Acne vulgaris

THIS IS THE MOST COMMON SKIN DISORDER SEEN IN CLININICS THIS IS SAID TO BE THE DISEASE OF TEEN AGE WHICH IS PARTIALY TRUE. THERE IS A COMMON WRONG BELIEF THAT IT WILL GET BETTER AFTER MARRIAGE THIS HAS THE POTENTIAL TO MAKE THE FACE COSMETICALLY BAD THUS PRODUCING LIFE LONG PYCHOLOGICAL DISABILITY

Epidemiology
Onset? Males 10-17 yrs Females 14-19 yrs May persist through 4th decade or older Prevalence? Asians 10% African-American 25% Caucasians 29%

Causes?
Majority of patients have a family history of acne Emotional stress Androgens Dioxins, lithium Occlusion and pressure acne mechanica NOT DUE TO CHOCOLATE OR FATTY FOODS!

Pathogenesis:

Acne vulgaris is a disease of pilosebaceous follicles.

Factors: Retention hyperkeratosis. Increased sebum production.

Propionibacterium acnes
within the follicle. Inflammation

Initial pathogenesis (reason unknown):

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

Terms/Definitions
Microcomedone: hyperkeratotic plug made of sebum and keratin in follicular canal

Whitehead and blackheads

Open comedo (blackhead)

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

Melanin + packed keratinocytes + oxidized lipids dark colour

Pustular

Cysts papules,pustules, nodules

Cysts:
when follicles rupture into surrounding tissues, resulting in papule/pustule/nod ule.

Cysts

 When was the onset? Adolescence Where? Face, neck, trunk & buttocks Does it itch or hurt? Pustules painful How have the individual lesions changed? Triggers? Milk,chocalates,corbohydrates,stres s,cosmetics use,working envirnoment? Hirsutism? Oligomenorrhea?

How to arrive at diagnosis

Differential Diagnosis
Face
Staph aureus folliculitis Rosacea Perioral dermatitis
Pityrosporum folliculitis Hot Tub folliculitis Appears after sun exposure

Trunk

Acne Aestivalis

Types of Acne
Comedonal Papulopustular Nodulocystic

Why is this important?

Directs treatment options

Comedonal Acne
Closed comedones (whiteheads)
Sebum accumulation results in a white papule visible at the skin surface

Open comedones (blackheads)

Plug protrudes from canal and turns dark

Non-inflammatory Usually responds to topical keratolytic

Papulopustular Acne
Papules/Pustules
Follicular wall ruptures Releases sebum and bacteria into dermis

Topical agents alone usually insufficient Consider topical retinoids plus systemic antibiotics

Diagnosis

Complete history Pay attention to endocrine function - Rapid appearance with virilization/menstrual irregularity PCOS and other syndromes Complete medication list Physical exam: - Location - scarring - Lesion type - keloid - pigmentation

Medications that can cause acne

ACTH Azathioprine Barbiturates Isoniazid Lithium phenytoin

Disulfiram Halogens Iodides Steroids Cyclosporine Vitamins B2,6,12

TREATMENT OPTIONS

SYSTEMIC DRUGS
-Tetracycline - erythromycin - minocycline - TMP-SMX - doxycycline - clindamycin SYNTHETIC VITAMIN A DERIVATIVES ISOTRETINOIN ANTIANDROGENS aldactone,diane 35,cimetidine,ketaconazole TOPICAL DRUGS ANTIBIOTICS,BENZYLE PEROXIDE,TRETINOIN,ADAPALENE. AZELOIC ACID SULPHUR,SALICYLIC ACID,GLYCOLIC ACID

 RECENT ADVANCES IN ACNE TREATMENT INCLUDES BLUE LIGHT THERAPY,LASER THERAPY ALL YET EXPERIMENTAL. ACNE SCARRING CAN BE MANAGED BY VARIOUS METHODS LASER THERAPY,CHEMICAL PEELING,DERMAROLERS.

Rosacea
Chronic inflammatory facial dermatoses characterised by erythema and pustules Cause unknown Middle aged Flushing Erythema, telangiectasia, papules, pustules, occasional lymphoedema : rhinophyma

Rosacea
Eye involvement blepharitis, conjunctivitis No comedones Treatment Topical metronidazole Systemic antibiotics, retinoids, Rhinophyma laser, plastic surgery Avoid topical steroids

PYODERMA GANGRENOSUM
ACQUIRED INFLAMMATORY IDIOPATHIC AUTOIMMUNE? NEUTROPHILIC INFILTRATE IN DERMIS WITH DESTRUCTION OF TISSUES

Clinical features
Non healing ulcers painful Bullous lesions Vegetative lesions Dirty looking deep ulcers with overhanging borders Atrophic scars seen after healing.

ASS0CIATIONS
BLOOD DYSCRASIAS INFLAMMATORY BOWEL DISEASES ARTHRITIS SLE MALIGNANCIES CHRONIC ACTIVE HEPATITIS

Different clinical presentations

TREATMENT
SYSTEMIC STEROIDS CYCLOSPORIN AZATHIOPRINE
CYCLOPHOSPHAMIDE

DAPSONE CLOFAZAMINE NURSING CARE

Fever,pruritus,polymorp hic vesicular rash

Pruritis,good response to steroids but the rash persists