Asthma Case Study #3 Analysis
Instructions:-
Evaluate the presence and effects of alteration in the homeostatic state secondary to gender, genetic, ethnic and temporal variables
Select one of the case studies below, and include in your discussion an evaluation of the presence and effects of alteration in the homeostatic state secondary to gender, genetic, ethnic, and temporal variables.
Requirements:
- Make sure all of the topics in the case study have been addressed.
- Cite at least three sources; journal articles, textbooks or evidenced-based websites to support the content.
- All sources must be within 5 years.
- Do not use .com, Wikipedia, or up-to-date, etc., for your sources.
Case Study 3
Disorders of Ventilation and Gas Exchange
Emmanuel and his mother live in an urban community housing complex. The building is worn down and dirty from the urban dust, cockroaches, and mold. Emmanuel is five years of age and has suffered from asthma for the last two years. One evening, his mother poured him some milk and put him to bed. Shortly afterward, Emmanuel woke up wheezing and coughing. As he gasped for air, he became more and more anxious. His mother ran for his inhaler, but he was too upset and restless to use it. Emmanuel’s skin became moist with sweat, and as he began to tire, his wheezing became quieter. His mother called 911 and waited anxiously for the ambulance to arrive.
- Emmanuel uses a corticosteroid inhaler for the management of his asthma. What is the mechanism of action of this drug? How is its action different from the β2-agonist inhalants?
- Why does someone with severe asthma become physically fatigued during a prolonged attack? What are the physiological events that occur during an attack?
- One of the complications of respiratory fatigue is the development of hypercapnia. How does the body compensate for an increase in CO2? What are the effects of hypercapnia on the central nervous system?
Assignment Requirements:
Before finalizing your work, you should:
- be sure to read the Assignment description carefully (as displayed above);
- consult the Grading Rubric (under the Course Home) to make sure you have included everything necessary; and
- Utilize spelling and grammar check to minimize errors.
- Follow the conventions of Standard American English (correct grammar, punctuation, etc.);
- be well ordered, logical, and unified, as well as original and insightful;
- display superior content, organization, style, and mechanics; and
- use APA 6th Edition format as outlined in the APA Progression Ladder.
Solution
Asthma Case Study #3 Analysis
Asthma is a chronic disorder that affects the airways, and it encompasses a complex relationship between the airflow obstruction, inflammation, and bronchial hyperactivity. These features of the condition interact and determines clinical presentation and the severity of asthma. Also, the features of asthma ascertain the response of treatment. The central tenet in the development of asthma is the presence of underlying inflammation. Development and expression of asthma are highly dependent on the interactions between genetic and environmental factors. Of the environmental factors, allergic reactions remain critical. In this case study, Emmanuel, a five-year-old is predisposed to the environmental conditions that could lead to allergy. He lives in a house that is worn down and dirty from the urban dust, cockroaches, and mold.
Corticosteroids and beta 2 agonist inhalants play a significant role in the treatment and management of bronchial asthma. Corticosteroids are, however, preferred in difficult cases of asthma (Tamm et al., 2014). The two classes of drugs have dissimilar mechanisms of action. While corticosteroids’ mechanism of action is mainly geared towards decreasing airway inflammation; a pathology in asthma, beta 2 agonists work exclusively to reduce bronchospasm by causing bronchodilation.
Corticosteroids inhalants act by reducing mucosal edema. It also decreases the permeability of the vasculature through vasoconstriction. As such, it has an effect of reducing the emigration of leukocytes and consequently leading to the decrease of inflammation. Corticosteroids inhalants also inhibit the release of cysteinyl leukotrienes: LTC4 and LTD4 (Tamm et al., 2014). Leukotrienes have been demonstrated to be potent bronchoconstrictor with an additional effect on the clearance of mucus, eosinophilic inflammation, and blood vessels.
Another mechanism of action of corticosteroids is to decreases mucus secretion by inhibiting macrophage secretagogue release. Corticosteroids inhalants prevent the late phase reaction through the inhibition of inflammation and chemotaxis. This action can be associated with the inhibition of the release of leukotrienes (Maslan, & Mims, 2014). Inhaled corticosteroids act to decrease the inflammation of the airway by inhibiting the actions of key players in the process: leukocytes, cytokines and other mediators of inflammation. In essence, corticosteroids decrease airway mucus secretion and bronchial hyperactivity.
On the other hand, beta 2 agonists selectively bind to beta 2 receptors on the bronchial smooth muscle resulting in bronchodilation. Beta 2 selective agents are preferred for asthma compared to non-beta 2 selective agents to avoid unwanted actions that are associated with the activation of beta 1 receptor, like tachycardia. Beta 2 receptors is a transmembrane receptor coupled to G protein, whose activation leads to a second messenger system signal cascade that involves cAMP (Tamm et al., 2014). This second messenger then causes smooth muscle relaxation leading to bronchodilation.
Asthma is associated with bronchospasms where the airways are narrowed. With increased bronchospasm, bronchial edema, pronounced mucus secretion, airway remodeling, and airway hyperresponsiveness, exhalation becomes difficult (Ozier et al., 2011). Emmanuel’s coughing and wheezing can be associated with the narrowing airway narrowing. This narrowing of the airways led to ventilation-perfusion mismatch, lung hyperinflation and increased effort or work of breathing causing muscle fatigue. With hyperinflation of the lungs, a higher amount of energy is required to overcome the tension building in the lungs. The use of the accessory muscles of respiration generated fatigue. Fatigue can also be caused by oxygen deprivation due to decreased oxygen tension and buildup of carbon dioxide. Oxygen is required for the generation of energy and therefore without it, or decreased levels cause fatigue.
In an obstructive pulmonary disease like asthma, there is increase the partial pressure of carbon dioxide leading to respiratory acidosis. The body compensates this by increasing renal absorption of bicarbonate that leads to the normalization of the pH. In acute respiratory acidosis, bicarbonate is rather generated from intracellular proteins which then compensates for the respiratory acidosis (Kaufman, 2011). Also, the body compensate for respiratory acidosis through hyperventilation to wash off the excess carbon dioxide.
The effects of carbon dioxide in the central nervous system complex and is a total effect observed is as a result of three major actions; it affects the cerebral blood flow; by causing vasodilation, it affects intracellular pH leading to secondary effects within the cell (especially cells in the reticular activating system and the hypothalamus) and inert gas narcotic effect.
Cerebral blood flow has a direct relationship with the level of carbon dioxide. In this case, hypercapnia cause vasodilation of the cerebral vasculature leading to increased cerebral blood flow which causes a headache (Busch et al., 2016). This then results in an increase in intracranial pressure and occasionally papilledema.
Hypercapnia causes a direct cortical depression, and this increases the threshold for seizures. Increased levels of carbon dioxide stimulate the hypothalamic and subcortical centers which lead to an increase in excitability and consequently seizures. Also, higher levels of carbon dioxide cause depression of cortical and subcortical centers similar to the effect of anesthetic agents. Hypercapnia also has a neurologic effect function. It possesses almost a sedative-like an effect on the central nervous system leading to disorientation, somnolence and in severe circumstances, coma or death.
References
Tamm, M., Richards, D. H., Beghé, B., & Fabbri, L. (2012). Inhaled corticosteroid and long-acting β 2-agonist pharmacological profiles: effective asthma therapy in practice. Respiratory Medicine, 106, S9-S19.
Ozier, A., Allard, B., Bara, I., Girodet, P. O., Trian, T., Marthan, R., & Berger, P. (2011). The pivotal role of airway smooth muscle in asthma pathophysiology. Journal of Allergy, 2011.
Maslan, J., & Mims, J. W. (2014). What is asthma? Pathophysiology, demographics, and health care costs. Otolaryngologic Clinics of North America, 47(1), 13-22.
Kaufman, G. (2011). Asthma: Pathophysiology, diagnosis, and management. Nursing Standard, 26(5), 48-56.
Busch, David R., Jennifer M. Lynch, Madeline E. Winters, Ann L. McCarthy, John J. Newland, Tiffany Ko, Mary Anne Cornaglia et al. “Cerebral blood flow response to hypercapnia in children with obstructive sleep apnea syndrome.” Sleep 39, no. 1 (2016): 209.
