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Chronic obstructive pulmonary disease

SNOMED: 171230000933 wordsUpdated 03/03/2026
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Exam Tips

  • Diagnosis is clinical plus spirometric: post-bronchodilator FEV1/FVC < 0.70 supports COPD; do not rely on bronchodilator reversibility testing alone.
  • In OSCEs, always quantify smoking exposure in pack-years and ask about occupational/biomass exposures.
  • Red flags are atypical for stable COPD: haemoptysis, chest pain, marked weight loss, or unilateral signs should trigger urgent evaluation for alternative pathology (for example malignancy).
  • Differentiate symptom burden and future risk: frequent exacerbator phenotype drives escalation (often LABA/LAMA then consider ICS-containing therapy).
  • Cor pulmonale clues (raised JVP, oedema, loud P2, parasternal heave) indicate advanced disease and poorer prognosis.
  • Image revision: review flow-volume loop patterns in obstructive disease and CXR hyperinflation signs (flattened diaphragms, increased lucency) in your core respiratory textbook figures.

Definition

Chronic obstructive pulmonary disease (COPD) is a common, preventable and treatable chronic respiratory disorder characterized by persistent respiratory symptoms and usually progressive airflow limitation that is not fully reversible on bronchodilator testing. It is an umbrella diagnosis that includes chronic bronchitis and emphysema, most often caused by long-term exposure to tobacco smoke or other noxious particles, with acute exacerbations causing stepwise clinical decline.

Pathophysiology

COPD develops through chronic airway and alveolar inflammation, driven by inhaled toxins (especially cigarette smoke), with contributions from oxidative stress and protease-antiprotease imbalance. Two overlapping processes dominate: small-airway disease (mucus hypersecretion, wall thickening, fibrosis, narrowing) and parenchymal destruction (emphysema with loss of elastic recoil), leading to expiratory flow limitation, air trapping and hyperinflation. Gas-exchange abnormalities cause ventilation-perfusion mismatch, hypoxaemia and in advanced disease hypercapnia; chronic hypoxic pulmonary vasoconstriction can progress to pulmonary hypertension and cor pulmonale. In alpha-1 antitrypsin deficiency, reduced antiprotease protection accelerates emphysematous destruction (often earlier onset, sometimes lower-lobe predominant).

Risk Factors

  • Cigarette smoking (most important), plus cigar/pipe/water-pipe/marijuana smoking
  • Passive smoke exposure
  • Occupational dust/fume exposure (for example coal, silica, grain dust, welding fumes, isocyanates, polycyclic aromatic hydrocarbons)
  • Indoor biomass smoke exposure (wood/coal burning, especially poorly ventilated homes)
  • Alpha-1 antitrypsin deficiency and family history of early lung/liver disease
  • Impaired lung growth/development (maternal smoking, prematurity, severe childhood respiratory infection)
  • History of asthma (increased later COPD risk)

Clinical Features

Symptoms

  • Progressive exertional breathlessness
  • Chronic or recurrent cough
  • Regular sputum production
  • Frequent lower respiratory tract infections/exacerbations
  • Wheeze
  • Fatigue, weight loss, reduced exercise tolerance (more severe disease)
  • Nocturnal breathlessness in advanced disease

Signs

  • Examination may be normal early on
  • Wheeze and/or crackles
  • Hyperinflated chest (barrel chest), prolonged expiratory phase
  • Accessory muscle use, pursed-lip breathing
  • Cyanosis (advanced disease)
  • Cachexia or low BMI
  • Peripheral oedema, raised JVP, loud P2, parasternal heave, hepatomegaly (suggesting cor pulmonale)

Investigations

Post-bronchodilator spirometry:FEV1/FVC < 0.70 confirms persistent airflow obstruction consistent with COPD in the right clinical context
Chest X-ray:May show hyperinflation/flattened diaphragms; mainly used to exclude alternative diagnoses such as lung cancer, heart failure, TB, bronchiectasis
Full blood count:Polycythaemia from chronic hypoxia or anaemia contributing to dyspnoea
Pulse oximetry (and arterial/capillary blood gas if indicated):Hypoxaemia; severe disease may show hypercapnic respiratory failure
ECG, natriuretic peptides, echocardiography (if cardiac disease suspected):Helps identify heart failure/pulmonary hypertension/cor pulmonale as comorbidity or differential
CT thorax:Assesses emphysema pattern/bullae, and evaluates disproportionate symptoms or suspected alternative pathology
Alpha-1 antitrypsin testing:Consider in younger patients (especially <40-45 years), minimal smoking history, or suggestive family history

Management

Lifestyle Modifications

  • Smoking cessation support (behavioural plus pharmacotherapy), as this most effectively slows FEV1 decline
  • Annual influenza vaccination and pneumococcal vaccination
  • Pulmonary rehabilitation for symptomatic patients with exercise limitation
  • Inhaler technique training, adherence review, and individualized self-management/exacerbation action plan
  • Nutritional optimization and exercise conditioning (address low BMI/cachexia)
  • Long-term oxygen therapy for chronic severe resting hypoxaemia after specialist assessment; strict fire-safety counselling (no smoking around oxygen)

Pharmacological Treatment

Short-acting bronchodilators (reliever)

  • Salbutamol inhaler 100-200 micrograms as required (up to 4 times daily)
  • Ipratropium inhaler 20-40 micrograms 4 times daily

Use for symptom relief and during exacerbation worsening; check inhaler technique and response.

Long-acting bronchodilators (maintenance)

  • Tiotropium 18 micrograms once daily via DPI (or 5 micrograms once daily via Respimat)
  • Salmeterol 50 micrograms twice daily
  • Umeclidinium/vilanterol 55/22 micrograms once daily

Escalate from single long-acting bronchodilator to LABA+LAMA for persistent breathlessness/exacerbations. Caution with antimuscarinics in narrow-angle glaucoma and urinary retention.

Inhaled corticosteroid-containing regimens (selected patients)

  • Fluticasone propionate/salmeterol 500/50 micrograms one inhalation twice daily
  • Fluticasone furoate/umeclidinium/vilanterol 92/55/22 micrograms once daily (triple therapy)

Consider when exacerbations persist despite dual bronchodilation (often with eosinophilic phenotype/asthma overlap). Safety: increased pneumonia risk, oral candidiasis, dysphonia, skin bruising; use lowest effective ICS exposure and review benefit regularly.

Phosphodiesterase-4 inhibitor (specialist add-on)

  • Roflumilast 500 micrograms once daily

For severe COPD with chronic bronchitis and frequent exacerbations despite optimized inhaled therapy. Avoid in moderate-severe hepatic impairment; use caution in underweight patients and those with depression/suicidal ideation.

Mucolytic therapy

  • Carbocisteine 750 mg three times daily initially, then reduce (for example 750 mg twice daily) if effective

Trial in chronic productive cough; continue only if symptomatic benefit.

Exacerbation medication (acute episodes)

  • Prednisolone 30 mg orally once daily for 5 days
  • Amoxicillin 500 mg three times daily for 5 days (if purulent sputum/clinical bacterial infection suspected)
  • Doxycycline 200 mg on day 1 then 100 mg daily for total 5 days (penicillin alternative)

Antibiotics are not routine for all exacerbations; target likely infective episodes. Safety: steroid hyperglycaemia, mood effects, fluid retention; review repeated courses and osteoporosis risk.

Smoking cessation pharmacotherapy

  • Varenicline: titrate to 1 mg twice daily
  • Nicotine replacement therapy (single or combination forms)

Combine with behavioural support for best quit rates; check neuropsychiatric history and renal dosing for varenicline.

Surgical / Interventional

  • Lung volume reduction surgery in carefully selected heterogeneous emphysema with hyperinflation
  • Bronchoscopic lung volume reduction (endobronchial valves) in selected cases
  • Bullectomy for giant bullae causing compression symptoms
  • Lung transplantation in end-stage disease after specialist assessment

Complications

  • Frequent infective exacerbations and recurrent pneumonia
  • Chronic respiratory failure
  • Pulmonary hypertension and cor pulmonale
  • Secondary polycythaemia
  • Pneumothorax (especially with bullous disease)
  • Muscle wasting/cachexia and reduced functional capacity
  • Anxiety and depression
  • Increased risk of lung cancer
  • Reduced quality of life and premature mortality

Prognosis

COPD is typically progressive, with prognosis shaped by airflow limitation severity, symptom burden, exercise capacity, exacerbation frequency, and hospital admissions. Ongoing smoking, low BMI/cachexia, chronic hypoxia/hypercapnia, and multimorbidity worsen outcomes, while smoking cessation, pulmonary rehabilitation, vaccination, and optimized inhaled therapy reduce exacerbations and slow functional decline. Severe exacerbations requiring admission carry substantial medium-term mortality risk.

Sources & References

💊BNF Drug References(30)

NICE Guidelines(1)

📖Textbook References(11)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1693, 1694)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1693)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 373, 374)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 587, 588)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 589, 590)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1814)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 549)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 502)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 549)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 502)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 872)[context]

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