Allergic Rhinitis

Question 1

Allergic Rhinitis Hypersensitivity Reactions I: Type 1

Answer 1

• IgE mediated hypersensitivity -antigens bind to IgE on the surface of mast cells
• resulting in the release of inflammation mediators

Question 2

Allergic Rhinitis Hypersensitivity Reactions I: Type 2

Answer 2

• Antibody-mediated
• IgG or IgM antibodies target endogenous cell surface proteins
• Results in inflammation and cytotoxicity

Question 3

Allergic Rhinitis Hypersensitivity Reactions I: Type 3

Answer 3

• Immune complex-mediated hypersensitivity

- IgG or IgM antibodies form immune complexes that are deposited in tissues resulting in inflammation

Question 4

Allergic Rhinitis Hypersensitivity Reactions I: Type 4

Answer 4

• Cell Mediated hypersensitivity

- Activated T Cells cause cellular damage

Question 5

Allergic rhinitis (hay fever)

Answer 5

• IgE mediated hypersensitivity

- Characterized by inflammation of the upper respiratory tract (nose, eyes, ears, sinuses, pharynx)

Question 6

Allergies Epidemiology

Answer 6

• Affects 30 to 40 million in the US and continues to rise
• Most common allergic condition in the US
• Prevalence varies with population factors
• Typically develops by age 20
• Costs nation 5.3 B

Question 7

Allergies Etiology: Atopic triad/atopy

Answer 7

atopic dermatitis plus asthma plus allergic rhinitis

Question 8

Allergies: Etiological Risk Factors

Answer 8

• Positive family history of atopy (70% if both parents, 48% if one parent)
• Indoors (dust mite infestation, chronic dampness)
• Outdoors (high pollen counts, hot/dry/windy days)
• Most common in the period of childhood through early adult

Question 9

Allergies Pathophysiology I (sensitization and priming)

Answer 9

-Excessive inflammatory reaction of upper respiratory tract in response to proteins

Initial exposure (sensitization and priming)

• Antigen inhaled, attaches to mucous lining
• Allergen +Th2 stimulates B cell production of IgE
• IgE complexes with FcR’s on mast cells

Question 10

Allergies Pathophysiology II

Answer 10

Subsequent exposure

• Allergen crosslinks IgE on mast cells
• Mast cells release chemical mediators of inflammation (histamine, bradykinin, cytokines and chemokine (recruit immune cells), prostaglandins and leukokines (vasodilation))
• Early and late phase response

Question 11

Allergies Timeline: Early Phase

Answer 11

Chemical mediators lead immediately to symptoms (minutes)

• Mucous secretion
• Increased vascular permeability leading to swelling
• Vasodilation leading to redness and pressure
• Nerve activity leading to sneezing and itching

Question 12

Allergies Timeline: Late Phase

Answer 12

• Release of chemokine recruits other immune cells leading to sustained response
• Primarily involves eosinophils
• Hyper responsiveness to airborne irritants (cigarette smoke, pollutants)

Question 13

Allergies Clinical Presentation

Answer 13

Upper resp signs and symptoms: Sneezing, itching, rhinorrhea, sniffling, postnasal drop, congestion, ansonia, headache, earache, tearing, red eyes, periorbital swelling/bruising, snoring, sore throat, cough, fatigue, drowsiness

• 40 percent of pt have lower respiratory tract symptoms (wheezing)
• Symptom pattern helps identify etiology (at work? at home? year round? seasonal?)

Question 14

Allergies Assessment

Answer 14

-Evaluate nasal secretions/biopsy

Allergen skin testing

• Under skin of forearm or upper back
• Response in 20 min

Radioallergosorbent test (RAST for IgE in the blood

Question 15

Allergies Prognosis

Answer 15

• Complications are typically not serious
• Can include middle ear infection, sinusitis, reduced Qol
• Long term condition but readily treated
• Occasionally outgrown, wanes after age 40