ACNE VULGARIS

selflimited chronic inflammatory disease of the pilosebaceous unit that is seen primarily in adolescents

common 14-17, 16-19

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

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

Comedon formationIncrease proliferation of

keratinocytes and their cohesion,Excess corneocytesPlugging of the follicular

openining retaintion and accumulation of cells, sebum, and bacteria,

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

As the forces increase,

rupture of the comedo wall with extrusion of the immunogenic keratin and sebum occurs, with resultant inflammation+ scarring

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

what stimulates keratinoryte hyperproliferation and increased adhesion ?

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,

CLINICAL FEATURES

CLASSIFICATION

comedonalMild papulo-pustular

Moderate papulo-pustular

Severe Nodular / conglobate

siteINFLAMMATORY VS NON INFLAMMATORY

COMPLICATION

four general types of acne scars: ice pick, rolling, boxcar, and hypertrophic Ice pick scars are narrow, deep scars that

arewidest at the surface of the skin and taper

to a point in the dermis. Rolling scars are shallow, wide scars that

havean undulating appearance. Boxcar scars are wide, sharply

demarcated scars. the width of boxcar scars is similar at the surface and base.

hypertrophic.

Psycological impact

MANAGMENT

Topical therapy

Systemic therapy

SURGICAL THERAPY

PHYSICAL THERAPY

Cleansing BPO or SA .

Bid washing with a gentle cleanser --- application of acne Rx.

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 o in dosages of 50 to 100 mg bid.

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

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

VARIANTS neonatal Infantile Acne Conglobata Acne fulminans SAPHO syndrome PAPA Acne Excoriee des jeunes Filles Acne Mechanica Acne form eruptions …….

ROSACEA

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

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,

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 hyperreactivity.

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...vasoactive

SUB TYPES Erythematotelangiectatic type

Papulopustular rosacea Phymatous rosacea Ocular mild moderate severe

ERYTHEMATOTELANGIECTATIC

VASCULARPersistent facial erythema and flushing along with telangiectases, central face edema, burning and stinging, roughness or scaling

PAPULOPUSTULAR ROSACEA

INFLAMMATORYpersistent,central-face erythema with papules andpustules

PHYMATOUS ROSACEA

Patulous follicular orifices,thickenedskin, nodularities, and irregular surface contourOvergrowth of sebaceous glands

OCULAR

BlepharitisConjunctivitiskeratitis

VARIANT

Granulomatous rosacea Yellowbrown or red papules or nodules thatare monomorphic and located on thecheeks and periorificial facial skin

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