Paper Example on Disorders of Ventilation and Gas Exchange

Introduction

The corticosteroid inhaler is used to suppress inflammation in the airway. According to Hossny, Rosario, Lee, Singh, El-Ghoneimy, Sou, and Souef (2016) affirm that the suppression occurs by regulating pro-inflammatory proteins. Moreover, the authors indicate that corticosteroid inhalers remodel the airway by increasing the vascularity of the bronchi walls. Also, the authors state that the cellular target for the corticosteroid inhaler is epithelial cells. As they add, at that cellular level, the inhaler minimizes the cells that are inflamed in the airway. They mention that some of these cells include eosinophils, T lymphocytes, mast cells, and dendritic cells. The authors affirm that the effects of the corticosteroid inhaler occur when it suppresses chemotactic mediators and adhesion molecules. Notably, the inhaler inhibits the production of inflammatory cells. The authors affirm that when using corticosteroid inhalers, there are genomic and non-genomic mechanisms. In the genomic mechanism of action, the action is mediated through the Cytoplasmic glucocorticoid receptor-a while the action in non-genomic is through direct interaction with the airway (Hossny et al., 2016). v2-agonists inhalants are also used to treat asthma and their mechanism of action differs with corticosteroid inhalers. Billington, Penn, and Hall (2017) affirm that v agonists exert their bronchodilatory effects through the v2 adrenoreceptors (v2ARs) that are found in the airway smooth muscle cells. As the authors indicate, when these receptors are activated, relaxation in the airway takes place. Moreover, the authors add that the binding between v2-agonists and v2AR structures the airway in a way that it allows the G-protein to separate and bind to the adenylyl cyclase. The activation of adenylyl cyclase takes place, which forms the cyclic AMP (cAMP) from Adenosine Triphosphate (ATP). The molecules present in cAMP bind to Protein Kinase A (PKA), which separates catalytic and regulatory subunits from each other (Billington, Penn, and Hall, 2017). Afterward, the subunits of the PKA introduce a phosphate molecule and many cellular targets are activated which results in dilation of the bronchi and the relation of the airways smooth muscle (Billington, Penn, and Hall, 2017).

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Someone with severe asthma becomes physically fatigued after a prolonged attack because the levels of oxygen in the blood are low. According to Binuyo (2013), when the oxygen levels are low, an asthmatic person struggles to move air in and out of their lungs. The author indicates that in the lungs, diffusion of oxygen takes place through the alveoli walls and waste products, particularly carbon dioxide diffuses through the capillary walls and move to the alveoli. Also, the author adds that if anything prevents oxygen from reaching the alveoli, body cells receive an insufficient supply of oxygen and carbon dioxide piles up in the blood. Evidently, an asthmatic person gets tired because they are trying to bring oxygen from their lungs into the blood. Besides, the shortness of breath causes overall tiredness in a person. During an asthma attack, the bronchi become inflamed. A person may experience an asthma attack because of an irritant such as cigarette smoke that accumulates in the airway. Binuyo (2013) affirms that when the body detects a harmful irritant, the immune system sends mast cells to the area of irritation, which is the airway. The mast cells produce histamine, which causes an inflammation characterized by swelling and redness (Binuyo, 2013). Also, the author affirms that histamine contracts the lining of the airway, which is a condition known as bronchospasm. The inflammation causes the airway to become narrow thus inhibiting the air that travels to the lungs (Binuyo, 2013). The author articulates that asthma begins with a dry cough and mild chest pressure. As the attack intensifies, the author mentions that wheezing begins to occur and it increases in pitch over time. Over time, breathing becomes difficult and the coughing produces mucus that appears thick (Binuyo, 2013). The author indicates that goblet cells, which produce mucus secret an excessive amount that clogs the bronchioles. The airway becomes inflamed and prevents oxygenated air from reaching the alveoli (Binuyo, 2013).

In every human body, carbon dioxide is present. When the concentration becomes high, then it is considered a medical condition that is known as hypercapnia, which can either be acute or chronic. According to the PHC Editorial Team (2012), the normal level of carbon dioxide in the blood is 40 mm Hg. When the levels of CO2 exceed 45 mm Hg, hypercapnia begins to occur. In a severe case of hypercapnia, the CO2 in the blood is 75 mm Hg or more (PHC Editorial Team, 2012). Porth (2011) affirms that the body compensates for an increase in carbon dioxide levels by increasing renal bicarbonate (HCO3) retention. The author affirms that the increase in HCO3 increases serum HCO3 and pH levels. The author explains that as long as the pH in the blood is normal, the complications of hypercapnia that will occur are those that take place s a result of hypoxia. Also, the author adds that people who have chronic hypercapnia may not have symptoms of the complication unless carbon dioxide becomes elevated. Hypercapnia results in the damage of the central nervous system. Nin, Angulo, and Briva (2018) affirm that hypercapnia results in the dysfunction of the respiratory muscle. As the author affirms, the respiratory muscles are controlled by the central nervous system. As they add, the activity in the central nervous system must adapt to both physiologic and pathologic situations to control the exchange of gases. Also, the authors affirm that the dysfunction causes hypoventilation of the alveoli that retain carbon dioxide within the system. Furthermore, the authors state that hypercapnia damages the diaphragm. They examine the study of Juan et al. who did a clinical research on acute hypercapnia over the diaphragm. In Juan et al.'s study, rats were used as the subjects (Nin, Angulo, and Briva, 2018). According to the authors, results from Juan et al' study found that a prolonged exposure of carbon dioxide in rats damages the diaphragm. However, their results found that when the diaphragm of rats was exposed to carbon dioxide, type 1 fibers were produced, which the authors presumed was an adaptive mechanism to overcome the excessive carbon dioxide caused by hypercapnia. Regarding another effect of hypercapnia on the central nervous system, Nin, Angulo, and Briva (2018) aver that it affects the limbs. As they affirm, hypercapnia depresses the limb muscles, which eventually results in muscle fatigue. The authors assert that the mechanism underlying muscle compromise takes place when hypercapnia triggers the muscle atrophy. PHC Editorial Team (2012) indicates that some other effects of hypercapnia on the central nervous system include dizziness, confusion, blurred vision, increased intracranial pressure, breathing difficulties, and increased pressure in the skull.

References

Billington, C. K., Penn, R. B., & Hall, I. P. (2017). v2-agonists. Handbook of Experimental Pharmacology, 237, 23-40. http://doi.org/10.1007/164_2016_64

Binuyo, M. (2013). Asthma; Causes and Treatment. Retrieved from https://www.researchgate.net/publication/256132817_Asthma_Causes_and_Treatment_I_INTRODUCTION

Hossny, E., Rosario, N., Lee, B., Singh, M., El-Ghoneimy, D., Sou, J., & Souef, P. (2016). The use of inhaled corticosteroids in pediatric asthma: update. World Allergy Organization Journal, 9:26.

Nin, N., Angulo, M., & Briva, A. (2018). Effects of hypercapnia in acute respiratory distress syndrome. Annals of Translational Medicine, 6(2), 37. http://doi.org/10.21037/atm.2018.01.09

PHC Editorial Team. (2012). Hypercapnia. Prime Health Channel. Retrieved from https://www.primehealthchannel.com/hypercapnia.html

Porth, C. (2011). Essentials of Pathophysiology: Concepts of Altered Health States. New York, NY: Lippincott Williams & Wilkins.