Atopic Dermatitis Flashcards
Atopic dermatitis (atopic eczema)
Chronic inflammatory skin disease that primarily begins in childhood
- hallmark symptom is pruritus on the infected skin
- often also present with atopic comorbidities such as asthma and allergic rhinitis
Is a familial transmitted skin disease caused by interactions amoung genetic and environmental risk factors
Pathogenesis behind atopic dermatitis
1) Damage to epidermal barrier and activation of immune responses by skin microbes/allergens or irritants. Leads to penetration of skin barrier
2) impaired stratum corneum (SC) barrier function is then induced by:
- decreased filaggrin and genetic barrier proteins
- increased proteases which leads to core oocyte dysadhesion
- increased production of abnormal lipids which increases SC permeability
3) infection leads to acute TH2 responses and chronic TH1 responses
Genetic components of atopic dermatitis (AD)
Accounts for 90% of susceptibility to early onset AD
- higher concordance rates in monozygotic than dizygotic
- also parental history of AD is a strong risk factor
Essential features of AD diagnosis
Pruritus
Rubbing/scratching that initiates or exacerbates flare ups
(“The itch that rashes”)
Eczematous dermatitis Found in face/neck/extensor extremities
- spares the groin and axilla and trunk usually
Flexure site specific eczema or lichenification in children/adults
Triggers for AD
Climate: low humidity or extreme temps
Irritants: wool/rough fabrics/perspiration/detergents/solvents
Infections: cutaneous or systemic
Environmental allergies
Food allergies: eggs/mils/peanuts/soy/wheat
Causes of decreased skin barrier function in AD
1) adding soap and detergents to skin and raising the pH
- increases activity of endogenous proteases
2) scratching of the epidermal barrier adds on to the damage and further exposes the barrier to exogenous proteases and S. Aureus infections
- also increases allergen absorption Into the skin and microbial colonization
Why is atopic dermatitis itchy?
Increased amount of histamine and IL-31
- TH2 mediated response
Also decreased FLG expression in keratinocytes
Cutaneous findings in atopic dermatitis
Acute = eczematous lesions that are erythematous papulovesicle lesions that have pinpoint crusting
Chronic = scale, excoriation and lichenification of the eczematous lesions
often patients will present with both in separate ares of the body
Differential diagnosis of atopic dermatitis
Seborrheic dermatitis
Contact dermatitis
Psoriasis
Asteatotic eczema
Scabies
Dermatophytosis
Impetigo
Darker skin cutaneous findings in atopic dermatitis
Follicular accentuation and flat topped papules in lichenified areas
- often presents with hyperpigmentation but can in rare situations show vitiligo-like depigmentation of the skin
Complications of atopic dermatitis
2 most common is molluscum contagiosum and warts
#1 most common = staph aureus superinfection - staph aureus presence often leads to increased skin inflammation and increases AD severity
Treatment of staph aureus super infections = dilute sodium hypochlorite baths (bleach baths)
Eczema herpeticum presence in atopic dermatitis
Most serious virally mediated complication in atopic dermatitis
Incubates for 5-12 days and then erupts into multiple pruritic vesiculopustular lesions in a disseminated pattern
- these lesions can cluster and become hemorrhagic
Ocular issues associated with atopic dermatitis
Eyelid dermatitis and chronic blepharitis are the most commonly associated ocular issues with AD
- can result in visual impairment from corneal scarring if untreated
Atopic keratoconjunctivits is less common but present with more disabling symptoms (burning, itching, tearing, mucous discharge)
Vernal conjunctivitis is very rare but results in severe bilateral recurrent chronic inflammatory processes assocaited with papillary Hypertrophy or cobblestoning of the upper eye lid
Hand dermatitis
Frequently caused by repeated wetting/washing of hands with soap, detergents or disinfectant agents
- often is recurrent and can lead to palmoplantar vesicular dermatitis
Exfoliating dermatitis
Caused by superinfection with toxic producing S. Aureus or HSV subtypes.
Symptoms= generalized redness, scaling, weeping, crusting and systemic toxicity signs with lymphadenopathy
Treatment of atopic dermatitis
1) not active or low level maintenance = daily use of emollient (thick creams with low water content or petroleum jelly) to skin sites and avoidance of triggers
2) High level maintenance =
Tropical corticosteroids, calcineurin inhibitors.
3) active eczema = daily use of topical corticosteroid
- can add antihistamine (intense itching) or antibiotic courses (superinfection present) as well as needed
What is the mainstay of treatment for atopic dermatitis
1) Fragrance-free emollients such as thick creams or ointments with little-no water
- Prevents water evaporation and xerosis
2) low grade topical steroids
- to prevent/limit inflammation
Treatment specific for puritis
Oral antihistamines NOT recommended
No sedating antihistamines = can try for a month in mild-moderate AD with severe itching
Sedating antihistamines = can try for 7-14 days as long as child is older than 6 months and complains of inability to sleep due to pruritis
When do you use high potency topical steroids?
For intense exacerbations of AD
- use for up to 7-14 days and then switch back to low grade
Types of steroids to use for AD
Low potency = hydrocortisone cream (1-2.5%)
Moderate potency = fluocinolone 0.025%/triamcinolone 0.1%
Topical calcienurin inhibitors
NOT 1st line therapy and NOT used in mild AD treatment
Approved for patients 2 years and older and particularly useful for cosmetically sensitive areas (face/neck)
Treatment of eczema herpeticum
Systemic acyclovir and referral out to dermatology and/or ophthalmology
Probiotic supplementation in mothers/infants for AD
Helpful in preventing and reducing severity of AD
Includes:
- lactobacillus rhamnosus GG
- y-linolenic acid and omega-3 fatty acids
Nummular/discoid eczema
Coin-shaped plaques that have numerous etiologies and a predilection for school-age children with AD
Very commonly shows flare ups in wintertime
others irritants:
- house dust mites
- Candida species
- mercury exposure
- high emotional distress
- isotretinoin, interferon a-2b, ribavirin, infliximab therapies
patients show higher rates of dental abscesses and paradental diseases
Differential diagnosis of nummular eczema
Allergic contact dermatitis
Stasis dermatitis
Atopic dermatitis
Tinea corporis (MUST RULE THIS OUT)
Impetigo
Psoriasis
My oasis fungoides
Paget disease of Nipple (if on the nipple)
What tests are NOT USEFUL in nummular eczema diagnosis?
Serum IgE levels
Bacterial cultures (unless you think there is a superinfection)
Antistreptolysin-O titers
Treatment of nummular eczema
Topical corticosteroids = mainstay
- lesions are often refractory to mid-potency topical corticosteroids and in which case need to be given high potency corticosteroids
Topical calcineurin inhibitors (Tacrolimus/pimecrolimus) = 2nd line and usually only for severe nummular eczema
Allergic contact dermatitis (ACD)
Cell-mediated (type-4) hypersensitivity caused by skin contact with an environmental allergen
- requires initial prior sensitization event first (first exposure your okay, 2nd exposure = dermatitis)
Accounts for 20% of new incident cases of contact dermatitis
- over 3700 possible irritants can cause this
- common is nickel and other metals as well as neomycin
requires patch testing to diagnosis (diagnostic test)
Clinical symptoms of ACD
Always presents with eczematous dermatitis
- pruritis, erythema, edema, vesicles
- always shows Some sort of focal pattern
Chronic exposure from recurrent contact = lichenification erythematous plaques that presents with fissuring and pigment changes
Specifics on rash
- forms within 24-72 hrs and peaks within 1 week of contract exposure (can last as long as 3 weeks though)
- is patches or streaks of red raised blisters
- is contagious only with contact though
- often is bilateral but can be unilateral
What is the substance in poisonous plants that leads to Allergic contact dermatitis?
Urushiol
- can also be aerosolized if plants that possess it are burnt
3 phases of ACD
Acute phase - lesions are marked by edema, erythema and vesicle formation
Subacute phase = vesicular rupture which leads to oozing, scaly papules that crust
Chronic phase = scaling fissuring and lichenification
What are the two approaches to ACD diagnosis
Topographic approach = based on the distribution of dermatitis on the patients skin
- periumbilical or infraumbilical rashes = belt metal
- distrusted around the hairline and beh8nd ears = hair product allergies
Allergen-specifc approach = based on knowledge of trends in dermatitis and patients history
Cosmetic associated allergens include
Fragrances
Para-phenylenediamine (PPD)
- very prominent in hair dyes
Preservatives
Lanolin alcohols
Glyceryl monothioglycolate (GMT) - very prominent in wave solutions
Phenylmeruric acetate
Benzalkonium cholride
can be hand-to-face, hand-to-body or airborne
Cellphone dermatitis signals allergies to what metal?
Nickel
What ingredient in nail lacquer can cause ectopic dermatitis of the eyelids?
Tosylamide formaldehyde resin
What are the main cosmetic allergens to cause isolated eyelid dermatitis?
Fragrances and preservatives
Usually contain phenylmercuric acetate and/or benzalkonium chloride
Treatment of allergic contact dermatitis
Identification of the allergen and avoid it
Give topical corticosteroids for 2-3 week s
Severe or widespread eruptions = 3 week dose of oral prednisone (1mg/kg/day for 1 week and then tapered weekly for the next week
also put the patient in the contact allergen management program (CAMP) and the contact allergen replacement database (CARD).
GMT
Chemical substance used in permanent wave solutions
Produces ACD of the scalp and face if a patient is allergic
