Chronic obstructive pulmonary disease (COPD) is a major global health issue ranked the third leading cause of mortality worldwide. The disorder is characterized by progressive and irreversible airflow limitation resulting from chronic inflammation of the airways, lung parenchyma, and pulmonary vasculature. This chapter explores the intricate pathophysiological mechanisms of COPD, focusing on chronic inflammation driven by neutrophils, macrophages, and CD8+ T-lymphocytes, which release pro-inflammatory cytokines and proteases, disrupting the balance between proteases and antiproteases and leading to tissue degradation and emphysema. Oxidative stress, exacerbated by reactive oxygen species from tobacco smoke and inflammatory cells, further contributes to cellular damage and disease progression. Structural lung changes, including airway remodeling and emphysema, are detailed, highlighting the consequences of goblet cell hyperplasia, subepithelial fibrosis, and loss of elastic recoil. The epidemiology of COPD is influenced by both genetic factors, such as alpha-1 antitrypsin deficiency, and environmental exposures, with smoking being the primary risk factor in developed countries and biomass fuel exposure in developing countries. Diagnostic approaches rely on symptomatic evaluation, spirometry, and imaging, with spirometry being the gold standard. Management involves a combination of pharmacological treatments, including bronchodilators and inhaled corticosteroids, and non-pharmacological strategies, such as smoking cessation and pulmonary rehabilitation. Advanced cases may require surgical interventions. We emphasize the complexity of COPD and the critical need for early diagnosis and targeted therapies to improve patient outcomes and quality of life. Ongoing research into the genetic, environmental, and molecular factors driving COPD is essential for future advancements in treatment have also been highlighted in this chapter.