Y5 - Acne vulgaris Flashcards
acne vulgaris
def
a skin disease affecting the pilosebaceous unit
-characterised by comedones, papules, pustules, cysts
epi
most common in adolescents
- boys>girls in adolescence
- girls>boys in adulthood
what do lesions in acne vulgaris consist of
non-inflammatory comedones (whiteheads and blackheads), inflammatory papules, pustules, cysts
four main pathogenetic factors:
- sebaceous gland hyperplasia and excess sebum production
- abnormal follicular differentiation
- cutibacterium acnes colonisation
- inflammation and immune response
aetiology
what stimulates sebaceous glands to enlarge and produce more sebum
androgens (puberty)
what happens to keratinocytes in acne vulgaris
karatinocytes are retained and accumulate
what sort of bacteria is cutibacterium
gram positive non-motile rods
what does cutibacterium stimulate
the production of pro-inflammatory mediators and lipases
what happens in inflammation and immune response in acne vulgaris
inflammatory cells and mediators efflux into the disrupted follicle causing development of papules, pustules, and cysts
what external factors may contribute to acne
- mechanical trauma
- cosmetics
- corticosteroids
- hyperandrogenism
pathophysiology
- formation of the microcomedo
- follicular keratinocytes with increased cohesiveness do not shed normally and lead to accumulation
- androgens stimulate enlargement of sebaceous glands and increased sebum production
- pressure build-up occurs and whorled lamellar concretions develop - proliferation of c acnes
- capable of metabolising triglycerides and releasing FFAs
- activates complement and pro-inflammatory mediators - microcomedo ruptures due to increased pressure and recruitment of inflammatory mediators
signs and symptoms
RFs
skin tenderness
RFs for acne vulgaris
adolescence
genetic predisposition
greasy skin/ increased sebum production
what medications can increase risk of acne vulgaris
androgens, corticosteroids, antiepileptics