NURS 6501 Week 4 Assignment Case Study Analysis

NURS 6501 Week 4 Assignment

Case Study Analysis

Student Name

Walden University

NURS 6501

Professor Name

Date

Case Study Analysis

Factors Contributing to COPD Development

Smoking forty packs of cigarettes over the course of a lifetime is the primary cause of the patient’s COPD. When smoking stimulates immune cells and produces tissue-damaging radicals in the lungs, it damages the alveoli and alters the airways (De Cunto et al., 2020). In addition to smoking, occupational health hazards are a significant contributor to the development of COPD. Even if they do not smoke, mine workers and other workers who regularly come into contact with certain irritants, such silica dust, run the risk of developing chronic airway inflammation and fibrosis (Ike-Samuel et al., 2025). Because these irritants affect cilia function and trigger comparable inflammatory responses in the lungs, exposure to them has the same negative health effects as smoking.

Smoking-Induced Lung Changes

The toxic chemicals in cigarette smoke cause the lung’s neutrophils and macrophages to become activated, producing inflammatory agents and reactive oxygen species. Lung elasticity is decreased as a result of the cells’ digestion of elastin and alveolar walls by proteases such elastase (Heinz, 2020). Because elastic tissue degrades and keeps the lungs too full of air, ineffective breathing results. In order to create a barrel-shaped chest, the diaphragm flattens and the chest wall expands outward. Patients have to rely on more muscles to exhale, which makes breathing more difficult and changes the anatomy of their chest.

Mechanisms of Productive Cough

Patients with COPD who have irritated airways generate excessive mucus that is unable to adequately leave their bodies. Smoking causes the glands beneath the mucosal tissue to enlarge, producing more mucus, and it also causes an excess of goblet cells (Gui et al., 2021). Because the cilia are damaged by the harmful compounds, mucus cannot be removed by the regular cleaning process. The cough reflex is activated to clear blocked airways of mucus. Chronic inflammation’s negative health effects increase nerve sensitivity, which encourages coughing fits. Sputum is produced daily as a result of the ongoing airway alterations that characterize chronic bronchitis.

Alveolar Destruction and Gaseous Exchange

The available gas exchange surface area is decreased when alveoli are destroyed by emphysematous degradation, which leads to hypoxemia (a reduced capacity to diffuse oxygen) and hypercapnia (a reduced capacity to expel carbon dioxide) (Cho & Stout-Delgado, 2020). Hypoxemia impairs the supply of oxygen to muscles, resulting in obvious exhaustion while exerting oneself. Patients can breathe at large lung volumes, which are less effective for the diaphragm, and residual volume rises in hyperinflation. It makes breathing more difficult and develops into dyspnea. Breathlessness causes compensatory tachypnea, which further stresses the respiratory muscles. Chronic hypercapnia maintains anomalies of gas exchange by desensitizing chemoreceptors and decreasing respiratory drive (Palmer & Clegg, 2023).

Susceptibility to Respiratory Infections

Patients with COPD have nearly nonexistent immunological responses (airway defenses), making them vulnerable to a variety of infections. Because of mucus accumulation and ciliary failure, airway pathogens invade the airways. Prolonged inflammation inhibits the removal of pathogens, interferes with the phagocytic activity of alveolar macrophages, and interferes with the generation and recycling of antioxidants (Lugg et al., 2021). Additionally, structural damage like thickening of the bronchial wall prevents the recruitment of immune cells. Recurrent infections in this patient exacerbate the decrease in lung function and raise the likelihood of hospitalization.

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