Chronic obstructive pulmonary disease classification: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 4: Line 4:


==Overview==
==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.<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> 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 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. In England, an estimated 842,100 of 50&nbsp;million people have a diagnosis of COPD.<ref name="BJGPref">{{cite journal |author=Simpson CR, Hippisley-Cox J, Sheikh A| title= Trends in the epidemiology of chronic obstructive pulmonary disease in England: a national study of 51 804 patients | journal=Brit J Gen Pract |volume=60 |issue=576 |pages=483–488| year=2010 |pmid=20594429 |pmc=2894402| doi= 10.3399/bjgp10X514729}}</ref>  
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.<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> 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 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. In England, an estimated 842,100 of 50&nbsp;million people have a diagnosis of COPD.<ref name="BJGPref">{{cite journal |author=Simpson CR, Hippisley-Cox J, Sheikh A| title= Trends in the epidemiology of chronic obstructive pulmonary disease in England: a national study of 51 804 patients | journal=Brit J Gen Pract |volume=60 |issue=576 |pages=483–488| year=2010 |pmid=20594429 |pmc=2894402| doi= 10.3399/bjgp10X514729}}</ref>  
==Classification==
==Classification==
===Chronic Bronchitis===
===Chronic Bronchitis===
{{Main|chronic bronchitis}}
{{Main|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&nbsp;months of a year, for 2 consecutive years.<ref name="ohcm">{{cite book |author=Longmore, J. M.; Murray Longmore; Wilkinson, Ian; Supraj R. Rajagopalan |title=Oxford handbook of clinical medicine |publisher=Oxford University Press |location=Oxford [Oxfordshire] |year=2004 |pages=188–9 |isbn=0-19-852558-3 }}</ref> 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. [[Microscope|Microscopically]] there is [[Infiltration (medical)|infiltration]] of the airway walls with [[Inflammation|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.<ref name=kc>{{cite book |author=Kumar P, Clark M |title=Clinical Medicine |publisher=Elsevier Saunders |year=2005 |isbn=0702027634 |pages=900–1 |edition=6th }}</ref>
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&nbsp;months of a year, for 2 consecutive years.<ref name="ohcm">{{cite book |author=Longmore, J. M.; Murray Longmore; Wilkinson, Ian; Supraj R. Rajagopalan |title=Oxford handbook of clinical medicine |publisher=Oxford University Press |location=Oxford [Oxfordshire] |year=2004 |pages=188–9 |isbn=0-19-852558-3 }}</ref> 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. [[Microscope|Microscopically]] there is [[Infiltration (medical)|infiltration]] of the airway walls with [[Inflammation|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.<ref name="kc">{{cite book |author=Kumar P, Clark M |title=Clinical Medicine |publisher=Elsevier Saunders |year=2005 |isbn=0702027634 |pages=900–1 |edition=6th }}</ref>


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.<ref>{{cite book |author=Chung C, Delaney J, Hodgins R |chapter=Respirology |editor=Somogyi, Ron; Colman, Rebecca |title=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 |publisher=Toronto Notes for Medical Students |location=Toronto |year=2008 |page=R9 |isbn=0-9685928-8-0 }}</ref> The [[Hypoxia (medical)|hypoxia]] and [[Water retention (medicine)|fluid retention]] leads to them being called "Blue Bloaters".
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.<ref>{{cite book |author=Chung C, Delaney J, Hodgins R |chapter=Respirology |editor=Somogyi, Ron; Colman, Rebecca |title=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 |publisher=Toronto Notes for Medical Students |location=Toronto |year=2008 |page=R9 |isbn=0-9685928-8-0 }}</ref> The [[Hypoxia (medical)|hypoxia]] and [[Water retention (medicine)|fluid retention]] leads to them being called "Blue Bloaters".
Line 14: Line 14:
===Emphysema===
===Emphysema===
{{Main|emphysema}}
{{Main|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.<ref name="ohcm"/> 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.
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.<ref name="ohcm" /> 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:<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:
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.
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.
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. There may be congenital extrinsic compression, commonly by an abnormally large pulmonary artery. This causes malformation of bronchial cartilage, making them soft and collapsible. CLE is a potentially reversible (yet possibly life-threatening) cause of respiratory distress in the neonate.
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.


There are 4 types of emphysema:
# Centriacinar / centrilobular: proximal to central parts of [[Acinus#The Lungs|acini]] (air spaces closer to bronchioles) are affected
# Panacinar / panlobular: enlargement of all air spaces (from bronchioles to terminal blind alveoli). This type is associated with alpha-1-antitrypsin deficiency
# Distal acinar / [[Emphysema#Paraseptal emphysema|paraseptal]]: proximal acinus normal, distal acinus affected
# Irregular: various parts of acinus involved. Associated with fibrosis.<ref>{{cite book |author=Kumar V, Abbas AK |title=Robbins Pathologic Basis of Disease |year=2009 |page=684 }}</ref>


==References==
==References==

Revision as of 14:40, 13 November 2017

Chronic obstructive pulmonary disease Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Chronic obstructive pulmonary disease from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

Echocardiography or Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Future or Investigational Therapies

Case Studies

Case #1

Chronic obstructive pulmonary disease classification On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Chronic obstructive pulmonary disease classification

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Chronic obstructive pulmonary disease classification

CDC on Chronic obstructive pulmonary disease classification

Chronic obstructive pulmonary disease classification in the news

Blogs on Chronic obstructive pulmonary disease classification

Directions to Hospitals Treating Chronic obstructive pulmonary disease

Risk calculators and risk factors for Chronic obstructive pulmonary disease classification

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. 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. 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. There may be congenital extrinsic compression, commonly by an abnormally large pulmonary artery. This causes malformation of bronchial cartilage, making them soft and collapsible. CLE is a potentially reversible (yet possibly life-threatening) cause of respiratory distress in the neonate. 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.


References

  1. "What is COPD?". National Heart Lung and Blood Institute. U.S. National Institutes of Health. June 01, 2010. Check date values in: |date= (help)
  2. Template:Cite doi [1]
  3. 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. 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.
  5. Kumar P, Clark M (2005). Clinical Medicine (6th ed.). Elsevier Saunders. pp. 900–1. ISBN 0702027634.
  6. 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.
  7. Kumar V, Abbas AK (2009). Robbins Pathologic Basis of Disease. p. 684.


Template:WikiDoc Sources