atopic dermatitis Flashcards
AD is more common in ____ (high/low) income areas possibly due to____
- high income - urban environments (exposure to pollutants) and lack of exposure to infectious agents may trigger development of AD
Prevalence of AD in children? Adults?
- 25% in children -3% adults
Early onset AD arises by ___ age
1-2 years old
___ % of AD resolves by 12 years of age
60% (remember the 60’s for AD)
Senile onset arises at ____ age
after 60 y/o
___% of AD occurs within the first year of life, and ___% by 5 y/o
- 60% within first year - 90-95% by 5 y/o
What is the general pathogenesis of AD?
interplay between: - poor epidermal barrier - immune dysregulation - environment - genetics (if child has AD, high chance one or both of parents did)
Gene mutation associated with development of AD and severe early onset AD:
- Filaggrin mutation, leads to barrier dysfunction, transepidermal water loss and xerosis, allowing penetration of allergens
Immunologic proteins and cytokines increased in AD include:
- Th2>Th1 - IL-4, IL-5, IL-12, IL-13
Acute AD is ____ predominant state w/ eosinophilia and increased ____ production
- Th2 - IgE - remember that pregnancy is Th2 state and this is why pregnant patients can get atopic eruption of pregnancy
Chronic atopic derm is a ____ predominant state with increased ____.
- Th1 - IFN-gamma
Mediators of itch in AD are:
- neuropeptides - proteases - kinins - histamines (less important)
Clinical criteria for AD are:
- 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
What will you see clinically in acute AD lesions?
- erythema, edema, vesicles, oozing and crusting
What will you see clinically in subacute/chronic AD lesions?
- lichenification, papules, nodules, and excoriations
Pediatric/infantile AD occurs from ___ to ___ age
- birth to 6 months
Pediatric/infantile AD favors which body parts?
- face, scalp, EXTENSOR surfaces
Childhood AD occurs from ___ to ____ age
- 2 years to puberty
Childhood AD favors ____ areas of body
- flexural (infantile favors extensors, face, scalp)
Diffuse xerosis in AD patients tends to become more prominent in which age group?
- childhood (2 y/o to puberty)
Adolescent/Adult AD starts at age ____
- 12
clinical findings of adolescent/adult AD?
- lichenified plaques > weeping eczematous lesions
Adolescent/adult AD favors which body parts?
- flexures, face, neck, upper arms, back and acral sites - adults tend to have more hand involvment
AD beginning during childhood is associated with ___ (more/less) severe disease as adults
- more severe, treatment-resistant disease
Senile AD presents as:
- marked xerosis rather than typical AD lesions
Name the associated features of AD:
- 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
Children, especially those with darker skin types, have increased incidence of _____, which is more visible after ____
- pityriasis alba - more visible after sun exposure
Bacterial impetiginization is most often with ____ > _____
- S. aureus > S. pyogenes
Viral complications that can occur secondary to disrupted barrier in AD include:
- eczema herpeticum (usually HSV1 or 2) - molluscum dermatitis - eczema vaccinatum (Seen with smallpox vaccination)
Ocular complications of AD are:
- atopic keratoconjunctivitis - vernal keratoconjunctivitis (children in warmer climates) - posterior subcapsular cataracts - keratoconus (elongation of cornea) - retinal detachment
_____ occurs in spring/summer in boys on elbows/knees and appears as clusters of small 1-2mm lichenoid papules
- frictional lichenoid eruption (regional variant of AD)
Dyshidrotic eczema occurs on _____ parts of body and is described clinically as____
- lateral fingers and palms - “tapioca-like” firm and deep-seated pruritic vesicles
Histopath of acute AD:
- prominent spongiosis!! - intraepidermal vesicles/bullae - perivascular lymphohistiocytic inflammation with eosinophils
Histopath of subacute AD
- milder spongiosis vs acute. - increased acanthosis!! - lacks vesicles/bullae of acute AD
Histopath of chronic AD
- marked irregular to psoriasiform acanthosis!! (Key feature - minimal to no spongiosis - +/- dermal fibrosis and hyperkeratosis
In some patients, identifications of allergens using which tests can be of use?
- Fluorescence enzyme immunoassays - RAST testing - Skin prick testing - atopy patch testing
When can you consider testing for food allergies for AD?
- severe/refractory AD, or if worsening dermatitis after an ingestion
What percent of AD patients have coexisting food allergy?
- 10-15%
Common exacerbating factors of AD:
FADS - fragrances, fabrics, food allergies -other Allergens (pet dander, dust mites) - Dry environments, Detergents - Smoking, Sweating, Showers to hot, too long, too often, stress
60% rule for AD:
- 60% have onset within first year of life, 60% resolve by age 12.
3 clinical features critical for diagnosis of AD:
- Pruritis 2. chronic relapsing and remitting course 3. eczematous rash
RAST testing detects:
- antigen specific IgE in blood
Skin prick/patch testing works by:
- detecting allergen specific IgE that activates mast cells and leaves pt with contact dermatitis or wheal.
What is general trend on histopathology as you move from acute to chronic AD?
- acute has more spongiosis, less acanthosis - the more chronic, the less spongiosis and more acanthosis you will get.
How to educate for AD patients?
- 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)
Mainstay of tx for AD is:
- topical corticosteroids
Child is having itch and it is keeping him up at night, what medication can you add
- sedative antihistamine
treatment ladder for AD
topicals (steroids, calcineruin inhibitors), light therapy , systemic meds (systemic corticosteroids, cyclosporine, azathioprine, MMF, MTX)
Primary prevention of AD is via ____ after birth
Breast feeding or formulas w/ hydrolyzed milk products for first 4-6 months
What other supplementation can be used prenatally and postnatally to reduce risk of atopic dermatitis?
- probiotics
Prognosis of AD:
Tends to clear by puberty in most children - 60% cleared by age 12
