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Dermatology Board Prep > DERM (02) Eczematous Disease > Atopic Dermatitis > Flashcards

Atopic Dermatitis Flashcards

1
Q

What is it called when you have superinfected (with HSV) AD diffusely?

A

Kaposi’s varicelliform eruption/Eczema herpeticum

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2
Q

Dx criteria for AD?

A

Pruritus essential!

  • History of xerosis personal hx of allergic rhinitis or asthma
  • Onset <2yo
  • History of skin crease involvement
  • Visible flexural dermatitis
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3
Q

Subsets of AD?

A

Early-onset (MC), Late-onset, and Senile-onset

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4
Q

What type of response (TH1 or Th2) is involved in AD?

A

Acute = Th2

Chronic = Th1, Th17, Th22 responses

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5
Q

What IL’s are involved in acute AD?

A

IL-4, IL-5, IL-13, IL-31, IgE

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6
Q

Strongest risk factor for AD?

A

A parent with AD

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7
Q

Which protein is known as the “master-switch of allergic inflammation”

A

Thymic stromal lymphopoinetan

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8
Q

What happens with cutaneous antimicrobial peptides?

A

They are decreased

This is one reason why pts with AD tend to get super infections of their lesions

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9
Q

4 stages of AD (By ages)?

A

infantile *2mos-2yrs childhood AD, 2 to 12 yrs Adolescent/adult AD Senile >60

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10
Q

Areas that infantile AD tends to favor?

A

Face, scalp, and extensor surfaces

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11
Q

Prominent areas of adolescent/adult AD?

A

Flexures, face, neck, retorauricular, upper arms, back and aural sites

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12
Q

What type of cataract is related to AD

A

Anterior subcapsular cataracts are more classically associated w/ AD but the posterior subcapsular cataracts are more common within this population in general (just are as specific)

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13
Q

Causes of lip chelitis?

A

lip-lickers eczema > allergic contact >AD

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14
Q

What is the HAPPY ddx eosinophilic spongiosis?

A

H: Herpes gestationis

A: Arthropod, allergic contact, AD

P: Pemphigus

P: Pemphigoid

I: Incontinea pigmentosa

E: Erythema toxicum neonatorum

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15
Q

Most common s/e of dupilumab?

A

Conjunctivitis

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16
Q

Targets of dupilumab?

A

IL-4 and IL-13 receptors

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17
Q

What are the essential features for AD diagnosis?

A

Pruritus, typical eczematous morphology and age-specific distribution patterns, chronic or relapsing course.

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18
Q

What are the typical distributions for AD?

A

Spares the groin and axillae face, neck and extensor extremities in infants and young children flexural lesions at any age

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19
Q

When is the pruritus often worst for patients with AD?

A

Nightime

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20
Q

Prevalence of AD in kids vs adults?

A

Kids=~25%

Adults = 3%

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21
Q

What are the 3 subsets of AD by onset time and the epidemiology of these?

A

Early-onset (m/c) : 1-2 y/o, 50% have allergen-specific IgE antibodies, 60% resolve by 12 years of age. 50-60% have onset in the first year of life, 90-95% by 5 years of age.

Late-onset: Arises after puberty

Senile onset: Arises after 60 y/o

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22
Q

3 general components of AD pathogenesis?

A

Epidermal barrier dysfunction, immune dysregulation, and alteration of the microbiome.

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23
Q

Which is the strongest risk factor (family history) for AD between: history of AD, History of asthma, or history of allergic rhinitis?

A

Parental history of AD

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24
Q

How is transepidermal water loss effected in AD?

A

Defective epidermal permeability barrier is a consistent feature of AD and is evident in nonlesional and lesional skin.

**The level of transepidermal water loss in the nonlesional skin of children with AD correlates with disease severity.

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25
Q

What mutation is associated with AD development, especially severe early-onset AD?

A

Genes encoding epidermal proteins filaggrin (FLG) and SPINK

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26
Q

Mutations in the FLG gene/protein is also responsible for which disease?

A

Icthyosis Vulgaris

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27
Q

Which cytokines are heavily involved in AD?

A

IL-4, IL-5, IL-12, and IL-13

28
Q

What cytokines are important in the acute phase of AD?

A

IL-4, IL-5 and IL-13 (Th2 based cascade)

29
Q

Which keratinocyte-derived cytokines are involved in promoting the Th2 response?

A

IL-1, thymic stromal lymphopoietin (TSLP), IL-25, IL-17E, and IL-33

30
Q

What cytokine is the “master switch of allergic inflammation?”

A

TSLP (thymic stromal lymphopoietin). This is highly expressed in acute and chronic lesions.

31
Q

Which cytokine is key in driving Th2 cell differentiation and IgE production and eosinophil recruitment?

A

IL-4! Of note, the heterodimeric receptors for IL-4 and IL-13 both contain the IL-4 receptor a subunit (IL-4Ra) and activates signal tranducer and activator of transcription 6 (STAT6). This promotes differentiation of naive t cells into Th2 effector cells.

32
Q

What two cytokines are blocked by dupilumab?

A

IL-4/IL-13. It targets both because it targets the IL-4Ra which is downstream from both cytokines and is what leads to activation of STAT6

33
Q

What immune Th response is predominant in chronic AD?

A

Th1 response predominates w/ increased levels of IFN-gamma

34
Q

What bacteria is increased in those with AD usually?

A

Staph Aureus, 90% of AD patients have skin colonized with S. Aureus, whereas only 5% of unaffected patients do.

35
Q

How do levels of S. Aureus relate to AD disease activity?

A

The proportion of the microbiome that is S. Aureus increases from ~35% to ~90%

36
Q

What age is considered more the childhood time when AD goes more to the flexural surfaces?

A

2 years old

37
Q

What do we call the hypopigmentation seen on the face/neck that can occur in kids with AD?

A

Pityriasis alba

38
Q

In what skin type is pityriasis alba more common?

A

Darker skin types

39
Q

What are Dennie-morgan lines?

A

These are accentuations of the lines under the lower eyelid

40
Q

What are some other associated features/conditions seen in AD?

A

Xerosis, ichthyosis vulgaris, keratosis pilaris, palmoplantar hyperlinearity

41
Q

What is it called when you see diminished lateral eyebrows in the setting of AD?

A

Hertoghe sign

42
Q

What pattern of cataracts are seen in AD?

A

Posterior subcapsular cataracts occur most commonly, subcapsular anterior cataracts are more specific for AD

43
Q

What is the condition that is often shown with a young boy showing bumps located on the elbows in the summer?

A

Frictional lichenoid eruption: occurs during spring and summer in boys on elbows (mc)/knees/dorsal hands

44
Q

What is Id reaction?

A

Autosensitization, a classic example is a vesicular eczematous reaction of the hands arising in a pt w/ tinea pedis.

45
Q

What is Juvenile plantar dermatosis?

A

Repetitive frictional movements, as the foot moves up and down in a shoe

The occlusive effect of covered footwear, especially synthetic shoes (eg, nylon or vinyl)

Excessive sweating (hyperhidrosis), which when followed by rapid drying leads to cracking and fissuring

Genetic sensitivity of the skin

Climatic changes: with worsening during the summer months due to heat and sweating, and in colder months due to the wearing of winter boots.

What are the clinical features of juvenile plantar dermatosis?

Juvenile plantar dermatosis presents with shiny, red and dry skin on the weight-bearing areas of the sole of the feet.

It usually affects both feet symmetrically.

Painful fissures, cracking and scaling occur when juvenile plantar dermatosis is longstanding.

Common sites are the plantar aspect of the great toe, forefoot and heel; toe-webs and instep are often spared.

It can rarely affect the palms and fingertips.

46
Q

What treatment is first-line for AD in infants?

A

Low-potency steroid ointments, such as hydrocortisone 1% or 2.5% are preferred.

47
Q

Which calcineurin inhibitor (topical) is more effective for AD?

A

Tacrolimus (protoic) is more effective than pimecrolimus

48
Q

What steroid is tacrolimus equivalent to?

A

Triamcinolone acetonide 0.1%

49
Q

What steroid cream is pimecrolimus (Elidel) equivalent to?

A

Class V or VI topical steroid.

50
Q

What is the mechanism of crisaborole ointment?

A

This is brand name Eucrisa, is a PDE-4 inhibitor that is for mild to moderate AD in patients >2 years of age.

51
Q

What is the most common type of phototherapy used to treat AD?

A

Narrowband UVB

52
Q

Dosing of dupilumab?

A

600mg initially SubQ then 300mg every other week after that.

53
Q

What is the most common subtype of atopic dermatitis?

A

Early onset

  • This arises by 1-2 years of age
  • 50% have allergen-specific IgE antibodies and 60% resolve by 12 years of age
54
Q

What are the main mediators of itch in AD?

A

Histamines less important than neuropeptides, proteases, kinins, and certain cytokines

Anti-histamines don’t often work well

55
Q

What are important triggers of pruritus in AD?

A

Avoid wool clothing, sweat and stress

56
Q

What viral complications can occur in AD?

A

Eczema herpeticum, molluscum dermatitis, and eczema vaccinatum (seen w/ smallpox vaccination)

57
Q

Should IgE testing be routinely performed in AD?

A

No!

Level I evidence showing no benefit to this

58
Q

When should food allergy be considered in patients w/ AD?

A

In severe/refractory AD w/ a reliable hx of immediate reaction or worsening after ingestion of certain foods

59
Q

What type of allergic reaction is food usually associated with?

A

This is the most common cause of type I immediate hypersensitivity reaction

60
Q

What percentage of pediatric/children pts w/ AD have coexistent food allergies?

A

10-15%

61
Q

What should be tested in teens/adults w/ severe or refractory AD on exposed skin surfaces?

A

Aeroallergens (dust mites, pollen, animal dander, and fungi)

Incidence of airborne allergy increases with age

62
Q

What type of AD does dupilumab address?

A

The acute phase!!

It alters the Th2 response. The chronic phase is largely Th1 and thus you need to use other treatments (topical steroids, TCI, etc) to address the long term (lichenification, psoriasiform lesions, etc) sequelae

63
Q

What is the general therapeutic ladder in AD?

A

Topicals (steroids/TCI) –> light therapy –> Systemic medications

64
Q

How should low and mid/high potency steroids be used in AD?

A

Mid/high potency –> flares

Low potency –> maintence

65
Q

The general prognosis of AD?

A

75% resolve by adolescence is the classic teaching

  • Newer studies may suggest that only 50% remit by early adulthood however
  • If AD does persist to adulthood then it is more likely to be chronic

DERM (02) Eczematous Disease (6 decks)

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