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Dermatology > Atopic Dermatitis > Flashcards

Atopic Dermatitis Flashcards

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Dermatology Board Prep flashcards
1
Q

Define atopic dermatitis

A
  • genetically inherited, relapsing pruritic dermatitis
    • most commonly assoc. w/ IgE against environmental allergens
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2
Q

What is the pathogenesis of atopic dermatitis?

A

Multiple different mechanisms

  • Type I hypersensitivity (IgE)
  • T cell imbalances
  • Primary skin barrier defect
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3
Q

What is released when a mast cell degranulates?

A
  • pre-formed mediators
    • proteases (e.g. typtase)
    • heparin
    • histamine
  • newly-formed mediators
    • ​prostaglandins
    • leukotrienes
    • cytokines (e.g. IL1/6, TNF-a)
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4
Q

What is the pathogenesis of acute atopic dermatitis regarding an imbalance in T cell populations?

A

Many more T helper 2 cells (IL 4/5/31) than helper 1’s –> increased IgE production

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5
Q

What is the pathogenesis of chronic atopic dermatitis regarding an imbalance in T cell populations?

A

more T helper 1 cells than helper 2s

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6
Q

Describe the pathogenesis of atopic dermatitis regarding a disease of the skin barrier

A
  • abnoramilities in upper layers of the epidermis
    • incr skin permeability and allergen penetration
    • higher risk for allergic sensitization
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7
Q

What are the two routes of allergen access for AD?

A
  • inhalation
    • inhaled, then systemically absorbed, IgE migrates to tissue and binds to mast cells
  • percutaneous absorption
    • allergen captured by LC in the skin –> local production of IgE
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8
Q

What are the clinical signs of atopic dermatitis?

A
  • familial hx
  • strong breed predilection
    • terriers, shar-peis, setters, retrievers, beagles, dalmatians, cockers
  • onset b/t 1-3 yr
  • seasonal signs at first
    • progressive worsening w/ time
  • pruritis and erythema: face, feet (front first), ears, groin, axillae
  • with chronicity:
    • excoriations, lichenification, hyperpigmentation
    • secondary ear and skin infections
      • pyoderma
      • malassezia dermatitis and otitis
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9
Q

Describe atopic dermatitis in cats

A
  • young adults
  • progressive worsening with age
  • C/S:
    • pruritis
    • symmetrical alopecia
    • miliary dermatitis
    • eosinophilic granuloma complex
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10
Q

How do you diagnose atopic dermatitis?

A
  • hx, c/s, exclusion of other pruritic diseases
    • scabies, food allergy, flea allergy, etc.
  • at least 3 major and 3 minor criteria:​
  • Major:
    • pruritis
    • facial and/or digital involvement
    • lichenification of the flexor surfaces
    • chronically relapsing dermatitis
    • familial hx
    • breed predilection
  • Minor:
    • onset of C/S before 3 yrs of age
    • facial erythema
      bacterial conjunctivitis
    • superficial pyoderma
    • hyperhydrosis
    • positive skin test
    • elevated allergen specific IgE
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11
Q

What is the purpose of allergy testing and what are the two types of testing?

A
  • to select allergens to use for immunotherapy
  • Two types: IDST and serology
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12
Q

Describe intradermal skin testing (IDST)

A
  • evaluate the presence of IgE in the skin
  • small amounts of allergens are injected in the skin
    • evaluation of mast cell degranulation
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13
Q

What is the procedure for intradermal skin testing?

A
  • before skin testing:
    • treat all concurrent dz (e.g. infections)
    • off steroids for 2 mo
    • off antihistamines for 2 wks
  • select allergens of the area
  • clip an area on the lateral thorax
  • sedate the patient (xylazine)
  • inject 0.05 cc ID
    • negative control (saline)
    • postive control (histamine)
    • allergens
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14
Q

What are you evaluating for after a skin test?

A
  • immediate reactions - 15 min
  • subjective: erythema, induration, size
  • objective - measurement of wheal
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15
Q

What are examples of false positive reactions after a skin test?

A
  • irritant allergens
  • contaminated allergens
  • skin sensitizing antibodies
  • poor technique
  • substances that trigger mast cell degranulation
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16
Q

What are some causes of false negative reactions to intradermal skin testing?

A
  • subcutaneous injections
  • too little allergen
  • outdated allergen
  • steroids
  • antihistamines
  • tranquilizers
  • progestational compound
  • anergy (peak of the season)
  • off season testing
  • estrus, pseudopregnancy, severe stress
17
Q

Describe in vitro testing (serology)

A
  • measurement of circulating allergen specific IgE
    • ​radioallergosorbent test (RAST)
    • enzyme linked immunosorbent (ELISA)
  • usually poor correlation with IDST
18
Q

What are the advantages of serology?

A
  • no need to clip
  • no need to discontinue drugs
  • no need to keep in stock allergens
19
Q

What are the disadvantages of serology?

A
  • poor correlation with IDST
  • false positive (non specific binding)
  • not reproducible results
20
Q

Compare and contrast skin testing and in vitro testing

A

Skin test

  • more specific
  • cheap/quick
  • assess MC function
  • assess IgE level (skin)
  • inhibited by steroids/antihistamines
  • clipping, sedation

In vitro

  • more sensitive/expensive
  • takes weeks
  • does not assess MC function
  • assess IgE level (serum)
  • Is not inhibited by steroids/antihistamine
  • does not require clipping/sedation
21
Q

How do you treat atopic dermatitis?

A
  • treat any concurrent dz (other allergies, skin infections)
  • allergen avoidance
  • hyposensitization (allergy vax)
  • systemic tx
  • topical tx
    • keep animal below pruritic threshold
22
Q

Describe hyposensitization

A
  • effective in 60-80% of cases
  • good option if prolonged season of pruritis
  • no results for first 3 months
  • life long tx
  • based on positive rxns
  • no more than 12 allergens/vaccine
  • adverse effects: rare, incr pruritis, anaphylaxis, urticaria
23
Q

Describe glucocorticoid treatment for AD

A
  • palliative therapy
  • only oral steroids
  • decr efficacy over time
  • long term side effects
  • indicated only in case of:
    • short season
    • no concurrent pyoderma/demodicosis
24
Q

Describe Cyclosporine treatment for AD

A
  • immunomodulant
    • suppresses T cells and cytokine production
  • life long therapy
  • initial dose: 5 mg/kg SID
  • monitor for infections (skin and urinary)
  • efficacy not related to blood values
  • drug interactions
  • adverse effects
    • GI, papillomatous dermatitis
25
Q

Describe Oclacitinib (Apoquel) treatment

A
  • recently released drug that targets pruritis of various causes
  • janus kinase inhibitor
  • extremely effective
  • fast acting
  • may precipitate demodicosis
26
Q

Describe IL-31 monoclonal antibody (Cytopoint) treatment

A
  • injectable, SQ, 1x/month
  • for dogs only
  • blocks IL-31, which is important in transmission of pruritis
  • very effective in some dogs, may not work in others
27
Q

Describe antihistamine treatment for AD

A
  • effective in 40-50% of cases
    • histamine is not the main mediator of AD in dogs!
  • more effective for prevention rather than treatment of pruritus
  • try different types
  • side effects
28
Q

Describe essential fatty acid treatment for AD

A
  • anti-inflammatory
  • barrier function
  • restoration of normal lipid composition
  • essential fatty acids
    • linoleic acid
    • alpha-linoleic acid
    • dihomo-gama-linoleic
    • eicosapentanoic acid
  • e.g. cold water marine oil, evening primrose, borage, black currant oil
29
Q

Describe topical therapy for AD

A
  • frequent cold baths
  • oatmeal
  • topical anesthetic/antihistamine
  • lime sulfur
  • topical steroids
  • capsaicin
  • topical calcineurin inhibitors
30
Q

Describe topical steroid therapy for AD

A
  • Triamcinolone spray (0.015%)
    • reported to be safe for long term use
    • effective in 67% of allegic dogs
    • alcohol may be irritating
  • Leave on hydrocortisone
    • safe for long-term use
    • efefctive for mild to moderate cases
31
Q

Describe Capsaicin treatment

A
  • active ingredient of chilli pepper
  • proposed mechanism of action
  • 0.05%
  • used for localized pruritius
    • lick granuloma
  • initial worsening
  • prolonged relief
32
Q

Describe tacrolimus

A
  • topical calcineurin inhibitor
  • mechanism similar to cyclosporine
  • minimally absorbed - extremely safe
  • effective esp. for localized cases
  • improvement seen after 1-2 wks
  • initial burning sensation
33
Q

What are some treatments to restore barrier function?

A
  • phytospingosine
  • topical tx with ceramides, essential FA, emollients

Dermatology (13 decks)

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