Chronic Obstructive Pulmonary Disease (COPD)

 

Chronic Obstructive Pulmonary Disease (COPD)  

Definition:

  • Persistent respiratory symptoms (cough, dyspnea) + airflow limitation (post-bronchodilator FEV1/FVC < 0.70).

  • Caused by small airway obstruction + parenchymal destruction.

Key Conditions:

  • Chronic bronchitis: Productive cough ≥ 3 months/year for ≥ 2 consecutive years.

  • Emphysema: Permanent dilatation of airspaces distal to terminal bronchioles, destruction of alveolar walls.

  • PRISm: FEV1 < 80% predicted, FEV1/FVC ≥ 0.70.


Epidemiology:

  • Male:female ratio ≈ 3:2

  • Prevalence ~6% in the US


Etiology:

Exogenous:

  • Tobacco smoking (major risk factor)

  • Passive smoking, air pollution, occupational dust (organic & inorganic)

Endogenous/Genetic:

  • α1-antitrypsin deficiency (AATD)

  • Abnormal lung development, premature birth, recurrent infections

  • Airway hyperresponsiveness, antibody deficiencies, primary ciliary dyskinesia


Pathophysiology:

  1. Chronic inflammation:

    • Neutrophils, macrophages, CD8+ T-cells → cytokines → tissue damage

    • Goblet cell hyperplasia → mucus hypersecretion → chronic cough

  2. Tissue destruction:

    • Protease/antiprotease imbalance (↑ elastase) → alveolar wall destruction

    • ↓ Elastic recoil → airway collapse → air trapping, hyperinflation

    • ↓ DLCO → hypoxemia & hypercapnia

  3. Pulmonary hypertension & cor pulmonale:

    • Hypoxic vasoconstriction, smooth muscle hypertrophy


Clinical Features:

  • Early: Chronic productive cough, dyspnea on exertion

  • Advanced: Dyspnea at rest, tachypnea, cyanosis, accessory muscle use

  • Signs: Barrel chest, prolonged expiration, decreased breath sounds, peripheral edema, weight loss/cachexia

  • “Pink puffer” vs “Blue bloater”:

    FeaturePink PufferBlue Bloater
    Main mechanismEmphysemaChronic bronchitis
    AppearanceCachectic, noncyanotic, pursed-lip breathingOverweight, cyanotic, peripheral edema
    PaO2Slightly reducedMarkedly reduced
    PaCO2Normal (late ↑)↑ early

Emphysema Subtypes:

  • Centrilobular: Upper lobes, smokers as pic below:

     

  • Panlobular: Lower lobes, AATD


  • Other: Cicatricial (quartz dust), Giant bullous, Age-related


Diagnosis:

  • Clinical + Pulmonary function tests (↓ FEV1/FVC)


  • Imaging: Assess severity, complications


  • GOLD classification:
    Spirometric Grades:

    • GOLD 1 ≥ 80% FEV1

    • GOLD 2 50–79%

    • GOLD 3 30–49%

    • GOLD 4 < 30%
      Groups (A, B, E): Based on symptoms + exacerbations


Management:

Non-pharmacologic:

  • Smoking cessation (most effective)

  • Pulmonary rehabilitation, physical activity, nutrition

  • Vaccinations: Influenza, pneumococcal, COVID-19, Tdap, RSV, zoster

Pharmacologic:

  • Bronchodilators: Mainstay (SABA/SAMA, LABA/LAMA)

  • ICS: Only with long-acting bronchodilators or asthma overlap

  • Follow-up: Adjust based on treatable traits (dyspnea, exacerbations)

Advanced disease:

  • Oxygen therapy (PaO2 ≤ 55 mmHg or SaO2 ≤ 88%)

  • Noninvasive ventilation for hypercapnia

  • Surgical options: Bullectomy, lung volume reduction, transplantation

  • Palliative care: Symptom control for breathlessness


Complications:

  • Acute exacerbations (most significant)

  • Chronic respiratory failure (hypoxemia, hypercapnia)

  • Pulmonary hypertension / cor pulmonale

  • Spontaneous pneumothorax (bullae rupture)


Prognosis:

  • 5-year survival: 40–70%, depending on severity

  • BODE index (BMI, Obstruction, Dyspnea, Exercise) predicts prognosis

  • Improved survival: Smoking cessation, long-term oxygen therapy in severe hypoxemia

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