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Endocrine > Acne Vulgaris > Flashcards

Acne Vulgaris Flashcards

1
Q

What is acne vulgaris?

A

Common disorder of the pilosebaceous unit primarily seen in adolescents.

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2
Q

What is the most notable factor that affects acne?

A

Testosterone

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3
Q

What are the lamellar granules?

A

Oil synthesizing cells that form protective layer to protect against infection

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4
Q

What do melanocytes do?

A

Form pigment

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5
Q

What are merkel cells?

A

Sensory cells that respond to touch; connected to sensory neuron

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6
Q

What does the epidermis extend into?

A

Hair follicle

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7
Q

Within what unit does acne occur?

A

Pilosebaceous unit

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8
Q

What are the four key elements of pathogenesis in acne vulgaris?

A
  1. Follicular epidermal hyperproliferation
  2. Sebum production
  3. Presence and activity of Propionibacterium acnes/Cutibacterium acnes
  4. Inflammation and immune response
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9
Q

What are the clinical features of acne?

A
  • Comedones (clogged pores)
  • Papules
  • Pustules
  • Nodules on face, chest, and back
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10
Q

What type of comedome is a blackhead?

A

Open

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11
Q

What type of comedome is a whitehead?

A

Closed

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12
Q

What is important to know about pustules?

A

Infection involved

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13
Q

What is important to know about cysts?

A

Bacterial growth and tissue erosion

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14
Q

Name the steps of progression to a pimple

A
  1. Microcomedone
  2. Comedone
  3. Inflammatory papule or pustule
  4. Nodule
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15
Q

What are noteworthy features about the microcomedone?

A
  • Hyperkeratotic infundibulum (by the opening)
  • Sebum secretion
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16
Q

What are noteworthy features about the comedone?

A
  • Accumulation of shed corneocytes and sebum
  • Dilation of follicular ostium
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17
Q

What are noteworthy features about the inflammatory papule or pustule?

A
  • Further expansion of follicular unit
  • Proliferation of Propionibacterium acnes
  • Perifollicular inflammation
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18
Q

What are noteworthy features about the nodule?

A
  • Rupture of follicular wall
  • Marked perifollicular inflammation
  • Scarring caused by erosion of tissue
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19
Q

What is something that regulates follicular keratinocyte proliferation?

A

Linoleic acid (essential fatty acid in the skin) - low levels can induce follicular keratinocyte hyperproliferation and the production of proinflammatory cytokines

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20
Q

Are linoleic acid levels decreased, increased, or normal in patients with acne?

A

Decreased

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21
Q

When do linoleic acid levels normalize in patients with acne?

A

After successful treatment with isotretinoin (vitamin A derivative, linoleic acid)

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22
Q

What hormones are significant promotors of cell proliferation, hyperkeratinization, sebum, and acne?

A

Androgens (testosterone and DHEA)

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23
Q

What does DHEA stand for?

A

Dehydroepiandrosterone

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24
Q

What stimulates the ovary to make androstenedione (which can then be made into testosterone or estrogen)?

A

FSH and LH

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25
Q

What stimulates the adrenal gland (which can eventually make testosterone or DHEA)?

A

ACTH

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26
Q

What are the pharmacologic mechanisms for acne treatment?

A
  • Reduce inflammation
  • Reduce cell proliferation/cohesion (sticks to itself)/keratinization
  • Reduce sebum production
  • Reduce bacterial population
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27
Q

What type of agent is benzoyl peroxide?

A

Topical

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28
Q

What does benzoyl peroxide do?

A
  • Generates reactive oxygen species, which bombards bacteria with electrons and can be bacteriocidal (unpaired electron is bacteriocidal!)
    *Dissolves keratin, opens pores, and allows sebum to drain
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29
Q

How is benzoyl peroxide used?

A

Used in combination with antibiotics and with adapalene (retinoid - this is the only retinoid it can be used with)

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30
Q

What is an alternative use for benzoyl peroxide?

A

BPO is a bleach! Can be used as a teeth whitener

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31
Q

What is azelaic acid?

A

Dicarboxylic acid (produced by plants following a wound); white powder component of a cream

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32
Q

What does azelaic acid treat?

A
  • Acne
  • Rosacea
  • Skin spots
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33
Q

What is the MOA of azelaic acid?

A

Unknown! What we do know:
* Antibacterial activity, maybe by inhibiting protein synthesis
* Inhibits keratin synthesis
* Inhibits tyrosinase enzyme necessary for skin pigment
* Inhibits a hyperactive protease activity that converts cathelicidin into antimicrobial skin peptide LL-37

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34
Q

What is salicylic acid’s MOA?

A

Inhibits cyclooxygenase-1 (COX-1); plant derivative

35
Q

What does salicylic acid do?

A

Facilitates the sloughing of skin cells which helps open pores

36
Q

Which drugs are considered retinoids?

A
  • Tretinoin
  • Isotretinoin
  • Adapalene
  • Tazarotene (Avage)
  • Trifarotene (Aklief)
37
Q

Which retinoid is also known as a “all-trans retinoic acid” (atra)?

A

Tretinoin (1st gen product)

38
Q

Which retinoid is a 13-cis retinoic acid?

A

Isotretinoin (1st gen, carbon in different position)

39
Q

Which retinoids are 3rd generation?

A

Adapalene and tazarotene

40
Q

Which retinoid is tolerant to benzoyl peroxide?

A

Adapalene (can be used in combination with benzoyl peroxide!)

41
Q

Which retinoid is 4th generation?

A

Trifarotene

42
Q

What does further generations of retinoids mean?

A

Later in generations = more specific more retinoid receptors that are for acne

43
Q

Several signal transduction pathways converge on what?

44
Q

What does CBP p300 lead to?

A

Alterations in gene expression (which ones are changed depends on the cell)

45
Q

Which group is retinoic acid a part of?

A

Group I Hormones -> retinoic acid -> nuclear receptors -> CBP p300 -> alterations in gene expression

46
Q

What does a canonical retinoic acid receptor (RAR) signaling mean?

47
Q

What does a non-canonical retinoic acid receptor (RAR) signaling mean?

A

Not so ordinary

48
Q

What can RARs combine and form a dimer with?

A

Retinoic X receptor

49
Q

As dimers, what can RAR/RXR do?

A

Regulate retinoic acid response elements (RARE), which activate the transcription of certain genes depending on the subtypes

50
Q

What are the three subtypes of RARs?

A

Alpha, beta, and gamma (they are no uniformly spread across each cell type)

51
Q

What are the desired targets in treating acne?

A

RAR-gamma receptors (these are the RAR subtypes predominant in skin cells)

52
Q

What are the effects of retinoids?

A
  • Decrease cell differentiation and proliferation
  • Decrease sebum production
  • Result in dry, scaly skin, redness, and irritation
  • Other side effects if taken orally
53
Q

What acne drug class is contraindicated in pregnancy?

A

Retinoids - teratogenic! Interfere with fetal organ development, and must sign iPledge program

54
Q

What is the oral form of isotretinoin approved for?

A

Treatment of recalcitrant and nodular ance vulgaris

55
Q

How is the efficacy of isotretinoin’s oral form?

A

Remarkable efficacy in severe acne and may induce prolonged remissions after a single course of therapy

56
Q

When are clinical effects generally noted with isotretinoin?

A

1-3 months after starting therapy

57
Q

How many patients relapse with isotretinoin?

A

One third of patients, typically within 3 years of stopping therapy

58
Q

What are some toxic systemic side effects of isotretinoin?

A
  • Altered plasma lipids
  • Liver damage
  • Premature closure of epiphyseal plate = short stature and other bone abnormalities
59
Q

What are some common side effects of isotretinoin?

A
  • Dry skin
  • Dry eye
  • Nose bleed
  • Muscle pain
  • Reduced visual accuity
60
Q

What are some characteristics of tretinoin?

A
  • Topical retinoid
  • Legacy product (used to use, not really anymore, cheap)
  • Not photo-stable, so must be used at night!
  • Not stable with BPO (new formulation is being with BPO is being worked on)
61
Q

What concentration of adalapene is OTC?

62
Q

What concentration of adalapene is with BPO?

63
Q

What is adalapene considered?

A

“Workhorse”

64
Q

How efficacious is tazarotene topical?

A

Potent and efficacious compared to tretinoin, but not as well tolerated at the usual dose

65
Q

What is something significant about trifarotene?

A

4th generation = high specificity for the RAR-gamma receptor, which is found predominantly in the skin cells. Therefore, very low concentration is used (0.005%)

66
Q

Which oral tetracyclines can be used to treat acne?

A

Minocycline, doxycycline, and sarecycline (Seysara)

67
Q

Which oral tetracycline is approved in ages 9 and older?

A

Sarecycline (Seysara)

68
Q

What form of erythromycin and clindamycin can be used to treat acne?

A

Cream with BPO

69
Q

What is erythromycin and clindamycin’s MOA?

A

Attaches to ribosome and prevents it from moving (translocation); protein synthesis inhibitor, used less due to resistance

70
Q

What form of sulfacetamide-sulfur can be used to treat acne?

71
Q

What is sulfacetamide-sulfur’s MOA?

A

Inhibits dihydropteroate synthase

72
Q

What form of Bactrim can be used to treat acne?

73
Q

What form of dapsone can be used to treat acne?

74
Q

What is dapsone’s MOA?

A

Inhibits dihydropteroate synthase; PABA agonist = same MOA as sulfa drugs

75
Q

What form of minocycline (Amzeeq) can be used for acne?

76
Q

How can birth control pills help control acne?

A

Reduce androgen production

77
Q

What is flutamide’s MOA?

A

Blocks testosterone receptors (primary use is in prostate cancer)

78
Q

What does flutamide have a boxed warning for?

A

Liver damage

79
Q

What is spironolactone’s MOA?

A

K-sparing diuretic, also blocks androgen receptors

80
Q

What is clascoterone (Winlevi)’s MOA?

A

Blocks testosterone receptors

81
Q

Why are flutamide and spironolactone not used in men?

A

Inhibits secondary sexual characteristics

82
Q

Is clascoterone (Winlevi) ok for males?

83
Q

What form does clascoterone (Winlevi) come in?

Endocrine (4 decks)

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