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
third generation retinoids
less local irritation as compared with tretinoin
Polyaromatic compounds such as adapalene and tazarotene
Commonly prescribed Retinoids
Tretinoin
Adapalene - least potent
Tazarotene
Can act both as comedolytic and anti-inflammatory
Salicylic acid
-Lipophilic characteristics facilitte peeling of the exterior layer of the dermis and open follicles that are plugged
Can interfere with arachidonic acid cascade of the inflammatory process-> reduces inflammation
Salicylic Acid
Most effective acne medication
Oral isotretinoin
-hits on all 4 processes of acne devt. but with many side effects
Potential Side effects of oral Isotretinoin
Xerosis, Chelitis
Teratogenicity, Hypertriglyceridemia, hepatotoxicity, depression
Bacteriostatic agents
ERYTHROMYCIN
CLINDAMYCIN
chloramphenicol
sulfonamides
trimethoprim
Tetracyclines
Bactericidal agents
Benzoyl Peroxides
Aminoglycosides Beta lactams Vancomycin Quinolones Rifampicin Metronidazole
Lipophilic
Applied topically
Only bactericidal medication - others are bacteriostatic
Breaks down into benzoic acid and oxygen upon contact with skin
Both bactericidal and anti-inflammatory
Benzoyl peroxide
Intereferes with the synthesis of bacterial capsule, rendering it susceptible to phagocytosis
Clindamycin
Reversible binding to ribosomal subunits will inhibit protein synthesis
Erythromycin
First Generation Cycline Antibiotic
tetracycline, oxytetracycline
- impaired by food and milk, very cheap
- 500 mg BID
second generation cycline antibiotics
Doxycycine 100mg - 200mg OD
Minocycline 100 mg-200mg OD
Lymecycline 300mg - 600mg OD
Anti-inflammatory Agents
BPO - Reduces P. acnes
Clindamycin - acts on pro inflammatory cytokines
Erythromycin - inhibitory effect on neutrophil chemotactic factor activity of P. acnes
- Inhibitory effect on production of ROS
Retinoids - Activity against TLR; isotretinoin can reduce conc. of MMPs in sebum
Corticosteroids
Oral antibiotics
Increasing sex hormone binding globulin and decrease circulating free testosterone
Oral Contraceptives
Androgen receptor blocking properties
Decreasing sebum production in acne
Spironolactone
Treatment consideration of TOPICAL RETINOIDS
Use of sunscreen and protective clothing to reduce photosensitivity induced by retinoids
BPO and retinoids are not applied at the same time because BPO oxidizes and colored fabrics
Treatment consideration of BPO
May bleach hair and colored fabrics
treament consideration of BPO and topical retinoids
May irritate skin - start on alternate day dosing
Use of moisturizer to reduce irritancy
Rationale of combination therapy
Improved efficacy
Minimized complications
Enhanced tolerability
Most common cause of treatment failure (ACNE)
Lack of adherence
Topical agents take ____months to see effects
2-3 months
Therapy should be continued for at least _____ weeks before treatment response can be accurate
8 weeks
Grades of Acne
Grade 1: Comedones (Open or closed), ocassionaly pustules or papules, no scarring
Grade 2: Papules, comedones, few pustules; mild scarring
Grade 3: Predominant pustules, nodules, abscesses, moderate scarring
Grade 4: Mainly cysts, abscesses, scars; severe scarring.
(Add oral treatment for grades 2, 3, 4)
Onset of Neonatal Acne
birth to 6 weeks
Onset of Infantile acne
6 weeks to 1 year
Onset of Mid-childhood acne
1 year to 7 years
Onset of Pre adolescent acne
7 to 12 years or menarche in girls
Onset of Adolescent acne
12 to 19 years or after menarche in girls
Neonatal acne
2 weeks of age
Spontaneously resolves within 3 months
Not true acne: comedone formation is absent
Transiently elevated sebum excretion rate
Baby has high risk of having severe acne later on
Infantile acne
3-6 months
Resolves at 1-2 years of age
True acne: Comedones are present
transient elevation of DHEA
TREATMENT: topical retinoids, BPO (lower concentrations are given)
Mid Childhood acne
between 1 to 7 years old
very rare
Possible sequelae of excess androgens
Treatment of Acne variants
1-7 year olds : rule out underlying systemic abnormality
Preadolescent acne: similar to older age except!!!
<8 : avoid oral tetracycline - damage to enamel and bones
Retinoids: ADAPALENE, BPO 2.5% for >9 years old
Tretinoin 0.05%: FDA approved for >10 years old
Post adolescent women (Androgens in acne)
Serum hormone levels usually normal
Acne lesions often perioral and along the jaw line
Hormonal Acne
DHEAS :
4000-8000 ng/ml : congenital adrenal hyperplasia
>8000 ng/ml: adrenal tumor
SERUM TOTAL TESTOSTERONE
>150 ng/ml : Ovarian source of excess (150-200 :PCOS)
INCREASED LH/FSH ratio
>2.0: polycystic ovary disease
Teenage male
Draining lesion discharge
Subcutaneous dissection with formation of multichannel sinus tracts.
can outgrow this condition (but scarring acne)
Acne Conglobota
-treatment: isotretoin, antibiotic or intralesional steroids
Most severe form, associated with systemic sypmtoms
Sudden, explosive appearance
Appears in the back and chest (Face and neck are usually spared)
Acne Fulminans
TreatmentL systemic steroids
Young women
Extensive neurotic excoriations leaving crusted erosions that scar.
Acne Excoriee
Sports induced acne
Combination of heat, pressure, occlusion of the skin areas and repetitive fictional rubbing (fiddler’s acne)
Acne Mechanica
Chloracne
Chorinated hydrocarbons
Comedone, cysts, and pigmentary changes
Can occur as early as 2 week after steroids are started,
Monomorphous papules and/or pustules.
Note Hx: constant application of topical steroids or intake of oral steroids, you will have more acne
Also a differential for acne vulgaris, steroid-induced acne
Steroid Folliculitis
Drug-induced Acne
Testosterone, Progesterone, Steroids
Lithium, Phenytoin, Isoniazid
Vitamins B2, B6, and B12
Halogens: Bromides , iodides
Pre existing acne on long term oral antibiotics especially tetracyclines .
Enterobacter, Klebsiella, Escherichia, Proteus
Tx: oral antibiotics with gram (-) coverage, oral isotretinoin, oral cephalosporin
may look like acne but comedones are absent
Not related to hormones
Flushing
Telangiectasia
Triggers: Alcohol, sunlight, hot beverages, picy food, emotional stress
Rosacea
Papules, pustules, with scaling around mouth, nose and eyes
Absence of comedones
HPI: History of prior or current use of topical steroids
Periorificial Dermatitis (Perioral Dermatitis)
