Atopic Dermatitis Flashcards

1
Q

What is atopic dermatitis

A

Chronic relapsing skin disorder with intense itch
Usually associated with family history of atopic disease
-atopic march (AD, asthma, rhinitis)

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2
Q

Describe the epidemiology of AD

A

Generally found in childhood
-most within 1st year of life, 1 to 5

Rarely occurs for the 1st time during adulthood

Prevalence increasing

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3
Q

What 3 factors contribute to the aetiology of AD

A

Environmental

  • allergens, irritants, dietary factors
  • infections, stress
  • pollutants, weather change

Genetic

  • FHx, genetic disposition
  • defective skin barrier
  • abnormal Th2, IgE immune response
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4
Q

Describe how gene mutations contribute to barrier dysfunction
-how common is this mutation

A

Normal functioning of filaggrin

  • converted from profilaggrin between the stratum granulosum and corneum
  • in corneum => incooporated into lipid envelope for skin barrier function
  • releases AA that aid in water retention

Abnormal functioning

  • abnormal barrier => increased AG entry, Th2 response
  • increased dryness

10% of us have the mutation
40% of mutation carriers have eczema
-more likely to have atopic triad

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5
Q

Describe the pathophysiology behind AD

A

Impaired stratum corneum barrier function

  • decreased functional filaggrin =>
  • increased protease => corneocyte dysadhesion
  • abnormal lipids => increased SC permeability

Environmental factors

  • altered skin microbiome (more S aureus)
  • damage to epidermal barrier and increased skin barrier penetration of AG => immune activation

Both contribute to immune dysregulation
-keratinocyte derived pro Th2, ILC cytokines => acute innate, adaptive and chronic responses

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6
Q

Describe the presentation of AD in different age group[s

  • infant
  • child
  • adults
A

Infant => forehead, cheeks, extensor surfaces
-papules, vesicles that crust

Child => flexor surfaces, face, neck

Adult => hands, neck, shoulders, flexor surfaces

May also have

  • periorbital eczema
  • xerosis (general dryness)
  • excoriations and prurigo (due to intense itch)
  • impetiginization

If chronic
-lichenification (increased skin markings)

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7
Q

Describe the prognosis of AD

A

Chronic disease with recurrent flares

  • most children outgrow it
  • adults may continue to have localised dermatitis on hands

Frequent skin infections, S aureus colonization
-eczema herpeticum <= herpes virus

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8
Q

Describe the comorbidities that accommpany AD

A

Obesity, smoking => increased risk for AD

Atopic

  • atopic triad
  • allergic conjunctivitis, rhinosinusitis, esophagitis
  • allergy contact dermatitis

Infection (cutaneous, extracutaneous)

AI

Skin pain and itch

Sleep disturbances

Neuropsych

  • anxiety, depression, suicide
  • ADHD
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9
Q

How would you treat AD

  • topical
  • systemic
A

Topical

  • Emollients
  • CS
  • calcineurin inh (inhibits Tcell activation)
  • antiseptic wash (for frequent infections)

Systemic

  • short course prednisolone
  • phototherapy
  • methotrexate, ciclosporin, azothiopurine
  • mycophenolate mofetil
  • biologics
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10
Q

What is dulipumab

  • how does it work
  • what are the side effects
A

IL4, 13 inh

Normally IL4 => Th2 activation

  • produces IL4, IL5, IL13, IL31 => activates eosinophils, basophils, mast cells, IgE releasing B cells, T cells
  • +ve feedback loop of IL4
  • leads to weakening of epidermal barrier, reduction in antimicrobial peptides

Conjunctivitis
Enthesitis, arthritis

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11
Q

When would you use dulipumab

A

Only recommended in

  • moderate/severe AD in adults if
    • no response/contraindicated/not tolerant to at least 1 other systemic therapy

Stop dupilumab at 4 months if no response

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