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eczematous dermatoses > atopic dermatitis > Flashcards

atopic dermatitis Flashcards

1
Q

AD is more common in ____ (high/low) income areas possibly due to____

A
  • high income - urban environments (exposure to pollutants) and lack of exposure to infectious agents may trigger development of AD
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2
Q

Prevalence of AD in children? Adults?

A
  • 25% in children -3% adults
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3
Q

Early onset AD arises by ___ age

A

1-2 years old

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4
Q

___ % of AD resolves by 12 years of age

A

60% (remember the 60’s for AD)

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5
Q

Senile onset arises at ____ age

A

after 60 y/o

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6
Q

___% of AD occurs within the first year of life, and ___% by 5 y/o

A
  • 60% within first year - 90-95% by 5 y/o
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7
Q

What is the general pathogenesis of AD?

A

interplay between: - poor epidermal barrier - immune dysregulation - environment - genetics (if child has AD, high chance one or both of parents did)

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8
Q

Gene mutation associated with development of AD and severe early onset AD:

A
  • Filaggrin mutation, leads to barrier dysfunction, transepidermal water loss and xerosis, allowing penetration of allergens
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9
Q

Immunologic proteins and cytokines increased in AD include:

A
  • Th2>Th1 - IL-4, IL-5, IL-12, IL-13
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10
Q

Acute AD is ____ predominant state w/ eosinophilia and increased ____ production

A
  • Th2 - IgE - remember that pregnancy is Th2 state and this is why pregnant patients can get atopic eruption of pregnancy
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11
Q

Chronic atopic derm is a ____ predominant state with increased ____.

A
  • Th1 - IFN-gamma
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12
Q

Mediators of itch in AD are:

A
  • neuropeptides - proteases - kinins - histamines (less important)
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13
Q

Clinical criteria for AD are:

A
  • Essential: pruritis - plus >/= 3 of the following: - history of xerosis - personal history of allergic rhinitis or asthma - onset< 2 y/o - history of skin crease involvement (antecubital, popliteal, ankle, neck, periorbital) - visible flexural dermatitis
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14
Q

What will you see clinically in acute AD lesions?

A
  • erythema, edema, vesicles, oozing and crusting
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15
Q

What will you see clinically in subacute/chronic AD lesions?

A
  • lichenification, papules, nodules, and excoriations
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16
Q

Pediatric/infantile AD occurs from ___ to ___ age

A
  • birth to 6 months
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17
Q

Pediatric/infantile AD favors which body parts?

A
  • face, scalp, EXTENSOR surfaces
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18
Q

Childhood AD occurs from ___ to ____ age

A
  • 2 years to puberty
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19
Q

Childhood AD favors ____ areas of body

A
  • flexural (infantile favors extensors, face, scalp)
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20
Q

Diffuse xerosis in AD patients tends to become more prominent in which age group?

A
  • childhood (2 y/o to puberty)
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21
Q

Adolescent/Adult AD starts at age ____

A
  • 12
22
Q

clinical findings of adolescent/adult AD?

A
  • lichenified plaques > weeping eczematous lesions
23
Q

Adolescent/adult AD favors which body parts?

A
  • flexures, face, neck, upper arms, back and acral sites - adults tend to have more hand involvment
24
Q

AD beginning during childhood is associated with ___ (more/less) severe disease as adults

A
  • more severe, treatment-resistant disease
25
Q

Senile AD presents as:

A
  • marked xerosis rather than typical AD lesions
26
Q

Name the associated features of AD:

A
  • xerosis - ichthyosis vulgaris - Keratosis Pilaris - palmoplantar hyperlinearity - Dennie-Morgan lines (underneath eyelid from medial canthus) - allergic shiners - white dermatographism - diminished lateral eyebrows - circumoral pallor - anterior neck folds
27
Q

Children, especially those with darker skin types, have increased incidence of _____, which is more visible after ____

A
  • pityriasis alba - more visible after sun exposure
28
Q

Bacterial impetiginization is most often with ____ > _____

A
  • S. aureus > S. pyogenes
29
Q

Viral complications that can occur secondary to disrupted barrier in AD include:

A
  • eczema herpeticum (usually HSV1 or 2) - molluscum dermatitis - eczema vaccinatum (Seen with smallpox vaccination)
30
Q

Ocular complications of AD are:

A
  • atopic keratoconjunctivitis - vernal keratoconjunctivitis (children in warmer climates) - posterior subcapsular cataracts - keratoconus (elongation of cornea) - retinal detachment
31
Q

_____ occurs in spring/summer in boys on elbows/knees and appears as clusters of small 1-2mm lichenoid papules

A
  • frictional lichenoid eruption (regional variant of AD)
32
Q

Dyshidrotic eczema occurs on _____ parts of body and is described clinically as____

A
  • lateral fingers and palms - “tapioca-like” firm and deep-seated pruritic vesicles
33
Q

Histopath of acute AD:

A
  • prominent spongiosis!! - intraepidermal vesicles/bullae - perivascular lymphohistiocytic inflammation with eosinophils
34
Q

Histopath of subacute AD

A
  • milder spongiosis vs acute. - increased acanthosis!! - lacks vesicles/bullae of acute AD
35
Q

Histopath of chronic AD

A
  • marked irregular to psoriasiform acanthosis!! (Key feature - minimal to no spongiosis - +/- dermal fibrosis and hyperkeratosis
36
Q

In some patients, identifications of allergens using which tests can be of use?

A
  • Fluorescence enzyme immunoassays - RAST testing - Skin prick testing - atopy patch testing
37
Q

When can you consider testing for food allergies for AD?

A
  • severe/refractory AD, or if worsening dermatitis after an ingestion
38
Q

What percent of AD patients have coexisting food allergy?

A
  • 10-15%
39
Q

Common exacerbating factors of AD:

A

FADS - fragrances, fabrics, food allergies -other Allergens (pet dander, dust mites) - Dry environments, Detergents - Smoking, Sweating, Showers to hot, too long, too often, stress

40
Q

60% rule for AD:

A
  • 60% have onset within first year of life, 60% resolve by age 12.
41
Q

3 clinical features critical for diagnosis of AD:

A
  1. Pruritis 2. chronic relapsing and remitting course 3. eczematous rash
42
Q

RAST testing detects:

A
  • antigen specific IgE in blood
43
Q

Skin prick/patch testing works by:

A
  • detecting allergen specific IgE that activates mast cells and leaves pt with contact dermatitis or wheal.
44
Q

What is general trend on histopathology as you move from acute to chronic AD?

A
  • acute has more spongiosis, less acanthosis - the more chronic, the less spongiosis and more acanthosis you will get.
45
Q

How to educate for AD patients?

A
  • use emollients - short lukewarm baths with minimal soap - can do bleach baths (especially if history of infections) - wet dressings +/- topical steroids - avoid irritants (And common FADS triggers)
46
Q

Mainstay of tx for AD is:

A
  • topical corticosteroids
47
Q

Child is having itch and it is keeping him up at night, what medication can you add

A
  • sedative antihistamine
48
Q

treatment ladder for AD

A

topicals (steroids, calcineruin inhibitors), light therapy , systemic meds (systemic corticosteroids, cyclosporine, azathioprine, MMF, MTX)

49
Q

Primary prevention of AD is via ____ after birth

A

Breast feeding or formulas w/ hydrolyzed milk products for first 4-6 months

50
Q

What other supplementation can be used prenatally and postnatally to reduce risk of atopic dermatitis?

A
  • probiotics
51
Q

Prognosis of AD:

A

Tends to clear by puberty in most children - 60% cleared by age 12

eczematous dermatoses (8 decks)

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