Pathophysiology of COPD, Acute Exacerbation, Pneumonia, and Interventions for COPD Management

Nursing
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1.1. Pathophysiology of COPD
Chronic Obstructive Pulmonary Disease (COPD) is manifested by airflow limitation which is persistent
and rarely reversible. It is related to chronic inflammatory response in the lungs and airways due to
some gases or particles particularly from smoking. Presence of these smoke particles in the lungs trigger
inflammatory response which leads to increased macrophage and neutrophil infiltration into the lungs.
Cytokines, chemokines and elastases are released by these immune cells and this eventually damage the
parenchyma with time (Wells, & Dransfield, 2013).
Besides inflammation, there are two other processes involved in the pathogenesis of COPD. One is the
imbalance between proteases and antiproteases and the other is imbalance between oxidants and
antioxidants in the lungs. The first, that is, protease-antiprotease imbalance has been associated with
pathogenesis of emphysema. Emphysema is a disease of alveoli whereby the fibers that forms the walls
of alveoli becomes destroyed. The destructions render them less elastic and unable to function during
exhalation. Proteases like elastase and matrix metalloproteinase (MMPs) released by the inflammatory
cells breaks down the connective tissue of alveolar walls and the septae. This loss of the elasticity leads
to reduced rates of expiratory flow, air trapping and collapsing of the airway.
Inflammation from smoke exposure also leads to fibrosis of bronchiolar walls, hypersecretion of mucus,
airway edema and bronchoconstriction. This generally may be referred to chronic bronchitis. In chronic
bronchitis, the epithelium of the central airways and also the mucus-producing glands are inflamed. This
is associated with mucus production, reduced mucociliary clearance and increased permeability of the
airspace epithelial barrier. Goblet cells hyperplasia, mucous gland enlargement and mucociliary
dysfunction causes excessive mucus production in larger airways and build up reducing the airway
lumen. Despite the fact that these changes occur in the larger airway, it is evident that the increased
airway resistance is majorly in the small airways(≤2mm) (Kim, & Criner,2013). Fibrosis and smooth

muscle hypertrophy likely occur together with increased mucus production and also cellular infiltration
in the peripheral airways.
1.2.Acute exacerbation of COPD
Acute exacerbations of COPD is when there an abrupt worsening of the symptoms of COPD that is,
shortness of breath, amount and color of sputum which likely last for many days. Acute
exacerbations of chronic bronchitis (AECB) is another term for Acute exacerbation of COPD. This
condition may be caused by an infection with microorganisms such as bacteria or viruses or even by
pollutants of the environment. Basically most of the causes is due to infections either by bacteria or
viruses or both. During exacerbation, there is an increased airway inflammation which leads to
increase in hyperinflation, reduce in air flow during exhalation and also decreased gas exchange.
(Ko, Chan,Hui, Goddard, Shaw, Reid & Yang,2016)
Robert is diagnosed with exacerbation of COPD due to community acquired pneumonia which can
be due to infections with bacteria, fungi, viruses and parasite with little contact with the healthcare
system (Vestbo, Hurd, Agustí, Jones, Vogelmeier, Anzueto & Stockley, 2013). Factors that can put
patient like Robert at high risk for exacerbation of COPD may include; obstruction of airway part and
lung disease. When the bronchus is obstructed for example by mucus, the lung cannot eliminate
fluid and hence this can lead to pneumonia which in turn cause exacerbations. Underlying lung
diseases such as emphysema and habits such as smoking as in for Robert’s case also lead to more
frequent and even more severe bouts of pneumonia.
Other factors that can cause exacerbations may include severe allergy or heavy air pollution.
Weather changes, too much activity, lack of enough sleep, undergoing stress or anxiety also triggers
exacerbations. In some cases, however, the exact cause is unknown.
1.3.Pathophysiology of pneumonia and the differences between Community Acquired, Hospital
Acquired and Health Care Associated Pneumonia.