ce allergies or NOT?
Common outdoor aeroallergens include pollen and mold spores. Other nonairborne pollens have also been identified as triggers. Pollutants, such as ozone, tobacco smoke, and diesel exhaust particles are considered environmental triggers and are becom- ing more of a concern in highly populated areas. Common indoor aeroallergens include those from house-dust mites and cockroaches, pet dander, and mold spores. Occupational aeroallergens include latex, biologic enzymes, wool dust, resins, organic dust (flour), and various chemicals (glutaralde- hyde, isocyanate). There are many proposed risk factors that contribute to the development and severity of allergic rhinitis. Potential risk factors are listed below: • Family history of atopy (genetic predisposition to develop allergic diseases) • Male sex • Birth during the pollen season • Firstborn status • Early use of antibiotics • Maternal smoking exposure in the first year of life • Exposure to indoor allergens, such as dust mite allergen • Serum immunoglobulin E (IgE) > 100 international units/mL before age 6 • Presence of allergen specific IgE • Filaggrin (skin barrier protein) gene mutation • Higher socioeconomic level • Eczema • Positive reaction to allergy skin tests • Poor diet in children and adolescents (consuming three or more fast-food meals per week) CLINICAL PRESENTATION OF ALLERGIC RHINITIS Allergic rhinitis can be classified as intermittent, persistent, and episodic. The condition’s specific classification depends on the timing and duration of symptoms. The symptoms of aller- gic rhinitis can be further classified as mild or moderate/severe. Below describes the different classifications of allergic rhinitis: Intermittent • Symptoms occur < 4 days per week or < 4 weeks • Mild severity • Symptoms do not impair sleep or daily activities, no troublesome symptoms • Moderate/severe severity • One or more of the following occurs: impairment of sleep; impairment of daily activities; trouble- some symptoms Persistent • Symptoms occur > 4 days per week and > 4 weeks • Mild severity • Symptoms do not impair sleep or daily activities, no troublesome symptoms • Moderate/severe severity • One or more of the following occurs: impairment of sleep; impairment of daily activities; trouble- some symptoms
INTRODUCTION
Colds, allergic rhinitis, and sinus infections are some of the most common conditions for which patients self-medicate and initiate access to the health care system. Many individuals have difficulty differentiating these conditions as they all have similar manifestations and incorporate the same symptoms. However, it is vital to be able to distinguish between these upper respiratory disorders in order to take the appropriate treatment approach. Therefore, the purpose of this continued education program is to aid health care workers in appropriately identifying key dif- ferences between colds, allergic rhinitis, and acute bacterial rhinosinusitis and appropriately managing these conditions.
ALLERGIC RHINITIS INTRODUCTION
Allergic rhinitis, also known as allergic rhinosinusitis, is a systemic disease with prominent nasal symptoms. It is a worldwide problem that affects both adults and children. It is estimated that 8% of adults and 10% of children in the United States are newly diagnosed with allergic rhini- tis annually. Direct costs are estimated to be roughly $3.4 billion per year, which includes medications and office visits. When accounting for indirect costs, such as related work and school absenteeism, the annual costs rise to $11 billion. People suffering from allergic rhinitis have the poten- tial to have an impaired quality of life. Symptoms of the condition generally begin after the second year of life and continue to be prevalent in children and adults 18-64 years of age. After the age of 65 years, the number of cases tends to decrease. The prevalence of allergic rhinitis is higher in the southern United States than in any other region.
PATHOPHYSIOLOGY OF ALLERGIC RHINITIS
Allergic rhinitis affects the upper respiratory system. The condi- tion is triggered by indoor and outdoor environmental allergens. Upon exposure to an allergen, atopic individuals first undergo a sensitization phase. The allergen stimulates beta-lympho- cyte-mediated IgE production. After the sensitization phase, the individual then undergoes the early phase, which occurs within minutes of subsequent allergen exposure. The early phase consists of a rapid release of preformed mast cell mediators (histamine, proteases, etc.) as well as the production of addi- tional mediators, such as prostaglandins, kinins, leukotrienes, and neuropeptides. After the early phase, cellular recruitment occurs. Circulating leukocytes, especially eosinophils, are attracted to the nasal mucosa and release more inflammatory mediators. Lastly, the late phase begins 2-4 hours after aller- gen exposure and includes signs and symptoms of mucus hypersecretion secondary to submucosal gland hypertrophy and congestion. Continued persistent inflammation primes the tissue and results in a lower threshold for allergic- and non-allergic-mediated triggers (strong odors, cold air, etc.).
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