Pathology, pathogenesis, and pathophysiology

Chronic obstructive pulmonary disease (COPD) is characterised by poorly reversible airflow obstruction and an abnormal inflammatory response in the lungs. The latter represents the innate and adaptive immune responses to long term exposure to noxious particles and gases, particularly cigarette smoke. All cigarette smokers have some inflammation in their lungs, but those who develop COPD have an enhanced or abnormal response to inhaling toxic agents. This amplified response may result in mucous hypersecretion (chronic bronchitis), tissue destruction (emphysema), and disruption of normal repair and defence mechanisms causing small airway inflammation and fibrosis (bronchiolitis). These pathological changes result in increased resistance to airflow in the small conducting airways, increased compliance of the lungs, air trapping, and progressive airflow obstruction—all characteristic features of COPD. We have good understanding of the cellular and molecular mechanisms underlying the pathological changes found in COPD. View this table: Pathological changes found in COPD Inflammation is present in the lungs, particularly the small airways, of all people who smoke. This normal protective response to the inhaled toxins is amplified in COPD, leading to tissue destruction, impairment of the defence mechanisms that limit such destruction, and disruption of the repair mechanisms. In general, the inflammatory and structural changes in the airways increase with disease severity and persist even after smoking cessation. Besides inflammation, two other processes are involved in the pathogenesis of COPD—an imbalance between proteases and antiproteases and an imbalance between oxidants and antioxidants (oxidative stress) in the lungs. The pathogenesis of COPD; dashed bars represent inhibitory effects This is the second in a series of 12 articles COPD is characterised by increased numbers of neutrophils, macrophages, and …