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OS 212 DERMATOLOGY > Acne > Flashcards

Acne Flashcards

1
Q

Epidemiology of Acne

A

90% of adolescents
Usually (+) Fmhx

Typically presents at ages 8-12 years old

For women -> first outbreak at 20-35 years old

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2
Q

2 types of morphology of Acne

A

Non-inflammatory papules

Inflammatory papules

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3
Q

Non inflammatory papules

A

Comedones:

Open - blackheads
Closed - whiteheads

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4
Q

Inflammatory papules

A

Erythematous papules

Erythematous nodules and cysts (PIC)

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5
Q

History of acne

A

When does it start?

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6
Q

4 Basic event that occur during acne formation

A

Increased sebum production

Follicular epithelial hyperproliferation

Colonization of P. acnes

Production of inflammation

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7
Q

Main stimuli for Pathogenesis for Acne

A

Androgenic Stimuli

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8
Q

Increased Sebum Production

A

Sebaceous gland hyperactivity

5a-reductase -> testosterone to 5a testosterone -> receptors in SG -> increase SS -> hyperseborrhea or oily skin

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9
Q

Composition of sebum

A

Free fatty acid

Lower concentration of linoleic acid

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10
Q

How does sebum induces follicular hyperkeratosis

A

Through IL-1 secreted by the sebocytes

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11
Q

Increased production of dead skin

A

Hyperkeratiniation

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12
Q

Follicular Epithelial Hyperproliferation

A

more dead skin cells from stratum corneum are being formed in the follicle, while the sebum plugs the follicle ->microcomedone formation

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13
Q

Sebum + dead skin

A

Microcomedone

-precursor of other acne lesions

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14
Q

Earliest microscopid manifestation (histologic inflammation)

A

Microcomedone

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15
Q

Follicular Epithelial Hyperproliferation is triggered by..

A

Androgen hormones

Alterations in follicular linoleic acid and IL-1

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16
Q

Gram negative, anaerobic diphtheroid. Constituent of normal cutaneous flora, Produces LIPASE that digest the free fatty acid in sebum

A

P. acnes

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17
Q

Three pathways in the production of Inflammation

A

Inciting of inflammatory by P. acnes

Rupture of follicular epithelium

Exces sebum production (linoleic acid deficiency)

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18
Q

Inciting of inflammation by P. acnes

A

innate immunity

TLR-2 (homologous to IL-1)

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19
Q

part of the innate immune system that recognizes stimuli (endotoxin, bacteria, neuropeptidases) including P. acnes stimulating the immune response

A

TOLL receptors

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20
Q

Rupture of Follicular epithelium

A

Expansion of the follicular unit -> plug -> build up -> RUPTURE -> foreign body response -> more perifollicular inflammation

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21
Q

Causes infundibular rupture

A

EGF/TGF

-levels of EGF receptor decreases with age

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22
Q

Not clinically inflamed but histologic inflammation exists

A

Comedonal acne

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23
Q

Treatment to normalize follicular hyperkeratinization

A

Comedolytic/keratolytic agents

Topic retinoids
BPO
SA
AHA

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24
Q

Treatment to decrease sebum production

A

Sebostatic agents

Oral isotretenoin
OC pills
Anti-androgens

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25
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
26
Treatment for the Inflammation
Intralesional steroids or oral (use with caution; acne ironically is a side effect) Topical isotretinoin Topical erythromycin, clindamycin, tetracycline
27
MOA for retinoids
Keratolytic and has activity against TLr (both keratolytic and anti-inflammatory)
28
fIRST GENERATION rETINOIDS
Retinol, tretinoin, isotretinoin
29
Reduces concentration of MMPs in sebum
Isotretinoin
30
Second generation Retinoids
etretinate, acitretin | manoaromaticcompounds
31
third generation retinoids
less local irritation as compared with tretinoin Polyaromatic compounds such as adapalene and tazarotene
32
Commonly prescribed Retinoids
Tretinoin Adapalene - least potent Tazarotene
33
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
34
Can interfere with arachidonic acid cascade of the inflammatory process-> reduces inflammation
Salicylic Acid
35
Most effective acne medication
Oral isotretinoin -hits on all 4 processes of acne devt. but with many side effects
36
Potential Side effects of oral Isotretinoin
Xerosis, Chelitis | Teratogenicity, Hypertriglyceridemia, hepatotoxicity, depression
37
Bacteriostatic agents
ERYTHROMYCIN CLINDAMYCIN chloramphenicol sulfonamides trimethoprim Tetracyclines
38
Bactericidal agents
Benzoyl Peroxides ``` Aminoglycosides Beta lactams Vancomycin Quinolones Rifampicin Metronidazole ```
39
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
40
Intereferes with the synthesis of bacterial capsule, rendering it susceptible to phagocytosis
Clindamycin
41
Reversible binding to ribosomal subunits will inhibit protein synthesis
Erythromycin
42
First Generation Cycline Antibiotic
tetracycline, oxytetracycline - impaired by food and milk, very cheap - 500 mg BID
43
second generation cycline antibiotics
Doxycycine 100mg - 200mg OD Minocycline 100 mg-200mg OD Lymecycline 300mg - 600mg OD
44
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
45
Increasing sex hormone binding globulin and decrease circulating free testosterone
Oral Contraceptives
46
Androgen receptor blocking properties Decreasing sebum production in acne
Spironolactone
47
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
48
Treatment consideration of BPO
May bleach hair and colored fabrics
49
treament consideration of BPO and topical retinoids
May irritate skin - start on alternate day dosing Use of moisturizer to reduce irritancy
50
Rationale of combination therapy
Improved efficacy Minimized complications Enhanced tolerability
51
Most common cause of treatment failure (ACNE)
Lack of adherence
52
Topical agents take ____months to see effects
2-3 months
53
Therapy should be continued for at least _____ weeks before treatment response can be accurate
8 weeks
54
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)
55
Onset of Neonatal Acne
birth to 6 weeks
56
Onset of Infantile acne
6 weeks to 1 year
57
Onset of Mid-childhood acne
1 year to 7 years
58
Onset of Pre adolescent acne
7 to 12 years or menarche in girls
59
Onset of Adolescent acne
12 to 19 years or after menarche in girls
60
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
61
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)
62
Mid Childhood acne
between 1 to 7 years old very rare Possible sequelae of excess androgens
63
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
64
Post adolescent women (Androgens in acne)
Serum hormone levels usually normal | Acne lesions often perioral and along the jaw line
65
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
66
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
67
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
68
Young women Extensive neurotic excoriations leaving crusted erosions that scar.
Acne Excoriee
69
Sports induced acne Combination of heat, pressure, occlusion of the skin areas and repetitive fictional rubbing (fiddler's acne)
Acne Mechanica
70
Chloracne
Chorinated hydrocarbons Comedone, cysts, and pigmentary changes
71
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
72
Drug-induced Acne
Testosterone, Progesterone, Steroids Lithium, Phenytoin, Isoniazid Vitamins B2, B6, and B12 Halogens: Bromides , iodides
73
Pre existing acne on long term oral antibiotics especially tetracyclines . Enterobacter, Klebsiella, Escherichia, Proteus
Tx: oral antibiotics with gram (-) coverage, oral isotretinoin, oral cephalosporin
74
may look like acne but comedones are absent Not related to hormones Flushing Telangiectasia Triggers: Alcohol, sunlight, hot beverages, picy food, emotional stress
Rosacea
75
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)

OS 212 DERMATOLOGY (9 decks)

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