Asthma’s Diagnosis and Treatment

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Introduction

Asthma is one of the ailments that cause persistent morbidity and deaths across the globe. Studies show that its dominance has augmented in the past two decades. This chronic disease affects the lungs and causes reversible airway barriers due to swellings along the lung airways as well as contraction of the muscles surrounding the lungs.

The airway obstruction is present in most asthma patients, but a number of triggers exacerbate this condition depending on the patient’s environment. Some of these triggers include smoke, pollen grains, dust, industrial chemicals, fur, and cold air. Asthma can be managed successfully; however, most of its morbidity is due to bad management and particularly when taking preventive medication.

Pathophysiology of Asthma

The pathology observed in the lungs of asthmatic patients who succumb to the disease indicates that a high degree of lung inflation. A closer view of this over-inflation shows a striking alveoli distention. The smooth muscles located in the bronchi undergo substantial hyperplasia whilst the submucosal layers become dangerously thick.

Furthermore, mucosa is present in the lungs with a bogged mucosal epithelium due to the inadequate quantity of ciliated epithelium cells. The submucosa undergoes an upsurge in mucus gland hypertrophy. The upsurge in quantity of muscle, mucous glands, and tissue edema causes the airway wall to congeal while the caliber minimizes (Harver & Kotses, 2010).

The alteration of the latter structures is known as remodeling, which generally explains the intricate morphological modifications in the bronchial wall. The changes in the bronchial wall make the columnar cells detach themselves from basal attachments (Clark, 2010). The inconsistent quantity of mucous in the lumen of a patient’s airway triggers the airway obstruction that can even utterly block the airway. The complete occlusion of the airway can lead to growth of a distal at the atelectasis in the lung parenchyma.

Inflammation

Most patients who succumb to asthma have acutely inflamed airways. Inflammation is caused by a convoluted multifactorial process that entails the collaboration of various cells coming from disparate tissues and organs such as bone marrow, the lymphoid, and nervous system among other organ systems.

The cells, which include respiratory cells, CD4 helper T- lymphocytes, and leukocytes, produce cytokine that causes inflammation. Two possible pathways facilitate asthma inflammation. In the first pathway, large amount of immunoglobulin E (IgE) facilitates allergic inflammation. The second pathway is structural change in the bronchial wall (remodeling), which is by caused enzymes, proinflammatory cytokines, and the destroyed bronchial epithelium (Clark, 2010).

The indicators of inflammation include calor and rubor, tumour, and dolor. In the case of asthma, inflammation occurs when triggered by IgE-dependent agents. This allergic reaction is facilitated by eosinophils that accumulate when worms or parasites attack the body. Apart from providing a severe protection against harm, inflammation helps in healing and restituting tissues following an attack by toxins. Nevertheless, in the case of asthma, inflammatory reaction is triggered in an erroneous way, which leads to harm rather than gain.

Medical practitioners do not have a conclusive research on the link between inflammation and indicators of asthma. Probably, the level of inflammation is influenced by the airway responsiveness (AHR). The level of AHR is connected to the signs of asthma and the urgency of one to seek medical attention. Swelling of the airways has the potential to raise AHR and thus enable triggers that compress the airways even when such triggers did not initially have the potential (Harver & Kotses, 2010).

Inflammation can also be an express indication for asthma in various ways such as cough and chest constriction. Apart from inflammatory mechanisms, some anti-inflammatory mechanisms can exacerbate inflammatory responses. Endogenous cortisol can act as a good controller of allergic inflammatory reactions.

Diagnosis

Detecting asthma in children can be difficult particularly in children below the age of 5 years. There is no definite form, severity, or regularity of indication. The ambiguity in the description implies that the evidence-based recommendations are not likely to be certain.

However, common symptoms in children include wheezing, cough, obscurity breathing, and chest constriction (Redwood & Neil, 2013). During the initial clinical assessment, the latter signs are checked, and if most observations are linked with getting consistent wheezing or other respiratory symptoms, then it can be deduced that the patient has asthma.

Nursing Management of Asthma

As aforementioned, poor management of Asthma leads to high morbidity cases; however, following doctors’ prescriptions can help in managing the condition. The prescriptions differ from one patient to another. Two forms of treatment can be offered including quick relief and prolonged management. Quick-relief medication plan helps in relieving the patient from the signs of asthmatic attacks. Patients who aspire to have a longer quick-relief plan should consult their doctors to check if the medication needs to be changed.

In the case of long-term management plan, a patient protects him/herself from frequent attack, but it cannot relieve one from asthmatic attacks. The medications often have side effects and patients should seek the relevant information from their doctors (Clark, 2010). Patients should develop asthma management plan to ensure that the treatment is in line with the symptoms. Patients should share their management plan with individuals that they trust in a bid to monitor them.

Special Treatment for Particular Asthma Patients

Pregnant asthmatic patients should be given specific treatments, as at the time of pregnancy, the condition becomes very severe, hence the need for a closer supervision and modifications in medications. The unborn child is at risk if the mother does not adhere to the doctor’s prescription. Obese patients should receive similar treatment as those who are not, as a reduced weight in obese patients enhances lung function and reduces asthma severity.

The pharmacology treatment of occupational asthma is similar to management of other kinds of asthma, but it does not act as a replacement for sufficient exposure. Asthma patients who undergo thoracic or respiratory surgeries are likely to have trouble during and after the surgery. Doctors should conduct a lung function test prior to the surgery and in case it is below the 80% of the patient’s best, then he or she should take glucocorticosteroids drugs (Redwood & Neil, 2013).

Patients with other respiratory infections apart from asthma should also have special attention. Patients suffering from aspirin-induced asthma also deserve special consideration. Most asthmatic adults are allergic to aspirin and several nonsteroidal anti-inflammatory medicines. Doctors should carryout checkups first before prescribing the medication. Checkups can be done using cardiopulmonary which are able to do resuscitation (Redwood & Neil, 2013).

Conclusion

Asthma is an intricate disease. Evidently, it is not a single disease, but a combination of interaction between different phenotypes that encompass disparate cells and mediators. Currently, the treatment of asthma emphasizes on managing inflammation.

Perhaps, as further studies are done on the subject, medical practitioners will develop more a definite treatment. However, the existing management methods can reduce morbidity as long as patients are loyal to take their treatment as advised. Moreover, application of non-pharmacological management interventions can reduce the dominance of asthma.

References

Clark, M. (2010). Asthma: A Clinician’s Guide. Sudbury, MA: Jones & Bartlett Learning.

Harver, A., & Kotses, H. (2010). Asthma, Health and Society: A Public Health Perspective. New York, NY: Springer.

Redwood, T., & Neill, S. (2013). Diagnosis and treatment of asthma in children. Practice Nursing, 24(5), 222-229.

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