Asthma Flashcards
Where are the highest rates of asthma
Ontario and Nova Scotia
Prevalence of Asthma
- asthma is increasing (major cause of hospitalization in children)
- prevalence increased as more people are living with asthma due to decreased mortality of disease
- incidence decline
- Higher prevalence in boys and women
Where are the lowest rates of asthma
Northwest Territories, Yukon, Nunavut
Annual Canadian asthma trends
- 20-25% of asthma exacerbation occur in September (back to school)
- Adults tend to experience more exacerbations in winter (flu season)
Causes of Childhood Asthma
- susceptible in first 3-5 years of life
- family hx of allergy and allergic disorders
- high exposure to airborne allergens
- exposure to tobacco smoke
- low birth weight and respiratory distress syndrome
What is Asthma?
An inflammatory disorder of the airways characterized by paroxysmal or persistent symptoms
Characterizing symptoms of Asthma
dyspnea, chest tightness, wheezing, sputum production and cough
Main mechanism causing development and persistence of asthma
Inflammation of the airways and consequential damage
What are the main effects of asthma on the airways?
Inflammation, bronchospasm, increased mucus production, airway remodelling, extrinsic and intrinsic factors, early and late phase response
What are the extrinsic triggers for asthma?
Type I IgE mediated hypersensitivity reaction
What are intrinsic triggers for asthma
respiratory tract infections, exercise, hyperventilation, cold air / weather, drugs (NSAIDs & chemicals), irritants, hormonal changes, emotional upset, airborne pollutants, GERD
Early Phase Response
Occurs within 10-20 minutes to 2 hours
- Allergen binds to performed IgE on sensitized mast cells on mucosal surface of airways
Mast cell activation releasing inflammatory mediators
- Pre-formed granules —> Histamine, chemotactic chemokine (mast cell degranulation)
Leukotrienes, prostaglandin D2, cytokines
- Cause infiltration of inflammatory cells, opening intracellular cell junctions allowing access to submucosal mast cells = further inflammation, Increase mucus secretion, increased vascular permeability and bronchoconstriction
Late Phase Response
Occurs 4-8 hours to days after trigger
- Release of inflammatory mediators causing recruitment of neutrophils, eosinophils, basophils, T lymphocytes (TH2)
- Inflammatory cells cause epithelial injury and edema, increased mucus, change in mucociliary functions —> accumulation go mucus and increased airway responsiveness and bronchospasm
- Change in mucociliary function due to toxic effects of cells (eosinophils) causing local autonomic parasympathetic nerves to be stimulated = further inflammation
What causes bronchospasm
due to parasympathetic stimulation through vagal pathways
- Histamine (early phase)
- Leukotrines (late phase)
- PAF (platelet activating factor)
- Prostaglandins
- Autonomic nervous system dysregulation (PNS)
Increase Cholinergic mediator responsiveness —> due to alteration of muscarinic receptor function = increase in acetylcholine = bronchial smooth muscle constriction & more mucus secretion
What causes mucus hyper-secretion?
goblet cell hyperplasia and submucosal gland atrophy