Acne Flashcards
Epidemiology of Acne
90% of adolescents
Usually (+) Fmhx
Typically presents at ages 8-12 years old
For women -> first outbreak at 20-35 years old
2 types of morphology of Acne
Non-inflammatory papules
Inflammatory papules
Non inflammatory papules
Comedones:
Open - blackheads
Closed - whiteheads
Inflammatory papules
Erythematous papules
Erythematous nodules and cysts (PIC)
History of acne
When does it start?
4 Basic event that occur during acne formation
Increased sebum production
Follicular epithelial hyperproliferation
Colonization of P. acnes
Production of inflammation
Main stimuli for Pathogenesis for Acne
Androgenic Stimuli
Increased Sebum Production
Sebaceous gland hyperactivity
5a-reductase -> testosterone to 5a testosterone -> receptors in SG -> increase SS -> hyperseborrhea or oily skin
Composition of sebum
Free fatty acid
Lower concentration of linoleic acid
How does sebum induces follicular hyperkeratosis
Through IL-1 secreted by the sebocytes
Increased production of dead skin
Hyperkeratiniation
Follicular Epithelial Hyperproliferation
more dead skin cells from stratum corneum are being formed in the follicle, while the sebum plugs the follicle ->microcomedone formation
Sebum + dead skin
Microcomedone
-precursor of other acne lesions
Earliest microscopid manifestation (histologic inflammation)
Microcomedone
Follicular Epithelial Hyperproliferation is triggered by..
Androgen hormones
Alterations in follicular linoleic acid and IL-1
Gram negative, anaerobic diphtheroid. Constituent of normal cutaneous flora, Produces LIPASE that digest the free fatty acid in sebum
P. acnes
Three pathways in the production of Inflammation
Inciting of inflammatory by P. acnes
Rupture of follicular epithelium
Exces sebum production (linoleic acid deficiency)
Inciting of inflammation by P. acnes
innate immunity
TLR-2 (homologous to IL-1)
part of the innate immune system that recognizes stimuli (endotoxin, bacteria, neuropeptidases) including P. acnes stimulating the immune response
TOLL receptors
Rupture of Follicular epithelium
Expansion of the follicular unit -> plug -> build up -> RUPTURE -> foreign body response -> more perifollicular inflammation
Causes infundibular rupture
EGF/TGF
-levels of EGF receptor decreases with age
Not clinically inflamed but histologic inflammation exists
Comedonal acne
Treatment to normalize follicular hyperkeratinization
Comedolytic/keratolytic agents
Topic retinoids
BPO
SA
AHA
Treatment to decrease sebum production
Sebostatic agents
Oral isotretenoin
OC pills
Anti-androgens
treatment to reduce P. acnes Proliferation
Use antibiotics
BPO
Topical/oral antibiotics (Clindamycin, lindocyclin)
Bacteriostatics preferably used because P. acnes is part of normal flora so it should not be completely eradicated
Treatment for the Inflammation
Intralesional steroids or oral (use with caution; acne ironically is a side effect)
Topical isotretinoin
Topical erythromycin, clindamycin, tetracycline
MOA for retinoids
Keratolytic and has activity against TLr (both keratolytic and anti-inflammatory)
fIRST GENERATION rETINOIDS
Retinol, tretinoin, isotretinoin
Reduces concentration of MMPs in sebum
Isotretinoin
Second generation Retinoids
etretinate, acitretin
manoaromaticcompounds