Chronic Obstructive Pulmonary Disease

COPD is a major cause of morbidity and mortality in the UK, strongly linked to smoking and socioeconomic deprivation. Diagnosis is confirmed by post-bronchodilator spirometry showing an FEV1/FVC ratio < 0.70. Clinical features include progressive dyspnoea, chronic sputum production, and frequent winter chest infections. Severity is graded by FEV1 % predicted (GOLD: Mild >80%, Moderate 50-79%, Severe 30-49%, Very Severe <30%). Patients often exhibit 'pink puffer' (emphysematous, high drive, breathless) or 'blue bloater' (bronchitic, low drive, cyanosed, oedematous) phenotypes. Management according to NICE NG115 starts with smoking cessation and vaccinations (influenza and pneumococcal). Pharmacotherapy follows a pathway: SABA/SAMA for breathlessness, then adding LABA+LAMA if no asthmatic features, or LABA+ICS if features of asthma/steroid responsiveness (e.g., high eosinophils) exist. Triple therapy (LABA+LAMA+ICS) is used if symptoms or exacerbations persist. Pulmonary rehabilitation is recommended for all patients with a mMRC score >=2. Long-term oxygen therapy (LTOT) is considered if pO2 <7.3 kPa when stable. Acute exacerbations are treated with increased bronchodilators, steroids (5 days prednisolone), and antibiotics if purulent sputum is present.

COPD involves chronic inflammation throughout the airways, parenchyma, and pulmonary vasculature. In the large airways, irritants cause goblet cell hypertrophy and mucus hypersecretion (chronic bronchitis). In the small airways (bronchioles), inflammation leads to fibrosis and narrowing. Emphysema is the destruction of the gas-exchanging surfaces (alveoli) resulting from an imbalance between proteases (such as elastase) and anti-proteases (such as alpha-1 antitrypsin). Smoking recruits neutrophils and macrophages which release elastase; if this outweighs the protective effects of alpha-1 antitrypsin, the lung parenchyma is 'digested,' leading to reduced elastic recoil and bullae formation. This airway collapse during expiration causes air trapping and lung hyperinflation, which increases the work of breathing and flattens the diaphragm. Pathological patterns include centriacinar emphysema (common in smokers, upper lobes) and panacinar emphysema (characteristic of alpha-1 antitrypsin deficiency, lower lobes).

Patients typically present in their 50s or 60s with 'smoker's cough' and exertional dyspnoea. Signs include tachypnoea, a prolonged expiratory phase, pursed-lip breathing, and use of accessory muscles. Hyperinflation may cause a 'barrel chest,' hyper-resonant percussion, and decreased cricosternal distance (<2 fingers). Auscultation reveals quiet breath sounds and occasional coarse crackles or wheeze. Advanced disease may show signs of cor pulmonale (raised JVP, peripheral oedema, parasternal heave). Red flags include weight loss, hemoptysis (requiring lung cancer exclusion), and sudden worsening (suggestive of pneumothorax or PE). Complications include Type 2 respiratory failure (hypercapnia), polycythaemia (compensatory response to chronic hypoxia), and secondary spontaneous pneumothorax (rupture of bullae).

Bedside: Post-bronchodilator spirometry (FEV1/FVC < 0.7); Pulse oximetry; mMRC Dyspnoea scale. Bloods: FBC (polycythaemia/eosinophilia), Alpha-1 antitrypsin level (especially if <45 yrs or non-smoker). Imaging: Chest X-ray (hyperinflation, >6 anterior ribs, flattened diaphragms, decreased lung markings); CT Thorax (gold standard for emphysema and assessing for lung cancer/bronchiectasis). Special Tests: ABG (assess for hypoxia/hypercapnia if SpO2 <92%); ECG (looking for P-pulmonale or RVH).

**Conservative:** Smoking cessation (Varenicline/NRT — most effective intervention), Pulmonary Rehabilitation, Vaccinations (annual Influenza, Pneumococcal, COVID-19 boosters).

**Medical (Stable COPD) — GOLD 2024 / NICE NG115:**
GOLD 2024 revised stable COPD classification from A/B/C/D groups to A/B/E groups based on symptoms and exacerbation history (C and D merged into 'E' for frequent exacerbators):
- **Group A** (low symptoms, low exacerbation risk): SABA or SAMA prn.
- **Group B** (high symptoms, low exacerbation risk): Long-acting bronchodilator — LABA + LAMA preferred over monotherapy. Initiate dual bronchodilation early.
- **Group E** (frequent exacerbators ≥2/year or ≥1 requiring hospitalisation): LABA + LAMA. If eosinophils ≥300 cells/µL or asthmatic features: LABA + ICS (or triple LABA/LAMA/ICS).
Other stable management: Mucolytics (Carbocisteine) for chronic productive cough. Long-term Azithromycin (250mg OD or 500mg 3×/week) for frequent exacerbators not responding to inhaled therapy — check QTc, hearing, and exclude NTM infection before starting.

**Acute Exacerbation:** Increased SABA via spacer/nebuliser; Prednisolone 30mg PO for 5 days; Antibiotics (e.g. Amoxicillin/Doxycycline) if purulent sputum or clinical signs of infection; Controlled Oxygen via Venturi mask (24% or 28%) — target SpO2 88-92% if CO2 retention risk; NIV (BiPAP) if pH <7.35 and pCO2 >6.0kPa despite optimal medical therapy.