Case Scenario-A 61-year-old Male with Complaints of Shortness of Breath Are the spirometry results consistent with obstructive or restrictive pulmonary disease? What is the most likely pulmonary diagnosis for this patient?

The patient’s spirometry results are harmonious with obstructive pulmonary disease. This is evidenced by a forced expiratory volume in the first second (FEV1) of less than 80 percent of the predicted value (64 percent), a lower forced vital capacity (FVC), and an FEV1: FVC ratio of less than 0.7 (0.56).

The patient’s diagnosis is chronic obstructive pulmonary disease (COPD). This is evidenced by insignificant changes in the spirometry readings of the FEV1/FVC ratio after administering a bronchodilator (Celli & Wedzicha, 2019).

1. Explain the pathophysiology associated with the chosen pulmonary disease.

COPD manifests with limitation of airflow, impaired gaseous exchange, excessive mucus secretion, and pulmonary hypertension. Notably, limited airflow is caused by perpetual inflammation, exudation, and fibrosis (Celli & Wedzicha, 2019). This leads to a decrease in the FEV1 and a subsequent decline in the FEV1: FVC ratio (Celli & Wedzicha, 2019). Also, limited airflow leads to the retention of inhaled air and increases the risk of hypercapnia (Celli & Wedzicha, 2019). This triggers hyperinflation. Inflammation associated with COPD is attributed to oxidative stress and proteases (Stockley et al., 2019). Proteases mediate the breakdown of elastin and predispose an individual to emphysema and airway inflammation (Stockley et al., 2019). Findings demonstrate that oxidative stress is exacerbated in patients with COPD. Excessive mucus secretion results from increased goblet cells and enlargement of submucosal glands due to persistent airway inflammation (Stockley et al., 2019). Other mediators, such as proteases, may increase mucous secretion by activating the epidermal growth factor (Stockley et al., 2019). Pulmonary hypertension represents a poor prognosis of COPD; it is triggered by vasoconstrictor pulmonary arteries secondary to hypoxia. Both viral and bacterial respiratory infections worsen COPD.

COPD occurs in two forms: chronic bronchitis (CB) and emphysema. CB is caused by the destruction of the endothelium and compromised mucociliary clearance (Celli & Wedzicha, 2019). This leads to the accumulation of mucus, bacteria, and neutrophils. A continuous inflammatory response leads to fibrosis via hyperplasia and metaplasia of goblet cells (Celli & Wedzicha, 2019). The structural changes limit gaseous exchange. On the other hand, emphysema is characterized by enlarged airspaces and a decrease in the volume of the air sacs. The destruction of alveoli impairs elastic recoil and gaseous exchange (Celli & Wedzicha, 2019). It also constricts the airways and compounds impaired gaseous exchange.