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ACNE     SKIP S- Excess sebum production K-altered keratinization I- inflammation P-Proprionibacterium acnes proliferation and activity EPIDEMIOLOGY     Worldwide

distribution Mild degrees seen at birth (from follicular stimulation by adrenal androgens ;) may continue up to neonatal period Greatest prevalence in adolescent population Starts at puberty, incidence decreases by early 20’s, may persists until third decade or beyond Disorder of pilosebaceous unit face chest and back Most frequent in adolescents, may persist to adulthood Self-limiting course but with lifelong sequelae ( atrophic/hypertrophic scarring)

CLINICAL PRESENTATION:  Morphologic characteristics-non inflammatory: Comedones : (the primary lesions of acne) -inflammatory Papules, pustules, nodules, cysts Locations- areas rich in sebaceous glands-face, chest, upper back, upper arms Symptoms-usually asymptomatic unless inflamed(tender)

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DIFFERENTIAL DIAGNOSIS     Acneform erosion Gram negative folliculitis Peri-oral dermatitis Rosacea

COURSE AND PROGNOSIS   Flares may occur just before the menses Inflammatory type: atrophic/hypertropic scars

compound irritancy potential of many topical acne treatments MILD ACNE  Topical  Retinols tretinoin  adapaline  isotretinoin  antibiotics  erythromycin  clindamycin  benzoyl peroxide  keratolytics  salicylic acid  resarcinol  sulfur  sodium sulfacetamide  combination: BEST results Oral.disrupts cutaneous lipid barrier.MANAGEMENT  Tailoring each patient’s acne regimen:  -knowledge of acne pathogenesis  -MOA of the available acne treatments Maximum therapeutic response  Local therapy  Cleansing: Bid washing with gentle cleanser followed by acne treatment application  Avoid alkaline soaps.not needed  MODERATELY SEVERE ACNE   Topical ( as above) Oral  Antibiotics  Tetracycline 500 mg OD  Doxycycline 100 mg OD  Minocycline 100 mg OD  Lymecycline 300 mg OD  Hormonal  Cyproterone acetate with ethinyl estradiol  Desogestrel with ethinyl estradiol .

PATIENT EDUCATION  Correct perceived myths .SEVERE ACNE  Oral isotretinoin 0. peeling. premature pubarche Hirsutism Steady weight despite caloric intake . severe or of late onset. laser resurfacing  Hypertrophic scarring:ILSI      PREVENTION. liver function test  TG. dermabrasion. laser  Atrophic scarring: fillers.0 mkd  Teratogenic  Do pregnancy test  May cause elevation s in lipid profile. total cholesterol  AST. ALT  Risk of pseudotumor cerebri if used withtetracycline Local therapy Intralesional steroid injections (ILSI) Comedone extraction Photodynamic therapy Management of sequelae  Pigmentation: bleaching agents.does not correct within 2 years post menarche Acne vulgaris-persistent.Generally unaffected by the diet Discourage squeezing/ pricking pimples at home  SUSPECT PCOS IN ADOLESCENTS     Oligomenorrhea.5-1.Acne is not due to poor hygiene .

Trauma(“koebner’s” phenomenon) .Infection( MC streptococcus or HIV) . IL 17) -Inflammation -accelerated epidermopoeisis Trigger factors . NSAID’S)  Clinical features:      Chronic inflammatory lesion on the skin Classic: Circumscribed erythematous plaques covered with thick.Deforming arthritis( extremities and spine) Classically begins as erythematous macules covered with dry silvery scales that extend periperhally.TNF α. anti.malaria’s. lobulated. IL-1/2/12. silvery white scales May have permanent itching/burning sensation No permanent cure Involves skin and joints .blockers.Skin sites of predilection .Drugs(beta. lithium. or gyrated with involution at the center   . several susceptible genes found Early onset (type 1 psoriasis)  Positive family history  HLA-CW6 M=F Start at any age ( peak at 2nd and 5th decades) Flare ups during colder months Less frequent in tropics Tends to improve/temporarily disappear but may flare up after delivery Pathogenesis  Autoimmune T-cell mediated reaction -Over expression of pro-inflammatory TH1 and TH17 cytokines (TH 1.Stress .PSORIASIS Epidemiology      Etiology   Autoimmune T-Cell mediated reaction triggered by still unknown factors Heredity. coalesce and become thicker May become annular.

hydroxychloroquine. edge of psoriatic plaques) White plaques on mucosa (tongue. palms.Exanthematous febrile eruption of pustules . According to morphology of skin lesions I. minocycline. acetazolamide. Generalized pustular type (Von Zumbusch)        Fever with appearance of skin lesions Erythema in flexures-generalized pustular eruption Lake of pus( periungual. coal tar. steroid widrawal.Continuous fever.AUSPITZ SIGN   Pinpoint bleeding when a psoriatic scale is forcibly removed Severe thinning of the epidermis over the tips of dermal papillae KOEBNER’S PHENOMENON  Appearance of typical lesions of psoriasis at sites of even trivial injuries PSORIASIS TYPES: A.terbinafine. Localized pustular type     Most common type is palmoplantar Fused putules resemble “Lakes of pus” Sterile pustules Variant: acrodermatitis continua of Hallopeau ( digits associated with osteolysis) III. erythroderma. Chronic Plaque Type   Most common Circumscribed. salicylates Stages: .Flare ups of fever and pustules . cachexia Systemic complications: -pneumonia -CHF -Hepatitis -ARDS  . dry plaques covered by silvery white scales II. mouth) Usually associated with hypocalcemia Maybe triggered by drugs : iodide. erythematous.

moist. Nails V. fissured little scaling Autspitz sign usually negative “Napkin psoriasis”. Exfoliative dermatitis/ Erythroderma    generalized scaling on diffusely erythematous skin no normal skin nor discrete psoriasis plaques maybe accompanied by extropion (eversion of the eyelids) B.IV. red demarcated plaques -eczematized. Psoriatic arthritis     Seronegative arthritis Presence of HLA B 27 in nearly half of all patients “Sausage shape” digits 5 clinical patterns CO-MORBIDITIES     Highly associated with depression Chron’s disease Lymphoma . Guttate    size of water drops (2-5 mm) acute infection (streptococcal pharyngitis)- abrupt eruption more common in patients under the age of 30 V. According to location: I.8 mos III. Scalp   Most common site of initial involvement Marked prediclection. Inverse/ Flexural      exclusive involvement salmon. Classic extensor II.usually 2.frontal scalp margin usually no hair loss D. Palmoplantar IV.

PAF-1) DIFFERENTIAL DIAGNOSIS        Fungal infections Seborrheic dermatitis Pityriasis rosea Lichen planus Psoriasiform subset of SCLE Contact Dermatitis and dyhidrotic eczema Parapsoriasis and CTCL Management A. Topical treatment( limited/localized disease) Moisturizers Salicylic acid  Keratolytic  Widespread dse in pedia group (risk for salicylism) Corticosteroids (topical)  Limited quantity/ duration (to avoid atrophy. trigger factors. hirsutism. non psoriatic persons  Increase risk for DM and atheroscleroticdisease  Cluster signs: -obesity (abdominal) -HPN -hyperlipidemia -elevated FBS -pro inflammatory factors (CRP. calcitriol)  Controls keratinocyte proliferation. promotes differeantiation  Most common side effect: irritation (face. flexures) Tar Calcineurin inhibitors (Tacrolimus. treatment options and risks  Lifestyle modifications to avoid metabolic syndrome B. thus safe and effective for facial and flexural . acne. Metabolic syndrome  Occurs at higher rate in psoriatic vs. Patient education  Nature and course. Screening for comorbidities and appropriate management C. telangectasias. striae.HPA ax is supression Vit. Pimecrolimus)   Malodorous. D Analogs (calcipotriol. may stain Free from steroidal side effects.

Ustekinumab)   Selectively target a portion of immune reaction leading to psoriasis( thus preventing generalized non selective immunosuppression) May target T. mucocutaneous dryness  Biologic Agents (Ifliximab. short contact use D. Etanercept. bone marrow supression Cyclosporine  Immunosuppressive  S/E: HPN. Systemic therapy (generalized/recalcitrant to topical)  Periodic organ function monitoring required (due to cumulative toxicities) Methotrexate  anti. Phototherapy (generalized/recalcitrant to topical)  Series of controlled exposures to non-ionizing radiation (UV light) to modulate T cell immune mediated reaction  Broadband and Narrowband UBV(311 nm wavelength)  Psoralen+ UVA (PUVA)  Excimer laser therapy targeted at few lesions of localized psoriasis E.cells or cytokines(TNFα) parenteral . Alefacept. Nephrotoxicity Acitretin  Anti-proliferative & enhance keratinocyte differentiation  S/E teratogenicity.Adalimumab.Anthralin Tazarotene    psoriasis Anti-proliferative Irritating( short contact use) may stain Irritating. hyperlipidemic.inflammatory & suppresses DNA synthesis  Oral DOC for psoriatic arthritis  S/E: teratogenicity. hepatotoxicity.