pathology and mechanism of airflow obstruction

Last edited 12/2018 and last reviewed 02/2021

Pathological changes in COPD seen in the airways, lung parenchyma and in pulmonary vasculature.  These changes include:

• chronic inflammation
• increased numbers of specific inflammatory cell types in different parts of the lung
• results from an enhanced or abnormal inflammatory response to chronic irritants such as cigarette smoke
• structural changes due to repeated injury and repair (1)

These pathological changes in turn results in the following physiological abnormalities:

• mucous hypersecretion
• an increase in the number of goblet cells and size of bronchial submucosal glands (caused by noxious particles and gases) is the cause
• causes a chronic productive cough which is characteristic of chronic bronchitis
• not necessarily associated with airflow limitation (1)
• all COPD patients do not have symptomatic mucous hypersecretion
  
  
• ciliary dysfunction
• caused by squamous metaplasia of epithelium
• results in dysfunction of the mucociliary escalator and difficulty expectorating
  
  
• airflow limitation and hyperinflation/air trapping
• airflow limitations are seen mainly in the small airways (<2mm in diameter) caused by
• inflammation, narrowing (airway remodelling) and inflammatory exudates
• loss of lung elastic recoil (due to destruction of alveolar walls)
• destruction of alveolar support (from alveolar attachments)
• progressive air trapping during expiration causes hyperinflation of the lungs at rest and dynamic hyperinflation during exercise
• hyperinflation is thought to develop early in the disease and is the main mechanism for exertional dyspnoea (1,2)
  
  
• gas exchange abnormalities
• characterised by arterial hypoxaemia with or without hypercapnia
• results from an abnormal distribution of ventilation/perfusion ratios
  
  
• pulmonary hypertension
• occurs in late COPD where there is severe gas exchange abnormalities
• contributing factors include
• small pulmonary arterial vasoconstriction (due to hypoxia)
• endothelial dysfunction
• remodelling of the pulmonary arteries smooth muscle (hypertrophy and hyperplasia)
• destruction of the pulmonary capillary bed (1,2)

Reference:

• (1) Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2018. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease.
• (2) Currie GP. ABC of COPD. 2nd ed. West Sussex, UK. Wiley-Blackwell; 2011.