Author(s): Saetta M, Turato G, Maestrelli P, Mapp CE, Fabbri LM
Chronic obstructive pulmonary disease (COPD) is defined as a disease state characterized by poorly reversible airflow limitation that is usually both progressive and associated with an abnormal inflammatory response of the lung (1). Cigarette smoking is the most important risk factor for the development of COPD. However, only a minority of smokers develop COPD and the reason is still unknown.
The pathological hallmarks of COPD are inflammation of the peripheral airways and destruction of lung parenchyma or emphysema. The functional consequence of these abnormalities is expiratory airflow limitation. Since the major determinants of expiratory flow are a driving pressure that promotes flow (elastic recoil of the lung) and an opposing resistance that inhibits flow (airway obstruction), the reduction in flow occurring in COPD is more correctly defined as airflow limitation rather than airflow obstruction, since both loss of elastic recoil and increase in airway resistance play an important role in the observed decrease in flow. Emphysema will contribute to the airflow limitation by reducing the elastic recoil of the lung through parenchymal destruction, as well as by reducing the elastic load applied to the airways through destruction of alveolar attachments. On the other hand, inflammation of the peripheral airways will contribute to the airflow limitation by increasing the thickness of the airway wall which, together with fibrosis and smooth muscle hypertrophy, may cause airway narrowing. The role of mucus hypersecretion in the development of chronic airflow limitation is still controversial (2, 3). The main site of mucus hypersecretion, expressed clinically as chronic bronchitis, is the central airways, and there is increasing evidence that the central airways are inflamed in patients with COPD.
Referred From: https://www.atsjournals.org/doi/10.1164/ajrccm.163.6.2009116
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