Atopic Dermatitis Flashcards

1
Q

What is associated with more severe atopic dermatitis

A

Older children, eldest child in family, Hispanic/African American background

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2
Q

Genetic mutations associated with AD

A

Loss of function mutation in Profilaggrin (10-30% of patients)

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3
Q

Three main components behind pathogenesis of AD

A
  1. Immune dysregulation
  2. epidermal barrier dysfunction
  3. environmental interactions with skin
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4
Q

What contributes to increased amount of superinfections

A

Th2 cells activated to express IL4, 5, and 13 which promote eosinophilia and IgE production but also suppress antimicrobial peptides such as Beta-defensins and cathelicidin

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5
Q

What is presumed to mediate pruritus in AD

A

TSLP (thymic stromal lymphopoeitin) and IL31

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6
Q

Clinical criteria for AD

A
  1. Must have pruritus
  2. Must have 3 of the following
    - hx of dry skin in past year
    - personal hx of allergic rhinitis/asthma or in first degree relative if <4yo
    - Onset before 2yo
    - Hx of skin crease involvement
    - visible flexural dermatitis
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7
Q

Role of ceramides

A

Long chain lipids that are decreased in AD (likely contribute to defective epidermal barrier)

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8
Q

Infantile AD

A

Age 0-6mo and usually on cheeks/forehead/scalp before possibly involving extensor surfaces around 8 mo as they begin to crawl

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9
Q

Childhood AD

A

From 2yo to puberty, usually less exzematous and more lichenified that in infantile form
- facial involvement changes from cheeks/chin to perioral

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10
Q

Adult AD

A

prurigo nodularis commonly seen in adolescence

- dorsal hands and feet commonly affected

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11
Q

Associated clinical signs

A
  • white/regular dermatographism
  • keratosis pilaris
  • Lichen spinulosus (round collections of tiny flat-topped papules more common in AA children)
  • atopic pleat (Dennie-Morgan fold)
  • allergic shiners
  • allergic salute
  • hyperlinear palms
  • Allergic keratoconjunctivitis (requires optho)
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12
Q

Bacterial Superinfections

A

MCC: Staph Aureus (MSSA)

- others include Strep pyogenes (classically see more facial/periorbital involvement, fever, cellulitus, +/- bacteremia)

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13
Q

Non-bacterial superinfections

A
  • Molluscum
  • Eczema herpeticum (punched out erosions and umbilicated vesicles)
  • Eczema vaccinatum (after contact with person recently vaccinated against smallpox)
  • Eczema coxsackium
  • Malassezia (particularly suspect in adolescents with recalcitrant AD in head and neck region)
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14
Q

DDx for Ad

A
  • Seborrheic dermatitis
  • Irritant/allergic contact dermatitis
  • nummular dermatitis
  • psoriasis
  • Scabies
  • Langerhans cell histiocytosis
  • Acrodermatitis enteropathica
  • Scabies
  • IPEX syndrome
  • Wiskott-Aldrich (WAITER aka immunodeficiency, thrombocytopenia, eczema, recurrent pyogenic infections)
  • Hyperimmunoglobulinemia E
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15
Q

Management of mild AD

A

bathing and barrier repair
Avoidance of irritating/allergic triggers
Intermittent short term Class VI or VII topical steroids +/- calcineurin inhibitors
Treat superinfection

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16
Q

Management of moderate AD

A

bathing and barrier repair
Avoidance of irritating/allergic triggers
Intermittent short term Class III to V topical steroids +/- calcineurin inhibitors
Treat superinfection
Oral antihistamines

17
Q

Management of severe AD

A

bathing and barrier repair
Avoidance of irritating/allergic triggers
Intermittent short term Class III or V topical steroids +/- tacrolimus
Treat superinfection
Consider systemic anti-inflammatory agents, UV tx

18
Q

When to food allergy test in AD

A

Test to milk/peanuts/soy/eggs/wheat if kids <5 with moderate to severe AD who wither 1) do not respond to maximum topical therapy or 2) have reliable history of flair just after ingesting certain foods

19
Q

Age cut-off for Class I steroids

A

Typically not given in children <12yo

20
Q

What to warn parents about with topical calcineurin inhibitors

A

Burning/pruritus on application

Practice food sun protection

21
Q

Equivalency of topical calcineurin inhibitors to topical steroids

A

Tacrolimus 0.1% ointment comparable to mid-strength steroid. Tacrolimus 0.03% and Pomecrolimus comparable to low potency steroids

22
Q

MOA of crisaborole

A

Phosphodiesterase 4 inhibitor

23
Q

Treatment of secondary bacterial infections

A

Bleach baths for maintenance

Keflex for extensive involvement

24
Q

Systemic Immunosuppresive therapy in AD

A
Narrow band UVB
Cyclosporine (greatest efficacy but highest risk)
Azathioprine: check TPMT levels before 
Methotexate
CellCept
Dupilumab (IL-4 antibody)