Free Essay on Asthma: Inflammatory Cells and Mechanisms of Bronchospasms

Introduction

Inflammatory cells in the lungs cause the development of asthma, eosinophils, mast cells, lymphocytes, and neutrophils (Subramanya, 2014). This mechanism inflames the infiltrate and pronounced modifications in bronchial composition, severe bronchospasm, mucosal edema, mucus plug forming, and airway wall restructuring: thickening of the basement membrane. It induces frequent coughing at night or early morning, chest tightness, shortness of breath, and wheezing (Ekim, 2016). Asthma can be regulated by medications and by avoiding the sources of an attack. Patients are categorized into 4 categories. These categories are severe persistent, moderate persistent, mild persistent, and intermittent asthma types (Subramanya, 2014).

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Asthma can also contribute to a rise in mucus-secreting cells with mucosal gland enlargement. Increased mucus production can trigger thick airway-blocking mucus plugs (Kumari, 2014). Epithelial damage may contribute to epithelial peeling, which may result in severe degradation of the airway. Loss of the epithelium's barrier role causes allergens to invade and induce a hyperresponse to airways, which is a significant aspect of asthma (Ekim, 2016). The extent of hyperactivity depends primarily on the degree of inflammation and the immunological retort of the person.

Asthma also induces enzyme deficiency that usually breaks down inflammatory mediators, resulting in reflexive neuronal responses from sensory nerve stimulation (Subramanya, 2014). Without proper care and monitoring, asthma can lead to airway restructuring, causing modifications in lower respiratory tract cells and tissues; these effects create irreversible fibrotic disruption. Such remodeling may be permanent, culminating in gradual lung function decline, and diminished treatment responsiveness (Kumari, 2014).

Symptoms That Support the Diagnosis of Asthma

The patient was whizzing and was unresponsive to his fluticasone/salmeterol (Advair) inhaler. The patient also had difficulty breathing, which is why he started breathing with accessory muscles. These events are usually synonymous with airflow obstruction that requires sudden reversal or treatment (Kumari, 2014). Asthma may also have contributed to a spike in mucus-secreting cells with the widening of mucus-secreting glands. Enlarged mucus secretion can create thick airway-blocking mucus plugs (Ekim, 2016). Epithelium damage can cause epithelial peeling, leading to severe airway obstruction.

The Treatment Provided in The Emergency Department and Additional Therapies Needed to Mitigate the Symptoms and Return the Patient to Wellness

Oxygen treatment can help normalize oxygen content when reducing fixed airway congestion due to airway irritation and mismatched ventilation perfusion. This process decreases the reaction of catecholamine to tachycardia and blood pressure (Subramanya, 2014).

Inhaled β2-agonists should provide the quickest remedy for acute bronchospasm with the least side effects (Subramanya, 2014). A reverse airflow cap in the emergency department will not be stopped until treatment with β2-agonists inhaled (using a metered-dose inhaler [MDI] or wet nebulizer) (Kumari, 2014). Salbutamol is safer and more effective in inhalation than intravenous salbutamol. Bronchodilator intravenous use should only be considered when there is a bad reaction to the inhaled drug or when the patient coughs heavily or is showing signs of possibly dying, even after the treatment with the inhalation (Ekim, 2016).

The dose of the bronchodilators inhaled should be balanced according to realistic airflow-controlling precautions and symptoms. It may take one puff every 30-60 seconds to raise the dosage (Ekim, 2016). Depending on the medication's reaction, an optimum dosage will not be relevant, although others have recommended 20-40 puffs (Subramanya, 2014). Consistent therapy with a wet nebulizer can sometimes be indicated. Bronchospasm relief will be best accomplished by adopting the cumulative dose principle: consecutive doses are based on the therapeutic efficacy of previously given doses (Ekim, 2016). Pre-hospital therapy of inhaled β2-agonists (using an MDI or a wet nebulizer) does not prohibit a complete reversal of breathing obstruction in the emergency room (Kumari, 2014).

If a plateau has been reached (i.e., no further progress has been observed following successive doses), either method's continued use of bronchodilators is unlikely to have any therapeutic benefit. It may result in harmful effects (Ekim, 2016). Patients with extreme asthma (i.e., FEV1 or PEF < 40% of the previous maximum or anticipated value) that struggle to progress through therapeutic or rational measurement need more regular use of bronchodilators and constant supervision (Subramanya, 2014). The stagnation must be described in terms of attack intensity. The other hand's progress should be described in terms of a series of clinical and objective measures (≥ 15% improvement in FEV1 or PEF) (Ekim, 2016).

Meta-analysis findings of children and adults testing MDI and wet nebulization show that the use of chamber or spacer MDI is associated with a quicker initiation of bronchodilation, shorter period of emergency treatment, fewer side effects, and greater patient satisfaction (Ekim, 2016). Faster and smoother bronchodilation will be accomplished with adequate doses provided with an MDI plus spacer system than with traditional doses provided with a wet nebulizer (Subramanya, 2014).

Concerns with The Numbers

There is a crucial concern with the patient’s numbers since they indicate signs of a severe asthma attack, and death could occur if quick action is not taken.

The Causes of The Exacerbation of Asthma

I believe what triggers asthma to worsen is an unpleasant environmental regulation. The patient lives in the Midwest, an area prone to high amounts of dust and pollen. Another factor adding to the patient's severe asthma attack is that the patient has a history of mild asthma (Ekim, 2016).

Conclusion

In conclusion, prospective nurses must be able to diagnose respiratory system disorders. Understanding the clinical signs allows one to offer outstanding care for the illness of the person. It will also allow for the discovery of the dynamics of knowing the pathophysiology of asthma conditions.

References

Ekim, A. (2016). Allergen Control in Asthma. Asthma - From Childhood Asthma to ACOS Phenotypes. https://doi.org/10.5772/62767Kumari, K. (2014). A Review on Epidemiology, Pathophysiology, and Management of Asthma. Journal of Applied Pharmaceutical Science. https://doi.org/10.7324/japs.2012.2737

Subramanya, N. (2014). Management of acute Bronchial Asthma. Management of Childhood Bronchial Asthma, 41–41. https://doi.org/10.5005/jp/books/12216_5