ACNE & ADNEXAL DISORDERS Diany Nurdin
DISORDER OF ADNEXAL ADOLESCENS SKIN SEBACEOUS GLANDS APOCRINE GLANDS ECCRINE GLANDS
PHYSIOLOGY OF REGULATORY MECHANISM
INSURANCE ? Acne vulgaris Is it important or just Trivial ? Is it a disease ? INSURANCE ?
Embarrasing Devastating
Why it is important – serious disease The morbidity - the prevalence 85% – 95% (100% teenager) adult acne- women > 21th -the most common dermatologic disorder in US, RSS the II nd The embarrasing disease The cost - skin care - treatment of complication - scar
MOST FREQUENT QUESTIONS DIET –CHOCOLATE -SPICY -FRIED FOODS -MILK STRESS SEXUAL ACTIVITY
What is ACNE ? Not an infectious but Inflammatory skin condition Common, chronic, recurring disease Self limited disease Influences Quality of Life Constitute a socioeconomic problem
ACNE VULGARIS DEFINITION: CHRONICALLY INFLAMMATION OF SEBACEOUS FOLLICLE 2. LESSION COMEDONE-PAPULE-PUSTULE- NODULE-CYST-SCAR (PLEOMORPHIC) 3. PREDILECTION SEBORRHOIC AREA 4. AGE -PUBERTY
Prevalence ( 85 %) mild ( 15 %) need medical treatment
PREVALENCE THE MOST COMMON VISIT DERMATOLOGIST AGE 15-45 MAN > WOMAN ------- VISIT OF WOMEN 80% > FREQUENT > AGE 19 YRS US DATA PRESCRIPTION ANTIBIOTICS $ 5 MILLION ISOTRETINOIN $ 1.4 MILLION
PATHOGENESIS: ANDROGEN DHT 5ar type 1 MICROCOMEDONE Linoleic acid IL-1 alpha ABNORMAL KERATINIZATION Acroinfundibulum INFLAMMATION RUPTURE FOLLICLE WALL TNF -ALPHA LIPASE P.ACNE SEBUM SECRETION
Gollnick H et al J.Am.Acad.Dermatol 2003:;49(1 Suppl) S1-S37
MICROBIOLOGY OF PILOSEBACEOUS UNIT STAPHYLOCOCCI, MICROCOCCI GRAM (+), COAGULASE (-) SUPERFICIAL AEROBIC PORTION OF SEBACEOUS UNIT PITYROSPOSPORUM OVALE, PITYROSPORUM ORBICULARE. LIPOFILIC YEAST PROPIONEBACTERIUM ACNES, ANEROBIC PLEOMORHIC DIPHTEROID. MOST PREVALENT ORGANISM IN FOLLICULAR INFRAINFUNDIBULUM ANAEROBIC CONDITION OF SEBACEOUS UNIT INFLAMATORY REACTION OCCURS IN ACNE MICROBIOLOGY OF PILOSEBACEOUS UNIT
PATHOGENESIS: THE DEVELOPMENT OF ACNE LESSION MIKROCOMEDO COMEDO INFLAMMATION LESSION
CLINICAL SIGN: PRIMARY LESSION COMEDO 1.OPEN 2.CLOSED
DIAGNOSE OF ACNE VULGARIS: 1. PREDILECTION 2. LESSION 3. SEBORRHOE 4. TEENAGE
CLINICAL VARIATION: NEONATAL ACNE
ADULT ACNE
ACNE IN COLORED SKIN
SUBTYPES OF ACNE: CYSTIC ACNE
SUBTYPE ACNE : ACNE FULMINAN
SUBTYPES ACNE: MECHANICAL ACNE ACNE COSMETICA – POMADE ACNE
ACNE EXCORIEE
ROSACEA DIFFERENTIAL DIAGNOSIS: ERYTHEMATOTELANGIETATIC PAPULOPUSTULAR
DIFFERENTIAL DIAGNOSIS: PHYMATOUS OCULAR
DIFFERENTIAL DIAGNOSIS: ACNEIFORM ERUPTION * CORTICOSTEROID * INH * BROMIDE. IODIDE * PHENYTOIN
DIFFERENTIAL DIAGNOSIS PERIORAL DERMATITIS
Perioral Dermatitis, Corticoid Damage
GRAM NEGATIVE FOLLICULITIS DIFFERENTIAL DIAGNOSIS: GRAM NEGATIVE FOLLICULITIS
TREATMENT: ANTI -ANDROGEN RETINOIC ACID ANTIBIOTIK ANTI INFLAMMATION ABNORMAL KERATINIZATION RETINOIC ACID ANTI INFLAMMATION INFLAMMATION P.ACNE ANTIBIOTIK SEBUM SECRETION
Actions of Anti-Acne Therapies Topical retinoids: Normalize follicular hyperproliferation and cohesiveness Reduce inflammatory response Oral Isotretinoin: Reduces sebum Normalizes hyperkeratinization Inhibits P. acnes growth (indirect) Reduces inflammatory response Antibiotics: Reduce microorganisms Reduce inflammatory response Hormones: Reduce sebum production Reduce proliferation of follicular keratinocytes Benzoyl peroxide: Reduces microorganisms
CURRENT ACNE TREATMENT TOPICAL -RETINOIDS -ANTIBIOTICS : CLINDAMYCIN, ERYTHROMYCIN, NADIFLOXACIN, NA SULFACETAMIDE, DAPSONE -BENZOYL PEROXIDE -AZELAIC ACID -SALICYLIC ACID, SULFUR -NICOTINAMIDE, ASCORBIC ACID SYSTEMIC -ANTIBIOTICS -HORMONAL -ISOTRETINOIN ADJUVANT -CHEMICAL PEELING -LASER & LIGHT -CRYO THERAPY -DIET
Actions of Anti-Acne Therapies Sebum production Hyper- keratinization Inflammation Reduction in P.acnes Topical therapies Retinoids - ++ + Benzyl peroxide +++ Antibiotics Azelaic acid +/- Nicotinamide Systemic therapies Hormonal therapy Indirect Layton AM. A review on the treatment of acne vulgaris. Int. J. Clin. Pract. 60(1), 64–72 (2006).
TREATMENT: NON INFLAMMATION TOPICAL KERATOLYTIC COMEDOLYTIC BACTERICIDAL
TREATMENT: INFLAMMATION TOPICAL = ACNE NONINFLAMMATION BENZOIL PEROKSIDE ANTIBIOTIC SYSTEMIC ANTIBIOTIC ANTI INFLAMMATION HORMON
BROMHIDROSIS APOCRINE ECCRINE
BROMHIDROSIS APOCRINE : BROMIDROSIS OSMIDROSIS ECCRINE : KERATINOGENIC-- BACTERIAL DEGRADATION OF MACERATED STRATUM CORNEUM--ODOROGENIC FATTY ACID
BROMHIDROSIS EXCESSIVE –ABNORMAL BODY ODOR FOUL SMELLING SWEAT-MALODOR ARISE FROM THE APOCRINE GLAND
BROMHIDROSIS YOUNG ADULTS BLACK SUMMER FAMILY HISTORY CULTURAL SUBJECTIVE -RACES
BROMHIDROSIS PATHOGENESIS Increase number & size apocrine glands, increase ratio apocrine/eccrine -----increase production Axillary bacteria ------- e-3-methyl 2 hexenoic acid Short chain fatty acids & ammonia. Trimethylaminuria- FISH ODOR
PREDISPOSING FACTOR HYPERHYDROSIS OBESITY INTERTRIGO DIABETES MELLITUS FOODS - GARLIC - ALCOHOL HERITABLE AMINOACIDURIA
BROMHIDROSIS TREATMENT HYGIENE –SOAP & WATER DEODORANT REDUCING BACTERIA REDUCING APOCRINE /ECRINE SWEAT -ANTIPERSPIRANT -ABSORBENT POWDERS -SURGERY- CURRETAGE SUBCUTANEOUS - EXCISION - SYMPATHECTOMY -BOTULINUM TOXIN INJECTION -IONTOPHORESIS
ANTIPERSPIRANT Aluminum chloride hexahydrate Aluminum chlorhydrate Aluminum sesquichlorohydrate Aluminum chlorohydrex Aluminum zirconium tetrachlorohydrate Formaldehyde 10% Glutaraldehyde 10% Methenamine 8% Glycopyrrolate Metal ions form precipitating complexes with mucopolysaccharides --damage to luminal epithelial cell -- obstructive conglomerate -- completely plugs the acrosyringium..
DEODORANT Triclosan Benzalkonium chloride, Chlorhexidine. Propylene glycol Fragrances
Iontophoresis with tap water by producing a physical blockage of the sweat ducts at the level of the stratum
Botulinum toxin injection Botulinum toxin, a neurotoxin, acts by blocking the release of acetylcholine from the presynaptic terminal of the neuromuscular junction. It enters the cytosol and very specifically cleaves protein components of the neuroexocytosis apparatus; consequently, acetylcholine cannot be released. The use of Botulinum toxin to block sympathetic innervation of eccrine sweat glands