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chronic obstructive pulmonary disease

progressive, largely irreversible airflow obstruction caused by chronic bronchitis and/or emphysema, overwhelmingly linked to smoking

respiratorycommonchronic

About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

The Bottom Line

  • Diagnosis: post-bronchodilator FEV₁/FVC <0.7 in a patient with appropriate exposure history (usually smoking)
  • NOT fully reversible (unlike asthma) — <12% reversibility on spirometry
  • NICE inhaler pathway: SABA/SAMA → if asthmatic features (eosinophils/atopy) add ICS+LABA; if not, add LABA+LAMA
  • Acute exacerbation: nebulised bronchodilators, prednisolone 30 mg for 5 days, antibiotics if purulent sputum, controlled O₂ (target 88–92%)
  • LTOT criteria: PaO₂ ≤7.3 kPa on two ABGs ≥3 weeks apart when stable — use ≥15 h/day

Overview

COPD is a common, preventable, and treatable disease characterised by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases — predominantly cigarette smoke. It encompasses chronic bronchitis (productive cough ≥3 months in ≥2 consecutive years) and emphysema (destruction of alveolar walls distal to terminal bronchioles). Unlike asthma, the airflow limitation is progressive and not fully reversible.

Epidemiology

COPD affects approximately 1.2 million diagnosed patients in the UK, with an estimated further 2 million undiagnosed. It is the third leading cause of death worldwide. The overwhelming risk factor is cigarette smoking (~85% of cases). Other risk factors include occupational dust/fume exposure, biomass fuel exposure, alpha-1 antitrypsin deficiency (suspect in young/non-smoking patients), air pollution, and childhood respiratory infections. Prevalence rises steeply with age and is strongly correlated with socioeconomic deprivation.

Clinical Features

Symptoms
Progressive exertional breathlessness — the cardinal symptom
Chronic productive cough — often worse in the morning
Frequent winter "chest infections"
Wheeze
Reduced exercise tolerance and fatigue
Weight loss and muscle wasting (advanced disease)
Haemoptysis — must exclude lung cancer
Signs
Hyperinflated barrel chest, reduced cricosternal distance
Pursed-lip breathing, use of accessory muscles
Reduced breath sounds, expiratory wheeze
Hyperresonant percussion
Cyanosis (blue bloater phenotype)
Signs of cor pulmonale: raised JVP, peripheral oedema, hepatomegaly
Asterixis (CO₂ retention flap) in hypercapnic respiratory failure

Investigations

First-line
Post-bronchodilator spirometryFEV₁/FVC <0.7 confirms airflow obstruction. FEV₁ % predicted determines severity: mild ≥80%, moderate 50–79%, severe 30–49%, very severe <30%
Chest X-rayHyperinflation, flat hemidiaphragms, increased AP diameter, bullae. Also excludes other pathology (lung cancer, pneumonia)
FBCPolycythaemia (chronic hypoxia), eosinophilia (may guide ICS use)
Second-line
BMILow BMI is a poor prognostic marker — forms part of BODE index
Alpha-1 antitrypsin levelCheck in patients diagnosed <40 years, minimal smoking history, family history, or predominantly basal emphysema
Sputum cultureDuring exacerbations if not responding to empirical antibiotics
ABGType 2 respiratory failure (raised PaCO₂, low PaO₂) in severe disease or acute exacerbation
Specialist
CT thoraxConfirms emphysema distribution, excludes bronchiectasis and malignancy, pre-operative assessment
Transfer factor (TLCO)Reduced in emphysema; helps distinguish from asthma (normal/elevated in asthma)
EchocardiogramIf cor pulmonale or pulmonary hypertension suspected
1
Non-pharmacological (all patients)
  • Smoking cessation — single most important intervention, offer NRT/varenicline at every contact
  • Pulmonary rehabilitation — for all with MRC dyspnoea ≥3
  • Annual influenza and pneumococcal vaccination
  • Self-management plan for exacerbations (rescue pack)
2
Step 1 — short-acting bronchodilators
  • SABA (salbutamol) or SAMA (ipratropium) PRN
  • If persistently symptomatic → step up based on phenotype
3
Step 2 — determine pathway by phenotype
  • Asthmatic/eosinophilic features (previous asthma diagnosis, eosinophils ≥300, atopy): LABA + ICS
  • No asthmatic features: LABA + LAMA (e.g. tiotropium + olodaterol)
  • NICE emphasises checking eosinophil count and asthma history before starting ICS
4
Step 3 — triple therapy if still symptomatic
  • LABA + LAMA + ICS (triple inhaler e.g. Trimbow, Trelegy)
  • Consider roflumilast in severe COPD with frequent exacerbations (FEV₁ <50%) and chronic bronchitis phenotype
  • Azithromycin prophylaxis for frequent exacerbations (specialist decision, check ECG and LFTs)
5
Advanced/specialist
  • Long-term oxygen therapy (LTOT): if PaO₂ ≤7.3 kPa on two ABGs ≥3 weeks apart, use ≥15 h/day. Must have stopped smoking
  • NIV for chronic hypercapnic respiratory failure
  • Lung volume reduction surgery or endobronchial valves for selected emphysema patients
  • Lung transplantation in end-stage disease
6
Acute exacerbation (AECOPD)
  • Controlled oxygen: target SpO₂ 88–92% via Venturi mask (24–28%)
  • Nebulised salbutamol 5 mg + ipratropium 500 mcg
  • Prednisolone 30 mg OD for 5 days
  • Antibiotics if purulent sputum: amoxicillin, doxycycline, or clarithromycin
  • NIV (BiPAP) if pH <7.35 and PaCO₂ >6.0 despite initial treatment
  • Do NOT give high-flow oxygen — risk of CO₂ retention and respiratory arrest

Complications

  • Acute exacerbations: Accelerate lung function decline — each exacerbation increases mortality risk
  • Cor pulmonale: Right heart failure secondary to chronic pulmonary hypertension
  • Respiratory failure: Type 2 (hypercapnic) — may require long-term NIV
  • Pneumothorax: Rupture of bullae, especially in emphysema
  • Lung cancer: Smoking is the shared risk factor — maintain high index of suspicion
  • Depression and anxiety: Highly prevalent — screen and treat
  • Polycythaemia: Secondary to chronic hypoxia
  • Osteoporosis: From systemic steroids and physical inactivity
UKMLA Exam Tips
  • 1COPD: FEV₁/FVC <0.7 post-bronchodilator with LESS than 12% reversibility (>12% = think asthma)
  • 2Target SpO₂ in COPD exacerbation is 88–92% — NOT 94–98%. This is the most commonly tested oxygen target
  • 3LTOT criteria: PaO₂ ≤7.3 kPa on TWO stable ABGs ≥3 weeks apart — and patient must not be smoking
  • 4Alpha-1 antitrypsin: suspect if COPD in a young non-smoker with basal emphysema and liver disease
  • 5TLCO is LOW in emphysema but NORMAL/HIGH in asthma — useful differentiator in exams
  • 6Never give high-flow O₂ to a COPD patient without monitoring — risk of suppressing hypoxic respiratory drive
  • 7NIV (BiPAP) is indicated when pH <7.35 despite maximal medical therapy — know this threshold
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Verified Sources & References

NICE NG115 — COPD
GOLD 2024 Report
BNF — COPD