Chronic obstructive pulmonary disease classification: Difference between revisions
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There are 4 types of emphysema:<ref>{{cite book |author=Kumar V, Abbas AK |title=Robbins Pathologic Basis of Disease |year=2009 |page=684 }}</ref> | There are 4 types of emphysema:<ref>{{cite book |author=Kumar V, Abbas AK |title=Robbins Pathologic Basis of Disease |year=2009 |page=684 }}</ref> | ||
Emphysema can be classified by location into three categories: | Emphysema can be classified by location into three categories: | ||
Panacinary (panlobular): | === '''Panacinary (panlobular):''' === | ||
The entire respiratory acinus, from respiratory bronchiole to alveoli, is expanded. Occurs more commonly in the lower lobes (especially basal segments) and in the anterior margins of the lungs. | * The entire [[respiratory]] [[acinus]], from [[respiratory bronchiole]] to [[Pulmonary alveolus|alveoli]], is expanded. Occurs more commonly in the lower lobes (especially basal segments) and in the anterior margins of the [[Lung|lungs]].<ref name="urlEmphysema">{{cite web |url=http://www.meddean.luc.edu/Lumen/MedEd/MEDICINE/PULMONAR/pathms/mpath6.htm |title=Emphysema |work= |accessdate=2008-11-20}}</ref> | ||
=== '''Centroacinary (panacinar and centriacinar):''' === | |||
* The [[respiration|respiratory bronchiole]] (proximal and central part of the [[acinus]]) is expanded. The distal [[acinus]] or [[Pulmonary alveolus|alveoli]] are unchanged. Occurs more commonly in the upper lobes.<ref name="urlEmphysema">{{cite web |url=http://www.meddean.luc.edu/Lumen/MedEd/MEDICINE/PULMONAR/pathms/mpath6.htm |title=Emphysema |work= |accessdate=2010-01-20}}</ref><ref name="pmid4784376">{{cite journal |author=Anderson AE, Foraker AG |title=Centrilobular emphysema and panlobular emphysema: two different diseases |journal=Thorax |volume=28 |issue=5 |pages=547–50 |year=1973 |month=September |pmid=4784376 |doi= 10.1136/thx.28.5.547|pmc=470076}}</ref> | |||
=== Other types: === | |||
===== Congenital lobar emphysema (CLE) ===== | |||
CLE results in over-expansion of a [[Pulmonary|pulmonary lobe]], and resultant compression of the remaining lobes of the ipsi-lateral lung (and possibly also the contralateral [[lung]]). There is [[bronchus|bronchial]] narrowing because of weakened or absent bronchial [[cartilage]].<ref name="Wood">[http://emedicine.medscape.com/article/407635-overview eMedicine Specialties > Radiology > Pediatrics --> Congenital Lobar Emphysema] Author: Beverly P Wood, MD, MS, PhD, University of Southern California. Updated: December 1, 2008</ref> There may be [[congenital]] extrinsic compression, commonly by an abnormally large [[pulmonary artery]]. This causes malformation of [[bronchial]] [[cartilage]], making them soft and collapsible.<ref name="Wood" /> CLE is a potentially reversible (yet possibly life-threatening) cause of [[Acute respiratory distress syndrome|respiratory distress]] in the [[infant|neonate]].<ref name="Wood" /> | |||
=====Paraseptal emphysema===== | |||
Para-septal emphysema is a type of emphysema which involves the alveolar ducts and sacs at the [[lung]] periphery. The emphysematous areas are sub-pleural in location and often surrounded by inter-lobular septa (hence the name). It may be an incidental finding in young adults, and may be associated with spontaneous [[pneumothorax]]. It may also be seen in older patients with centri-lobular emphysema. Both centri-lobular and para-septal emphysema may progress to bullous emphysema. A bulla is defined as being at least 1 cm in diameter, and with a wall less than 1 mm thick. Bullae are thought to arise by [[air trapping]] in emphysematous spaces, causing local expansion.<ref>Webb WR, Higgins CB. ''Thoracic Imaging''. Lippincott, Williams & Wilkins 2005.</ref> | |||
==References== | ==References== |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Philip Marcus, M.D., M.P.H. [3]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [4]
Overview
Chronic obstructive pulmonary disease is the co-occurrence of chronic bronchitis and emphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed.[1] 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. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD.[3]
Classification
Chronic Bronchitis
Lung damage and inflammation in the large airways results in 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.[4] In the airways of the lung, the hallmark of chronic bronchitis is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.[5]
Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as "Blue Bloaters" because of the bluish color of the skin and lips (cyanosis) seen in them.[6] The hypoxia and fluid retention leads to them being called "Blue Bloaters".
Emphysema
Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.[4] The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It also reduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung. These airways are more likely to collapse causing further limitation to airflow.
There are 4 types of emphysema:[7] Emphysema can be classified by location into three categories:
Panacinary (panlobular):
- The entire respiratory acinus, from respiratory bronchiole to alveoli, is expanded. Occurs more commonly in the lower lobes (especially basal segments) and in the anterior margins of the lungs.[8]
Centroacinary (panacinar and centriacinar):
- The respiratory bronchiole (proximal and central part of the acinus) is expanded. The distal acinus or alveoli are unchanged. Occurs more commonly in the upper lobes.[8][9]
Other types:
Congenital lobar emphysema (CLE)
CLE results in over-expansion of a pulmonary lobe, and resultant compression of the remaining lobes of the ipsi-lateral lung (and possibly also the contralateral lung). There is bronchial narrowing because of weakened or absent bronchial cartilage.[10] There may be congenital extrinsic compression, commonly by an abnormally large pulmonary artery. This causes malformation of bronchial cartilage, making them soft and collapsible.[10] CLE is a potentially reversible (yet possibly life-threatening) cause of respiratory distress in the neonate.[10]
Paraseptal emphysema
Para-septal emphysema is a type of emphysema which involves the alveolar ducts and sacs at the lung periphery. The emphysematous areas are sub-pleural in location and often surrounded by inter-lobular septa (hence the name). It may be an incidental finding in young adults, and may be associated with spontaneous pneumothorax. It may also be seen in older patients with centri-lobular emphysema. Both centri-lobular and para-septal emphysema may progress to bullous emphysema. A bulla is defined as being at least 1 cm in diameter, and with a wall less than 1 mm thick. Bullae are thought to arise by air trapping in emphysematous spaces, causing local expansion.[11]
References
- ↑ "What is COPD?". National Heart Lung and Blood Institute. U.S. National Institutes of Health. June 01, 2010. Check date values in:
|date=
(help) - ↑ Template:Cite doi [1]
- ↑ Simpson CR, Hippisley-Cox J, Sheikh A (2010). "Trends in the epidemiology of chronic obstructive pulmonary disease in England: a national study of 51 804 patients". Brit J Gen Pract. 60 (576): 483–488. doi:10.3399/bjgp10X514729. PMC 2894402. PMID 20594429.
- ↑ 4.0 4.1 Longmore, J. M.; Murray Longmore; Wilkinson, Ian; Supraj R. Rajagopalan (2004). Oxford handbook of clinical medicine. Oxford [Oxfordshire]: Oxford University Press. pp. 188–9. ISBN 0-19-852558-3.
- ↑ Kumar P, Clark M (2005). Clinical Medicine (6th ed.). Elsevier Saunders. pp. 900–1. ISBN 0702027634.
- ↑ Chung C, Delaney J, Hodgins R (2008). "Respirology". In Somogyi, Ron; Colman, Rebecca. The Toronto notes 2008: a comprehensive medical reference and review for the Medical Council of Canada Qualifying Exam — Part 1 and the United States Medical Licensing Exam — Step 2. Toronto: Toronto Notes for Medical Students. p. R9. ISBN 0-9685928-8-0.
- ↑ Kumar V, Abbas AK (2009). Robbins Pathologic Basis of Disease. p. 684.
- ↑ 8.0 8.1 "Emphysema". Retrieved 2008-11-20.
- ↑ Anderson AE, Foraker AG (1973). "Centrilobular emphysema and panlobular emphysema: two different diseases". Thorax. 28 (5): 547–50. doi:10.1136/thx.28.5.547. PMC 470076. PMID 4784376. Unknown parameter
|month=
ignored (help) - ↑ 10.0 10.1 10.2 eMedicine Specialties > Radiology > Pediatrics --> Congenital Lobar Emphysema Author: Beverly P Wood, MD, MS, PhD, University of Southern California. Updated: December 1, 2008
- ↑ Webb WR, Higgins CB. Thoracic Imaging. Lippincott, Williams & Wilkins 2005.