Acne vulgaris Flashcards
cause
multifactorial
acne pathogenesis
normal hair follicle has a wide opening
- narrowing of HF
- increased sebum production, and increased on skin so feels greasy
- sebum is blocked in –> stagnates
- bacterium multiply in stagnant sebum –> irritation + inflammation –> pus formation
critical factors in pathological process
- Follicular epidermal hyperproliferation
- Blockage of pilosebaceous units with surrounding inflammation
- Increased sebum production
- Infection with propionibacterium acnes
epidemiology
occurs in 85% of adolescents
can continue into early and mid adulthood
presentation areas and 3 cardinal signs
face, back, sternal area (where theres lots of sebaceous glands)
- open comedones (blackheads)
- closed comedones (whiteheads)
- pustules
skin may be greasy
premenstrual exacerbation
what pathway makes scarring more likely?
rupture of inflamed lesions, deep-seated dermal inflammation + nodulocystic lesions
1st line treatment
topical agents
- kertolytics e.g. benzoyl peroxide, azelaic acid
- topical retinoids (tretinoin, isotretinoin)
- topical antibiotics e.g. erythromycin for inflammatory acne
side effects of topical agents
irritation
2nd line therapy
low-dose oral antibiotics for 3-4 months e.g. oxytetracycline
cyproterone acetate/co-cyprindiol - contraceptive pill that also is anti-androgenic
- UVB phototherapy
3rd line therapy
retinoid drug - isotretinoin
when to use 3rd line therapy?
if 1st and 2nd line fail
nodulocystic with scarring
severe psychological disturbance
caution of 3rd line therapy?
VERY teratogenic
hospital-only drug in most countries