Chronic bronchitis overview: Difference between revisions
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==Historical perspective== | ==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. | 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== | |||
* 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.<ref name=ohcm>Longmore M, Wilkinson I, Rajagopalan S (2005). ''Oxford Handbook of Clinical Medicine'', 6ed. [[Oxford University Press]]. pp 188-189. ISBN 0-19-852558-3.</ref> | |||
* Chronic bronchitis is hallmarked by [[hyperplasia]] (increased number) and [[hypertrophy]] (increased size) of the goblet cells ([[mucous gland]]) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction. [[Microscope|Microscopically]] there is [[Infiltration (medical)|infiltration]] of the airway walls with [[Inflammation|inflammatory]] cells, particularly [[neutrophils]]. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to [[metaplasia]] (abnormal change in the tissue) and [[fibrosis]] (further thickening and scarring) of the lower airway. The consequence of these changes is a limitation of airflow.<ref name=kc>Kumar P, Clark M (2005). ''Clinical Medicine'', 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.</ref>. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 18:48, 28 March 2012
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Bronchitis is an inflammation of the bronchi (medium-size airways) in the lungs. Acute bronchitis is usually caused by viruses or bacteria and may last several days or weeks. Chronic bronchitis is not necessarily caused by infection and is generally part of a syndrome called chronic obstructive pulmonary disease (COPD); it is defined clinically as a persistent cough that produces sputum (phlegm) and mucus, for at least three months in two consecutive years.
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
- 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.[1]
- Chronic bronchitis is hallmarked by hyperplasia (increased number) and hypertrophy (increased size) of the goblet cells (mucous gland) of the airway, resulting in an increase in secretion 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 remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to metaplasia (abnormal change in the tissue) and fibrosis (further thickening and scarring) of the lower airway. The consequence of these changes is a limitation of airflow.[2].
References
- ↑ Longmore M, Wilkinson I, Rajagopalan S (2005). Oxford Handbook of Clinical Medicine, 6ed. Oxford University Press. pp 188-189. ISBN 0-19-852558-3.
- ↑ Kumar P, Clark M (2005). Clinical Medicine, 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.