Derm2- Atopic Dermatitis

  1. What are the characteristics of atopic dermatitis? (4)
    pruritus, chronicity, typeical lesion distribution, family history/breed predilection
  2. What is atopic dermatitis?
    genetically predisposed inflammatory dermatosis associated with IgE antibodies to environment allergens
  3. Atopic dermatitis is mediated by a(n) ________________.
    type I (IgE-mediated) hypersensitivity
  4. If an animal has a _______ predisposition, it will be allergic b/c it will activate mast cells and eosinophils, IgE mediated HS.
  5. How does percutaneous allergen entry occur?
    loss of function/mutations in filaggrin--> impaired permeability barrier [decreased/altered lipid content]
  6. What are possible triggers for pruritus? (6)
    allergens (pollens, mold spores, dust/mites, food), bacteria (Staph), yeast (Malassezia), irritants, temperature, humidity
  7. What is the most outstanding feature associated with atopic dermatitis?
    severe intense pruritus
  8. What is the most common age of onset of atopic dermatitis?
    6 months- 3 years
  9. What is the seasonality of atopic dermatitis?
    seasonal (seasonal initially but most become nonseasonal), seasonally-nonseasonal (worse during one part of the year)
  10. Describe the response to glucocorticoids with atopic dermatitis? How does this compare to CAFR?
    • atopic dermatitis: excellent initially +/- may become refractory
    • CAFR: some respond, but not nearly as dramatically as with AD
    • *This does not give you a diagnosis
  11. What is the lesion localization of AD?
    [same as CAFR] ventrum, face, ears, paws, distal limbs, perianal
  12. What are the primary lesions of atopic dermatitis?
  13. What lesions are associated with atopic dermatitis? (7)
    alopecia, lichenification, hyperpigmentation, seborrhea, crusts, secondary infections (pyoderma or yeast), otitis
  14. Describe the unique characteristics of feline atopic dermatitis. (7)
    6-12 months of age onset, seasonal, rare to have secondary infection and otitis; symmetrical alopecia, miliary dermatitis, head and neck pruritus, eosinophilic granuloma complex
  15. What are the 3 components of feline eosinophilic granuloma complex?
    eosinophilic plaque, indolent ulcer, linear granuloma
  16. How do you diagnose atopic dermatitis? (4)
    diagnosis of exclusion, suggestive history, dietary trial to rule out CAFR, rule out flea allergy in cats
  17. When is allergy testing useful?
    only once we have diagnosed atopic dermatitis, and we want to use it to determine allergens for allergen-specific immunotherapy
  18. What is it called when an animal has an allergy test reaction with no atopic dermatitis? What is the significance of this?
    subclinical hypersensitivity; allergy tests do NOT tell you if the animal has atopic dermatitis!!!! it only tells you what allergens are involved when an animal has a history of atopic dermatitis
  19. What are the seasonal allergens?
    • Spring- trees
    • Summer- grasses
    • Fall- weeds
    • Summer, fall- outdoor molds (Aspergilus, Alternaria, Cladosporium, Fusarium)
  20. What are non-seasonal allergens? (5)
    house dust mites (Dermatophagoides farinae and pteronyssinus), storage mites, indoor molds, cockroachs/moths, danders
  21. What is the most common cause of nonseasonal atopic dermatitis?
    house dust mites- Dermatophagoides farinae and pteronyssinus
  22. What drugs need to be cleared from the animals system before allergy testing (b/c they will interfere with the test)? (2)
    antihistamines (only for intradermal testing), glucocorticoids
  23. What type of serum allergen testing is better?
    heska Fc epsilon receptor testing is much more specific; conventional monoclonal and polyclonal testing has more false positives
  24. How do you interpret an allergy test? (6)
    • do the positive reactions fit with when the animal is pruritic [seasonality]
    • if no--> animal does not have AD, alternative allergy test may be better, interference of other drugs (glucocorticoids), allergens of significance not tested, some AD dogs are never positive (atopic-like disease- unknown reason)
  25. What are the 2 types of allergen-specific immunotherapy?
    subcutaneous immunotherapy (SCIT), sublingual immunotherapy (SLIT)
  26. What is an important factor when using allergy immunotherapy? How does this differ from symptomatic therapy?
    allergy vaccines are YEAR ROUND, even if the allergy is seasonal; symptomatic therapy can be given only when the animals is symptomatic
  27. What are options for controlling atopic dermatitis (not immunotherapy)? (8)
    antihistamines, antidepressants, essential fatty acids, antimicrobials (secondary infection), topicals, steroids, atopica, apoquel
  28. What treatments have weak evidence of efficacy? (5)
    antihistamines, antidepressants, essential fatty acids, topicals, lipid-replacement therapy
  29. When would you use treatments with weak evidence of efficacy?
    used b/c inexpensive, readily available, and have few side effects; used for seasonal, mild allergies
  30. Omega-3 fatty acids are useful for ________; omega-6 fatty acids are useful for _________.
    anti-pruitic; barrier protection
  31. What is the difference in timing b/w antihistamines and essential fatty acids?
    • antihistamines will work within 10-14 days (if not working within that period, won't ever work)
    • essential fatty acids need up to 2 months to show effects
  32. What kinds of topicals can be used to manage mild AD? (3)
    glucocorticoids, pramoxine, oatmeal
  33. Lipid-replacement therapy help to maintain ____________; __________ is a component of ceramide that is replaced with this therapy.
    barrier function of skin; phytosphingosine
  34. Medications with fair evidence of efficacy. (2)
    Tacollimus (protopic, blocks transcription of inflammatory cytokines), glucocorticoid spray
  35. What is Talcolimus used for?
    twice a day on LOCALIZED lesions
  36. What is glucocorticoid spray useful for?
    generalized pruritus
  37. What medications are within the group with STRONG evidence of efficacy? (5)
    systemic glucocorticoids, cyclosporine (Atopica), Oclacitinib (Apoquel), K9 AD immunotherapy, allergen-specific immunotherapy
  38. What are indications for medications with strong evidence of efficacy? (3)
    non-seasonal atopic dermatitis, seasonal AD if other therapies were not effective or had too many side effects, acute/chronic cases (GC, apoquel, CADI)
  39. What medications with strong efficacy CANNOT  be used in acute cases of AD? (2)
    cyclosporine and allergen-specific immunotherapy (takes a while to work)
  40. What is the safest medication with strong efficacy?
    allergen-specific immunotherapy
  41. What is the fastest working medication with strong efficacy?
  42. What is the crisis buster for severe pruritus?
    3 day course of 0.5-1mg/kg SID of prednisone
  43. What are the short-term side effects of systemic glucocorticoids? (5)
    PU/PD, polyphagia, panting, vomiting, diarrhea
  44. What are the long-term side effects of systemic glucocorticoids therapy? (8)
    UTI, liver enzyme elevations, predisposition to DM, calcinosis cutis, poor wound healing, muscle weakness, increased infections/demodecosis, iatrogenic cushing's
  45. What follow up is necessary for patients on systemic glucocorticoids, Atopica, Apoquel, CADI?
    once a year: CBC/Chem and urine culture
  46. What can be added as adjunctive therapy to systemic glucocorticoids to reach the lowest possible GC dose? (3)
    omega-3 fatty acids, antihistamines, topicals
  47. How does Atopica (cyclosporine) work?
    block transcription of cytokine genes in activated T cells
  48. Cyclosporine should be given...
    orally 2 hours before or after a meal (better absorption on empty stomach)
  49. What are side effects of cyclosporine? (7)
    vomiting, diarrhea, [much less common] decreased appetite, lethargy, UTIs, gingival hyperplasia, papillomatosis
  50. What is a contraindication for using Atopica (cyclosporine)?
    history of neoplasia
  51. Why would you administer ketoconazole with Atopica?
    both eliminated by P450 mechanism- can half the dose of Atopica (which is $$$) and it will  be eliminated more slowly
  52. How does Apoquel work?
    synthetic JAK inhibitor, inhibiting the function of pruritogenic and pro-inflammatory cytokines (IL-31) that are dependent on JAK enzyme activity
  53. Apoquel shouldn't be used on... (5)
    dogs less than a year old, with glucocorticoids, pregnant/lactating dogs, history of demodicosis, history of neoplasia
  54. Side effects of Apoquel. (9)
    vomiting, diarrhea, anorexia, lethargy, pyoderma, otitis, interdigital cysts, demodicosis, BM suppression
  55. How does CADI work?
    caninized (only for use in the dog) monoclonal antibody that inhibits IL-31
  56. Side effects of CADI. (3)
    vomiting, diarrhea, lethargy
  57. How does allergen-specific immunotherapy work?
    desensitization, hyposensitization to the allergen [the only treatment that modulates the immune system to take it from hypersensitive to tolerant]
  58. What are the advantages of allergen-specific immunotherapy? (2)
    low risk of long term side effects, lower cost
  59. What is the rule of third for ASIT?
    • 1/3 patients only need ASIT
    • 1/3 need adjunctive therapies with ASIT
    • 1/3 no response ever
  60. How quickly do most patients respond to ASIT?
    usually within 6-9 months, some earlier; failure is determined after 1 year
  61. Why is it important to do rechecks?
    owners don't understand that ASIT doesn't work have to keep them on board! [at a MINIMUM, 3 and 12 month rechecks]
  62. How is SLIT administered?
    two pumps twice a day orally for line
  63. How is SKIT administered?
    usually every 20 days SQ, concentration changes over lifetime
  64. What are the main points of regionally-specific immunotherapy? (4)
    no allergy testing required (as opposed to ASIT), formulated based on region/not individualized, all contain weeds/trees/grasses/molds/dust mites, no studies on efficacy
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Derm2- Atopic Dermatitis
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