acne vulgaris


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acne vulgaris

  1. 1. Acne Vulgaris TSMU
  2. 2. Definition Acne vulgaris, more commonly referred to simply as acne, is a chronic inflammatory disorder of the pilocebaceous unit.characterized by: abnormalities in sebum production follicular desquamation bacterial proliferation inflammation
  3. 3. Overview Acne vulgaris is the most common cutaneous disorder. It affects more than 17 million Americans. Patients can experience significant psychological morbidity and, rarely, mortality due to suicide. Important that physicians are familiar with Acne Vulgaris and its treatment. affects all races and ethnicities with equal significance. Darker skinned patients at increased risk for developing post-inflammatory hyper-pigmentation and keloids.
  4. 4. Etiology Acne is polygenic and multi-factorial. Four main pathogenetic factors contribute to the disease:• Propionibacterium acnes and Staphylococcus epidermidis colonisation. : bacteria found deep in follicles and stimulate the production of pro-inflammatory mediators and lipases.• Inflammation and immune response. Inflammatory cells and mediators efflux into the disrupted follicle, leading to the development of papules, pustules, nodules, and cysts.• Sebaceous gland hyperplasia and excess sebum production.• Abnormal follicular differentiation.
  5. 5. Propionibacterium AcnePropionibacterium acne is a gram-positive, non-motil rods relativelyslow growing typically aerotolerant anaerobic gram positive bacterium
  6. 6. Staphylococcus epidermidis• S. epidermidis is a very hardy microorganism, consisting of nonmotile, Gram-positive cocci, arranged in grape-like clust- part of human skin flora and consequently part of human flora. Although S. epidermidis is not usually pathogenic, patients with compromised immune systems are often at risk for developing acne.
  7. 7. Pathophysiology• The initial step in the development of acne is the formation of the microcomedo.Follicular keratinocytes that exhibit increas- ed cohesiveness do not shed normally, leading to retention and accumulation.• Androgens stimulate enlargement of sebaceous glands and increased sebum production, and the abnormal keratinaceo- us material and sebum collect in the microcomedo.• This leads to a build-up of pressure, and whorled lamellar concretions develop. At this stage, a non-inflammatory comedo may be seen clinically.
  8. 8. • This micro-environment allows the proliferation of bacterium, which is part of the normal flora of follicles. This gram-positive rod has low virulence but is capable of metabolising triglycerides and releasing free fatty acids.This metabolism, as well as its ability to activate complement, produces pro- inflammatory mediators, including neutrophil chemo- attractants.• With increased pressure and recruitment of inflammatory mediators, the microcomedo may rupture and release immunogenic keratin and sebum, thus stimulating an even greater inflammatory response
  9. 9. • Depending on the specific inflammatory cells present,suppur- ative pustules or inflamed papules, nodules, or cysts may develop. If a sufficient amount of inflammation and tissue damage results, post-inflammatory hyperpigmentation and scarring may result.
  10. 10. Clinical Manifestations:• Closed comedone (whitehead) - a clogged follicle. Whiteheads usually appear on the skin as small, round, white bumps.• Open comedone (blackhead) - a plugged follicle that opens and turns dark at the surface of the skin. Blackheads do not indicate the presence of dirt.• Papules - inflamed lesions that appear as small, pink bumps on the skin.• Pustules (pimples) - inflamed pus filled lesions that are red at the base.• Cysts and nodules - large, inflamed, pus filled lesions deep under the skin that can cause pain and scarring.
  11. 11. • Local symptoms : include pain tenderness.• Systemic symptoms : most often absent Severe acne with associated systemic signs and symptoms such as Fever, Psychological impact on any patient
  12. 12. Closed comedones (whiteheads)Accumulation of sebum converts a microcomedo into this.
  13. 13. Open comedones (blackhead)when follicular orifice is opened and distended. Melanin + packed keratinocytes + oxidized lipids  dark colour
  14. 14. Whitehead and blackheads
  15. 15. Pustules inflamed pus filled lesions that are red at the base.
  16. 16. Cysts• Cysts: when follicles rupture into surrounding tissues, resulting in papule/pustule/nodule.
  17. 17. Classification• Classification system generally as follows• Type 1 — Mainly comedones with an occasional small inflamed papule or pustule; no scarring present• Type 2 — Comedones and more numerous papules and pustules (mainly facial); mild scarring• Type 3 — Numerous comedones, papules, and pustules, spreading to the back, chest, and shoulders, with an occasional cyst or nodule; moderate scarring Type 4 — Numerous large cysts on the face, neck, and upper trunk; severe scarring
  18. 18. Diagnosis• Complete history• Pay attention to endocrine function- Rapid appearance with virilization/menstrual irregularity• Complete medication list• Physical exam:- Location - scarring- Lesion type - keloid- pigmentation
  19. 19. LABORATORY EXAMINATIONNo laboratory examinations required. If there is suspicion ofan endocrine disorder, free testosterone, follicle-stimulatinghormone, luteinizing hormone, and DHEAS should be deter-mined to exclude hyperandrogenism and polycystic ovarysyndrome.majority of acne patients, hormone levels are normal.Laboratory examinationstransaminases(ALT, AST), triglycerides, and cholesterollevels may be required if systemic isotretinoin treatment isplanned DHEAS - Dehydroepiandrosterone
  20. 20. DIFFERENTIAL DIAGNOSIS• Comedones are required for diagnosis of any type of acne. Comedones are not a feature of acne-like conditions and of the conditions listed below.• Face - S. aureus folliculitis, pseudofolliculitis barbae, rosacea, perioral dermatitis.• Trunk -Malassezia folliculitis, “hot-tub” pseudomonas folliculitis, S. aureus folliculitis, and
  21. 21. TreatmentThe goals of pharmacotherapy for acne vulgaris are to reducemorbidity and to prevent complications.Medication: Benzoyl Peroxide Antibiotics,Topical and OralretinoidsBenzoyl Peroxide :Benzoyl peroxide is a first-line treatment for mild andmoderate acne vulgaris due to its effectiveness and mild side-effects
  22. 22. Antibiotics:• Topical and systemic antibiotics used in the treatment of acne vulgaris are directed at Propionibacterium acnes. They also have anti-inflammatory properties. Minocycline Doxycycline Tetracycline
  23. 23. Retinoids:• These agents decrease the cohesiveness of abnormal hyperproliferative keratinocytes, and they may reduce the potential for malignant degene- ration. They also modulate keratinocyte differentiation. isotretinoin Tretinoin topical Adapalene Tazarotene
  24. 24. Alternative treatments• Phototherapy with blue and red light emitted from special fluorescent lights, LEDs, lasers, or dichroic bulbs.• Photodynamic therapy involving intense blue or violet light,• zinc, teat tree oil, heat therapy, salt water therapy are all used for treating acne.
  25. 25. PrognosisAcne of any severity usually remits spontaneously by theearly to mid-20s,but a substantial minority of patients,usually women, may have acne into their 40s.