Chronic obstructive pulmonary disease overview: Difference between revisions
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==Causes== | ==Causes== | ||
It is most often due to [[tobacco smoking]],<ref name="dev">Devereux G. ''ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors.'' [[British Medical Journal|BMJ]] 2006;332:1142-1144. PMID 16690673</ref>, <ref>{{cite web |title=What is COPD? |date=June 01, 2010 |work=National Heart Lung and Blood Institute |publisher=U.S. National Institutes of Health |url=http://www.nhlbi.nih.gov/health/health-topics/topics/copd/}}</ref>, <ref name="pmid17507545">{{cite journal |author=Rabe KF, Hurd S, Anzueto A, ''et al.'' |title=Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary |journal=Am. J. Respir. Crit. Care Med. |volume=176 |issue=6 |pages=532–55 |year=2007 }}</ref> but can be due to other airborne irritants such as coal dust, [[asbestos]] or solvents, congenital conditions such as [[alpha-1-antitrypsin deficiency]] and as well as preserved meats containing nitrites. | It is most often due to [[tobacco smoking]],<ref name="dev">Devereux G. ''ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors.'' [[British Medical Journal|BMJ]] 2006;332:1142-1144. PMID 16690673</ref>, <ref>{{cite web |title=What is COPD? |date=June 01, 2010 |work=National Heart Lung and Blood Institute |publisher=U.S. National Institutes of Health |url=http://www.nhlbi.nih.gov/health/health-topics/topics/copd/}}</ref>, <ref name="pmid17507545">{{cite journal |author=Rabe KF, Hurd S, Anzueto A, ''et al.'' |title=Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary |journal=Am. J. Respir. Crit. Care Med. |volume=176 |issue=6 |pages=532–55 |year=2007 }}</ref> but can be due to other airborne irritants such as coal dust, [[asbestos]] or solvents, congenital conditions such as [[alpha-1-antitrypsin deficiency]] and as well as preserved meats containing nitrites. | ||
==Differential diagnosis== | |||
In clinical practice, COPD is defined by its characteristically low airflow on [[lung function test]]s.<ref name=Nathell>{{cite doi|10.1186/1465-9921-8-89}} [http://respiratory-research.com/content/8/1/89]</ref> In contrast to [[asthma]], this limitation is poorly reversible and usually gets progressively worse over time. It should be differentiated from certain conditions that have similar presentation for instance [[congestive heart failure]], [[chronic asthma]], [[bronchiectasis]], and [[bronchiolitis obliterans]]. | |||
==Diagnosis== | ==Diagnosis== | ||
The diagnosis of COPD requires [[lung function tests]]. | The diagnosis of COPD requires [[lung function tests]]. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editors-In-Chief: Cafer Zorkun, M.D., Ph.D. [3], Priyamvada Singh, MBBS [4]
Overview
Chronic obstructive pulmonary disease (COPD), also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), is characterized by the pathological limitation of airflow in the airway that is not fully reversible [1]. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other lung disorders. This leads to a limitation of the flow of air to and from the lungs, causing shortness of breath (dyspnea). In clinical practice, COPD is defined by its characteristically low airflow on lung function tests.[2] In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time.
Historical perspective
The terms chronic bronchitis and emphysema were formally defined at the CIBA guest symposium of physicians in 1959. COPD has probably always existed but has been called by different names in the past. Bonet described a condition of “voluminous lungs” in 1679. Matthew Baillie illustrated an emphysematous lung in 1789 and described the destructive character of the condition. The term COPD was first used by William Briscoe in 1965 and has gradually overtaken other terms to become established today as the preferred name for this disease.
Pathophysiology
Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in the large (central) airways, the bronchioles, and the lung parenchyma. Increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases, proteinase-3 and macrophage-derived matrix metalloproteinases (MMPs), cysteine proteinases, and a plasminogen activator resulting in lung destruction. The antiprotease in the body cannot counteract effectively these elastases. Additionally, increased oxidative stress caused by free radicals in cigarette smoke, phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis. In addition to macrophages, T lymphocytes, particularly CD8+, play an important role in the pathogenesis of smoking-induced airflow limitation.
Epidemiology and demographics
Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries.[3] COPD is the third leading cause of death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.[4][5]
Risk factors
Chronic obstructive pulmonary disease is a group of diseases characterized by the pathological limitation of airflow in the airway that is not fully reversible. A full comprehensive diagnosis is needed to eliminate related conditions and isolate the influence of lifestyle and behavior risk factors on condition outcome. Some common risk factors are cigarette smoking, occupational pollutants, air pollution and genetics. Other risk factors are increasing age, male gender, allergy, repeated airway infection.
Causes
It is most often due to tobacco smoking,[6], [7], [8] but can be due to other airborne irritants such as coal dust, asbestos or solvents, congenital conditions such as alpha-1-antitrypsin deficiency and as well as preserved meats containing nitrites.
Differential diagnosis
In clinical practice, COPD is defined by its characteristically low airflow on lung function tests.[2] In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time. It should be differentiated from certain conditions that have similar presentation for instance congestive heart failure, chronic asthma, bronchiectasis, and bronchiolitis obliterans.
Diagnosis
The diagnosis of COPD requires lung function tests.
Treatment
Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation.[8]
References
- ↑ Mannino DM, Homa DM, Akinbami LJ, Ford ES, Redd SC (2002). "Chronic obstructive pulmonary disease surveillance--United States, 1971-2000". MMWR. Surveillance Summaries : Morbidity and Mortality Weekly Report. Surveillance Summaries / CDC. 51 (6): 1–16. PMID 12198919. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 2.0 2.1 Template:Cite doi [1]
- ↑ Mathers CD, Loncar D (2006). "Projections of Global Mortality and Burden of Disease from 2002 to 2030". PLoS Med. 3 (11): e442. doi:10.1371/journal.pmed.0030442. PMC 1664601. PMID 17132052. Unknown parameter
|month=ignored (help) - ↑ COPD (Chronic Obstructive Pulmonary Disease)
- ↑ "2007 NHLBI Morbidity and Mortality Chart Book" (PDF). Retrieved 2008-06-06.
- ↑ Devereux G. ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors. BMJ 2006;332:1142-1144. PMID 16690673
- ↑ "What is COPD?". National Heart Lung and Blood Institute. U.S. National Institutes of Health. June 01, 2010. Check date values in:
|date=(help) - ↑ 8.0 8.1 Rabe KF, Hurd S, Anzueto A; et al. (2007). "Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease: GOLD Executive Summary". Am. J. Respir. Crit. Care Med. 176 (6): 532–55.