Chronic Obstructive Pulmonary Disease

RA Stockley, Queen Elizabeth Hospital Birmingham, Edgbaston, Birmingham, UK

Published online: June 2011

DOI: 10.1002/9780470015902.a0002131.pub2

Chronic obstructive pulmonary disease is a group of conditions characterised by the presence of persistent airflow obstruction during expiration, primarily owing to narrowing of the smaller airways. Its prevalence is increasing and soon it will be the third most common cause of illness and death worldwide. The condition is a slowly progressive one punctuated by acute episodes of deterioration (exacerbations) and there is currently no specific therapy confirmed to slow the progression. The underlying pathophysiology is believed to be uncontrolled inflammation owing to a combination of genetic and environmental factors. Although classically associated with smoking, increasing pollution in the industrialised world and the burning of biomass fuels indoors in the third world also influences its prevalence.

Key Concepts:

  • COPD is a group of conditions in which airflow obstruction cannot be fully reversed.
  • The pathophysiology is owing to uncontrolled inflammation in the lung.
  • COPD is associated with an increased risk of co-morbidities such as arteriosclerosis, type II diabetes and osteoporosis probably as a result of common inflammatory processes.
  • Thoracic imaging is being increasingly used to identify different pathological processes that contribute to COPD.
  • Large clinical trials of inhaled therapy have demonstrated a reduction in the number of acute episodes of deterioration and possibly mortality.

Keywords: lung disease; bronchitis; emphysema; COPD; 1-antitrypsin; smoking

Figure 1. Representation of a spirometric trace for forced expired volume against time. The solid line indicates a normal pattern of expiration with more than 80% of the total forced expired volume being delivered in the first second (FEV1). The dashed trace is a representation of the forced expired pattern in an individual with airflow obstruction. The volume expired within the first second is significantly less than 70% of the total volume expired with time.
Figure 2. Family screening for 1-antitrypsin deficiency. The diagram indicates the most common mode of inheritance occurring in a family where a patient (in the highlighted box) with PiZZ (homozygote) 1-antitrypsin deficiency is identified. Most commonly the parents are heterozygotes and siblings of the index case stand a 1 in 4 chance of having normal 1-antitrypsin activity, a 1 in 2 chance of being heterozygotic, and a 1 in 4 chance of being homozygotic for the Z gene. In addition, screening partners of the siblings will identify other heterozygote pairing that may lead to the second generation of severe 1-antitrypsin deficiency. As the heterozygotic state is relatively common (approximately 3% of the general population), it is clearly important to identify the genetic state of the index patient's spouse, again determining risks to any children, and so on.
Figure 3. Representation of connective tissue destruction by neutrophils. The development of a chemoattractant gradient to cytokines such as interleukin 8 (IL-8) and leucotriene B4 (LTB4) recruits neutrophils from the vascular space through the endothelial cell layer. The neutrophils then pass through connective tissue, eventually passing through the epithelial layer into the airway. As the cells migrate, high concentrations of destructive enzymes are released in the immediate vicinity, digesting connective tissue and resulting in a path for cell migration (a) represents the process in normal subjects where the destruction around the migrating neutrophil is carefully limited by normal concentrations of proteinase inhibitors such as 1-antitrypsin. (b) The much larger area of connective tissue degradation that occurs when there is a deficiency of protective inhibitors, such as in genetic 1-antitrypsin deficiency.
Figure 4. Flow volume loop, with expiratory flow plotted against the volume expired. The normal loop is shown as a solid line; the dashed line indicates the loop in patients who have effort-dependent airways collapse during expiration, usually as a result of loss of connective tissue in extensive emphysema.
Figure 5. High-resolution computed tomogram from a patient with extensive emphysema. Density mask analysis highlights low-attenuation areas (areas with a density close to that of air) in white. These areas are consistent with the marked pathological changes of emphysema.
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    book Stockley RA (1999) "1-Antitrypsin deficiency". In: Stockley RA (ed.) Molecular Biology of the Lung, Vol. I: Emphysema and Infection, pp. 37–53. Boston, MA: Birkhauser.
    book Stockley RA, Rennard SI, Rabe K and Celli B (2007) Chronic Obstructive Pulmonary Disease, 1st edn. Oxford, UK: Blackwell Publishing Ltd.
    other The Lancet (2009) 374(9691), August 29–September 4.

Related Sub-Topics:

Inflammation | Molecular Genetics of Common and Complex Disease | Specific Genetic Disorders
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Article Title: Chronic Obstructive Pulmonary Disease
 
How to Cite close
Stockley, RA(Jun 2011) Chronic Obstructive Pulmonary Disease. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0002131.pub2]