Pilosebaceous Disorders including Acne vulgaris

Pilosebaceous Disorders including Acne vulgaris

1. PILOSEBACEOUS DISORDERS

2. Acne V ulgaris

3. Self limiting chronic inflammatory disease of the pilosebaceous unit that is seen primarly in adolescents characterized by seborrhea, open and closed commedons, papules and pustules In severe cases nodules and pseudocysts

4. Very common –affect 85% of population lifetime 14 to 17 F , 16 - 19 M 2O – 25 yrs it resolves slowly In 20% persists beyond age 25 2% of male and 5% of female continues to have the lesion at 40 years of age

5. Etiology & Pathogenesis four basic steps (1) follicular epidermal hyperproliferation , (2) excess sebum production , ( 3) inflammation, and (4) the presence and activity of Propioni bacterium acne

6. the corneocytes , are normally shed into the lumen of the follicle and extruded through the follicular ostium ,

7. Comedon formation Increase proliferation of keratinocytes and their cohesion, Excess corneocytes Plugging of the follicular openining retaintion and accumulation of cells, sebum, and bacteria ,

8. further expansion of the follicular unit + baccterial proliferation  perifollicular inflamation , PAPULE

9. As the forces increase, rupture of the comedo wall with extrusion of the immunogenic keratin and sebum occurs, with resultant inflammation+ scarring

10. Melanin deposition and lipid oxidation within the debris may be responsible for the black coloration.

11. what stimulates keratinocyte hyperproliferation and increased adhesion ?

12. Androgen receptors, found in the cells of the basal layer of the sebaceous gland and the outer root sheath of the hair follicle, are responsive to testosterone and dihydrotestosterone ,

13. CLINICAL FEATURES Gradual onset Face, back, chest,neck ,shoulder Polymorphic lesions- commedons, papules, pustules,nodules,cysts Usually asyptomatic but can be pruritic and painful

14. Classification comedonal Mild papulo-pustular Moderate papulo-pustular Severe Nodular / conglobate Site– face,chest ,back INFLAMMATORY VS NON INFLAMMATORY

15. Differential dx Rosacea Periorficial dermatitis Sebaceous hyperplasia Millia Nevus comedonicus

16. Complication scar hyperpigmentation psychological impact

17. MANAGMENT Topical therapy Systemic therapy SURGICAL THERAPY PHYSICAL THERAPY

18. SYSTEMIC THERAPY Antibiotics and Antibacterial Agents for moderate-to-severe acne, with inflammatory disease. for Rx chest, back or shoulder acne. takes 6 to 8 wks to see efficacy. keeping pts free of disease for 1 to 2 mos before each decrease in dosage is best to prevent flaring. Most courses of oral therapy are of at least 3 to 6 months duration doxycycline in dosages of 50 to 100 mg bid.

19. Cleansing To minimize sebum Wash 2x daily Use gentle cleansers Use Medicated cleansers that contain benzyle peroxide or salicylic acid

20. Drug induced acne Inflamed papules and pustules develop on a background of erythema that favors the distribution of corticosteroid application. Lesions resolve with discontinuation of the corticosteroid, although steroid dependency can lead to prolonged and severe flares post withdrawal

21. Acne fulminans is the most severe form of cystic acne and is characterized by the abrupt onset of nodular and suppurative acne in association with variable systemic manifestations. Severe, eruptive nodulocystic acne without systemic manifestations is termed acne conglobata Acne mechanica occurs secondary to repeated mechanical and frictional obstruction of the pilosebaceous outlet

22. VARIANTS neonatal Infantile Acne Conglobata Acne fulminans Acne Excoriee des jeunes Filles Acne Mechanica Acne form eruption s …….

23. Rosacea

24. Rosacea chronic disorder affecting the facial convexities, characterized by frequent flushing, persistent erythema and telangiectasia , interspersed by episodes of inflammation during which swelling, papules and pustules are evident

25. epidemiology most common in fair-skinned individuals, but it can occur in any skin type. The peak in both incidence and disease severity is in the third and fourth decades of life, occasionally in children,

26. Pathophysiology Antimicrobial peptides-- Cathelicidins Neoangiogenesis and vascular endothelial growth factor (VEGF) overexpression Reactive oxygen species-Nu Ferritin expression Microbial organisms-D F- Demodex folliculorum Perivascular versus perifollicular inflammation Chemicals and ingested agents Dermal matrix degeneration Climatic exposures Vasculature  hyper reactivity

27. Pathophysiology Induced by the use of topical corticosteroids on the face UV light hot or cold temperature, sunlight, wind, hot drinks, spicy food, exercise, alcohol, emotions, cosmetics, topical irritants, Menopausal flushing, and medications _ Niacin ...

28. SUB TYPES Erythematotelangiectatic type Papulopustular rosacea Phymatous rosacea Ocular mild ,moderate and severe

29. Erythemato telangiectatic VASCULAR Persistent facial erythema and flushing along with telangiectases , central face edema, burning and stinging, roughness or scaling

30. Papulopustular rosacea INFLAMMATORY persistent, central-face erythema with papules and pustules

31. Phymatous rosacea Patulous follicular orifices,thickened skin, nodularities , and irregular surface contour  Overgrowth of sebaceous glands

32. Ocular Blepharitis Conjunctivitis keratitis

33. VARIANT Granulomatous rosacea Yellowbrown or red papules or nodules that are monomorphic and located on the cheeks and periorificial facial skin

34. Periorficial dermatitis

35. POD Xized by small discrete papules & pustules in a periorificial distribution predominantly around the mouth Perioral dermatitis is a chronic papulopustular and eczematous facial dermatitis Earlier in young women 15-25 yrs of age but now recognized to occur in children as well

36. POD … periorbital skin → periocular dermatitis Has a worldwide distribution Etiology & pathogenesis POD related to misuse of potent topical corticosteroids ( fluorinated or non fluorinated) Patients report a hx of an acute steroid responsive eruptions around the mouth, nose and/or eyes that worsens when the steroid is d/c

37. POD There has been histological similarity of granulomatous POD with acne rosacea Clinical Feature Eruption begins abruptly in the nasolabial area Spreads rapidly to the periorbital zone Spares the lip margin(vermillion border) at least 5mm clear zone Lesions are symmetrical

38. POD A background of erythema and scale may occur Lesions reported to appear on the ears, scalp, trunk, labia majora & extremities Rarely burning or itching sensation Intolerance to moisturizers & other topical products

39. TREATMENT Avoid steroid Photoprotection Topical treatment 0.75 to 1% metronidazole Erythromycin Systemic treatment-in severe cases doxcyclin , tetracyclin , erythromycin

40. Thanks