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Chronic Obstructive Pulmonary Disease


3.1. Definition of Chronic Obstructive Pulmonary Disease (COPD)
COPD is a chronic pulmonary disease characterized by obstruction of air flow
in the airways that is progressive nonreversive or partially reversible. COPD consists
of chronic bronchitis and emphysema atau a combination of both. 4
3.2 Epidemiology
Globally , it is estimated that about 3 million deaths were caused by COPD in
2015 which is 5% of all global deaths that year. More than 90% of COPD deaths
occur in developing countries. The main cause of COPD is exposure to tobacco
smoke (either active smoking or passive smoking. Other risk factors include
exposure to indoor and outdoor air pollution and dust and working fumes
(WHO,2015). The prevalence of COPD is expected to increase with respect to the
increase in the life expectancy of the world's population. According to WHO
predictions, COPD, which is currently the 4th leading cause of death worldwide, is
estimated that by 2030 it will be the 3rd cause of death worldwide. 5th
3.3 Risk Factors
1. Smoking is the only causal cause that is the most important, much more
important than other causal factors.
In recording the history of smoking, it is necessary to pay attention to:
a. History of smoking
- Active smoker
-Passive smoking
-Former smoker
2.History of exposure to air pollution in the environment and workplace
3.Hypereaktiviti of the bronchi
4.History of recurrent lower respiratory tract infections
5.Alpha-1 antitrypsin deficiency, generally rare in Indonesia. 5th


3.4 Pathophysiology



1

, In COPD, airflow barriers are the main physiological changes caused by
changes typical of the airways proximal, peripheral, parenchymal and vascularization
of the lungs due to chronic inflammation and structural changes in the lungs. The
occurrence of thickening of the small airway with an increase in lymphoid follicle
formation and deposition of collagen within the outer wall of the airway results in
restrictions on airway opening. The lumen of the small airway is reduced due to
thickening of the mucosa containing inflammatory exudate, which increases
according to the severity of the pain. 2


The inflammatory process will activate alveolar macrophage cells, the
activation of these cells will lead to the release of neutrophil chemotactic factors
such as interleukin 8 and B4 leukotrienes, tumuor necrosis factor (TNF), monocyte
chemotactic peptide (MCP)-1 and reactive oxygen species (ROS). 2


The dominant paradigm of emphysema pathogenesis consists of four
related events: (1) Chronic exposure from smoking will lead to the recruitment of
inflammatory cells into the terminal air chamber in the lungs. (2) These
inflammatory cells release elastonic proteinases that damage the extracellular matrix
in the lungs. (3) Cell death structurally results from oxidative stress and loss of cell
matrix bonds. (4) The repair of elastin and the components of the extracellular matrix
that are ineffective results in an enlargement of the air chamber defined as
pulmonary emphysema. 2
Exposure to cigarette smoke can affect the large respiratory tract, small
respiratory tract (≤2mm in diameter), and alveoli. Changes in the large respiratory
tract cause coughing and sputum, while in the small respiratory tract and alveoli are
responsible for physiological changes. 2
COPD patients are said to experience acute exacerbations when the
patient's condition worsens the acute nature of the previously stable condition and
with a variation in normal daily symptoms so that the patient requires changes in the
treatment that is commonly used. These exacerbations are usually caused by
infections (bacterial or viral), bronchospasm, air pollution or sedative class drugs. 4



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