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OS 212 DERMATOLOGY > Acne > Flashcards

Flashcards in Acne Deck (75):
1

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

2 types of morphology of Acne

Non-inflammatory papules

Inflammatory papules

3

Non inflammatory papules

Comedones:

Open - blackheads
Closed - whiteheads

4

Inflammatory papules

Erythematous papules

Erythematous nodules and cysts (PIC)

5

History of acne

When does it start?

6

4 Basic event that occur during acne formation

Increased sebum production

Follicular epithelial hyperproliferation

Colonization of P. acnes

Production of inflammation

7

Main stimuli for Pathogenesis for Acne

Androgenic Stimuli

8

Increased Sebum Production

Sebaceous gland hyperactivity

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

9

Composition of sebum

Free fatty acid
Lower concentration of linoleic acid

10

How does sebum induces follicular hyperkeratosis

Through IL-1 secreted by the sebocytes

11

Increased production of dead skin

Hyperkeratiniation

12

Follicular Epithelial Hyperproliferation

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

13

Sebum + dead skin

Microcomedone

-precursor of other acne lesions

14

Earliest microscopid manifestation (histologic inflammation)

Microcomedone

15

Follicular Epithelial Hyperproliferation is triggered by..

Androgen hormones

Alterations in follicular linoleic acid and IL-1

16

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

P. acnes

17

Three pathways in the production of Inflammation

Inciting of inflammatory by P. acnes

Rupture of follicular epithelium

Exces sebum production (linoleic acid deficiency)

18

Inciting of inflammation by P. acnes

innate immunity

TLR-2 (homologous to IL-1)

19

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

TOLL receptors

20

Rupture of Follicular epithelium

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

21

Causes infundibular rupture

EGF/TGF

-levels of EGF receptor decreases with age

22

Not clinically inflamed but histologic inflammation exists

Comedonal acne

23

Treatment to normalize follicular hyperkeratinization

Comedolytic/keratolytic agents

Topic retinoids
BPO
SA
AHA

24

Treatment to decrease sebum production

Sebostatic agents

Oral isotretenoin
OC pills
Anti-androgens

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)