Shortness of breath: COPD
Table of Contents
Introduction.....................................................................................................................................2
Epidemiology...................................................................................................................................2
Pathogenesis....................................................................................................................................3
Pathology.........................................................................................................................................7
Pathophysiology.............................................................................................................................10
Risk Factors....................................................................................................................................12
Approach to Patient.......................................................................................................................15
History........................................................................................................................................15
Physical Findings........................................................................................................................16
Laboratory Findings....................................................................................................................17
References.....................................................................................................................................23
,Chronic Obstructive Pulmonary Disease
Introduction
COPD is defined as a disease state characterized by persistent respiratory symptoms and
airflow limitation that is not fully reversible.
COPD includes
o Emphysema: anatomically defined condition characterized by destruction of the
lung alveoli with air space enlargement
o Chronic bronchitis: - a clinically defined condition with chronic cough & phlegm
o Small airway disease: - a condition in which small bronchioles are narrowed and
reduced in number.
The classic definition of COPD requires the presence of chronic airflow obstruction,
determined by spirometry, that usually occurs in the setting of noxious environmental
exposures, most commonly cigarette smoking.
o Patients with a history of cigarette smoking without chronic airflow obstruction
may have chronic bronchitis, emphysema, and dyspnea.
Although these patients are not included within the classic definition of
COPD, they may have similar disease processes.
o Respiratory symptoms and other features of COPD can occur in subjects who do
not meet a definition of COPD based only on airflow obstruction determined by
spirometric thresholds of normality.
Epidemiology
COPD is the 3rd leading cause of death and affects >10 million persons in the US.
COPD (Loscalzo & Jameson, 2022) is also a disease of increasing public health
importance around the world.
Estimates suggest that COPD will rise to the 3rd most common cause of death worldwide
by 2020.
, Pathogenesis
Airflow limitation is a major physiologic change, can result from small airway disease
and/or emphysema.
Small airways may become narrowed by cells (hyperplasia & accumulation), mucus, and
fibrosis, and extensive small airway destruction has been demonstrated to be a hallmark
of advanced COPD.
Although the precise biological mechanisms leading to COPD have not been determined,
a number of key cell types, molecules, and pathways have been identified from cell-
based and animal model studies.
The pathogenesis of emphysema is more clearly defined than the pathogenesis of small
airway disease.
The dominant current pathogenesis of emphysema comprises a series of 4 interrelated
events:
1. Chronic exposure to cigarette smoke in genetically susceptible individuals
triggers inflammatory & immune cell recruitment within large & small airways
and in the terminal air spaces of the lung.
2. Inflammatory cells release proteinases that damage the ECM(extracellular
matrix) supporting airways, vasculature, and gas exchange surfaces of the lung.
3. Structural cell death occurs through oxidant-induced damage, cellular
senescence, and proteolytic loss of cellular-matrix attachments leading to
extensive loss of smaller airways, and alveolar destruction.
4. Disordered repair of elastin and other ECM components contributes to air space
enlargement and emphysema.
Table of Contents
Introduction.....................................................................................................................................2
Epidemiology...................................................................................................................................2
Pathogenesis....................................................................................................................................3
Pathology.........................................................................................................................................7
Pathophysiology.............................................................................................................................10
Risk Factors....................................................................................................................................12
Approach to Patient.......................................................................................................................15
History........................................................................................................................................15
Physical Findings........................................................................................................................16
Laboratory Findings....................................................................................................................17
References.....................................................................................................................................23
,Chronic Obstructive Pulmonary Disease
Introduction
COPD is defined as a disease state characterized by persistent respiratory symptoms and
airflow limitation that is not fully reversible.
COPD includes
o Emphysema: anatomically defined condition characterized by destruction of the
lung alveoli with air space enlargement
o Chronic bronchitis: - a clinically defined condition with chronic cough & phlegm
o Small airway disease: - a condition in which small bronchioles are narrowed and
reduced in number.
The classic definition of COPD requires the presence of chronic airflow obstruction,
determined by spirometry, that usually occurs in the setting of noxious environmental
exposures, most commonly cigarette smoking.
o Patients with a history of cigarette smoking without chronic airflow obstruction
may have chronic bronchitis, emphysema, and dyspnea.
Although these patients are not included within the classic definition of
COPD, they may have similar disease processes.
o Respiratory symptoms and other features of COPD can occur in subjects who do
not meet a definition of COPD based only on airflow obstruction determined by
spirometric thresholds of normality.
Epidemiology
COPD is the 3rd leading cause of death and affects >10 million persons in the US.
COPD (Loscalzo & Jameson, 2022) is also a disease of increasing public health
importance around the world.
Estimates suggest that COPD will rise to the 3rd most common cause of death worldwide
by 2020.
, Pathogenesis
Airflow limitation is a major physiologic change, can result from small airway disease
and/or emphysema.
Small airways may become narrowed by cells (hyperplasia & accumulation), mucus, and
fibrosis, and extensive small airway destruction has been demonstrated to be a hallmark
of advanced COPD.
Although the precise biological mechanisms leading to COPD have not been determined,
a number of key cell types, molecules, and pathways have been identified from cell-
based and animal model studies.
The pathogenesis of emphysema is more clearly defined than the pathogenesis of small
airway disease.
The dominant current pathogenesis of emphysema comprises a series of 4 interrelated
events:
1. Chronic exposure to cigarette smoke in genetically susceptible individuals
triggers inflammatory & immune cell recruitment within large & small airways
and in the terminal air spaces of the lung.
2. Inflammatory cells release proteinases that damage the ECM(extracellular
matrix) supporting airways, vasculature, and gas exchange surfaces of the lung.
3. Structural cell death occurs through oxidant-induced damage, cellular
senescence, and proteolytic loss of cellular-matrix attachments leading to
extensive loss of smaller airways, and alveolar destruction.
4. Disordered repair of elastin and other ECM components contributes to air space
enlargement and emphysema.
