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Pathology and mechanism of airflow obstruction

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

Reference:


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