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Note: COPD may also refer to RAO in horses.
Chronic obstructive pulmonary disease
Classification and external resources
ICD-10 J40. - J44., J47.
ICD-9 490 - 496
OMIM 606963
DiseasesDB 2672
MedlinePlus 000091
eMedicine med/373  emerg/99
MeSH C08.381.495.389

Chronic obstructive pulmonary disease (COPD) is a group of diseases characterised by limitation of airflow in the airway that is not fully reversible. COPD is the umbrella term for chronic bronchitis and/or emphysema. It is most often due to tobacco smoking [1] but can be due to other airborne irritants such as coal dust or solvents.

Contents

[edit] Signs and symptoms

The main symptoms of COPD include shortness of breath (dyspnea) lasting for months or perhaps years, possibly accompanied by wheezing, and a persistent cough with sputum. [2]

COPD is particularly characterised by a ratio of forced expiratory volume over 1 second (FEV1) to forced vital capacity (FVC) being < 70% and the FEV1 < 80% of the predicted value.[3] Other signs include a rapid breathing rate (tachypnea) and a wheezing sound heard through a stethoscope.

[edit] Causes

The leading cause of COPD is smoking. Continuous smokers have at least a 25% risk of developing COPD.[4] Working or living in a polluted environment is a possible cause of COPD. For example, many people develop COPD after working in the coal mining industry and being exposed to high levels of respirable coal dust.

Rarely, there may be a deficiency in an enzyme known as alpha 1-antitrypsin deficiency.[5]

[edit] Pathophysiology

[edit] Chronic Bronchitis

Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.[6]

Chronic bronchitis is hallmarked by the increased number (hyperplasia) and increased size (hypertrophy) of the mucus-secreting (goblet) cells of the airway. This, along with enlargement of the mucous gland, results in an increase in production of mucus which contributes to the airway obstruction. Microscopically there is infiltration of the airway walls with inflammatory cells, particularly neutrophils. Inflammation is followed by scarring and remodelling that thickens the walls resulting in narrowing of the small airway. Further progression leads to an abnormal change (metaplasia) in the nature of the tissue along with further thickening and scarring (fibrosis) of the lower airway. The consequence of these changes is a limitation of airflow. [7]

[edit] Emphysema

Main article: Emphysema

Emphysema is defined histologically as the enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.[6]

The enlarged air sacs (alveoli) of the lungs reduces the surface area available for the movement of gases during respiration. This can cause breathlessness in severe cases. The exact mechanism for the development of emphysema is not understood, although it it known to be linked with smoking and age.

[edit] Diagnosis

The diagnosis of COPD is usually suggested by symptoms; it is a clinical diagnosis and no single test is definitive. A comprehensive history from the patient (particularly related to smoking), physical examination, and confirmation of airflow obstruction using spirometry (see above) are all vital in establishing the diagnosis.

The severity of COPD can be classified through spirometry:

Severity Post-bronchodilator FEV1/FVC FEV1 % predicted
At risk >0.7 ≥80
Mild COPD ≤0.7 ≥80
Moderate COPD ≤0.7 50-80
Severe COPD ≤0.7 30-50
Very Severe COPD ≤0.7 <30

[edit] Management

Although COPD is not curable, it can be controlled in a variety of ways.

[edit] Smoking cessation

Main article: Smoking cessation

Smoking cessation is one of the most important factors in slowing down the progression of COPD. Even at a late stage of the disease it can reduce the rate of deterioration and prolong the time taken for disability and death.[7]

[edit] Drug therapy

[edit] Bronchodilators

There are three types of bronchodilators used clinically: β2-agonists, anticholinergics and methylxanthines.[8]These drugs relax the smooth muscles of the airway allowing for improved airflow. The change in FEV1 may not be substancial, but changes in the lung volumes are often larger. Many patients feel less breathless after taking bronchiodilators.

[edit] Corticosteriods

Inhaled corticosteriods (specifically glucocorticoids) act in the inflammatory cacade and may improve airway function considerably,[7] however the long term value has not been proven. Corticosteroids are often combined with bronchodilators in a single inhaler.

[edit] Vaccination

Patients with COPD should be routinely vaccinated against influenza to prevent illness and the possibility of death.[8]

[edit] Pulmonary rehabilitation

Pulmonary rehabilitation is a programme of disease management, counselling and exercise coordinated to benefit the individual.[9] Pulmonary rehabilitation has been shown to relieve difficulties breathing and fatigue. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.[10]

[edit] Prognosis

A good prognosis of COPD relies on an early diagnosis and prompt treatment. Most patients will have improvement in lung function once treatment is started, however eventually signs and symptoms will worsen as COPD progresses. The median survival is about 10 years if two-thirds of expected lung function was lost by diagnosis.[11]

[edit] Epidemiology

According to the World Health Organisation (WHO), 80 million people suffer from moderate to severe COPD and 3 million died due to it in 2005. The WHO predicts that by 2030, it will be the 4th largest cause of mortality worldwide.[12]

Since COPD is not diagnosed until it becomes clinically apparent, prevelance and mortality data greatly underestimate the socio-economic burden of COPD.[8] In the UK, COPD accounts for about 7% of all days of sickness related absence from work.[7]

[edit] References

  1. ^ Devereux G. ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors. BMJ 2006;332:1142-1144. PMID 16690673
  2. ^ U.S. National Heart Lung and Blood Institute - Signs and Symptoms
  3. ^ PatientPlus - Spirometry
  4. ^ Lokke A, Lange P, Scharling H, Fabricius P, Vestbo J. Developing COPD: a 25 year follow up study of the general population. Thorax. 2006 Nov;61(11):935-9. PMID 17071833
  5. ^ MedlinePlus Medical Encyclopedia
  6. ^ a b Longmore M, Wilkinson I, Rajagopalan S (2005). Oxford Handbook of Clinical Medicine, 6ed. Oxford University Press. pp 188-189. ISBN 0-19-852558-3.
  7. ^ a b c d Kumar P, Clark M (2005). Clinical Medicine, 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.
  8. ^ a b c American Thoracic Society / European Respiratory Society Task Force (2005). Standards for the Diagnosis and Management of Patients with COPD. Version 1.2. New York: American Thoracic Society. http://www.thoracic.org/go/copd
  9. ^ U.S. National Heart Lung and Blood Institute - Treatment
  10. ^ Lacasse Y, Goldstein R, Lasserson T J, Martin, S. Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews. (4):CD003793, 2006. PMID 12137716
  11. ^ Prognosis of COPD
  12. ^ WHO - COPD