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Acne- definition, etiology, classification, lab diagnosis and management.

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  1. 1. What is it? 0 Disorder of pilosebaceous complex which predominantly affects the peripubertal population and manifest as comedones, papules, nodules, pustules and cysts and heals with scars.
  2. 2. ETIOLOGY 0 Increased sebum secretion. 0 Follicular duct hypercornification. 0 Increased colonization with Propionibacterium. 0 Inflammation.
  3. 3. PATHOGENESIS 0 Occlusion of pilosebaceous orifice. 0 Increased sebum secretion. 0 Microbial colonization. 0 Release of inflammatory mediators.
  4. 4. OCCLUSION OF PILOSEBACEOUS ORIFICE Occluded by keratinous plug induced by chemicals and reduced level of linoleic acid in sebum Retention of sebum encouraging growth of microbes. Distended follicle rupture, releasing proinflammatory chemicals into dermis Stimulate inflammation.
  5. 5. INCREASED SEBUM SECRETION 0Occurs due to end organ sensitivity to androgens. Increased activity of 5α reductase in sebaceous gland. Converts testosterone to 5 α testosterone Binds to receptors in sebaceous gland Increase sebaceous secetion.
  6. 6. Microbal colonization 0 Organisms involved-Propionibacterium , Malassezia furfur,Staph epidermidis Bacteria thrive Inflammation results Chemotactic factors attract neutrophils Depending on conditions Non-inflammatory open/closed comedones Inflammatory papule/ pustule/nodule
  7. 7. EPIDEMIOLOGY 0 PREVELANCE -affects all adolescents. 0 AGE- Onset-12-14 years. 0 GENDER- Both sexes equally but nodulocystic acne common in males.
  8. 8. FACTORS 1. GENETIC PREDISPOSITION Found to be familial Identical twins shows greater concordance of severity of acne. 2) DIET High glycemic diet. 3. COSMETICS Seen in women using oil based cosmetics for long time. Follows facial massage. 4. MENSTRUAL CYCLE Premenstrual edema of pilosebaceous duct. 5. PSYCHOLOGICAL FACTORS
  9. 9. MORPHOLOGY 0 Polymorphic eruption consisting of papules, pustules, nodules, cysts, and pathognomic open and closed comedones on a background of oilness.
  10. 10. COMEDONES 0 Hyperkeratotic plug made of sebum and keratin in follicular canal. 0 Pathognomic lesions of acne vulgaris. 0 2 types: 1. Open comedones. 2. Closed comedones.
  11. 11. OPEN COMEDONES 0 Also known as Black head. 0 Due to plugging of pilosebaceous orifice by keratin and sebum on the skin surface.
  12. 12. CLOSED COMEDONES 0 Due to keratin and sebum accretions plugging the pilosebaceous ducts below the skin surface. 0 SUBMARINE COMEDONES-deep seated and seen by stretching the skin.
  13. 13. Grades of Acne (Pillsburry’s classification)  Grade I: Comedones (open or closed), occasionally pustules or papules; no scarring.  Grade II: papules, comedones, few pustules; mild scarring.  Grade III: predominant pustules, nodules, abscesses; moderate scarring.  Grade IV: mainly cysts, abscesses, scars; severe scarring.
  14. 14. SCARS 0 Acne scars can be: Depressed scars 1. Ice pick scars- deep pits. 2. Box car scars-superficial/deep 3. Rolling scars Hypertrophic and keloidal scars.
  15. 15. VARIANTS
  16. 16. ACNE CONGLOBATA 0 Severe form of acne characterised by intercommunicating abscess, cysts, and sinuses loaded with serosanguinous fluid or pus. 0 Multiporous comedones. 0 Lesions take months to heal and on healing leave behind deep pitted or hypertrophic scars.
  17. 17. OCCUPATIONAL ACNE 0 Caused by exposure to industrial chemicals (tar, chlorinated hydrocarbons) and cutting oils. 0 Predominantly comedones
  18. 18. COSMETIC ACNE 0 Seen in women using cosmetics(oil based ones) 0 Comedones 0 Frequently on the chin
  19. 19. DRUG INDUCED ACNE 0 Steroids, androgens, oral contraceptives, antitubercular drugs, iodides, bromides and anticonvulsants. 0 Lesions are monomorphic, consisting of papules and pustules 0 Site- trunk especially back.
  20. 20. INFANTILE ACNE 0 Due to presence of maternal hormones in child. 0 Common in males.
  21. 21. LATE ONSET ACNE 0 Onset after 25 years of age. 0 Predominantly women. 0 Deep seated persistent lesions on lower half of face.
  22. 22. ACNE EXCORIEE 0 Seen in young girls, who obsessively pick their mild acne. 0 Results in discrete excoriations on face, while comedones, and papules are few and far between.
  23. 23. ACNE FULMINANS 0 Acute onset. 0 Crusted ulcerated lesions. 0 Associated with fever, myalgia and arthralgia.
  24. 24. ACNE AFTER FACIAL MASSAGE 0 3-6 weeks later as acneiform eruption. 0 Indolent deep seated nodules with vey few comedones. 0 Predominantly on cheeks along the mandible.
  25. 25. DIFFERENTIAL DIAGNOSIS 0 Rosacea 0 Folliculitis 0 Acne scarring may be mistaken for acne keloidalis, varioliform, atrophy and porphyria cutanea tarda
  26. 26. TREATMENT 0 General measures 0 Topical therapy 0 Systemic therapy 0 Physical therapy
  27. 27. GENERAL MEASURES 1. Local hygiene Regular cleansing with soap and water and avoiding use of oil based cosmetics. 2. Diet Avoid use of high glycemic diet. 3. Stress
  28. 28. TOPICAL THERAPY 0 Retinoids Most frequently used agent in acne. Effective against comedones and inflammatory acne. Reduces formation of microcomedo. Side effects include irritation and photosensitivity.
  29. 29. 0 Benzoyl peroxide Powerful antimicrobial which decrease population of Propionibacterium acnes. Used in both inflammatory acne and non inflammatory acne. Side effects include irritation and bleaching of hair.
  30. 30. 0 Topical antibiotics Clindamycin(1-2%) and erythromycin(2-4%) Used in inflammatory acne since it suppress P.acnes. Side effect: antibiotic resistance. So should be combined with retinoids or benzoyl peroxide.
  31. 31. Systemic treatment 0 Antibiotics Mostly Doxycycline and minocycline; Erythromycin and azithromycin. Inhibit growth of P.acnes and has direct anti inflammatory effect.
  32. 32. ADVERSE EFFECTS  Doxycycline - onycholysis, oesophagitis with ulceration, fixed drug eruptions, photosensitivity etc.  Minocycline - benign intracranial hypertension, pappiloedema, blue-black pigmentation and rarely hypersensitivity reactions  Macrolide group - gastritis, diarrhoea.
  33. 33. HORMONES 0 Act by decreasing sebum secretion rate. 0 Used only in females with late onset acne and menstrual irregularities.
  34. 34. Adverse effects of hormonal therapy  Weight gain  Menstrual irregularity  Occasional fluid retention  Melasma  Hypertension  Thrombophlebitis  Pulmonary embolism
  35. 35. ISORETINOIN 13-cis- retinoic acid (Vitamin A derivative )  Mechanism of action: ◦ Inhibiting sebum secretion. ◦ Alters the composition of sebum ◦ Lowers P.acnes concentration and has anti- inflammatory activity
  36. 36.  Indicated for : ◦ Nodulocystic/ severe Acne ◦ Pyoderma faciale ◦ Excessive seborrhoea ◦ Depression / Dysmorphophobia ◦ Acne conglobata / other unusual variants ◦ Scarring
  37. 37.  Dose: 0.5 – 1 mg/ kg per day is given after meals. Cumulative dose: 120-150 mgs/kg  Side effects ◦ Teratogenicity ◦ Mucocutaneous side effects, dryness ◦ Elevation of serum lipids ◦ Neurological : pseudotumor cerebri Optic Neuritis, depression, mood swing ◦ Arthritis, myalgia ◦ Acne flares
  38. 38. PHYSICAL MODALITIES 0 Intralesional corticosteroids 0 Cryotherapy 0 Laser therapy 0 Photodynamic treatment 0 Dermabrasion 0 Fillers
  39. 39. Thank You…..