Acne vulgaris Flashcards

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1
Q

cause

A

multifactorial

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2
Q

acne pathogenesis

A

normal hair follicle has a wide opening

  1. narrowing of HF
  2. increased sebum production, and increased on skin so feels greasy
  3. sebum is blocked in –> stagnates
  4. bacterium multiply in stagnant sebum –> irritation + inflammation –> pus formation
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3
Q

critical factors in pathological process

A
  • Follicular epidermal hyperproliferation
  • Blockage of pilosebaceous units with surrounding inflammation
  • Increased sebum production
  • Infection with propionibacterium acnes
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4
Q

epidemiology

A

occurs in 85% of adolescents

can continue into early and mid adulthood

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5
Q

presentation areas and 3 cardinal signs

A

face, back, sternal area (where theres lots of sebaceous glands)

  1. open comedones (blackheads)
  2. closed comedones (whiteheads)
  3. pustules

skin may be greasy
premenstrual exacerbation

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6
Q

what pathway makes scarring more likely?

A

rupture of inflamed lesions, deep-seated dermal inflammation + nodulocystic lesions

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7
Q

1st line treatment

A

topical agents

  • kertolytics e.g. benzoyl peroxide, azelaic acid
  • topical retinoids (tretinoin, isotretinoin)
  • topical antibiotics e.g. erythromycin for inflammatory acne
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8
Q

side effects of topical agents

A

irritation

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9
Q

2nd line therapy

A

low-dose oral antibiotics for 3-4 months e.g. oxytetracycline

cyproterone acetate/co-cyprindiol - contraceptive pill that also is anti-androgenic

  • UVB phototherapy
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10
Q

3rd line therapy

A

retinoid drug - isotretinoin

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11
Q

when to use 3rd line therapy?

A

if 1st and 2nd line fail
nodulocystic with scarring
severe psychological disturbance

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12
Q

caution of 3rd line therapy?

A

VERY teratogenic

hospital-only drug in most countries

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