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  1. Describe cells involved in antigen exposure and generation of IgE in type I allergic response.
    APCs (HLA class II) present processed peptides to helper T-cells, releasing interleukins (IL-4, IL-13) which transform B-cells to plasma cells that generate IgE.
  2. What is the primary reaction phase in an IgE mediated (type I) allergic response.
    • Sneezing, rhinorrhea, congestion, nasal pruritus
    • Occurs in minutes (max effect in 15 min)
    • IgE attaches to mast cells and basophils
    • release of preformed mediators (histamine, seratonin, proteases) and newly generated mediators (TNF-alpha and arachadonic acid derivatives - leukotrienes, prostaglandins)
  3. What is the secondary (late) phase of an IgE mediated allergic response?
    • 4-6 hours after exposure
    • peristent congestion, rhinorrhea, sneezing
    • migration of neutrophils and eosinophils
    • mast cells inactive, basophil releases mediators
  4. Describe a type I hypersensitivity (type, meditors, reactions)
    • Anaphylactic, IgE mediated response
    • immediate
    • stimulates mast cells and basophils to release histamine and other mediators
  5. Describe a type II hypersensitivity (type, meditors, reactions)
    • Cytotoxic (against self)
    • IgG, IgM binding to phagocyte or complement
    • eg: transfusion rxn, goodpastures
  6. Describe a type III hypersensitivity (type, meditors, reactions)
    • Immune complex
    • IgG, IgM, IgA complexes increase blood viscosity
    • removed by reticuloendothelial system
    • eg: glomerulonephritis, serum sickness
  7. Describe a type IV hypersensitivity (type, meditors, reactions)
    • T-cell mediated, delayed
    • eg: graft rejection, contact dermatitis
  8. What percentage of allergic rhinitis patients have asthma?
    • 1/3 (33%)
    • both involve mast cells and eosinophils in pathophysiology
    • nasal-bronchial reflex: nasal histamine provocation increases lower airway resistence
  9. Common allergens by season
    • Trees and grass (spring/summer)
    • ragweed, tumbleweed (fall)
    • dust mites (may increase in winter due to closed windows)
    • molds (perennial, may worsen when damp/humid)
  10. Describe skin prick testing.  What are its advantages?
    • allergen placed on skin, followed by prick through droplet into skin
    • most convenient, least expensive method
    • must avoid antihistamines 72 hours prior
    • risk of anaphylaxis, not as sensitive as RAST, subjective
  11. What is an "intradermal test", how does it compare to skin prick test?
    • Intradermal bleb introduced with 26 or 27 ga needle.
    • more sensitive
    • greater risk of anaphylaxis
  12. Describe radioallergosorbant testing.  What are its advantages of skin-prick testing?
    • react serum with series of known allergens
    • labelled anti-IgE identifies antigen-IgE complexes
    • highly specific (less sensitive)
    • no conflict with meds (antihistamines, B blockers)
    • no risk of anaphylaxis
    • disadv: expensive, takes weeks for results, less sensitive
  13. indications for RAST testing
    • high risk of anaphylaxis
    • skin disorders 
    • uncooperative patient
    • equivocal skin test (negative skin test NOT an indication)
    • failed immunotherapy
  14. How do beta blockers relate to allergy?
    increase sensitivity to allergens
  15. indications for immunotherapy?
    • severe persistent symptoms
    • unavoidable allergens
    • failed maximal medical management
    • wish to avoid chronic medication
    • coexisting asthma (that is not severe or unstable)

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2013-06-03 00:22:35

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