Corticosteroids and Inhalants in Asthma

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Table of Contents

The Mechanism of Action of Corticosteroid in an Asthma Attack
Variance in the Action of Corticosteroids From Β2-Agonist Inhalants
The Causes of Fatigue and Physiological Events During an Asthma Attack
Development of Hypercapnia
How the Body Compensates for an Increase in CO2
The Effects of Hypercapnia on the Central Nervous System
References

Asthma is a disorder in which the body airways narrow, swell, and generate excessive mucus. It causes coughing, wheezing, and shortness of breath and makes breathing difficult. The presence of indoor allergens aggravates this illness. However, there is evidence that not all allergen exposure has the same impact on children. Cockroach exposure, for instance, causes severe asthma symptoms and is a leading cause of asthma morbidity (Rabito et al., 2017). Although the mechanism by which cockroach allergen causes morbidity is unknown, it has been demonstrated to promote proliferative T-cell responses and to be extremely strong. Generating an IgE response at much lower levels than dust, mite, and cat allergen. Cockroaches are a major asthma trigger, especially for children with asthma who live in urban areas. Therefore, proper attention and medication for asthmatic patients is key to its control. In this regard, I purpose to discuss the mechanism of corticosteroid in asthma and how it differs from β2-agonist inhalants. As well as the causes of fatigue and physiological events during an asthma attack, and how the body compensates for an increase in CO2, with a focus on the effects of hypercapnia on the central nervous system.

The Mechanism of Action of Corticosteroid in an Asthma Attack

Corticosteroids are a vital and life-saving medication when anti-inflammatory or immunosuppressive effects are required. They have a wide range of effects on the inflammatory pathway, which increases their usefulness. The steroid molecule diffuses across cell membranes and attaches to glucocorticoid receptors, causing the receptor to undergo a conformational change (Busse, 2019). The receptor-glucocorticoid complex can enter the cell nucleus and dimerize before binding to glucocorticoid response elements. Trans-repression and transactivation are terms used to describe the effects of glucocorticoid response elements on genes that suppress or promote transcription, resulting in ribonucleic acid and protein production. Finally, these drugs block transcription factors that control the production of pro-inflammatory mediators in eosinophils, macrophages, mast cells, lymphocytes, and dendritic cells.

Inhibition of phospholipase A2 is another major impact of corticosteroids. According to Busse (2019), phospholipase A2 is responsible for the generation of various inflammatory mediators. Therefore, the corticosteroid inhaler is a long-acting anti-inflammatory medicine, which reduces the formation of inflammatory mediators such as prostaglandins, leukotrienes, and antihistamines. These messengers are important in the progression of asthma attacks. They work to diminish inflammation in two important areas: the site of inflammation and the site where the immune response is initiated (Busse, 2019). For instance, they limit the release of secretagogue from macrophages, hence lowering mucus secretion.

Variance in the Action of Corticosteroids From Β2-Agonist Inhalants

Corticosteroid inhalants have a distinct mode of action than β2-agonist inhalants. The corticosteroid inhaler is a long-acting anti-inflammatory medicine that helps avoid asthma attacks and lessens the intensity of those that do occur (Park et al., 2022). It acts by lowering inflammatory mediators such as leukotrienes, prostaglandins, and histamine production. Corticosteroids function by diminishing the body’s generation of inflammatory mediators, unlike β2-agonist inhalants, which are short-acting medicines that ease symptoms by boosting smooth muscle tone in the bronchial tree, hence decreasing airway resistance (Park et al., 2022). These mediators increase mucus secretion, constrict blood arteries throughout the body, cause vascular smooth muscle contraction, and activate airway inflammation and mucus secretion, all of which contribute to asthma attacks.

Additionally, Corticosteroids are used to treat asthma and other ailments. They function by lowering inflammation and airway hyper responsiveness, which forms two important elements that contribute to asthma attacks. They also inhibit the release of substances called leukotrienes in the body, which leads to inflammation (Park et al., 2022). The β2-agonist, on the other hand, like albuterol, is used to open up airways, by attaching to alpha-2 receptors on smooth muscle cells. This helps manage acute asthma attacks or possibly prevent them from happening in the first place. Therefore, in this case, I would prescribe a corticosteroid, to help curb Emmanuel’s condition.

The Causes of Fatigue and Physiological Events During an Asthma Attack

During a prolonged attack of severe asthma, the constriction of airways generates ventilation-perfusion imbalance, lung hyperinflation, and increased labor of breathing, all of which lead to ventilatory muscle exhaustion. Asthma attacks also cause the airways to enlarge and the muscles that surround them to tighten (Van Herck et al., 2018). It is much more difficult to breathe as a result of this, and it can also generate anxiety, as depicted in Emmanuel’s behavior. This is stressful for both the body and the mind, resulting in exhaustion once the asthma episode has ended.

During asthma attacks, there are various physiological events that occur. These events include the tightening of muscles surrounding the air pathways, known as bronchoconstriction, which reduces the amount of air entering the lungs. The second event involves the excessive production of mucus which clogs the air paths. The final event is the Inflammation of the air passages that occur as a result of the aberrant immunological response.

Development of Hypercapnia

Hypercapnia is a condition that develops when a person’s blood contains much more CO2. It is usually caused by hypoventilation or a lack of ability to breathe effectively and receive oxygen into the lungs. When the body does not obtain enough oxygen or cannot get rid of CO2, it may be necessary to gasp or breathe a large amount of air to bring the amounts of oxygen and CO2 back into balance. Symptoms of hypercapnia might be mild or severe. Mild symptoms such as headaches, shortness of breath, and unusual tiredness or exhaustion can be promptly addressed by the body in order to improve breathing and regulate CO2 levels.

How the Body Compensates for an Increase in CO2

To compensate for the excess carbon dioxide, the body employs a variety of methods. For instance, in the situations of an increase in the partial pressure of carbon dioxide, above the normal. Both the peripheral and chemoreceptors respond to the increased H+ ion and carbon dioxide concentration in the blood (Collins et al., 2021). They trigger the respiratory centers in the medulla to proliferate the respiratory capacity to foster the exchange of gasses.

They stimulate the respiratory centers to intensify the respiration work to reach the state of equilibrium, thereby increasing the respiratory efforts. The chemoreceptors transmit signals to the heart muscle to steer up the cardiac output and force of contraction to boost blood pressure. An impetus for vasoconstriction is then sent to escalate blood pressure thereby improving the exchange of gasses and restoration of homeostasis. Additionally, the body can compensate for an increase in Carbon dioxide by hyperventilation which involves increasing breathing to oust more carbon dioxide.

The Effects of Hypercapnia on the Central Nervous System

The buildup of carbon dioxide in the bloodstream causes hypercapnia. This triggers a proportional increase in the brain tissue [H+]. In pulmonary insufficiency, the combination of hypoxia and hypercapnia causes cerebral vasodilation and increased cerebral blood flow, which may lead to increased intracranial pressure and reduction of the seizure threshold (Shigemura et al., 2020). Moreover, acute hypercapnia raises sympathetic nervous system discharge. As a result, plasma adrenaline and norepinephrine levels rise, increasing myocardial contractility and cardiac output but simultaneously increasing the risk of cardiac arrhythmias. Thus posing risks and traumatic damage to the central nervous system.

Cockroach and dust exposure in towns have been a major cause of asthma symptoms among children. Furthermore, in severe cases, these exposures often cause morbidity. Corticosteroid inhalant is a multi-purpose and long-acting anti-inflammatory medicine that helps avoid asthma attacks and lessens its intensity. Its mechanism in controlling and managing asthma has a greater impact than the β2-agonist inhalants. As a result, in cases of cockroach and dust exposure, I recommend patients to use corticosteroids to efficiently and effectively manage their situations.

References

Busse, W. W. (2019). Biological treatments for severe asthma: a major advance in asthma care. Allergology International, 68(2), 158-166.

Collins, S. É., Phillips, D. B., Brotto, A. R., Rampuri, Z. H., & Stickland, M. K. (2021). Ventilatory efficiency in athletes, asthma and obesity. European Respiratory Review, 30(161).

Park, H. J., Huh, J. Y., Lee, J. S., Lee, J. S., Oh, Y. M., & Lee, S. W. (2022). Comparative efficacy of inhalers in mild-to-moderate asthma: systematic review and network meta-analysis. Scientific reports, 12(1), 1-9.

Rabito, F., John, C. C., He, H., Werthmann, D., & Schal, C. (2017). A single intervention for cockroach control reduces cockroach exposure and asthma morbidity in children. Allergy Clin Immunol, 140(2), 564-570.

Shigemura, M., Homma, T., & Sznajder, J. I. (2020). Hypercapnia: an aggravating factor in asthma. Journal of Clinical Medicine, 9(10), 3207.

Van Herck, M., Spruit, M. A., Burtin, C., Djamin, R., Antons, J., Goërtz, Y. M., & Van’t Hul, A. J. (2018). Fatigue is highly prevalent in patients with asthma and contributes to the burden of disease. Journal of clinical medicine, 7(12), 471.

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