COPD encompasses chronic bronchitis (airway disease) and emphysema (parenchymal destruction), typically coexisting. In chronic bronchitis, inhaled irritants (primarily cigarette smoke) activate epithelial cells and alveolar macrophages to release chemotactic factors (IL-8, LTB4, TNF-alpha) recruiting neutrophils to airways. Neutrophil-derived elastase, cathepsins, and matrix metalloproteinases (MMP-9, MMP-12) digest structural proteins of airway walls and parenchyma. Chronic neutrophilic inflammation causes goblet cell hyperplasia, submucosal gland hypertrophy, smooth muscle hypertrophy, and peribronchial fibrosis leading to small airway narrowing. Emphysema results from protease-antiprotease imbalance: excess neutrophil elastase overwhelms alpha-1 antitrypsin (A1AT) defense, destroying alveolar walls and elastin scaffolding, causing irreversible airspace enlargement, loss of elastic recoil, and gas exchange surface area. Centriacinar emphysema (smoking-related) affects respiratory bronchioles predominantly in upper lobes; panacinar emphysema (A1AT deficiency) involves entire acinus, predominantly lower lobes. Dynamic hyperinflation occurs during exercise: air trapping from expiratory flow limitation increases residual volume, flattening the diaphragm and reducing its mechanical advantage, causing dyspnea and exercise limitation. Unlike asthma, COPD inflammation is predominantly neutrophilic and CD8+ T-cell mediated, with poor response to corticosteroids (except during exacerbations and in eosinophilic phenotype).