Chronic Obstructive Pulmonary Disease Signs and Symptoms

Introduction

• Chronic obstructive pulmonary disease (COPD) should be suspected in any patient who has chronic cough, sputum production, or dyspnea with or without history of risk factors for the disease

Definition

• A preventable and treatable disease with overall severity contributed by exacerbations and comorbidities
• A group of lung conditions which is characterized by chronic respiratory symptoms of dyspnea, cough and sputum production, as a consequence of abnormalities of the airways (eg bronchitis, bronchiolitis) and/or alveoli (eg emphysema) which cause persistent and often progressive airflow obstruction
• The persistent airflow limitation is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases
• The chronic airflow limitation is caused by a mixture of small airways disease and parenchymal destruction

Epidemiology

• Estimated global prevalence is 10.3% based on the Burden of Obstructive Lung Disease (BOLD) study
  • Prevalence is higher is smokers and ex-smokers, individuals ≥40 years of age and in men
• Third leading cause of mortality worldwide

Pathophysiology

• Consequence of complex, cumulative and dynamic gene-environment interactions occurring over the individual's lifetime resulting to lung damage and/or alteration of normal lung development or aging process
• Inflammatory and structural changes lead to increased severity of airway obstruction
  • Increased number of inflammatory cells (eg macrophages in peripheral airways, lung parenchyma and pulmonary vessels, activated neutrophils and lymphocytes) together with epithelial cells and other structural cells release multiple inflammatory mediators attracting inflammatory cells from the circulation leading to amplification of the inflammatory process and causing structural changes
    • Chronic inflammation leads to structural changes, small airway narrowing, luminal exudates in small airways and lung parenchyma destruction causing loss of alveolar attachments to the small airways and decreasing elastic recoil of the lung, which in turn reduces the ability of the airways to remain open during expiration
  • May also be secondary to oxidative stress
  • Structural changes may be due to the imbalance between proteases from inflammatory and epithelial cells responsible for breaking down connective tissue components and antiproteases
    • Include peribronchial fibrosis and interstitial opacities
  • Structural abnormalities in the airways, alveoli and pulmonary circulation leads to abnormal pulmonary gas exchange
  • Inflammatory and structural changes can also lead to gas trapping and hyperinflation
    • Hyperinflation occurs due to the loss of elastic recoil and expiratory flow obstruction
  • Airflow obstruction is due to small airway disease increasing airway resistance and parenchymal destruction
    • May also be caused by loss of small airways
    • Parenchymal destruction secondary to emphysema can cause decreased lung diffusing capacity

Signs and Symptoms

A diagnosis of COPD should be considered in patients >40 years of age, with suggestive medical history (ie presence of risk factors) and present with any of the following:

• Chronic cough (present intermittently or daily)
  • Does not reflect the major impact of airflow limitation on the morbidity and mortality in patients with COPD
  • Cough may be unproductive
• Exertional breathlessness that is usually progressive, wheezing, pursed-lip breathing, dyspnea with or without wheezing
• Rhonchi, prolonged expiratory phase of respiration, chest hyperinflation, use of accessory muscles for respiration, decreased breath sounds
• Signs of cor pulmonale: Neck vein distention, increased pulmonic component of second heart sound, lower extremity edema, hepatomegaly
• The absence of wheezing or chest tightness does not rule out a diagnosis of COPD

Risk Factors

Host Factors

• Lung growth and development
  • Individuals may have reduced maximal attained lung function due to processes during gestation and childhood
• Infections
  • Reduced lung function can be associated with a history of severe childhood respiratory infections
  • Previous tuberculosis
• Genetic factors (eg deficiency of alpha-1 antitrypsin and other genetic conditions)
• Airway hyper-responsiveness
  • Can exist without a clinical diagnosis of asthma
  • In population studies, airway hyper-responsiveness has been shown to be an independent predictor of COPD and respiratory mortality
  • Can be an indicator of risk of excess decline in lung function in patients with mild COPD
• Chronic bronchitis

Exposures

• Tobacco smoke
  • Most commonly encountered risk factor
  • Includes history of tobacco use or prolonged exposure to second-hand smoke
  • Smoking during pregnancy can put the fetus at risk
• Occupational dusts and chemicals (eg pesticides, biomass fuels)
• Air pollution
• Smoke from home cooking and heating fuels
• Low socioeconomic status