Chronic obstructive pulmonary disease for the USMLE Step 2 Exam
Pathophysiology
- Chronic Inflammation:
- COPD is driven by chronic inflammation of the airways and lung parenchyma due to long-term exposure to irritants such as cigarette smoke.
- Neutrophils, macrophages, and CD8+ T cells predominate in the inflammatory response, causing airway narrowing and alveolar destruction.
- Airflow Limitation:
- Small Airway Disease: Inflammation and fibrosis narrow the bronchioles, increasing airway resistance.
- Emphysema: Destruction of alveolar walls leads to loss of elastic recoil, causing air trapping and hyperinflation.
- Protease-Antiprotease Imbalance:
- In smokers and alpha-1 antitrypsin deficiency, increased protease activity leads to destruction of alveoli and small airways.
- Oxidative Stress:
- Smoke and inflammatory cells release oxidants, further damaging lung tissue and worsening inflammation.
Clinical Features
- Chronic Cough and Sputum Production:
- Early signs of COPD, often worse in the morning with productive sputum.
- Dyspnea:
- Progressive shortness of breath is the most characteristic symptom, typically worsening with exertion.
- Wheezing and Chest Tightness:
- These symptoms may occur, especially during exacerbations.
Diagnosis
- Spirometry:
- Key diagnostic test showing:
- FEV1/FVC Ratio <0.70: Confirms persistent airflow obstruction.
- Reduced FEV1: Reflects the severity of obstruction.
- Chest X-ray:
- Common findings include hyperinflation, flattened diaphragms, and increased retrosternal air space.
- Arterial Blood Gas (ABG):
- In advanced cases or exacerbations, ABG may show hypoxemia or hypercapnia.
Management
- Smoking Cessation:
- The most effective intervention to slow COPD progression and improve survival.
- Bronchodilators:
- Short-acting beta-agonists (SABAs): Provide symptom relief during exacerbations.
- Long-acting beta-agonists (LABAs) and long-acting muscarinic antagonists (LAMAs): Maintenance therapy to reduce symptoms and exacerbations.
- Combination LABA/LAMA: Superior in improving lung function and reducing exacerbations compared to monotherapy.
- Inhaled Corticosteroids (ICS):
- Used in combination with bronchodilators (LABA/ICS) for patients with severe COPD or frequent exacerbations.
- Oxygen Therapy:
- Long-term oxygen therapy improves survival in patients with severe resting hypoxemia (PaO2 ≤55 mmHg or SaO2 ≤88%).
- Pulmonary Rehabilitation:
- A program of exercise and education that improves quality of life, especially in patients with moderate-to-severe COPD.
Exacerbations
- Definition:
- Acute worsening of respiratory symptoms beyond normal day-to-day variations, often triggered by infections.
- Management of Exacerbations:
- Bronchodilators: SABAs with or without short-acting anticholinergics (e.g., ipratropium).
- Systemic Corticosteroids: Short courses of prednisone (e.g., 40 mg for 5 days) improve lung function and reduce recovery time.
- Antibiotics: Used if there is increased sputum purulence, fever, or evidence of infection.
Complications
- Pulmonary Hypertension and Cor Pulmonale:
- Chronic hypoxia leads to pulmonary hypertension and eventually right heart failure (cor pulmonale).
- Acute Respiratory Failure:
- Exacerbations can result in acute respiratory failure, requiring mechanical ventilation or non-invasive positive pressure ventilation (NIPPV).
Key Points
- COPD is characterized by chronic inflammation, airflow limitation, and parenchymal destruction, primarily due to smoking.
- Spirometry (FEV1/FVC <0.70) is essential for diagnosis and staging, with chest X-rays supporting findings in advanced disease.
- Smoking cessation is the most critical intervention to halt disease progression.
- Pharmacologic treatment includes bronchodilators (SABAs, LABAs, LAMAs) and inhaled corticosteroids for maintenance and exacerbation prevention.
- Exacerbations are managed with bronchodilators, corticosteroids, and antibiotics when appropriate.
- Complications include pulmonary hypertension, cor pulmonale, and respiratory failure.