefit. ‘No response after 8-12 weeks: ‘Quinacrine hydrochloride, 100 me/day. ‘Can be added to HQ without the ‘enhancing the risk of retinopathy. Inadequate contro! after 4-5 weeks: Replace hydrachloroquine with Chloroquine diphosphate, 3mg/tg, ‘Adjust dose for decreased renal or hepatic function. ‘Side Effects: Quinacrine — headache, GI Intolerance, hematologic texiclty, ‘pruritus, ichenold drug eruptions, ‘mucosal or cutaneous plementary pigmentation; yellow discoloration of skin and sclera; significant hemolysis with G6PD deficiency ‘Antimalarials — bone marrow suppression, aplastic anemia Nom Immunosuppres sive options for antimalarial- refractory “Methotrexate: 10-25 mg oncea week, with fotic acid (adjust If CrCl <60 mi/min) Diaminodiphenysufone (Dapsone}: Initial dose 25mg 2 x @ day, can increase disease 0200-400 mg/day _| ‘SE hemolysis and/or methemoglobinemia, especially in G6PD deficient Isotretinoin, 0.5-2.0 mg/kg/day, and ‘Acteetin, 10-50 mg/day. SE: teratogenicity, mucocutaneous dryness, hyperlipidemia ‘Thalidomide, 50-200 mg/day (or Lenalidomide) SE: severe teratogenicity, sensory neuropathy, peripheral neuropathy, elapse, thromboembolism Systemic ‘Every effort should be made to avoid the Glucocorticoids | use of systemic glucocorticoids. intravenous pulse methylprednisotor severe and symptomatic skin disease ral glucocorticoids (Prednisone), 20-40 ‘mg/day, as a single morning dose ~ supplemental therapy during the loading phase of therapy with an antimalarial agent Controlled disease activity: daily dosage should be reduced to Smg to 10 mg decrements until activity flares again or until a daily dosage of 20me/day is achieved 2.5 mg decrements at 20 mg/day Prednisolone — significant liver disease (prednisone requires hydroxylation in the liver) Dose should be reduced at the earliest ble time because of side effects: ascular (aseptic) bone necrosis ~ susceptible to LE patient steroid-bone loss occurs most rapidly in the first 6 months of use agents to prevent osteoporosis with the Initiation of steroid therapy Prognosis and Course ‘Acute | Depends on underiying SLE activity cue Subacute | Intermittent recurrence of disease activity over cue long periods of time without significant. progression of systemic involvement Chronic | Untreated: indolent progression to large areas cue ‘of cutaneous dystrophy and scarring alopecia Psychosocial devastating and occupationally disabling ‘Treatment: skin disease can be controlled ‘Spontaneous remission occurs occasionally Older, inactive lesions can be active again Rebound after discontinuation of treatment. ‘SCCin chronic smoldering OLE lesions 5% of DLE patients > SLE Generalized DLE with abnormal laboratory findings > Increased risk of SLE DERMATOMYOSITIS (0M) ‘Thought to evolve through multiple sequential phases: * a genetically determined susceptibility phase ‘+ an induction phase triggered by an environmental stimulus ‘* an autoimmune expansion phase * Injury phase Involving multiple Immunologic effector ‘mechanisms. EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 38Idiopathic inflammatory myopathies (1IDMs) ‘+ Predominately target the skeletal musculature and/or skin and typically result in symptomatic skeletal muscle weakness and/or cutaneous inflammatory disease Dermatomyasttis (DM) ‘+ Only idiopathic inflammatory myopathy that expresses a ‘characteristic pattern of primary cutaneous inflammation Classic Dermatomyositis ‘+ Cutaneous involvement in 30% to 40% of adults and in 95% of children '* Occur most frequently inthe fifth and sixth decades ‘+ Environmental factors have been implicated 2s disease triggers Drug-induced Dermatomyositis ‘+ Caused or exacerbated by systemic medications ‘© Present with both myositis and pathognomonic ‘cutaneous findings and resolve with discontinuation of the medication * Long-term hydroxyurea therapy ‘* Can produce a DM-tke cutaneous eruption © Unique in that muscle weakness and other systemic symptoms are absent * Painful leg ulcers, xerosis and cutaneous atrophy are often seen Cutaneous Lesions ‘+ Gottron sign and gottron papules are pathognomonic ‘ Periorbital, confluent, macular, violaceous {hellotrope) erythema/edema and periungual telangiectasia with dystrophic cuticles, are highly characteristic © Gottron sign = confluent macular violaceous erythema, most Pronounced over the metacarpophalangeal/ Interphatangeal joints, extending In a linear array ‘overlying the extensor tendons of the hand and fingers ‘+ Early Gottron papules ~ seen over the distal interphalangeal joints along with periungual erythema and dystrophic cuticles Primary skin changes of DM ‘© Pruritic, symmetric, confluent, macular violaceous erythema variably affecting the skin overlying the extensor aspect of the fingers, hands, and forearms; the arms, deltoid areas, posterior shoulders, and neck (the shaw! sign); the V area of the anterior neck and upper ‘chest; and the central aspect ofthe face, periorbital areas, forehead, and scalp ‘© Lateral aspects of the hips and thighs (holster sign) are also frequently involved ‘+ Poikiloderma atrophicans vasculare and calcinosis cutis ‘are often present EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ++ Followed by upper extremity weakness manifested by difficulty in raising the arms above the head to perform routine activities such as combing the halt = (+) pain or tenderness in the affected muscle groups # Weakness involving the upper one-third of the esophagus and/or the laryngopharyngeal muscles may present as dysphagia or a hoarse voice (dysphoria) ‘= Some patients with severe diaphragmatic disease require ‘mechanical ventilation + Cardiac failure may be present in the terminal phase of the disease Diagnostic Criteria ‘The following are commonly used to define OM/PM skin lesions + Heliotrope rash (red-purple edematous erythema on the ‘upper palpebra) '» Gottron’s papules or sign (red-purple flat-topped papules, atropty, or erythema on the extensor surfaces, ‘and finger joints) ‘+ Proximal muscle weakness (upper or lower extremity and trunk) ‘© Elevated serum creatine kinase or aldolase level ‘© Muscle pain on grasping or spontaneous pain ‘+ Myogenic changes on EMG (short-duration, polyphasic motor unit potentials with spontaneous fibrillation potentials) Treatment Goal is to arrest Inflammation In the skin and muscles and ‘obtain a clinical remission. ‘© Local Treatment = Avoid excessive sun exposure = Use effective broadspectrum sunscreens = Topical glucocorticoids (classes | and Il) = Dally use of a medicated shampoo ~ Effective moisturization regimens = Topical antipruritic agents = Pulsed dye laser therapy © Systemic Treatment ~~ Nonsedating or sedating antihistamines = Anti-malarials ‘+ Hydroxychloroquine sulfate (6 mg/kg given as two divided doses per day) Systemic glucocorticoids remain the traditional first- line therapy * Prednisone is given in divided doses of 1.0-1.5 ‘ma/ke/day, whereas in children the dosage is 1-2 make/da ~ Methotrexate (7.5-25.0 mg) given once weekly ~ Cyclosporine and cyclophosphamide — Mycophenolate mofetil ~ High-dose intravenous y globulin therapy ~~ anti-TNF-« therapy has been used anecdotally to treat both the muscular and cutaneous manifestations of om Muscle Disease ‘+ Initial clinical finding include lower-extremity weakness Prognosis and Complications ‘manifested as dificulty in performing routine activities of Classic OM daily living, such as rising from a chair ‘ Pulmonary and cardiac complications were the most frequent causes of death EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY a9SS SSS SS SPUR Ue ee ee a y , P p p p » 7 » er 2 . > ‘© Cancer-associated myositis had the worst prognosis © Juvenile-onset and overlap myositis had the best prognosis + Cutaneous ulceration, internal malignancy, opportunistic Infections and lymphoma may occur SCLERODERMA (SYSTEMIC SCLEROS'S) ‘+ Rare multisystem disease based on: * Autoimmunological processes © Vascular endothelial Injury ‘+ Extensive activation of fibroblasts ‘+ Most frequently affected organs: Skin, esophagus, lung, heart, kidneys Epidemiology Worldwide distribution, afects all races ‘© Women are more frequently affected by systemic sclerosis (SSe) ‘+ Women > Men (3:1 to 14:1) ‘Age of disease onset ranges between 30 and $0 years males have earlier onset than females ‘+ SSc has the highest case-specific mortality of any of the ‘autoimmune rheumatic diseases, but itvaries individually depending on: = racial or ethnie differences presence and severity of organ involvement = $e subsets age at diagnosis ~ gender differences Etiology ‘¢ Several studies suggest that a (+) family history for Sis the strongest risk factor ‘= Ethnicity also contributes: Blacks with SSc are frequently ‘younger than whites ‘= Approximately 1.5% of $Sc patients have one or more + affected first-degree relatives: a 10- to 15-fold higher risk In family members than In the general population ‘© Several studies suggest an association of scleroderma With the following genes: = HUA-DRB1*2302 = 0Q81%0604/0605 haplotypes: (with anti brilarin positive patients) = HLASRB1*0303 (with antiPm-Scl antibodtes) Clinical Manifestations Depend toa large extent on the subset and stage of disease SKIN = involvement is'a cardinal feature of $Sc; usually appears first in the fingers and hands = nonpitting edema ofthe fingers (putty fingers) hands, and extremities = Sclerodactyly: induration and skin thickening of the fingers = Restricted mobility of joints (dermatogenous contractures), and/or restricted breath-excursion may be present ~ Typical facial features: * telangiectasias, a beak-shaped nose as well as reduced mouth-aperture (microstomia) H] EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY = Calcinosis cutis: abnormal deposition of cutaneous, and/or sub- cutaneous calcium; occurs over pressure points (acral, joints) = *Satt and pepper skin” = hypo and hyperpigmented skin = loss of hair follicles and sweat glands \VASCULOPATHY = Approximately 50% of patients with $Se are affected by digital ulceration associated with vasculopathy at some paint in thelr disease = Tender and painful pitting scars > ulcers + Finger/toe-tips, extensor surfaces of joints = Other complications: * Critical digital ischemia, paronychia, infections, gangrene, osteomyelitis, finger pull oss svsTeMic = Cardiopulmonary * Dyspnea, non-productive cough, asturbed diffusion-capacity and cyanosis * Palpitations, iregular hearbest + Pulmonary arterial hypertension: mosticommon cause of disease-related death ~ Gastrointestinal * Most common internal organ involvement * Problems with motility, digestion, absorption, excretion * Dysphagia, heart burn (reflux), nausea, vomiting, early satiety * Hypomotilty, bacterial ‘malabsorption, fecal incontinence + Constipation alternating with dlarrhea = Nephrologic * Systemic: renal crisis: Acute renal failure with abrupt onset of moderate to severe HPN (50/asmami) * Elevated serum creatine wie normal upper limit = Proteinuria of >/= 0.5g/day on two or more ‘occasions = End-organ damage: encephalopathy with ‘generalized seizures or pulmonary edema = Musculoskeletal * arthralgia, myalgia, loss In joint range of motion and joint contracture, symptoms of carpal tunnel, muscle weakness * For, Nose, Throat * Sicca syndrome, poor dentition, hoarseness = Neurologic * Facial pain” and decreased sensation, hand baresthesias and weakness, headache and stroke = Reproductive * Erectile dysfunction, dyspareunia = Constitutional * Fatigue, weight loss overgrowth, AST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 20Management = Skin findings = Physical therapy and regular exercise = Topical steroids, calcineurin inhibitors, moisturizing = Immunosuppressive drugs, systemic steroids (short time) ~ Phototherapy = Surgery (calcinosis cutis) = Laser therapies = Bleaching agents, salicylic acids and chemical peels ‘+ Vascular findings (Raynaud's phenomenon, digital ulcerations) = Consistent warm keeping, Paraffin-bath = Galeium channel blockers PO = Moprost iv = Bosentan PO = Sildenafil PO ~ Wound dressing (hydrocolloid membrane, mepitex) * Lung findings (dyspnea, dry cougt alveotitis/lung fibrosis) = Oxygen Cyclophosphamide PO or IV ‘Azathioprine PO = Glucocorticoid » Gastrointestinal findings (reflux, dysphagia, alarrhes, obstipation) ~ Proton Pump inhibitor = Ha-receptor-antagonists = Change habit of eating ~ Antibitis (Erythromycin) ‘+ Cardiac (pulmonary arterial hypertension, shortness of breath, palpitations, peripheral edema) = Oxygen = Diuretics = Bosentan PO bibasilar rales, ~ Sildenafi PO = Epoprostenol/tloprost/Beraprost PO ‘* Renal (scleroderma renal crisis, headache, hypertension) = Blood pressure control = ACE-inhibitors (Use ina stable patient is not recommended Monitoring + 1t(s recommended that the clinically stable patient have the following diagnostics: + Pulmonary function test annually 4 High-resolution CT Sean (HRCT) If pulmonary funtion is 30% BSA) SIS-TEN Overlap (involvement of 10-30% BSA) ‘© both are considered by some as parts of a disease spectrum based on the following: ~ most commonly induced by the same medications ~ patients initially presenting with SIS may progress to ‘extensive skin loss resembling TEN ~ histologic ~ both are increased by the same magnitude in HIV infection EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 2NSS td ood Perriae Teeeee eee eee High-risk drugs: antibacterial sulfonamides, aromatic anticonvulsants, allopurinol, oxicam non-steroidal anti- Inflammatory drugs, lamotrigine, nevirapine Complications ‘Sepsis (S. aureus, Pseudomonas} ‘© Ophthalmic complications. ‘+ Nall changes ‘+ Mouth sequelae ‘Vulvar and vaginal complications Chronic lung disease Prognosis and Clinical Course ‘+ The epidermal detachment progresses for 5 to 7 days. ‘Then, patients enter a plateau phase, which corresponds. to progressive re-epithelalization. This can take a few days to a few weeks, depending on the severity of the disease and the prior general condition ofthe patient. Hospital mortality rate = Overall: 22-25% = SIS: 5.12% ~ TEN: >30% Treatment Early recognition © Withdrawal of offending drug. ‘© ‘Supportive care ~ Fluid replacement and electrolyte correction = Nutritional support Corticosteroids IV immunoglobulin ‘© Cyclosporine A ‘© Plasmapharesis or Hemodialysis ‘© Antitumor Necrosis Factor Agents EXFOLIATIVE DERMATITIS. ‘© Diffuse erythema and scaling of the skin involving more than 90% of the total body skin surface area ‘© With male predominant (a male-to-female ratio: of approximately 2:1 to 4:1) ‘© Any: age group can be. affected with most ‘studies excluding children ‘© average age of disease onset varies from 42 to 61. ‘Occursin all races. Etlology and Pathogenesis ‘Pre-existing dermatosis Is the most frequent cause in adults + Followed by drug hypersensitty reactions and cutaneous Teel lymphoma (CTCL or Sézary syndrome + Noundertying etiology is identified in approximately 20% of ED cases and are classified as idiopathic '« Psoriasis is the most common underlying skin disease to cause ED followed by sponglotic dermatitis Possible triggers for psoriatic ED include the following: ‘Medications, such as. lithium, terbinafine, and ‘antimalarials ‘© Topical irtants including tars # ‘Systemic ilness EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ‘+ Discontinuation of potent topical or oral corticosteroids methotrexate, or biologic (efalizumab) «Infection including human immunodeficiency virus (HIV) ‘= Pregnancy ‘Emotional stress ‘= Phototherapy burns History '» History of dermatoses (psoriasis, atopic dermatitis) or 2 systemic medical condition ‘+ Medication history including naturopathic-and over the ‘counter therapies ‘= Patients with history of psoriasis and atopic dermatitis should be queried specifically regarding use of topical ‘and systemic corticosteroids, methotrexate, and other systemic medications; topical irritants; systemic illness; infection ‘= Primary skin diseases have ‘a slower course while drug, reactions usually have a rapid onset and resolution Cutaneous Lesions '* Classic presentation Is erythematous patches. that Increase in size and coalesce into generalized red. ‘erythema witha shiny appearance ‘+ Involves more than 90% of the patient's skin surface ‘+ Fine white or yellow scaling begins 2 few days after erythema, classically arising inthe flexures 1 Platestike scaling may occur acutely'and on the palmsiand soles, Related Physical Findings Related physical findings due to ED of any etiology may include the following: ‘© Tachycardia due to Increased biood flow to'the skin and. ‘uid loss due to disrupted epidermal barrier © High-output cardiac failure secondary to the high-flow state In ED. ‘© Thermoregulatory disturbances can hyperthermia or less commonly hypothermia ‘* Generalized lymphadenopathy ‘¢ Hepatomegaly which Is more'commionly Seen In drug- Induced ED ‘© Splenomegaly which has been associated with lymphoma ‘+ Peripheral pedal or pretibial edema result in most commonly Laboratory Tests ‘© Most often not diagnostic and not specific ‘+ Common laboratory abnormalities include. anemia, leukocytosis, lymphocytosis, eosinophilia, increased IgE, decreased serum albumin, and an elevated erythrocyte sedimentation rate ‘© Fluld loss may lead to electrolyte abnormalities: and abnormal renal function (elevated creatinine level) ‘Treatment ‘+ Patients presenting acutely with EO may require inpatient management due to significant fluid and electrolyte Imbalance and hemodynamic or respiratory compromise FAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY 2: EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY ‘© Children presenting with erythradarms and fever should be hospitalized and managed aggressively and nursed 19 ‘8 warm (preferably 30°C-32°C) and humid environment for comfort and skin moisture, as wall ax to prevent hypothermia # Gentle focal skin care, including oatmeal baths andl wet dressings to weeping or crusted lesions, bland emoliients, and low potency topleal sterols should be started © High-potency topical steroids and topical Immunomodulators, such as tacrolimus, should be avolded as systemic absorption may occur due to the Increased skin permeability and large surface area Involved ‘¢ Antihistamines for sedation and antipruriticaftects ‘+ Systemic ontiblotics are required for patients with ‘evidence of localized and systemic secondary Infection. Dluretics and adequate fluid Intake for pedal ond perlorbital edema ‘© All nonessential and possible offending medications should be discontinued + Folate supplementation and a diet of 130% of normal dietary requirements for proteln to replace nutrient losses * Determining the underiving etiology early Is essential for definitive treatment of ED ‘+ When the underlying cause of ED Is unknown, empitc therapy with systemic agents, including methotrexate, cyclosporine, acitretin, mycophenolate mofetll, and systemic corticosteroids, has been used Prevention ‘© Controlling the undertying couse ‘= Medications and irritants that have previously caused ED. should be avolded ‘© Systemic sterolds should be avolded in patients with Psoriasis to prevent rebound flares ‘© Educating patients with underlying diseases (e., psoriasis, atopic dermatitis) about possible triggers of ED (irritants, abrupt discontinuation of certain therapies) may also be helpful to prevent ED BLISTERING DISEASES ‘© range of chronic diseases wherein autoantibodies are directed against autoantigens in the epidermis or the basement membrane ‘© disorders of epldermal-dermal adhesions due to the involvement of adhesion proteins at the epidermis and the dermal-epidermal junction Pemphigus «characterized by Intraepidermal blisters due tothe loss ot celhcelladheston of keratinocytes (acantholysts) ~ Pamphigus Vulgaris ~ Pemphigus Follaceus + occursasaresult of circulating antibodies of the IgG clas; these antibodles bind to desmogleins = PV: desmogiein 3 In some, also desmoglen 1) = PF: desmoglein 1 + PV: Mlaceld bilters on skin and arosions on mucous membranes ‘PF: scaly and crusted skin lesions @ 4+ Inmostcosos, the disease inexorably progresses to death Unless treated aggressively with Immunosuppressive agents + Management = Glucocorticoids 2 to 3. mpeg body weight of prednisone until cessation of new bilster formation ‘and disappearance of Nikoisky sign, Concomitant immunosuppressive Therapy + Azathioprine , 2-3 mg/kg body weight « Methotrexate , either orally (PO) or IM at doses of 25 to 35 mg/weok + Cyclophosphamide , 100-200 mg dally * Plasmapherests * Gold therapy = Mycophenolate mofetil (1 g twice dally) High-dose intravenous Immunoglobulin, (HIVig) (26/kg body welght every 3~4 weeks) * Rituximab (monoclonal antibody to CD20) = Other Measures © Cleansing boths, wet dressings, topical and intralesional glucocorticoids, _antimicroblal therapy per documented bacterial Infections. * Correction of fluid and electrolyte imbalance Bullous Pemphigold teraction of autoantibody with bullous pemphigold antigen (BPAGL and 8PAG2 (collagen type XVt}] in hamidesmosomes of basal keratinocytes ‘+ Abullous autoimmune disease usually in elderly patients ‘+ Pruritle popular and/or urticarial lesions with large tense bullae * Management = Systemic prednisone with sterting doses of 50-100 ‘mg/d continued until cle = Azathioprine, 150 mg daily “= ING, plasmapheresis = sulfones (dapsone) = Low-doxe MTK 2.5 to 10 mg weekly = Patients often go into a permanent remission after ‘therapy and do not require further therapy = Local recurrences can sometimes be controlled with ‘opleal glucocorticoids Clcatricial Pempbigold ‘© Blisters that rupture easily and also erosions resulting from epithellal fragility in the mouth; oropharynx; and, ‘more rarely, the nasopharyngeal, esophageal, genital, and rectal mucosa ‘© Ocular Involvement may initially manifest as unilateral or bilaterat conjunctivitis with burning, dryness, and forelgn-body sensation, ‘© The skin Is involved in roughly 30% of patients. © Management ‘~ Most patients respond to dapsone In combination with low-dose prednisone Pemphigotd Gestationis ‘+ A rate pruritic and polymorphic Inflammatory bullous dermatosis of pregnancy and the postpartum period, ‘Extremely pruritic vesicular eruption mainly on the abdomen but also on other areas, with sparing of the ‘mucous membranes EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY aEAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY @ ' begins from the fourth to the seventh month of pregnancy but can also occur Inthe fist trimester and in ‘the immediate postpartum period can be exacerbated by the use of estrogen and rogesterone-containing medications = geared to suppressing blister formation and relieving the intense pruritus, = Prednisone, 20-40 me/d Dermatitis Herpetiformls ‘relates to IgA deposits in the skin «Patients have antibodies to tansglutaminases (TGs) that may be the major autoantigens in this disease ‘A chronie, recurrent, intensely pruritic eruption occurring symmetrically on the extremities and the trunk ‘+ Consists of tiny vesicles, papules, and urticarial plaques that ae arranged in groups ‘+ Associated with gluten-sensitive ‘+ Management = Systemic Therapy: Dapsone 100-150 mg dail = Obtain a glucose- 6-phosphate dehydrogenase evel = Sulfapyridine 1-15 9/4, with plenty of fluids = Agluten-free diet may suppress the disease or allow reduction of the dosage of dapsone or sulfapyridine, but response Is very slow znteropathy (GSE) Unear igA Dermotosis / Chronic Bullous Disease of Childhood ‘+ Arrare, immune-mediated, subepidermal blistering skin disease defined by the presence of homogeneous linear deposits of igh at the cutaneous basement membrane zone LAD most often occurs after puberty Patients present with combinations of annular or ‘grouped papules, vesicles, and bullae that are distributed symmetrically on trunk and extremities including elbows, knees, and buttocks ‘© The lesions are very pruritic ‘+ Mucosal involvement is Important and ranges from large ‘asymptomatic oral erosions and ulceration to severe oral disease alone, or severe generalized cutaneous Involvement and oral disease ‘+ It fs dentical with chronic bullous disease of childhood {CBDC), which Is a rare bilstering disease that occurs predominantly in children <5 years '* LADhas been associated with drugs: vancomycin, lithium, phenytoin, sulfamethoxazole/trimethoprim, furosemide, ‘captopril, diclofenac, and others ‘* There is a small risk of lymphoid malignancies, and associated ulcerative colts has been reported © Management = Patients respond to dapsone or sulfapyridine but in ‘addition, most may require low-dose prednisone Epidermolysis Bullosa Acquisita ‘+ A chronic subepidermal bullous disease associated with autoimmunity to the type Vil collagen within the anchoring fibrils in the basement membrane zone. '» Fourtypes Classic mechano-bullous presentation Bullous pemphigold-ike presentation = Cicatrcial pemphigold-ike presentation = IgA bullous dermatosis-iike presentation + Management = High doses of systemic glucocorticoids, azathioprine, methotrexate, and cyclophosahamide = Dapsone and high doses of eolehicine ~ Supportive therapy EAST AVENUE MEDICAL CENTER DEPARTMENT OF DERMATOLOGY“Treatment Algorithm for Aene Vulgar Mild Moderate Papular/ Comedonal Pustular Fst Topical Topical retinoid + Fetinoid or topical antimicrobial combination’ orcombination? second Topical ‘Topical dapsone dapsoneor or azelsic acid or mrelaicacid or salicylicacid salicylic acid Female - - ‘Additional Comedone _Laserfight therapy, options extraction photodynamic therapy ile tale Maids + Egat pesont gore wm oe. yard tang + eonatnene dost ge nd der 02 * bemene dete anen? 02% + Fuchonde eam 018 + Fammeeaie tape een? + Hebets pptrte rer andra 8 fe Sic Teanssh incramman ieee, + Amcor een 09% * Beamthasone dolor’ on and cimer 0.25% {Gti propane elton Pap poor O05 + Desoxnetsone Oitwat and ar 025% ane O05 * een det rer ad ean? O15 + Funchond tat cre and alton O08 + veneer, ceom ved hon < Moraine iret aner 0% "aman stares 03% SS ea aba BHAI IY: + Amxleonide cream andaion 0.9% * Betamethasone dproclonateceam and fen 0156 = Betumethuznevleate cbtment 1% + Diersone dace ce 28% + Fseaoneproplenat ene 0.08% "Tiamelncone atone Saran. and rea 05% Severe Conglobata/ Papular/Pustular Nodular Fulminans rel antibiotic+ Oral antiblotic+ Oral isotretinoin 3 oral topical etinoid BPO topical retinoid BPO corticosteroids ‘orcombination" Oral antibiotie-+ Oral isotretinoin High-dose oral topical retinoid BPO ororalantiblotic+ antibiotic + topical ‘orcombination” ‘topical retinoid retinoid + BPO or BPO/azelaic acid or —_combinatlon* combination* +0ralcontraceptive/ + Oral contraceptive/ + Oral contraceptive/ antiandrogen | antiandrogen antiandrogen ‘Comedone extraction, Comedone extraction; Intralestonal laserflight therapy, Intralesional corticosteroid, photodynamic corticosteroid, laser/light therapy, therapy laserfight therapy, photodynamic therapy photodynamic therapy J 2 ean NRO + Beaamathssone yea for 0.12% + Devximetaione coum 005% [gf | * Bkocloloneacatonce obament 028% SE8S | « Franérnolic setmant 003% + Hydioconone leat nian 02 * Mometiene sie cram and eto 01% Tamanna cement Ranlog®) nd cream or pay 02% 221 eantdaohcenen + Betertusone ieponete ion 005% “ aeuruthasonejlete Geum ad on 0% + Cocosene page err 01%. a + Fucinolone schon rn 0.025% ool and shampoo 001% + Fueasone ropfoat ram anton 005% + Funder rom and loton 105% + ydcortsonefuryateclatrert. ren anon 01% + Hycrocortene ey * drocortsone yt can 0.2% « Predeatbate obimeet sd ce 0.3% «Shani ti ota 05% ton 1% TAN evan a oor + Aoretasare dipropionate ortment and car 105% “Tamera ssf «+ Betamathasone tolerate bation 0.1% " "Shea ae eon a 05 “Probe sane sin ten Neca oo ee + Topan with recortione, deamethatone and pedrbolone "ogumans ese