L5 Rhinitis and Immunotherapy

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jknell
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198450
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L5 Rhinitis and Immunotherapy
Updated:
2013-02-06 16:56:26
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Pulm II
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Pulm II
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  1. Nasal Anatomy and Physiology
    • -3 turbinates in ea nostril
    • -epithelium
    • -mucus layer (Ig's, enzymes, albumin)
    • -cilia
    • -AV anastamoses and collapsible venous sinusoids
    • -nervous control of vascular permeability
  2. Types of Rhinitis
    • 1. Allergic
    •      -Seasonal (pollen)
    •      -Perennial (indoor allergens)

    • 2. Non-allergic (Inflammatory)
    •      -infectious
    •      -NSAID sensitivity (ASA)
    •      -NARES syndrome (eosinophilia)
    •      -irritant/occupational

    • 3. Non-Allergic-Non-Inflammatory
    •      -rhinitis medicamentosa (nasal spray)
    •      -vasomotor rhinitis (hormonal, gustatory)
    •      -Medication induced (PDE5 inhibitors)
  3. Rhinitis symptoms
    • -rhinorrhea
    • -obstruction
    • -anosmia

    Associated sx = eyes, lungs, throat
  4. Rhinitis: Physical Exam Findings
    • -edema
    • -pallor (allergic) vs erythema (infectious)
    • -secretions (water, purulent, bloody)
    • -Conjunctivae, pharynx, lungs

    • -peripheral blood
    • -local tissue eosinophilia vs. neutrophilia
    • -allergen skin test or RAST
  5. Allergic Sensitization
    First exposure to an allergen results in IgE production and sensitization

    1. Allergen is presented on an APC

    2. APC activates Th2 lymphocytes

    3. Th2 cells secrete IL4 and IL13 which cause B cell class switching to produce IgE

    • 4. Allergen specific IgE binds to mast cells via high affinity receptor
  6. Response to Allergen
    Reexposure to allergen triggers response

    1. Allergen binds IgE on mast cells

    2. Mast cells immediately release mediators

    3. Mediators activate MPs --> activated Th2 cells

    4. Th2 cells secrete IL4, IL5 and IL13 to activate basophils and eosinophils (Late phase inflammation)

    • 5. Eosinophils secrete toxic proteins, LTs, IL3 and IL6
  7. Seasonal Allergic Rhinitis
    • -due to pollen allergens
    • -"geographic disorder": timing varies by location
  8. Perennial Allergic Rhinitis
    • Generally indoor allergens:
    • -dust mites feces
    • -furred animals (esp cats)
    • -molds (uncommon)
    • -cockroaches
    • -occupational exposure (research animals)
  9. Morbidity of allergic rhinitis
    • -ppl don't die of allergic rhinitis
    • -but it is the number 1 cause of loss of productivity
  10. Treatment of Non-Allergic Rhinitis
    • Inflammatory forms:
    • 1. topical steroids (most effective tx)
    • 2. antihistamines (best with mast cell inflammation)
    • 3. decongestants (can have reliance)

    • Non-Inflammatory Forms:
    • 1. lavage
    • 2. topical anticholinergics
    • 3. topical steroids
    • 4. avoid topical decongestants
  11. Treatment of Allergic Rhinitis
    1. Allergen avoidance (often difficult)

    2. Short course topical decongestant (1-3d)

    3. Oral antihistamine (OTC doses are low in order to avoid sedation)

    4. Anti-leukotriene (for eosinophilic forms)

    5. Topical intranasal corticosteroid spray (by far most effective)

    6. Topical intranasal antihistamine spray (best for obstruction)

    7. Topical intranasal anticholinergic spray (best for rhinorrhea)
  12. Subcutaneous Immunotherapy
    • -only if medical therapy is ineffective
    • -only in disease caused by allergen
    • -benefit 3/4 of patients
    • -dosage over prolonged period (min 3 years)
    • -effects may persist for decades
    • -risk of anaphylaxis and death

    • BENEFITS:
    • -improved nasal sx
    • -possible improvement of allergic asthma
    • -prevention of new allergies in children
    • -prevention of development of asthma in children
  13. Subcutaneous Immunotherapy Immune Effects
    • Drive the immune response to the allergen away from Th2, toward Treg and Th1 response

    Both of these mechanisms help prevent an allergic response
  14. Immunomodulatory Effects of IL10
    1. Dampens Th2 response

    2. Increases Treg differentiation (inhibits Th2)

    3. Increases IgG4 production (decreases IgE antigen presentation)

    4. Decreases eosinophil survival and activation

    • 5. Decreases IgE receptor expression on mast cells (decreasing mast cell activation)

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