**1. Introduction**

116 Chronic Obstructive Pulmonary Disease – Current Concepts and Practice

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Schilmann, Rogelio Perez-Padilla, and Omar Masera. Improved Biomass Stove Intervention in Rural Mexico Impact on the Respiratory Health of Women Pulmonary emphysema is a chronic disease defined pathologically as an abnormal permanent destruction and enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of alveolar walls without predominant fibrosis. Emphysema frequently occurs in overlapping association with chronic bronchitis which is clinically defined as chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough have been excluded. Previously, emphysema and chronic bronchitis was regarded as distinct entities and grouped under the umbrella term Chronic obstructive pulmonary disease(COPD).

COPD is a collection of heterogeneous conditions characterized by persistent expiratory airflow limitation. There is significant overlap and co-existence of conditions like emphysema, chronic bronchitis and asthma(see Figure 1). COPD is heterogeneous clinically and at a pathophysiologic level and its recognition, has led to new initiatives to categorize and define COPD and its subsets.(American Thoracic Society[ATS],1995,2010;British Thoracic Society[BTS],1997)

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) does not emphasise on the distinction between emphysema and chronic bronchitis (GOLD,2006). This report produced by the National Heart, Lung, and Blood Institute (NHLBI) and the World Health Organization(WHO) emphasised on the common feature of altered lung function recognizes both the systemic nature and the heterogeneity of COPD and defines it as follows:

"Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation

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Current Overview of COPD with Special Reference to Emphysema 119

iii. "Protease-antiprotease hypothesis"("Swedish hypothesis") - association of homozygous alpha1 protease inhibitor deficiency with emphysema was discovered by Laurell and Eriksson in Sweden. (Laurell & Eriksson,1963;Snider et al.,1974 as cited in Shapiro

iv. "American hypothesis" - American pathologist Averill Liebow emphasised that altered repair mechanisms contribute to the development of COPD and that deficient maintenance of lung structure, could lead to emphysema.(Liebow,1959;Rennard,2004

COPD has been described and subclassified on various clinical, etiopathogenetic and pathological basis. Chronic bronchitis has been associated with a "blue bloater" clinical phenotype on basis of the concept that altered airway anatomy would lead to heterogeneity of airflow distribution within the lung, resulting in ventilation-perfusion imbalance, hypoxemia, and right heart failure. On the other hand, emphysema has been described with the "pink puffer" phenotype based on the concept that it primarily causes decreased airflow

Pathologic studies delineate inflammation of airway structures (bronchitis) from destruction of the alveolar wall (emphysema). Emphysema has been described as centriacinar, panacinar and paraseptal based on the location of emphysematous airspaces in an acinus. Centriacinar variety is common in cigarette smokers and panacinar emphysema is

COPD is a major public health problem with a high and continually increasing morbidity. The Burden of Obstructive Lung Disease (BOLD) study showed that the worldwide prevalence of COPD (stage II or higher) was 10.1%. This figure varied by geographic location and by sex with prevalence among men at 11.8% (8.6-22.2%) and among women at 8.5% (5.1-16.7%)(Buist et al.,2007). The wide differences noted was partly due to site and sex differences in the prevalence of smoking. The true prevalence is likely higher because COPD is both under-recognized and under-diagnosed. COPD was the sixth leading cause of death worldwide in 1990 and is expected to become the third leading cause of death by

COPD has higher prevalence in low-socioeconomic population(Fletcher,1976). Commonly, patients present in their fifth decade of life with productive cough or acute chest illness. Alpha-1 Protease Inhibitor (A1PI) deficient patients present earlier than other COPD patients in 3rd-4th decade of life. COPD progresses with age and is more prevalent in elderly populations. In the United States, 15% of the total population aged 55 to 64 will have moderate COPD (GOLD stage 2, FEV1 < 80% predicted), and this increases to over 25% for

Cigarette smoking is the most significant and predictable risk factor in pathogenesis of COPD. Almost 80% of individuals who have COPD and 80% who die from COPD in the

SD,2010)

**3. Epidemiology** 

**3.1 Risk factors** 

**3.1.1 Cigarette smoking** 

as cited in Shapiro SD,2010)

from the obstruction and less prominent hypoxia.

predominant in proteinase inhibitor deficiency.

2020(Murray & Lopez,1997 as cited in Shapiro SD,2010).

those older than 75(Stockley et al.,2009 as cited in Shapiro SD,2010).

that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases."(GOLD,2006)

Fig. 1. Schematic Venn diagram of subsets of COPD. This is a non-proportional Venn diagram adapted from *Am J Respir Care Med* (ATS,1995) showing subsets of patients with chronic bronchitis, emphysema, and asthma(circles) and their relationship to airflow obstruction (box). The subsets comprising COPD are 4,5,6,7,8 and 9. Asthma is depicted by subset 3, whose airflow obstruction is completely reversible and are not considered to have COPD.
