Chronic Obstructive Pulmonary Disease (COPD): Comprehensive Guide

Key Points

• COPD is a progressive respiratory disease characterized by persistent airflow limitation and chronic inflammation.
• Major risk factors include tobacco smoking, environmental pollutants, and genetic predisposition (e.g., alpha-1 antitrypsin deficiency).
• Pathogenesis involves oxidative stress, protease–antiprotease imbalance, and airway remodeling.
• Clinical features include chronic cough, sputum production, dyspnea, and frequent exacerbations.
• Diagnosis is based on spirometry, imaging, and symptom assessment.
• Management focuses on smoking cessation, pharmacotherapy (bronchodilators, inhaled corticosteroids), pulmonary rehabilitation, and prevention of exacerbations.

Introduction

Chronic Obstructive Pulmonary Disease (COPD) encompasses chronic bronchitis and emphysema. It leads to irreversible airflow limitation and is a leading cause of morbidity and mortality worldwide. Early diagnosis and comprehensive management can improve quality of life and reduce healthcare burden.

Epidemiology and Risk Factors

• Global Prevalence: Affects over 200 million people; fourth leading cause of death globally.
• Smoking: Primary risk factor; responsible for 80–90% of cases in developed countries.
• Environmental Exposures: Biomass fuel smoke, air pollution (sulfur dioxide, nitrogen dioxide, ozone), occupational dusts, and chemical fumes.
• Genetic Factors: Alpha-1 antitrypsin deficiency predisposes to early-onset panacinar emphysema.
• Other Risks: Recurrent respiratory infections, low socioeconomic status, childhood lung growth impairment.

Pathogenesis

1. Oxidative Stress and Inflammation

• Exogenous Oxidants: Tobacco smoke, pollution.
• Endogenous Oxidants: Reactive oxygen species from activated neutrophils and macrophages.
• Oxidative damage to airway epithelium and inactivation of antiproteases.
• Upregulation of proinflammatory mediators (IL-6, IL-8, TNF-α) and activation of transcription factors.

2. Protease–Antiprotease Imbalance

• Neutrophil elastase and matrix metalloproteinases degrade elastin and collagen in alveolar walls.
• Reduced alpha-1 antitrypsin activity exacerbates tissue destruction.

3. Airway Remodeling and Mucus Hypersecretion

• Goblet cell hyperplasia and submucosal gland enlargement lead to chronic bronchitis.
• Fibrosis and smooth muscle hypertrophy contribute to airway narrowing.

4. Airflow Limitation and Air Trapping

• Loss of elastic recoil and small airway collapse during expiration.
• Increased residual volume and hyperinflation, reducing ventilation efficiency.

Clinical Features

• Symptoms:
• Chronic productive cough (bronchitis phenotype).
• Progressive dyspnea on exertion.
• Wheezing and chest tightness.
• Exacerbations:
• Acute worsening of symptoms often triggered by infections or pollutants.
• Systemic Effects:
• Skeletal muscle dysfunction, weight loss, cardiovascular comorbidities.

Diagnosis

1. Spirometry:
2. Post-bronchodilator FEV₁/FVC < 0.70 confirms persistent airflow limitation.
3. FEV₁ quantifies severity (GOLD stages I–IV).
4. Imaging:
5. Chest X-ray: Hyperinflation, flattened diaphragm.
6. CT Scan: Emphysema