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BRONCHIAL ASTHMA
By Nwokoye Hilary Ekene U2017/4710064 083
And MIEBAKA GOLDEN PATHOPHYSIOLOGY
The pathophysiology of bronchial
asthma involves complex interactions between genetic predisposition, environmental triggers, airway inflammation, and bronchial hyperresponsiveness. Airway Inflammation: •Asthma is characterized by chronic inflammation of the airways, involving infiltration of various inflammatory cells, including eosinophils, mast cells, T lymphocytes, and macrophages. •Exposure to allergens, respiratory viruses, pollutants, or other triggers leads to the release of pro-inflammatory mediators, such as histamine, leukotrienes, prostaglandins, and cytokines. •These mediators promote inflammation, vasodilation, mucous secretion, and recruitment of inflammatory cells to the airway epithelium and submucosa. Bronchial Hyper responsiveness (BHR): •Individuals with asthma exhibit increased sensitivity of the airways to various stimuli, leading to exaggerated bronchoconstriction and airflow obstruction. •BHR results from multiple factors, including airway inflammation, smooth muscle hyper reactivity, altered neurohumoral regulation, and structural changes in the airway wall. •Exposure to triggers such as allergens, cold air, exercise, or respiratory infections can precipitate bronchoconstriction and asthma symptoms in susceptible individuals. Smooth Muscle Contraction: •Contraction of bronchial smooth muscle is a central feature of asthma pathophysiology, leading to airway narrowing and obstruction. •Mediators such as acetylcholine, histamine, and leukotrienes promote smooth muscle contraction, while bronchodilators such as β2-adrenergic agonists act to counteract this effect. Airway Remodeling: •Chronic inflammation and repeated episodes of bronchoconstriction can lead to structural changes in the airway wall, collectively termed airway remodeling. •Remodeling features include epithelial injury, subepithelial fibrosis, increased airway smooth muscle mass, mucous gland hyperplasia, and angiogenesis. •These changes contribute to fixed airflow obstruction, reduced responsiveness to bronchodilators, and progressive decline in lung function over time. Immunological Dysregulation: •Asthma is considered a heterogeneous disorder with various phenotypes and endotypes, reflecting diverse underlying immunological mechanisms. •Type 2 inflammation, characterized by increased levels of interleukin (IL)-4, IL-5, and IL-13, plays a central role in allergic asthma driven by allergen exposure. •Non-allergic asthma may involve different pathways, such as innate immune responses, Th1/Th17-mediated inflammation, or viral-induced exacerbations. COMPLICATIONS • Severe asthma attacks that require emergency treatment or hospital care. • Permanent decline in lung function. • Missed school days or falling behind in schoolwork. • Poor sleep and fatigue. • Symptoms that interfere with play, sports or other activities.