In this case, the presenting symptoms provide evidence of bacterial bronchitis associated with a long history of chronic obstructive pulmonary disease (COPD). COPD is a common, preventable disease characterized by reversible airflow obstruction that is usually progressive. The production of mucus is due to chronic bronchitis, which causes hypersecretion of mucus and chronic cough production during winter for at least two consecutive years (Newsome et al., 2018). Emphysema causes abnormal enlargement of acini and destruction of the walls of the alveoli. In both cases, there is an enhanced chronic inflammatory response in the airways in response to gases and particles.
The pathophysiological changes of COPD take place in the human small peripheral airways, large central airways, and parenchyma of the lungs. In this case, chronic exposure to the irritating molecules recruits lymphocytes, macrophages, and neutrophils to the lungs (Hatipoğlu, 2018). These cells react by causing inflammation followed by oxidative stress, proteolysis of the extracellular matrix, and autophagic and apoptotic cell death. In chronic bronchitis, bronchial inflammation causes bronchia edema and an increase in the number and size of the goblet cells and mucus glands in the epithelium.
In addition, hypertrophy of the smooth muscles with fibrosis and reduction in the diameter of the airways are common pathophysiological changes (Hatipoğlu, 2018). The hypersecretion of thick and tenacious mucus cannot be cleared because the ciliary function is impaired. Consequently, the immune defense mechanism of the lungs is greatly reduced, which increases susceptibility to bacterial and fungal infections. In turn, frequent infections with bacteria damage airways, which are further complicated by bronchospasm with productive cough and dyspnea (Newsome et al., 2018). The accumulation of the thick and tenacious mucus and the hypertrophy of bronchial smooth muscles lead to the narrowing of the air path and eventual obstruction. Obstruction can also proceed to ventilation-perfusion and hypoxemia.
The heart and the lungs work together in the distribution of oxygen to cells throughout the body via blood flow. Comorbidities of cardiac and COPD diseases are associated and share common risk factors, symptoms, and pathophysiological processes (Hatipoğlu, 2018). A high risk of COPD is associated with a high risk of myocardial infarction, which also applies to acute exacerbations. Cardiac markers such as fibrinogen, N-terminal proBNP, CRP protein, Brain-type natriuretic peptide, troponin, and vascular endothelial growth factor (VEGF) increase in patients with COPD as an immune response. These factors are all risk factors for cardiac infarction, albeit independently.
The incidence and prevalence of COPD in the US differ with ethnicity and racial differences. Compared to white populations, both prevalence and incidence are lower in black and Asian groups and higher in white populations. Studies have shown that black people and Asian Americans with COPD also have less severe symptoms, while white patients tend to have severe shortness of breath. Furthermore, some studies have shown that Hispanics tend to have high incident and prevalence rates and severe symptoms when compared to Latinos (Díaz, Celli & Celedón, 2018). Research has shown that the likely differences between the racial and ethnic groups are due to biological and genetic variations, increased exposure to tobacco because of different lifestyles, and disparities in diagnosis and treatment.
The variations due to ethnicity and race can be explained based on the differences in smoking among the different groups. For example, whites and Native Americans have a higher prevalence of smoking than people of Asian origin. In addition, although black people are more likely to become smokers, they normally smoke a small number of cigarettes in a day compared to white and native smokers (Gilkes et al., 2017). Consequently, COPD is more prevalent among the ethnic and racial groups with higher exposure to smoke than those with low exposure. In addition, the interactions between the biological and genetic variations in lifestyle and behavior mean that when whites and Native Americans have the same level of exposure to smoke as blacks and Asians, they are more likely to develop COPD and have severe symptoms.
References
Díaz, A. A., Celli, B., & Celedón, J. C. (2018). Chronic obstructive pulmonary disease in Hispanics. A 9-year update. American Journal of Respiratory and Critical Care Medicine, 197(1), 15-21. Web.
Gilkes, A., Hull, S., Durbaba, S., Schofield, P., Ashworth, M., Mathur, R., & White, P. (2017). Ethnic differences in smoking intensity and COPD risk: An observational study in primary care. NPJ Primary Care Respiratory Medicine, 27(1), 1-6. doi: 10.1038/s41533-017-0052-8
Hatipoğlu, U. (2018). Chronic obstructive pulmonary disease: More than meets the eye. Annals of Thoracic Medicine, 13(1), 1–6. Web.
Newsome, B. R., McDonnell, K., Hucks, J., & Dawson Estrada, R. (2018). Chronic obstructive pulmonary disease: Clinical implications for patients with lung cancer. Clinical Journal of Oncology Nursing, 22(2), 184–192. Web.