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Integumentary System > Atopic Dermatitis > Flashcards

Atopic Dermatitis Flashcards

1
Q

Atopic dermatitis (atopic eczema)

A

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

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2
Q

Pathogenesis behind atopic dermatitis

A

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

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3
Q

Genetic components of atopic dermatitis (AD)

A

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
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4
Q

Essential features of AD diagnosis

A

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

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5
Q

Triggers for AD

A

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

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6
Q

Causes of decreased skin barrier function in AD

A

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

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7
Q

Why is atopic dermatitis itchy?

A

Increased amount of histamine and IL-31
- TH2 mediated response

Also decreased FLG expression in keratinocytes

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8
Q

Cutaneous findings in atopic dermatitis

A

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

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9
Q

Differential diagnosis of atopic dermatitis

A

Seborrheic dermatitis

Contact dermatitis

Psoriasis

Asteatotic eczema

Scabies

Dermatophytosis

Impetigo

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10
Q

Darker skin cutaneous findings in atopic dermatitis

A

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

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11
Q

Complications of atopic dermatitis

A

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)

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12
Q

Eczema herpeticum presence in atopic dermatitis

A

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

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13
Q

Ocular issues associated with atopic dermatitis

A

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

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14
Q

Hand dermatitis

A

Frequently caused by repeated wetting/washing of hands with soap, detergents or disinfectant agents
- often is recurrent and can lead to palmoplantar vesicular dermatitis

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15
Q

Exfoliating dermatitis

A

Caused by superinfection with toxic producing S. Aureus or HSV subtypes.

Symptoms= generalized redness, scaling, weeping, crusting and systemic toxicity signs with lymphadenopathy

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16
Q

Treatment of atopic dermatitis

A

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

17
Q

What is the mainstay of treatment for atopic dermatitis

A

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

18
Q

Treatment specific for puritis

A

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

19
Q

When do you use high potency topical steroids?

A

For intense exacerbations of AD

- use for up to 7-14 days and then switch back to low grade

20
Q

Types of steroids to use for AD

A

Low potency = hydrocortisone cream (1-2.5%)

Moderate potency = fluocinolone 0.025%/triamcinolone 0.1%

21
Q

Topical calcienurin inhibitors

A

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)

22
Q

Treatment of eczema herpeticum

A

Systemic acyclovir and referral out to dermatology and/or ophthalmology

23
Q

Probiotic supplementation in mothers/infants for AD

A

Helpful in preventing and reducing severity of AD

Includes:

  • lactobacillus rhamnosus GG
  • y-linolenic acid and omega-3 fatty acids
24
Q

Nummular/discoid eczema

A

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

25
Q

Differential diagnosis of nummular eczema

A

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)

26
Q

What tests are NOT USEFUL in nummular eczema diagnosis?

A

Serum IgE levels

Bacterial cultures (unless you think there is a superinfection)

Antistreptolysin-O titers

27
Q

Treatment of nummular eczema

A

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

28
Q

Allergic contact dermatitis (ACD)

A

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)

29
Q

Clinical symptoms of ACD

A

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
30
Q

What is the substance in poisonous plants that leads to Allergic contact dermatitis?

A

Urushiol

- can also be aerosolized if plants that possess it are burnt

31
Q

3 phases of ACD

A

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

32
Q

What are the two approaches to ACD diagnosis

A

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

33
Q

Cosmetic associated allergens include

A

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

34
Q

Cellphone dermatitis signals allergies to what metal?

A

Nickel

35
Q

What ingredient in nail lacquer can cause ectopic dermatitis of the eyelids?

A

Tosylamide formaldehyde resin

36
Q

What are the main cosmetic allergens to cause isolated eyelid dermatitis?

A

Fragrances and preservatives

Usually contain phenylmercuric acetate and/or benzalkonium chloride

37
Q

Treatment of allergic contact dermatitis

A

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).

38
Q

GMT

A

Chemical substance used in permanent wave solutions

Produces ACD of the scalp and face if a patient is allergic

Integumentary System (29 decks)

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