A newborn exhibits signs of respiratory distress due to the lack of surfactant. She has signs of low oxygen and high carbon dioxide.Explain why the lack of surfactant would result in respiratory distress. Furthermore, what type of acid-base disorder might she develop and how would her body compensate. Be detailed in your explanation and support your answer with facts from your textbook, research, and articles from scholarly journals. In addition, remember to add references in APA format to your posts to avoid plagiarism.

Answer:

- The pulmonary surfactant decreases the surface tension in the lungs

- Protein-lipid interactions at air-liquid interfaces are influenced by pH changes, and therefore alter pulmonary surfactant function.  

- Mutations in the surfactant associated proteins SP-C may lead to respiratory acidosis

Explanation:

The pulmonary surfactant is a surface-active lipoprotein complex (phospholipoprotein) produced by type II alveolar pneumocytes that act to decrease the surface tension between gaseous-aqueous interphase in the lungs. Pulmonary surfactant is composed of 90% lipids and 10% of four lipid-associated proteins, SP-A, SPB, SP-C, and SP-D (Veldhuizen et al. 1998, Dieudonné et al. 2001). Protein-lipid interactions at the air-liquid interphase are influenced by pH changes, and therefore they may alter pulmonary surfactant function (Amirkhanian and Merritt, 1995). Surfactant dysfunction may be caused by mutations in one of the protein-encoding genes SFTPB, SFTPC, and ABCA3, which are involved in surfactant production (Peca et al. 2011). Respiratory acidosis is an acid-base disorder characterized by the failure of ventilation and an accumulation of carbon dioxide (Patel and Sharma 2020). It has been shown that one mutation in the surfactant protein C gene (SP-C) leads to neonatal respiratory failure associated with respiratory acidosis (Soraisham et al. 2006).

References (APA format)

1. Amirkhanian, J. D., & Merritt, T. A. (1995). The influence of pH on surface properties of lung surfactants. Lung, 173(4), 243-254.

2. Dieudonné, D., Mendelsohn, R., Farid, R. S., & Flach, C. R. (2001). Secondary structure in lung surfactant SP-B peptides: IR and CD studies of bulk and monolayer phases. Biochimica et Biophysica Acta (BBA)-Biomembranes, 1511(1), 99-112.

3.Patel, S., & Sharma, S. (2020). Respiratory acidosis. StatPearls.

4. Peca, D., Petrini, S., Tzialla, C., Boldrini, R., Morini, F., Stronati, M., ... & Danhaive, O. (2011). Altered surfactant homeostasis and recurrent respiratory failure secondary to TTF-1 nuclear targeting defect. Respiratory research, 12(1), 1-8.

5. Soraisham, A. S., Tierney, A. J., & Amin, H. J. (2006). Neonatal respiratory failure associated with mutation in the surfactant protein C gene. Journal of perinatology, 26(1), 67-70.

6. Veldhuizen, R., Nag, K., Orgeig, S., & Possmayer, F. (1998). The role of lipids in pulmonary surfactant. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1408(2-3), 90-108.

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