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MBBS 3: Pediatrics > Atopic Dermatitis > Flashcards

Atopic Dermatitis Flashcards

1
Q

What is atopic dermatitis?

A

Also called eczema, is a chronic, Pruritic, Relapsing inflammatory skin condition
- It is one of the most common and stressful of all chronic skin disorders in children

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2
Q

History taking in atopic dermatitis?

A
  1. Environmental interactions
  2. Infectious triggers
  3. Higher social economic class
  4. Family history of atopy
  5. Predisposed to the development of allergy and allergic rhinitis (atopic march)
  6. Asthma develops in up to 50% of children
  7. Anxiety and stress
  8. Climate (extremes of temperature and humidity)
  9. Irritants, allergens, and infections
  10. Coexisting food allergies (30% of patients)
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3
Q

Pathogenesis?

A
  1. Multifactorial
  2. Complex interplay of
    - Genetics
    - Immunologic abnormalities
    - Impaired skin barrier function
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4
Q

Describe the pathogenesis of AD?

A
  • There is an exaggerated cutaneous inflammatory response to environmental triggers, including irritants and allergens
  • Prevalence is lower in areas where industrial pollution is less and where eosinophil-mediated infections such as helminthic infections are endemic
  • It is now known that mutations in filaggrin, in addition to causing ichthyosis vulgaris, cause the barrier dysfunction, which is characteristic of atopic dermatitis in about 50% of patients
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5
Q

Describe how external factors cause AD?

A
  • In genetically predisposed individuals, external factors including environmental irritants and allergens, bacteria, fungi, viruses, and foods trigger the differentiation of Th2 lymphocytes from Th0 lymphocytes and the release of acute inflammatory mediators (IL-4, 5, 13, 31)
  • In chronic disease Th1 lymphocytes are activated and chronic inflammatory mediators are upregulated
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6
Q

What are the external factors that aggravate AD?

A
  1. Rubbing or scratching
    - The resultant scratching leads to acute and chronic changes typical of atopic dermatitis
  2. Contact with saliva or acidic foods
  3. Soaps and detergents
  4. Wool or other harsh materials
  5. Fragranced products
  6. Sweat
  7. Highly chlorinated pools
  8. Low humidity
  9. Tobacco smoke
  10. Dust mites, animal dander, environmental pollens, and molds
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7
Q

Genetic factors that cause AD and their effect?

A

Positive families history of allergic rhinitis or asthma
- One-third of the children develop atopic dermatitis

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8
Q

Common history of patients with atopic dermatitis?

A
  1. 1/3 have personal history of allergic rhinitis or asthma
  2. 2/3 have family history of atopic dermatitis
  3. ½ ultimately develop allergic respiratory symptoms
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9
Q

Infantile phase of AD?

A

6 weeks to 2–3 years

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10
Q

Describe the skin rash of AD?

A

dry, red, itchy papules and plaques, may ooze and crust

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11
Q

Distribution of rash?

A
  1. Symmetrical on cheeks
  2. Forehead
  3. Scalp
  4. Trunk
  5. Extensor surfaces of the extremities
  6. The diaper area is usually spared
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12
Q

Lesion distribution in the infantile group (0-3 years)?

A

face and extensor surfaces; often generalized

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13
Q

Lesion distribution in the childhood group (4-10 years)?

A
  1. flexural surfaces (antecubital and popliteal fossae)
  2. wrists, ankles, hands, and feet
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14
Q

Lesion distribution in adults?

A
  1. Flexural areas
  2. neck, the face, hands, fingers, toes, and the upper arms and back
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15
Q

What is lichenification?

A
  • thickening of the skin due to chronic scratching
  • post-inflammatory hyperpigmentation
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16
Q

What is Pityriasis alba?

A

Subtle inflammation may result in poorly demarcated areas of hypopigmentation
- subtle inflammation may result in poorly demarcated areas of hypopigmentation, known as pityriasis alba. Lesions are most prominent in darkly pigmented individuals

17
Q

Complications?

A
  1. Secondary bacterial infection (Staphylococcus aureus, Streptococcus pyogenes)
  2. Cutaneous viruses (e.g HSV; eczema herpeticum)
  3. Fungal infection
18
Q

Differential diagnosis of AD?

A
  1. seborrheic dermatitis
  2. contact dermatitis
  3. pityriasis rosea
  4. psoriasis
  5. fungal infections
  6. Langerhans cell histiocytosis
  7. acrodermatitis entropathica
19
Q

Treatment of AD?

A
  1. moisturizers to restore the skin barrier
  2. avoidance of triggers of inflammation
  3. topical anti-inflammatory medication (steroids)
  4. Systemic therapy with immunosuppressive agents or ultraviolet light therapy
20
Q

Side effects of steroids?

A
  1. Local side: skin atrophy, striae, acne, telangiectasias, hypopigmentation
  2. Systemic side effects: Adrenal suppression or Cushing syndrome
    - can result with application of a potent topical corticosteroid to large surface areas or occluded areas at risk of enhanced penetration
21
Q

What is the antihistamine treatment?

A

Sedating antihistamines
e.g., diphenhydramine, hydroxyzine

22
Q

Describe the antihistamine treatment?

A
  • Have only mild effect on pruritus
  • Improve the sleeplessness due to scratching at night
  • A dose before bedtime is most effective
  • Nonsedating antihistamines are of little benefit
23
Q

Holistic treatment for AD?

A
  1. Suitable clothing
    - wool; cotton is ideal
    - avoid perfumed products
  2. Aqueous creams and bath oils
  3. Emollients: applied regularly to hydrate skin
  4. Occlusive wet dressings
  5. Antibiotics for infected eczema
  6. Pets and dietary avoidance in selected cases
24
Q

Prognosis of AD?

A
  • 75% improve by 10–14 years of age
  • Most severe and widespread in infancy and early childhood
  • Relapse of disease in adults can occur (face or hand dermatitis)
  • Frequently, adults have generalized dry skin
  • Patients develop asthma and allergic rhinitis
  • Asthma commonly associated with severe skin disease
25
Q

Prevention of AD?

A
  1. Avoiding triggers of inflammation
  2. Frequent moisturizer application
  3. Breast feeding for at least 4 months ± formula decreases incidence/ severity

MBBS 3: Pediatrics (42 decks)

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