Common, preventable, and treatable disease characterized by persistent respiratory symptoms and airflow limitations due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases
COPD (practical definition)
>40 years old
Significant exposure (10 pack-year smoking history, biomass exposure, certain occupations)
No prior diagnosis of asthma
Post bronchodilator FEV1/FVC ratio of <70
Pathophysiology of COPD
1. Increased # of mucus secreting goblet cells→more mucus secretion
2. Lymphocytic infiltrate (CD8+)
3. Ulceration of epithelial layer→squamous cell metaplasia with time
4. Inflammation→scarring and thickening of walls→fibrosis →airflow limitation
Risk factors for COPD
Smoking
Second-hand smoke
Alpha1 antitrypsin deficiency
Chronic asthma
Infections (often the precipitating cause of acute exacerbations)
Diagnosis of COPD
Pulmonary function tests (decreased FEV1 and FEV1/FVC ratio, post bronchodilator FEV1/FVC ratio of <70, decreased vital capacity, increased TLC, residual volume & FRC)
Chest x-ray (useful in severe advanced emphysema and acute exacerbations)
ABG (hypercapnia, hypoxemia)
Alpha 1 antitrypsin level (in patients with family history of premature emphysema)
Significant reversibility after bronchodilator (200ml AND 12%) does NOT exclude COPD; some people may have variable reversibility
Chest x-ray (low sensitivity)
Useful in severe advanced emphysema which would show hyperinflation, flattened diaphragm, enlarged retrosternal space, diminished vascular markings
Useful in acute exacerbations to rule out: pneumonia, pneumothorax
ABG
Hypercapnia, hypoxemia
Alpha 1 antitrypsin level
In patients with family history of premature emphysema
Chronic bronchitis
Chronic productive (sputum) cough of at least 3 months per year for at least 2 consecutive years. (Clinical diagnosis)
Emphysema
Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls. (Pathologic diagnosis)
Pathogenesis of chronic bronchitis
1. Excess mucus production narrows the airways
2. Inflammation & scarring in airways + enlarged mucus glands + SM hyperplasia à obstruction
Pathogenesis of emphysema
1. Elastase enzyme released by PMNs and macrophages digests the human lung and is usually inhibited by alpha 1 antitrypsin
2. Decrease in alpha 1 antitrypsin à alveolar wall destruction
Symptoms
Chronic cough
Sputum production (white or clear unless infected)
Dyspnea, wheeze
More prone to infections
Signs of chronic bronchitis (Blue Bloaters)
End-expiratory wheezing on auscultation, decreased breath sounds
Hyperresonance on percussion
Prolonged expiratory time
Usually overweight
Cyanosis
RR normal
Tachycardia
Bounding pulse
Peripheral vasodilation
Course flapping tremor
Confusion/drowsiness
Signs of emphysema (Pink Puffers)
Thin due to increasedBMR
Barrel chest
Tachypnea
Breathing through pursed lips (to prevent alveolar and airway collapse)
Patient in distress with accessory muscle use
Treatment
Smoking cessation (most important)
Home oxygen therapy (if pO2 ≤55 or saturation ≤88%; mortality benefit is directly proportional to the number of hours oxygen is used)
Influenza and pneumococcal vaccinations
Inhaled bronchodilators (anticholinergics ex: ipratropium bromide or B-agonists ex: albuterol, salmeterol or combination of both)
If low exacerbation risk: LAMA
If frequent exacerbations, highly symptomatic, or eosinophils > 300 à Inhaled corticosteroids + LAMA or LABA
Pulmonary rehabilitation
Surgery for selected patients (lung resection/transplantation)
The two types (chronic bronchitis and emphysema) usually coexist
Complications of COPD
Acute exacerbations (due to infections, non-compliance and cardiac problems)
Secondary polycythemia (as compensation for chronic hypoxemia)