CASE STUDY: COPD Essay Example
CASE STUDY: COPD 5
Case Study: Chronic Obstructive Pulmonary Disease (COPD)
Case Study: COPD
COPD is a significantly irreversible and insidious condition primarily caused by chronic cigarette smoking (Mosenifar, 2014). Tobacco smoking is estimated to be the etiology behind over 90% of COPD cases, including Mrs White’s. Pathogenesis of COPD occurs through three processes that include airway inflammation, oxidative stress and protease-antiprotease imbalance (MacNee, 2005).
Cigarette smoke induces increased production of inflammatory cells. These cells include neutrophils some of which migrate and sequestrate in lung capillaries after their deformability is affected by smoke components (MacNee, 2005). Moreover, T-lymphocytes especially the CD8+ type and macrophages are other inflammatory cells activated by cigarette smoke. Chronic cigarette smoking perpetuates an excessive production of these inflammatory cells becoming injurious to the lungs rather than protective (Yoshida & Tuder, 2007). These cells release inflammatory mediators and cytokines that orchestrate progressive airways and lung deformation and destruction. Neutrophils may secrete serum proteinases such as neutrophil elastase and matrix metalloproteinase (MMP) 8 and 9 that cause slow, but progressive alveolar destruction and excessive mucus production and mucus accumulation in large airways and small airways respectively blocking or narrowing the airways (Tuder & Petrache, 2012). CD8+ T cells may release perforins and granzymes that mediate apoptosis of epithelial cells in the alveoli progressing towards emphysema (MacNee, 2005). The smoke also activates more macrophages to release more inflammatory mediators such as TNFα and leukotriene b4, and proteases such as MMPs that mediate elastolytic activity in the lungs. Repeated inflammatory bronchial injury causes epithelial cells, neutrophils and macrophages to release transforming growth factor beta (TGF β) that mediates fibroblast activation leading to airway fibrosis and narrowing (MacNee, 2005).
Cigarette smoke has more than 4000 chemicals including oxidants and free radicles. The smoke condensate may form reactive peroxide and superoxide oxygen radicles in the epithelial lining of the lungs (Mosenifer, 2014). Furthermore, the smoke components turn on «inducible nitric oxide synthase» consequently forming oxidants that include peroxynitrite (Tuder & Petrache, 2012). Since cigarette smoke moderately depletes glutathione, a physiological antioxidant, the oxidants and free radicles cause oxidative stress that slowly destroy alveoli and lung epithelia cells (MacNee, 2005).
An uneven protease-antiprotease activity in the lung parenchyma contributes to the loss of elasticity especially in the alveoli. This is mediated by elastases released by neutrophils and macrophages that overburden the elastic maintenance activity of α1-antitrypsin (α1-AT) leading to loss of alveoli elastic recoil (Yoshida & Tudor, 2007).
Mrs. White’s abnormal pulmonary function tests such as 55% FEV1/FVC is a result of the loss of the lungs’ elastic recoil pressures and fibrotic remodeling of airways that consequently result in substantial airway narrowing. Proteolytic activity of elastases released by inflammatory cells in the lung parenchyma destroy elastin, a significant component of the parenchyma’s elastin fibers (MacNee, 2005). Since the destruction is not sufficiently counterbalanced by antiprotease activity of enzymes such as α1-AT, the consequent is an ultimate loss of alveoli’s and general lungs’ elastic recoil that also results in airways narrowing, reduced bronchial airflow and trapping of air in the lungs (Brashier & Kodgule, 2012). These changes together with inflammatory cell’s fibrotic activity in the airways reduces airflow especially during expiration thereby lowering the FEV1/FVC ratio, a defining finding in patients with COPD.
Mrs. White also presents with decreased PaO2 and increased PaCO2 in addition to a low, 91% oxygen saturation. Fibroblastic, apoptotic activity and oxidative stress all contribute to the destruction of alveoli (Brashier & Kodgule, 2012). Damaged alveoli have lower surface area available for gaseous exchange especially to facilitate sufficient uptake of oxygen and elimination of CO2 across the pulmonary vasculature. The impaired gaseous exchange leads to chronic hypoxic and hypercapnic states that manifest as decreased PaO2 and increased PaCO2 respectively (Bourdin et al., 2009). Central cyanosis is also a manifestation of prolonged hypoxic states.
Bourdin, A., Burgel, P.R., Chanez, P., Garcia, G., Perez, T. & Roche, N. (2009). Recent advances in COPD: pathophysiology, respiratory physiology and clinical aspects, including comorbidities. European Respiratory Review, 18(114), 198-212.
Brashier, B.B. & Kodgule, R. (2012). Risk factors and pathophysiology of chronic obstructive pulmonary disease (COPD). Journal of Association of Physician of India, 60, 17-21.
MacNee, W. (2005). Pathogenesis of chronic obstructive pulmonary disease. Proceedings of the American Thoracic Society, 2, 258-256.
Mosenifar, Z. (2014). Chronic obstructive pulmonary disease. Retrieved from http://emedicine.medscape.com/article/297664-overview#aw2aab6b2b1aa
Tuder, R.M & Petrache, I. (2012). Pathogenesis of chronic obstructive pulmonary disease. The Journal of Clinical Investigation, 122(8), 2749-2755.
Yoshida, T & Tuder, R.M. (2007). Pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease. physiological Reviews, 87(3), 1047-1082.
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