Chronic Obstructive Pulmonary Disease (COPD) 

Definition 
COPD is a preventable and treatable disease characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases. 

Epidemiology 

Affects ~10% of adults over 40 worldwide. 
Smoking is the leading risk factor (80–90% of cases in developed countries). 
Other risk factors: occupational dust, air pollution, alpha-1 antitrypsin deficiency, recurrent respiratory infections in childhood. 

Pathophysiology 

COPD includes two main pathological processes: 

Chronic Bronchitis (“Blue Bloater”) 
Chronic productive cough >3 months/year for ≥2 consecutive years. 
Airway inflammation → mucus hypersecretion → airway obstruction. 

Emphysema (“Pink Puffer”) 
Destruction of alveolar walls → loss of elastic recoil → airflow limitation. 
Air trapping → hyperinflation → dyspnoea. 

Key mechanisms: 

Airflow limitation → primarily due to small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema). 
Inflammatory cells: neutrophils, macrophages, CD8+ T lymphocytes. 
Protease-antiprotease imbalance → alveolar destruction (esp. α1-antitrypsin deficiency). 
Oxidative stress → amplifies inflammation 

Clinical Features 

Symptoms: 
Chronic cough 
Sputum production 
Progressive dyspnoea (especially on exertion) 
Wheezing, chest tightness 
Weight loss in advanced emphysema 

Signs: 
Barrel chest 
Use of accessory muscles 
Prolonged expiratory phase 
Cyanosis (especially in chronic bronchitis) 
Hyper-resonant lungs 
Decreased breath sounds, wheezes, crackles 

Complications 
Respiratory infections (pneumonia) 
Pulmonary hypertension → right heart failure (cor pulmonale) 
Acute exacerbations 
Pneumothorax (in emphysema) 

Diagnosis 

1. Spirometry (Gold standard) 
Post-bronchodilator FEV₁/FVC < 0.70 confirms airflow limitation. 
FEV₁ helps stage severity (GOLD criteria). 

2. Imaging 
Chest X-ray: hyperinflation, flattened diaphragms, increased retrosternal air space. 
CT scan: better for emphysema evaluation. 

3. Laboratory Tests 

α1-antitrypsin level (if early onset or family history) 
ABG in advanced disease (hypoxemia, hypercapnia) 

GOLD Classification (Airflow Limitation Severity) 


 
Management 

1. Non-pharmacologic 

Smoking cessation (most important) 
Vaccinations: influenza, pneumococcal 
Pulmonary rehabilitation 
Oxygen therapy (if PaO₂ ≤ 6.7KPa (55 mmHg) or SaO₂ ≤ 88% as directed by medical staff) 

2. Pharmacologic 

Bronchodilators: 
Short-acting: SABA (salbutamol), SAMA (ipratropium) 
Long-acting: LABA (symbicort), LAMA (Spiriva) 
Inhaled corticosteroids (ICS): for frequent exacerbations (eg; beclomethasone, budesonide) 
Combination therapy: LABA + LAMA or LABA + ICS 
Phosphodiesterase-4 inhibitors: roflumilast (severe cases) 
Mucolytics: in select patients 

3. Surgical 
Lung volume reduction lung surgery 
Lung transplantation (end-stage disease and other organs functioning well) 

4. Management of Exacerbations 
Oxygen supplementation (target 88–92%) 
Short-acting bronchodilators 
Systemic corticosteroids (e.g., prednisolone 30–40 mg/day for 5–7 days) 
Antibiotics if bacterial infection suspected 

Prognosis 

COPD is progressive and incurable. 
Prognosis depends on severity, exacerbation frequency, comorbidities, and smoking cessation. 
BODE index (BMI, airflow Obstruction, Dyspnoea, Exercise capacity) predicts mortality better than FEV₁ alone. 
 
Key Points 

Emphasise smoking cessation and risk factor modification. 
Spirometry is essential for diagnosis. 
Recognize chronic bronchitis vs emphysema phenotypes, but most patients have mixed features. 
Manage exacerbations promptly; these significantly affect prognosis. 
Careful management through pulmonary rehabilitation and oxygen therapy improve quality of life and life expectancy.