Chronic Obstructive Pulmonary Disease (COPD)

Centrilobular emphysema 865 lores[1]


Presentation

Symptoms and signs may include:

Workup

Workup consists of a detailed history, tests and physical examination.

Laboratory Tests

  • Complete blood count
  • Arterial blood gases
  • Serum electrolytes
  • Spirometry
  • Serum BNP levels
  • Sputum culture
  • Pulmonary function tests
  • Pulse oximetry

Imaging Studies

  • Chest radiography
  • CT scan

Test Results

On the results of laboratory tests and radiography, diagnosis is made and treatment is immediately begun.

Treatment

Oxygen

In a cluster randomised, controlled parallel group trial, in 405 patients, titrated oxygen significantly reduced mortality, hypercapnia and respiratory acidosis [8].

Medications

Medications that can be used include:

  • Bronchodilators: These are given in pumps, to be inhaled as many times as prescribed. 
  • Corticosteroids: These are given to stop the inflammation from worsening. They can be used as inhalers (inhaled corticosteroids ICS) in mild to moderate disease, or given per oral in advanced disease. 
  • Leukotriene inhibitors: To stop action of leukotrienes in the inflammatory pathway 
  • Long-acting Beta 2 Agonists: Their use is associated with improved quality of life and reduced exacerbations, but they have not been shown to reduce mortality or serious adverse events significantly. [9]. 
  • Antibiotics: For prophylactic treatment.

Cessation of smoking

Smoking should be immediately stopped to prevent the disease from worsening.

Removal of pollutants

Prolonged exposure to pollutants, such as smoke, asbestos, silica, etc should be avoided.

Prognosis

COPD is due to irreversible damage to the airways. This means this disease can be managed, not treated. Prognosis depends upon the stage of the disease and the treatment started. With appropriate treatment and cessation of smoking, COPD can be prevented from worsening and a relatively healthy life style can be adopted.

Complications

Etiology

In most patients, COPD is the result of long-term heavy cigarette smoking; about 10% of patients are nonsmokers [3]. Other causes may include alpha-1 anti-trypsin deficiency, bronchiectasis and cystic fibrosis. Exposure to large amounts of air pollutants may also lead to development of COPD.

Whatever the exact cause may be, the common factor is airway irritation, which leads to inflammation and then damage. This results first in mucosal and glandular changes in the airways, and as the disease progresses, these changes are unable to match up with the continuously on going irritation, and irreversible damage occurs. The type of COPD depends upon the exact causative factor.

Epidemiology

Incidence

COPD is estimated to be the fourth leading cause of death in the United States and the sixth leading cause of death world wide.

Sex and Race

There is a clear cut association between heavy cigarette smoking and emphysema, and women and African-Americans are more susceptible than other groups [2]. However, generally men are much more commonly found to be suffering from COPD than women.

Age

COPD is more common in people, particularly men, aged 40 years and above.

Sex distribution
Age distribution

Pathophysiology

COPD is a vast term that is used to describe three prominent disorders collectively. These include the following:

Emphysema

Emphysema is a condition of the lung characterised by irreversible enlargement of the air spaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis [4].

Chronic bronchitis

It is defined clinically as persistent productive cough for at least 3 months in 2 (or more) consecutive years. The earliest feature of chronic bronchitis is hypersecretion of mucus in the large airways, associated with hypertrophy of the submucosal glands in the trachea and bronchi [5].

Asthma

It is a chronic inflammatory disorder in which patients suffer from recurrent episodes of wheezing, breathlessness and cough. Many cells play a role in the inflammatory response, in particular lymphocytes, eosinophils, mast cells, macrophages, neutrophils and epithelial cells [6].

Chronic bronchiolitis, or small airway disease, also comes under the COPD category and shares many characteristics with the former two conditions. In a recent study, the overlap between these three disorders was found to be substantial [7].

Prevention

The use of continuous prophylactic antibiotics results in a clinically significant benefit in reducing exacerbations in COPD [10].
COPD can be easily prevented by not smoking tobacco and other such harmful agents. Also, avoiding exposure to pollutants can also prevent this disease from occurring.

Summary

Chronic obstructive pulmonary disease (COPD) is a common respiratory condition involving the airways and characterised by airflow limitation [1]. It is diagnosed based on clinical findings and results of pulmonary function tests. In acute COPD, symptoms are mild and the disease is often missed. As the disease progresses, varying symptoms present in different people.

Patient Information

COPD is a collective term for many respiratory disorders such as asthma, emphysema and chronic bronchitis. It may also include other airway diseases.

The most common causative factor is heavy smoking. People exposed to a large amount of air pollutants are also at risk for developing this disease. It has no cure, but can be appropriately managed with cessation of smoking, removing pollutants (if any) and by taking prescribed medications.

Self-assessment

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References

  1. Buist AS, McBurnie MA,Volmer WM, et al. International variation in the prevalence of COPD (the BOLD study): a population based prevalence study. Lancet 2007;379:741
  2. Cazzola M et al. One hundred years of chronic obstructive pulmonary disease (COPD). Respir Med 101:1049, 2007
  3. Shaw RJ et al. The Role of small airways in lung disease. Respir Med 96:67, 2002
  4. Snider G:The definition of emphysema:report of the National Heart, Lung and Blood Institute, Division of Lung Diseases Workshop. Am Rev Respir Dis 132:182, 1985
  5. deMello DE, Reid L. Pathology of Pulmonary Disease. Philadelphia. JB Lippincott, 1994.
  6. Bloemen K, et al. The allergic Cascade: review of the most important molecules in the asthmatic lung. Immunol Lett 113:6,2007
  7. Ware LB: Pathophysiology of acute lung injury and the acute respiratory distress syndrome. Semin Respir Crit Care Med 27:337, 2006
  8. Austin MA, Wills KE, Blizzard L, Walters EH, Wood-Baker R: Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital settings:randomised control trial. BMJ. Oct 18 2010;341:c5462
  9. Kew KM, Mavergames C, Walters JA: Long acting beta2 agonists for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2013, Oct 15;10CD:010177. 
  10. Herath SC, Poole P; Prophylactic antibiotic therapy for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2013, Nov 28;11:CD009764 

Media References

  1. Centrilobular emphysema 865 lores, Public Domain

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