Chronic respiratory condition characterised by airflow obstruction, most commonly the result of a combination chronic bronchitis and emphysema

Aetiology

• Caused by long-term exposure to toxic particles and gases - smoking accounts for 90-98% of cases in developed countries
  • In developing countries, other factors are also implicated, such as inhalation of smoke from biomass heating fuels and cooking in poorly ventilated areas
• More common with increasing age (>40)
• Genetic predisposition - alpha-1 antitrypsin deficiency
  • Results in failure to break down neutrophil elastase
  • More likely to develop COPD at a younger age, especially if they smoke

Pathophysiology

Chronic bronchitis

• Chronic exposure to noxious particles such as smoking or air pollutants causes hypersecretion of mucus in the large and small bronchi
• Airway inflammation and fibrotic changes result in narrowing of the airways and subsequently chronic airway obstruction
• Cigarette smoke interferes with the action of cilia in removing noxious particles
• Cigarette smoke also dampens the ability of leukocytes in eliminating the bacteria in the airways

Emphysema

• Abnormal irreversible enlargement of the airspaces distal to the terminal bronchioles, due to destruction of their walls
• This reduces the alveolar surface area thus impeding efficient gaseous exchange
• Cigarette smoke stimulates accumulation of neutrophils and macrophages which produce neutrophil elastase that destroys alveolar walls
• In a normal lung, α1-antitrypsin is responsible for inhibiting excessive activity of neutrophil elastase
  • However, in emphysema, the normal balance of proteases and antiproteases is lost
  • The stimulated neutrophils release free radicals that inhibit the activity of α1-antitrypsin
• This results in loss of elastic recoil and subsequently airway collapse during expiration and air trapping

Clinical features

General features of COPD

• Productive cough with white or clear sputum