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    Acne Vulgaris: Nelson P. Tandayu 0 9 - 1 0 0

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    This document provides an overview of acne vulgaris, including its definition, pathogenesis, lesions, epidemiology, etiology, grading, differential diagnosis, management principles, and treatment options. It discusses the role of the pilosebaceous unit, various lesion types including comedones and inflammatory lesions, and acne's typical manifestation in adolescents. Treatment involves topical and oral medications as well as physical therapies, targeting factors like keratinization, sebum production, bacteria, and inflammation.

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    Acne Vulgaris: Nelson P. Tandayu 0 9 - 1 0 0

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    This document provides an overview of acne vulgaris, including its definition, pathogenesis, lesions, epidemiology, etiology, grading, differential diagnosis, management principles, and treatment options. It discusses the role of the pilosebaceous unit, various lesion types including comedones and inflammatory lesions, and acne's typical manifestation in adolescents. Treatment involves topical and oral medications as well as physical therapies, targeting factors like keratinization, sebum production, bacteria, and inflammation.

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    Acne Vulgaris Nelson

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    This document provides an overview of acne vulgaris, including its definition, pathogenesis, lesions, epidemiology, etiology, grading, differential diagnosis, management principles, and treatment options. It discusses the role of the pilosebaceous unit, various lesion types including comedones and inflammatory lesions, and acne's typical manifestation in adolescents. Treatment involves topical and oral medications as well as physical therapies, targeting factors like keratinization, sebum production, bacteria, and inflammation.

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    Download as ppt, pdf, or txt
    59 views39 pages

    Acne Vulgaris: Nelson P. Tandayu 0 9 - 1 0 0

    Uploaded by

    ntandayu
    This document provides an overview of acne vulgaris, including its definition, pathogenesis, lesions, epidemiology, etiology, grading, differential diagnosis, management principles, and treatment options. It discusses the role of the pilosebaceous unit, various lesion types including comedones and inflammatory lesions, and acne's typical manifestation in adolescents. Treatment involves topical and oral medications as well as physical therapies, targeting factors like keratinization, sebum production, bacteria, and inflammation.

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    of 39

    ACNE VULGARIS

    N E L S O N P. TA N D AY U 09-100
    FA K U LTA S K E D O K T E R A N U N I V E R S I TA S K R I S T E N I N D O N E S I A

    DEFINITION

    Acne vulgaris is a self-limited disorder of the pilosebaceous unit that is seen primarily in adolescents.
    Zaenglein et al, 2008.

    PILOSEBACEOUS UNIT

    LESION (1)

    Cases of acne present with a pleomorphic variety of lesions, consisting of comedones, papules, pustules, and nodules.

    LESION (2)

    Although the course of acne may be self-limiting, the sequelae can be lifelong, with pitted or hypertrophic scar formation

    EPIDEMIOLOGY

    Acne is often an early manifestation of puberty The greatest numbers of cases are seen during the middle-to-late teenage period. Afterward, the incidence steadily decreases.

    ETIOLOGY
    Normal physiological reaction in puberty Disease of the ovaries
    Polycystic ovarian syndrome Benign or malignant ovarian tumors

    Disease of the adrenal gland


    Partial deficiency of the adrenal enzyme 21 Hydroxylase Benign or malignant adrenal tumors

    Disease of the pituitary gland


    Cushings syndrome due to excessive adrenocorticotrophic hormone Acromegaly due to excessive growth hormone production Adenoma of the adrenal gland especially prolactinoma

    Obesity and the metabolic syndrome Medication-phenytoin, steroids, barbiturates, OC Pills.

    ETIOLOGY

    Keratinization Sebum Bacteria Hereditary Hormonal Diet Weather

    INITIAL PATHOGENESIS: follicular hyperkeratinization proliferation + decreased desquamation of keratinocytes hyperkeratotic plug (microcomedone)

    PATHOGENESIS Sebaceous glands enlarge Sebum production increases

    Growth medium for P. acnes


    Plugs provide anaerobic Lipid-rich environment

    PATHOGENESIS
    Bacteria thrive Inflammation results Chemotactic factors attract neutrophils Depending on conditions
    Non-inflammatory open/closed comedones Inflammatory papule/pustule/nodule

    1. FOLLICULAR PLUGGING
    Proliferation of ductal keratinocytes, with altered differentiation Result in comedones First observed at adrenarchy Probably androgen mediated

    2. SEBORRHOEA Increased sebum production and release May be mediated by


    Androgens Growth hormone

    3. BACTERIAL OVERGROWTH Colonization with Proprionibacterium acnes Normal commensal, anaerobic Increased growth in blocked sebumfilled follicles

    4. INFLAMMATION Mediated by activation of monocytes and neutrophils by P. acnes Release of inflammatory cytokines
    Interleukins TNF

    GRADING
    Plewig & Kligman (1975)1: Comedones: <10 comedones on 1 side of the face 10-24 comedones 25-50 comedones >50 comedones Papulopustular lesions: <10 papulopustular lesions on 1 side of the face 10-20 papulopustular lesions 21-30 papulopustular lesions >30 papulopustular lesions
    Wasitaatmadja (1982)1: Ringan, bila: Beberapa lesi tak beradang pada 1 predileksi Sedikit lesi tak beradang pada beberapa tempat predileksi Sedikit lesi beradang pada 1 predileksi Sedang, bila: Banyak lesi tak beradang pada 1 predileksi Beberapa lesi tak beradang pada lebih dari 1 predileksi Beberapa lesi beradang pada 1 predileksi Sedikit lesi beradang pada lebih dari 1 predileksi Berat, bila: Banyak lesi tak beradang pada lebih dari 1 predileksi Banyak lebih beradang pada 1 atau lebih predileksi

    WHITEHEAD AND BLACKHEADS

    CLOSED COMEDONES (WHITEHEAD)

    CLOSED COMEDONES (WHITEHEADS)

    OPEN COMEDONES (BLACKHEAD)


    open comedo (a blackhead): when follicular orifice is opened + distended.

    Melanin + packed keratinocytes + oxidized lipids dark colour

    OPEN COMEDONES (BLACKHEAD)

    OPEN COMEDONES (BLACKHEADS)

    CLOSE UP OF BLACKHEAD

    INFLAMMATORY LESIONS Papules (small red bumps) Pustules (white or yellow squeezable spots) Inflamed nodules (large red lumps)

    ACNE CONGLOBATA
    Unpleasant form of nodulocystic acne Interconnecting abscesses and sinuses, which result in unsightly hypertrophic (thick) and atrophic (thin) scars. There are groups of large macrocomedones and cysts that are filled with smelly pus.

    WHAT TESTS SHOULD BE DONE? In general, laboratory workup is not indicated for patients with acne unless hyperandrogenism is suspected. Many patients report that their acne flares during periods of stress.

    DIFFERENTIAL DIAGNOSIS

    Acneiform eruption Acne Venenata Rosacea Perioral dermatitis

    ACNEIFORM ERUPTION
    A drug induced acne.

    GENERAL PRINCIPLES OF MANAGEMENT

    Prevention
    Treatment

    PREVENTION OF ACNE
    Avoid the increasing amount of lipid sebum Avoid the triggering factors of acne Inform consent

    TREATMENT OF ACNE
    Topical Systemic

    Physical
    Diet

    TOPICAL MEDICATION
    Retinoid (tretinoin 0.1-0.25%, isotretinoin 0.05%, adapalene 0.1%)

    take out the mature comedones anti-inflammatory effect

    prevents comedone formation


    Salicylic acid

    Azelaic acid (20% cream or 15% gel)

    has both antimicrobial and comedolytic properties.


    Additionally, it is a competitive inhibitor of tyrosinase, thus decreasing pigmentation.

    Benzoyl peroxide
    a powerful antimicrobial agent. This effect is related

    to a decrease in the bacterial population and an


    accompanying triglycerides. decrease in the hydrolysis of

    TOPICAL ANTIBIOTICS
    Clindamycin 1% Erythromycin 2% or 4% with zinc acetate 1.2% most useful when inflammatory lesions predominate

    SYSTEMIC MEDICATIONS

    Oral vitamin A dan retinoid Hormonal therapy Oral antibiotics

    ORAL ANTIBIOTICS
    1st line - Tetracycline, doxycycline, minocycline
    2nd line - Erythromycin Cotrimoxazole

    PHYSICAL TREATMENT Comedones extraction Intralesion corticosteroids Liquid nitrogen Ultraviolet radiation

    REFERENCES
    Djuanda A, Hamzah M, Aisah S, editor. Ilmu penyakit kulit dan kelamin. Edisi keenam. Jakarta: Badan Penerbit FKUI; 2013. Hal. 254-9. Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ. Fitzpatrick's dermatology in general medicine. 7th Ed. New York: McGraw-Hill; 2008. p. 692-702. Buxton PK. ABC of dermatology. 4th Ed. London: BMJ Group; 2003. p. 47-9.

    Weller R, Hunter J, Savin J, Dahl M. Clinical Dermatology. 4th Ed. UK: Blackwell Publishing; 2008. p. 16270.
    Batra, Sonia. Acne. In: Ardnt KA, Hsu JT, editor. Manual of dermatology therapeutics. 7th Ed. Massachusetts: Lippincot Williams and Wilkins; 2007. p. 4-18. Schalock PC. Rosaceae and perioral (periorificial) dermatitis. In: Ardnt KA, Hsu JT, editor. Manual of dermatology therapeutics. 7th Ed. Massachusetts: Lippincot Williams and Wilkins; 2007. p.175-180 Dreno B, Poli F. Epidemiology of Acne. Dermatology, Acne Symposium at the World Congres of Dermatology Paris July 2002. p.7-9.

    James WD, Berger TG, Elston DM. Acne. In: James W, Berger T, ElstonDM, editor. Andrews disease of the skin Clinical Dermatology 10th Ed. Canada: Elsevier; 2000. p. 231-44.
    Gupta AK, Swan JE. Perioral dermatitis. In: Williams H, Bigbi MC, Diepgen T, Herxheimer H, Nalgi L, Rzany B. Evidence-Based Dermatology. London: BMJ Books; 2003. p. 125-131. Webster, Guy. Overview of the pathogenesis of acne. In: Webster GF, Rawlings AV, editor. Acne and its therapy. London:Informa Healthcare; 2007. p. 1-5. Zouboulis, Christos C. Update and future of systemic acne treatment. Dermatology, Acne Symposium at the World Congres of Dermatology Paris July 2002. p. 37-42.

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