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ACNE & ADNEXAL DISORDERS

ACNE & ADNEXAL DISORDERS. Diany Nurdin. DISORDER OF ADNEXAL ADOLESCENS SKIN. SEBACEOUS GLANDS APOCRINE GLANDS ECCRINE GLANDS. PHYSIOLOGY OF REGULATORY MECHANISM. Acne vulgaris Is it important or just Trivial ?. Is it a disease ?. INSURANCE ?. Embarrasing Devastating.

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ACNE & ADNEXAL DISORDERS

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  1. ACNE & ADNEXAL DISORDERS DianyNurdin

  2. DISORDER OF ADNEXALADOLESCENS SKIN SEBACEOUS GLANDS APOCRINE GLANDS ECCRINE GLANDS

  3. PHYSIOLOGY OF REGULATORY MECHANISM

  4. Acne vulgaris Is it important or just Trivial ? Is it a disease ? INSURANCE ?

  5. Embarrasing Devastating

  6. 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

  7. MOST FREQUENT QUESTIONS • DIET –CHOCOLATE • -SPICY • -FRIED FOODS • -MILK • STRESS • SEXUAL ACTIVITY

  8. WhatisACNE? Not an infectious but Inflammatory skin condition Common, chronic, recurring disease Self limited disease Influences Quality of Life Constitute a socioeconomic problem

  9. ACNE VULGARIS DEFINITION: CHRONICALLY INFLAMMATION OF SEBACEOUS FOLLICLE 2. LESSION COMEDONE-PAPULE-PUSTULE- NODULE-CYST-SCAR (PLEOMORPHIC) 3. PREDILECTION SEBORRHOIC AREA 4. AGE -PUBERTY

  10. Prevalence ( 85 %) mild ( 15 %) need medical treatment

  11. 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

  12. ANDROGEN DHT PATHOGENESIS: 5ar type 1 MICROCOMEDONE Linoleic acid IL-1 alpha ABNORMAL KERATINIZATION Acroinfundibulum INFLAMMATION RUPTURE FOLLICLE WALL TNF -ALPHA LIPASE P.ACNE SEBUM SECRETION

  13. Gollnick H et al J.Am.Acad.Dermatol 2003:;49(1 Suppl) S1-S37

  14. MICROBIOLOGY OF PILOSEBACEOUS UNIT

  15. PATHOGENESIS: THE DEVELOPMENT OF ACNE LESSION MIKROCOMEDO COMEDO INFLAMMATION LESSION

  16. CLINICAL SIGN: PRIMARY LESSION COMEDO 1.OPEN 2.CLOSED

  17. DIAGNOSE OF ACNE VULGARIS: 1. PREDILECTION 2. LESSION 3. SEBORRHOE 4. TEENAGE

  18. CLINICAL VARIATION: NEONATAL ACNE

  19. ADULT ACNE

  20. ACNE IN COLORED SKIN

  21. SUBTYPES OF ACNE: CYSTIC ACNE

  22. SUBTYPE ACNE : ACNE FULMINAN

  23. SUBTYPES ACNE: MECHANICAL ACNE ACNE COSMETICA – POMADE ACNE

  24. ACNE EXCORIEE

  25. ROSACEA DIFFERENTIAL DIAGNOSIS: ERYTHEMATOTELANGIETATIC PAPULOPUSTULAR

  26. DIFFERENTIAL DIAGNOSIS: PHYMATOUS OCULAR

  27. DIFFERENTIAL DIAGNOSIS: ACNEIFORM ERUPTION * CORTICOSTEROID * INH * BROMIDE. IODIDE * PHENYTOIN

  28. DIFFERENTIAL DIAGNOSIS PERIORAL DERMATITIS

  29. Perioral Dermatitis, Corticoid Damage

  30. DIFFERENTIAL DIAGNOSIS: GRAM NEGATIVE FOLLICULITIS

  31. TREATMENT: ANTI -ANDROGEN ABNORMAL KERATINIZATION RETINOIC ACID ANTI INFLAMMATION INFLAMMATION ANTIBIOTIK P.ACNE SEBUM SECRETION

  32. 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 proliferationof follicular keratinocytes • Benzoyl peroxide: • Reduces microorganisms

  33. 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

  34. Actions of Anti-Acne Therapies Layton AM. A review on the treatment of acne vulgaris. Int. J. Clin. Pract. 60(1), 64–72 (2006).

  35. TREATMENT: NON INFLAMMATION TOPICAL KERATOLYTIC COMEDOLYTIC BACTERICIDAL

  36. TREATMENT: INFLAMMATION TOPICAL = ACNE NONINFLAMMATION BENZOIL PEROKSIDE ANTIBIOTIC SYSTEMIC ANTIBIOTIC ANTI INFLAMMATION HORMON

  37. BROMHIDROSIS APOCRINE ECCRINE

  38. BROMHIDROSIS APOCRINE : BROMIDROSIS OSMIDROSIS ECCRINE : KERATINOGENIC-- BACTERIAL DEGRADATION OF MACERATED STRATUM CORNEUM--ODOROGENIC FATTY ACID

  39. BROMHIDROSIS EXCESSIVE –ABNORMAL BODY ODOR FOUL SMELLING SWEAT-MALODOR ARISE FROM THE APOCRINE GLAND

  40. BROMHIDROSIS YOUNG ADULTS BLACK SUMMER FAMILY HISTORY CULTURAL SUBJECTIVE -RACES

  41. 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

  42. PREDISPOSING FACTOR HYPERHYDROSIS OBESITY INTERTRIGO DIABETES MELLITUS FOODS - GARLIC - ALCOHOL HERITABLE AMINOACIDURIA

  43. BROMHIDROSIS TREATMENT HYGIENE –SOAP & WATER DEODORANT REDUCING BACTERIA REDUCING APOCRINE /ECRINE SWEAT -ANTIPERSPIRANT -ABSORBENT POWDERS -SURGERY- CURRETAGE SUBCUTANEOUS - EXCISION - SYMPATHECTOMY -BOTULINUM TOXIN INJECTION -IONTOPHORESIS

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