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Dermatology Board Prep > DERM (05) Diseases of Cutaneous Adnexa > Acne > Flashcards

Acne Flashcards

1
Q

4 main players in acne pathogenesis?

A

Abnormal follicular keratinization, inflammation, bacteria and hormones

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2
Q

Key difference between acneiform reactions and acne?

A

You have to see comedones in acne

If you do see comedones it doesn’t necessarily mean it has to be acne, but you can’t have acne w/o comedones

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3
Q

What deficiency can cause increased comedone formation?

A

linoleic acid –>increases follicular plug

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4
Q

How does bacteria affect acne?

A

Cutibacterium are gram + rods that produce lipases and coproporphyrin III and these cleave sebum –> FFA –> FFA binds TLR-2 –> increases inflamation and is chemotactic. -key is that FFA is both comedogenic and chemotactic

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5
Q

What is acne fulminans associated with (drug)

A

Anabolic steroids

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6
Q

What is acne fulminans?

A

severe form of nodulocystic acne –> m/c in young males. p/w sudden-onset suppurative nodular acne, systemic symptoms (myalgia, arthralgias, fever, elevated ESR, leukocytosis, sterile osteolytic bone lesions over clavicle and sternum, can be a complication of aggressive isotretinoin therapy.

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7
Q

Tx for acne fulminans

A

Low dose isotretinoin and prednisone or prednisone alone at first and then isotretinoin

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8
Q

What ovarian androgen can contribute to acne?

A

Testosterone

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9
Q

What adrenal androgens are a/w acne?

A

DHEA-S, 17-OH-progesterone

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10
Q

When should you check hormone labs in women if isotretinoin fails?

A

First 7 days of the menstrual cycle (Make sure they are not on OCP’s!)

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11
Q

What sx’s are seen with PCOS?

A

Alopecia, hirsutism, irregular menses, increased LH/FSH ratio, and testosterone

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12
Q

What is the morphology of acne in PCOS

A

Nodular around the jawline.

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13
Q

What TLR is affected by retinoids?

A

TLR-2

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14
Q

What does combining isotretinoin and tetracyclines increase the risk of?

A

pseudotumor cerebri

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15
Q

Can you use tretinoin and benzoyl peroxide together?

A

No the BPO inactivates the tretinoin, you can use adapelene.

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16
Q

What cytokines are increased in acne that drive the inflammation

A

IL-1, IL-8 (neutrophil attractant), TNF-a via TLR-2 activation. TLR-2 expressed on innate immune cells and keratinocytes

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17
Q

What effect does cutibacterium have on acne pathogenesis?

A

Gram-positive anaerobic rod –> produce lipases and coproporphyrin III –> cleave sebum –>FFA- FFA binds TLR-2 and increases ii- FFA is both comedogenic and chemotactic

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18
Q

What effect/s do hormones have on acne pathogenesis?

A
  • Increased sebum production 2/2 androgen
  • Growth of sebaceous gland
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19
Q

What is the presentation of acne conglobata and associated syndrome?

A

Similar to fulminans (abrupt onset, erosive, severe nodulocystic acne) but no systemic sxs - a/w follicular occlusion tetrad (dissecting cellulitis of scalp, HS, acne conglobata, pilonidal cyst)

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20
Q

What are the associated inflammatory syndromes with acne conglobata?

A

PAPA (pyogenic arthritis, pyoderma gangrenosum, Acne conglobata) - PAPASH (PAPA +HS + Acne conglobata) - SAPHO (synovitis, pustulosis, hyperostosis, osteitis)

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21
Q

What is solid facial edema variant of acne?

A

This is a synonym for Morbihan disease

  • P/w woody nonscaling edema of mid-face and cheeks
  • Tx is isotretinoin for up to 24 months
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22
Q

Presentation of neonatal acne?

A

P/w papulopustules NOT comedones (not true acne) during the first 2 weeks of life, resolves by 3 months

  • 2/2 yeast (M. furfur)
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23
Q

What is infantile acne?

A

Prominent comedones (true acne) with risk of pitting and scaring

  • 3-6 months of age
  • Resolves within 1-2 years and may require topical retinoids and BPO
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24
Q

Presentation of acneiform drug eruption?

A

No comedones

  • Monomorphous follicular papules and pustules
  • A/w corticosteroids, phenytoin, lithium, isoniazid, iodidies, EGFR-i (cetuximab, erlotinib, gefitinib)
25
Q

Presentation of acne and endocrine abnormalities?

A

check for signs of hirsutism, androgenic alopecia, irregular menses, hormonal abnormalities (LH, FSH, DHEA-S, free and total testosterone.

26
Q

what effect does estrogen have on sebum?

A

It decreases sebum production –> xerosis cutis

  • This is a problem for transgender women taking estrogen
27
Q

How do OCP’s improve hormone acne?

A

OCP increases sex-hormone-binding globulin –> decreased free testosterone

  • Decrease release of testosterone from the ovaries
28
Q

Most common triggers of industrial acne?

A

M/c from exposure to halogenated hydrocarbons and benzenes (chlorinate dioxins, dibenzofurans, insoluble cutting oils)

29
Q

What other facial findings is industrial acne a/w?

A

Facial hypertirchosis, milia/bullae on dorsal hands

30
Q

What is the clinical presentation of industrial acne?

A

Comedones, pustules, and cysts over malar cheeks, retroauricular region and scrotum, also appears over the retroauricular area

  • The retroauricular area can be important if you are differentiating between PCT (from milia/findings on dorsal hands/face) and industrial acne. This area is photoprotected thus should not be involved in PCT
31
Q

What is one important exam finding of inflammation in inflammatory acne?

A

PIH

This can be especially prominent in darker skin types

32
Q

Treatments for acne?

A

There should be a step ladder approach

  1. Things that can be used in any acne other than when you are using isotretinoin = Topical retinoid, BP, topical clindamycin, sulfur agents, azelaic acid
    - Just comedonal –> Topicals (retinoid, BP, sulfur agents, clindamycin (always use w/ BP!)
    - Inflammatory –> use the ones above, but for moderate and above you can add antibiotics, spironolactone (in women)
    - Inflammatory severe –> isotretinoin
33
Q

What effect do retinoids have on keratinocytes and immune cells?

A

Reduces TLR-2 expression on keratinocytes and innate immune cells

  • Comedolytic
34
Q

Why do you not want to combine isotretinoin and tetracyclines?

A

Pseudotumor cerebri

35
Q

What medication is safe for comedonal acne during pregnancy?

A

Azelaic acid

  • BPO is category C
36
Q

What skin structures have androgen receptors and how does this play into acne pathophysiology?

A
  1. Androgen receptors are on the basal layer of the sebaceous glands and outer root sheath of the hair follicle
  2. Increased androgens (DHT and testosterone) lead to growth of sebaceous glands and increased sebum production
37
Q

When are androgens elevated for acne?

A

Puberty and also the first 6 months to 1 year in infancy (not from mom)

38
Q

What type of bacteria is the C. acnes?

A

Gram + anaerobic/microaerophilic rod

39
Q

What color does C. acnes glow under woods lamp?

40
Q

How is C. acnes involved in the pathophysiology of acne?

A

Produces lipases that break down triglycerides to free fatty acids. These are pro-inflammatory and help induce comedones

  • Activates TLR-2 on macrophages –> IL-1, IL-8, IL-12, and TNF-alpha

These attract neutrophils

41
Q

What is the product of C. acnes that makes it glow orange under the woods lamp?

A

Coproporphyrin III

42
Q

What is the difference between a pustule/cyst in acne and a closed comedones?

A

Comedones are non-inflammatory lesions, whereas the pustules/cysts in acne are inflammatory in nature

43
Q

What is the progression of lesions (least–>most severe) in acne?

A

Starts w/ closed/open comedones –> inflammatory lesions papules, pustules –> Nodules/cysts –> plaques and sinus tracts

44
Q

When does acne tend to flair in regards to menstruation?

A

The week prior to menstruation

45
Q

In what population does spironolactone have a black box warning?

A

Women w/ breast cancer (this is called into question/safety is affirmed in newer studies)

46
Q

What drugs are a/w acneiform drug reaction?

A

Corticosteroids, phenytoin, lithium, isoniazid, iodides, EGFR-i (cetuximab, erlotinib, gefitinib)

47
Q

What is the morphology of acne fulminans?

A

Suppurative nodules and plaques

  • Lesions are friable and it leads to hemorrhagic crust –> ulcerates and can have eschar –>scarring
48
Q

What locations are more commonly seen in acne conglobata?

A

Usually more severe on the trunk, usually less severe on the face

49
Q

What is the history of solid facial edema in acne?

A

Usually occurs after 2-5 years of having acne

50
Q

In what population does acne excoriée occur in?

A

Often young women

  • Can be a/w underlying depression or anxiety disorder, OCD, body dysmorphic disorder or other psychiatric conditions, prudent to screen (regardless of sex)
51
Q

What is acne excoriée?

A

Self-induced excoriation of existing acne lesions –> look for mild acne w/ excoriated crusted erosions

52
Q

What are the common sites of neonatal acne?

A

Nasal bridge and cheeks are the most common

  • Can also occur on the face/head/neck
  • More common to have inflammatory pustules than comedones
53
Q

What would be the underlying cause of severe pustular eruption on the face in a neonate with trisomy 21?

A

Leukemoid reaction

54
Q

When should further workup be initiated in infantile acne?

A

If there are signs of pubertal development (pubarche, thelarche, etc)

  • Get DHEAS, androstenedione, 17-OH-progesterone, and bone age
55
Q

What chemicals predispose to acne cosmetica?

A

Frequent/heavy use of products containing: lanolin, petrolatum, vegetable oils, butyl stearate, isopropyl myristate, sodium lauryl sulfate, lauryl alcohol, or oleic acid

56
Q

What is the morphology of acne cosmetica?

A

Small closed comedones, small papules, and pustules

57
Q

What is Apert Syndrome?

A

Acrocephalosyndactyly

  • AD mutation in fibroblast growth factor receptor 2 (FGFR2) –> increased FGFR2 signally

This causes follicular hyperkeratosis and sebaceous gland hypertrophy so these pts have diffuse moderate to severe acne

58
Q

What areas of acne involvement are seen in Apert Syndrome

A

Moderate to severe acne on the extensor arms, buttocks and thighs

  • Also see nail dystrophy and cutaneous/ocular hypopigmentation

DERM (05) Diseases of Cutaneous Adnexa (5 decks)

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