Chronic Obstructive Pulmonary Disease Overview

Chronic Obstructive Pulmonary Disease (COPD) Pathophysiology

• COPD is a common, preventable, and treatable disease.
• Characterized by persistent respiratory symptoms.
• Airflow limitation, usually due to airway and/or alveolar abnormalities, often from significant exposure to noxious particles or gases.
• Can involve host factors
• Mix of small airway disease (like obstructive bronchiolitis) and parenchymal destruction (like emphysema).
• Includes inflammation, mucus hypersecretion etc

Epidemiology of COPD

• One of the top 3 causes of death worldwide.
• Causes 6% of global deaths.
• In Canada, 2011, COPD caused 4.4% of deaths for those aged 40 and older.
• Male death rate from COPD has decreased 1998 to 2011.
• Female death rate from COPD increased steadily from 1950-2011
• Smokers are 12-13x more likely to die from COPD than non smokers
• ~90,000 hospitalizations from COPD in 2016-2017.
• 1 in 5 COPD patients are readmitted within 30 days of hospitalization.
• Average COPD hospitalization related to exacerbations is 10 days at a cost of $10,000 per stay.
• Total cost of COPD hospitalizations estimated at $1.5 billion annually.
• Prevalence of COPD varies based on age and sex.
• COPD prevalence among Canadians aged 35+ shows an increasing trend with aging.

Pathogenesis of COPD

• Inhalation of noxious particles modify lung inflammation causing tissue destruction, disrupted defence mechanisms and gas trapping, eventually leading to progressive airflow limitation.
• Increased oxidative stress: Oxidants from irritants and inflammatory cells reduce endogenous antioxidants.
• Protease/antiprotease imbalance: An increase in proteases that break down tissue, and reduction of antiproteases that protect tissue. This disrupts tissue health.
• Inflammatory cells: Include increased numbers of macrophages, activated neutrophils, lymphocytes, and eosinophils, especially if comorbid asthma.
• Inflammatory mediators: Result in attraction of more inflammatory cells, amplify inflammation and cause structural changes in the lungs.
• Peribronchiolar and interstitial fibrosis: Excess growth factors precedes inflammation, repeats injuries within the airways lead to muscle and fibrous tissue production, contributing to small airways limitation.

Pathophysiology of COPD

• Airflow limitation/air trapping: Progressive gas-trapping during exhalation leads to hyperinflation, a decrease in inspiratory capacity, reduced exercise capacity, and increased dyspnea symptoms, and usually develops early.
• This can be relieved by bronchodilators.
• Extent of inflammation, fibrosis, and luminal exudates in the smaller airways correlates with reduced FEV1 and FEV1/FVC ratio, and an accelerated decline in FEV1.
• Gas exchange abnormalities: Result in hypoxemia and hypercapnia (CO2 retention), reduced ventilatory drive.
• Ventilatory muscle impairment and airway limitation can worsen V/Q abnormalities.
• Mucus hypersecretion: Inflammatory mediators and proteases can increased mucus hypersecretion, increased goblet cells, enlarged submucosal glands and chronic productive cough (chronic bronchitis). Mucus hypersecretion does not always cause airway limitation.

Airway changes in COPD

• Luminal occlusion by mucus glycoproteins and inflammatory exudates: Fluid build up in the airways.
• Fibrosis.
• Alveolar attachments are disrupted.
• Airway wall thickening.
• Lymphocytes and goblet cells.

Assessment and Diagnosis of COPD

• Spirometry is a reliable and objective measurement of airflow limitation.
• Spirometry should be performed before and after the administration of a short acting bronchodilator
• Evaluating and referencing against appropriate values based on age, height, sex and race.
• Comparing to age related normal values for avoiding over diagnosing in elderly individuals.
• COPD is diagnosed based on criteria, including symptoms, risk factor exposure, and a post-bronchodilator FEV1/FVC ratio below 0.70.

Key Indicators in COPD

• The characteristic symptoms of COPD are progressive dyspnea (shortness of breath) that worsens over time, and is often worse with exertion; Persistent dyspnea (present every day).
• Described by the patient as "increased effort to breathe", "heaviness", "air hunger" or "gasping".
• Chronic cough that may be intermittent, and unproductive.
• Recurrent wheezing.
• Chronic sputum production. Presence of cough and/or sputum production may indicate COPD.
• History of exposure to risk factors: Tobacco smoke; Occupational dusts and/or chemicals; Smoke from home heating and/or cooking fuels.
• Host factors; family history and childhood factors; recurrent lower respiratory infections.

###Additional Investigations for COPD

• Imaging: X-ray/CT used to rule out other conditions.
• Oximetry with arterial blood gas analysis; measures oxygen saturation (important for assessing gas exchange).
• Alpha-1-antitrypsin deficiency; Genetic issue relevant for younger individuals and/or lower-lobe emphysema.
• Exercise tolerance: measures response to exercise.
• Lung volume: measures gas volume.
• Diffusing capacity: Measures gas movement.

Classification of Severity of COPD Airflow Limitations

• Based on post-bronchodilator FEV1 in patients with FEV1/FVC <0.70.
• GOLD 1 (Mild) FEV1 ≥ 80% predicted.
• GOLD 2 (Moderate) 50% ≤ FEV1 < 80% predicted.
• GOLD 3 (Severe) 30% ≤ FEV1 < 50% predicted.
• GOLD 4 (Very Severe) FEV1 < 30% predicted.
• Correlation between FEV1 and symptoms is generally weak.

Specific COPD Severity Stages (Examples)

• Mild COPD: characterized by potentially present, but not always apparent, cough and/or sputum production. Patient often unaware of lung dysfunction. FEV1/FVC <0.70; FEV1 ≥ 80% predicted.
• Moderate COPD: Shortness of breath on exertion. Cough and sputum present, but not always Patients in this stage typically seek medical attention. FEV1/FVC <0.70; FEV₁ 50-79% predicted.
• Severe COPD: Patients experience increased shortness of breath (SOB), reduced exercise capacity, fatigue, and repeated exacerbations. Exacerbations significantly affect quality of life (QOL). FEV1/FVC <0.70; FEV₁ 30-49% predicted.
• Very Severe COPD: Patients have chronic respiratory failure where PaO2 < 60, and PaCO2 > 50, and potential symptoms of cor pulmonale. Quality of life is significantly affected by frequent exacerbations. QOL significantly impaired, potential life threatening aspects.. FEV1/FVC < 0.70; FEV₁ < 30% predicted

COPD vs Asthma

• COPD inflammation involves neutrophils, while asthma inflammation involves eosinophils.
• COPD airway fibrosis, while asthma involves bronchoconstriction.
• Airflow limitation in COPD are generally irreversible, while asthma can be reversible.

This quiz covers the pathophysiology and epidemiology of Chronic Obstructive Pulmonary Disease (COPD). It discusses the disease's characteristics, causes, and its significant impact on global health. Test your knowledge on the statistics and clinical aspects of COPD and its management.