Introduction COPD

 

Aim of Presentation

To critically evaluate the patient suffering from COPD in terms of its pathophysiology, etiologies, risk factors, diagnosis and complications.

To highlight the roles of various healthcare professionals, the importance of a multidisciplinary approach in improving patient outcomes and provide insights into the experiences of individuals affected by COPD.

To investigate the effectiveness of interventions provided by nurses in improving COPD patient’s and caregivers' understanding of the disease, enhancing self-management skills and ultimately improving quality of life outcomes.

Patient was having a debilitating lung condition that can cause significant morbidity and mortality.

A chronic patientà so there was a progressive airflow obstruction.

COPD is characterised by a reduced FEV₁/FVC ratio < 0.7.

It develops gradually over years and can become irreversible.

Patient was now showing acute exacerbation of COPD.

It has become third leading cause of death globally.

The patient is a known case of COPD, a chronic, debilitating lung condition and a major cause of morbidity and mortality worldwide. It is characterised by a decreased FEV₁/FVC ratio of less than 0.7 and is now believed to be the third leading cause of death globally (Bhatt et al., 2019).  As it develops gradually over several years, patients may progressively lose their lung function. This is evident in this patient, who now presented with acute exacerbation and severe respiratory distress.  Moreover, COPD is more common in men and smokers, and its incidence increases with age (Terzikhan et al., 2016).

Pathophysiology of COPD

Tissue destruction

Cellular senescence

Impairment of the defence mechanisms

Chronic inflammatory cells accumulation

Disturbance of the repair mechanisms

Genetic conditions

Exacerbation à increase in airway resistance, worsening of expiratory flow limitation (EFL) and prolonged lung emptying.

Mucosal oedema

Bronchospasm

Thickened sputum secretions

The molecular pathophysiology of COPD is associated with chronic inhalation of detrimental particles, like those present in cigarette smoking, cellular senescence and genetic conditions (Hikichi, Mizumura, Maruoka, & Gon, 2019). Cell signalling and antimicrobial activity are essential to maintain homeostasis. Nevertheless, when reactive oxygen species (ROS) get accumulated in an excessive amount, they destroy the DNA, proteins and lipids (Hikichi, Mizumura, Maruoka, & Gon, 2019). Research has revealed that certain cytokines also participate in the pathology of this disease. However, evidence that they are involved in the pathogenesis of COPD remains inconclusive (Faner et al., 2016). Additionally, In COPD, it has been seen that there is an inhibition of neutrophil apoptosis while there is a decrease in the phagocytic function of alveolar macrophages (Hikichi, Mizumura, Maruoka, & Gon, 2019). This brings about neutrophil-induced inflammation because of secondary necrosis. All of these factors lead to airway narrowing and loss of elastic recoil in the lungs, resulting in airflow restriction.

Exacerbation leads to greatly increase in airway resistance and worsening of expiratory flow limitation. This is mainly because of mucosal oedema, thickened sputum secretions and bronchospasm. Lung emptying becomes also affected i.e. it becomes prolonged (Leap, Arshad, Cheema, & Balaan, 2021). This explains the pathophysiology of COPD and its exacerbation in this patient.