This site is intended for healthcare professionals

Go to /sign-in page

You can view 5 more pages before signing in

Pathology and mechanism of airflow obstruction

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

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 obstruction 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
    • may develop late in the course of COPD
    • contributing factors include
      • loss of pulmonary capillary bed due to emphysema and/or hypoxic vasoconstriction of the small pulmonary arteries (1)
      • endothelial dysfunction
      • remodelling of the pulmonary arteries smooth muscle (hypertrophy and hyperplasia) and intimal hyperplasia


Create an account to add page annotations

Add information to this page that would be handy to have on hand during a consultation, such as a web address or phone number. This information will always be displayed when you visit this page