Chronic Obstructive Pulmonary Disease: An Overview of Pathology and Pathogenesis

  1. Derek Chadwick Organizer and
  2. Jamie A. Goode
  1. James C. Hogg

Published Online: 7 OCT 2008

DOI: 10.1002/0470868678.ch2

Chronic Obstructive Pulmonary Disease: Pathogenesis to Treatment: Novartis Foundation Symposium 234

Chronic Obstructive Pulmonary Disease: Pathogenesis to Treatment: Novartis Foundation Symposium 234

How to Cite

Hogg, J. C. (2000) Chronic Obstructive Pulmonary Disease: An Overview of Pathology and Pathogenesis, in Chronic Obstructive Pulmonary Disease: Pathogenesis to Treatment: Novartis Foundation Symposium 234 (eds D. Chadwick and J. A. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/0470868678.ch2

Author Information

  1. St Paul's Hospital, The University of British Columbia, McDonald Research Laboratories, 1081 Burrard Street, Vancouver, Canada V6Z 1Y6

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 28 NOV 2000

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780471494379

Online ISBN: 9780470868676

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Summary

A cigarette smoke-induced inflammatory process underlies the pathogenesis of the majority of pathologic lesions associated with chronic obstructive pulmonary disease (COPD). In chronic bronchitis, this process is located in the mucosa, gland ducts and glands of intermediate sized bronchi with an internal diameter of 2–4 mm. The mucus-containing exudate produced by the inflammatory response overpowers the normal clearance mechanisms, resulting in the cough and expectoration that characterize chronic bronchitis. In some cases of chronic bronchitis, the inflammatory process extends to smaller bronchi and bronchioles less than 2 mm in internal diameter. In this location, the inflammatory process thickens the wall, narrows the lumen and destroys the parenchymal support of the airways. These changes progressively increase peripheral airways resistance and eventually reduce the patient's ability to empty their lungs to a degree that can be measured by a reduction in FEV1 (forced expiratory volume in one second). The reduction in lung surface area produced by parenchymal inflammation contributes to the decline in FEV1 by reducing lung elastic recoil, which is the major force driving air out of the lung. It also contributes to the reduction in diffusing capacity by reducing the lung capillary bed. The purpose of this presentation is to review the quantitative aspects of these pathological changes and attempt to provide insight into factors which result in progression of these lesions.