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Bronchopulmonary Dysplasia - Assignment Example

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The paper “Bronchopulmonary Dysplasia” seeks to evaluate a type of chronic lung infection that is caused by damage of the tissues to the lungs. BPD is common in immature children who had a severe lung infection, for example, respiratory distress syndrome at birth…
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Bronchopulmonary Dysplasia
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Bronchopulmonary Dysplasia Introduction Bronchopulmonary dysplasia (BPD) is a type of chronic lung infection that is caused by damage of the tissues to the lungs. BPD is common in immature children who had severe lung infection, for example, respiratory distress syndrome at birth. After birth, these infants are usually given mechanical ventilation as well as supplemental oxygen for sometime after their birth. Overstretched air sacs caused by ventilation or high level of oxygen can injure the lungs’ delicate tissues. Consequently, the lungs swell leading to extra accumulation of fluids in it. BPD is characterized by inflammation, fibrosis as well as delayed development of the lungs in pre-term infants. This paper explores BPD’s Pathophysiology, epidemiology, causes, signs and symptoms, and its prevention among others. Pathophysiology According to D’Angio and Maniscalco (2004), the Pathophysiology of Bronchopulmonary dysplasia is much complex and is yet to be fully understood. The following are some of the factors connected with BPD: Inflammation: The infiltration of granulocyte into the lungs of newborns developing BPD is well documented (D’Angio & Maniscalco, 2004). Animal samples of infant lung injury provide evidence for the role played by granulocyte in BPD’s pathogenesis. There is fast development of Neutrophil in the bronchoalveolar lavage fluid of newborns with RDS (D’Angio & Maniscalco, 2004). In infants who are later diagnosed with BPD, the decline in Neutrophil counts is delayed. Proinflammatory mediators like cytokines, which attract inflammatory cells into the lungs have been connected with the development of BPD in infants (Mighten, 2012, p. 135; D’Angio & Maniscalco, 2004). Architectural Disruption: Cellular injury as well as the destruction caused when inflammatory cells discharge reactive oxygen and proteases result from granulocytes infiltration into the lung. “The lung protease/antiprotease balance appears to be tilted toward proteolysis in infants who develop BPD” (D’Angio & Maniscalco, 2004, p.309). Infants with high probability of developing BPD show higher elastase levels. Fibroproliferation: Transforming growth factor (TGF) - β has been shown by most studies to have serious inhibitory impact on lung development besides other fibrogenic effects (D’Angio & Maniscalco, 2004). Higher levels of TGFβ have been identified in infants who are later diagnosed with BPD (D’Angio & Maniscalco, 2004). Delayed development of the lung has also been connected with ‘new’ BPD. Epidemiology The vulnerability to BPD increases with declining birth weight. The values for determining incidence depend on the criteria used, for instance, based on the results of a resent research, roughly “half of all admissions, weighing Read More
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