Chronic obstructive pulmonary disease (COPD) is characterised as an inflammatory disease of the lung that is linked to limited airflow and disrupted outbreaks of severe exacerbation

Introduction

Chronic obstructive pulmonary disease (COPD) is characterised as an inflammatory disease of the lung that is linked to limited airflow and disrupted outbreaks of severe exacerbation (Bhatt & Dransfield, 2013; MacNee, 2006). It is widely accepted that smoking is the major cause of COPD and is commonly associated with each stage of pulmonary disease; initiation, progression, and consolidation (Tuder & Petrache, 2012). As the name suggests, COPD primarily influences the respiratory system, however researchers have recently recognised that the inflammatory state related to COPD is not simply restricted to the lungs, but extends to other significant non-pulmonary organs like the brain and heart (Bhatt & Dransfield, 2013). This paper aims to investigate the impact of COPD on the respiratory and circulatory systems among smokers and the strategies that are available to patients to help mitigate the influence of COPD. Chronic Obstructive Pulmonary Disease and its Impact on Selected Body Systems All smokers develop inflammation in their lungs, but those who suffer from COPD as a result have a heightened response to the inhalation of the toxic agents and chemicals present in cigarettes and cigars (MacNee, 2006). This elevated reaction adversely affects the anatomy and physiology of the respiratory system as sufferers experience increased susceptibility to chronic bronchitis [see Figure 1] (inflammation of the bronchi), emphysema (damage of the alveoli) and bronchiolitis (harm of the bronchioles) (MacNee, 2006). Further, smoking also damages the pleura, the layers of tissue which surround and protect the lungs. If damaged by smoking, the pleura no longer restricts air from escaping the lungs, thus increasing a sufferer’s likelihood of experiencing pneumothorax (Canter, 2021; Charalampidis et al., 2015). In addition, tissue damage can provoke oxidative stress, extracellular matrix proteolysis, and apoptotic and autophagic cell death (Tuder & Petrache, 2012).

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