Pathophysiological Mechanisms of Chronic Asthma

Pathophysiological Mechanisms of Chronic Asthma Order Instructions: Anatomy and Physiology;

Pathophysiological Mechanisms of Chronic Asthma
Pathophysiological Mechanisms of Chronic Asthma

Pathophysiological Mechanisms of Chronic Asthma and Acute Asthma Exacerbation

Week 6 Assignment

Application: Asthma
Complications of asthma can be sudden. Consider the case of Bradley Wilson, a young boy who had several medical conditions. He appeared in good health when he went to school, returned home, and ate dinner. However, when he later went outside to play, he came back inside wheezing. An ambulance took him to the hospital where he was pronounced dead (Briscoe, 2012). In another case, 10-year-old Dynasty Reese, who had mild asthma, woke up in the middle of the night and ran to her grandfather’s bedroom to tell him she couldn’t breathe. By the time paramedics arrived, she had passed out and was pronounced dead at the hospital (Glissman, 2012). These situations continue to outline the importance of recognizing symptoms of asthma and providing immediate treatment, as well as distinguishing minor symptoms from serious, life-threatening symptoms. Since these symptoms and attacks are often induced by a trigger, as an advanced practice nurse, you must be able to help patients identify their triggers and recommend appropriate treatment options. For this reason, you need to understand the pathophysiological mechanisms of chronic asthma and acute asthma exacerbation.
To prepare:
Review “Asthma” in Chapter 26 of the Huether and McCance text. Identify the pathophysiological mechanisms of chronic asthma and acute asthma exacerbation. Consider how these disorders are similar and different.
Select a patient factor different from the one you selected in this week’s Discussion: genetics, gender, ethnicity, age, or behavior. Think about how the factor you selected might impact the pathophysiology of both disorders. Reflect on how you would diagnose and prescribe treatment of these disorders for a patient based on the factor you selected.
Review the “Mind maps—Dementia, Endocarditis, and Gastro-oesophageal Reflux Disease (GERD)” media in the Week 2 Learning Resources. Use the examples in the media as a guide to constructing two mind maps—one for chronic asthma and one for acute asthma exacerbation. Consider the epidemiology and clinical presentation of both chronic asthma and acute asthma exacerbation.
To complete:
Write a 2- to 3-page paper that addresses the following:
Describe the pathophysiological mechanisms of chronic asthma and acute asthma exacerbation. Be sure to explain the changes in the arterial blood gas patterns during an exacerbation.
Explain how the factor you selected might impact the pathophysiology of both disorders. Describe how you would diagnose and prescribe treatment for a patient based on the factor you selected.
Construct two mind maps—one for chronic asthma and one for acute asthma exacerbation. Include the epidemiology, pathophysiology, and clinical presentation, as well as the diagnosis and treatment you explained in your paper.

Pathophysiological Mechanisms of Chronic Asthma Reference

Briscoe, K. (2012, May 12). Thetford: mother of Bradley Wilson, who died of an asthma attack, told there was nothing she could have done. East Anglian Daily Times. Retrieved from http://www.eadt.co.uk/news/thetford_mother_of_bradley_wilson_who_died_of_asthma_attack_told_there_was_nothing_she_could_have_done_1_1375128

ALL ATTACHMENTS HAVE ALL NECESSARY RESOURCES FOR PAPER PLEASE USE THESE RESOURCES ONLY FOR PAPER

VERY IMPORTANT SEE BELOW FOR THE GUIDE FOR THE MIND MAP

Media
Zimbron, J. (2008). Mind maps—Dementia, endocarditis, and gastro-oesophageal reflux disease (GERD) [PDF]. Retrieved from http://www.medmaps.co.uk/beta/
Gastro-oesophageal reflux disease. [Image]. Used with permission of MedMaps.

This media provides examples of mind maps for dementia, endocarditis, and gastro-oesophageal reflux disease (GERD).

Pathophysiological Mechanisms of Chronic Asthma Sample Answer

Anatomy and Physiology
Pathophysiological Mechanisms of Chronic Asthma and Acute Asthma Exacerbation

Asthma is one of the most common chronic disorders affecting the airways. The condition is characterized by some variable and recurring symptoms, the hyper-responsiveness of the bronchial as well as an underlying inflammation. It is the severity and the interaction of the characteristics that describe whether the asthma is acute or chronic also the symptoms can determine the course of treatment to be taken for the type as well as the severity of the condition. Various concepts underly the pathogenesis of asthma with a greater insight being taken of the various clinical features and the genetic patterns of the conditions (Bal, Ravanetti, Dijkhuis & Lutter, 2013).

The most common underlying feature of asthma is the fact that in almost the patients there is an underlying airway inflammation. This is the variable that has various overlying patterns that may have which ay then reflect the different aspects of the disease. For instance, there can be persistent or intermittent manifestations. Also, it is this variable that renders asthma as either acute or chronic (Bal, Ravanetti, Dijkhuis, & Lutter, 2013). Some of the acute symptoms of asthma may manifest beginning with a bronchospasm. Such a symptom may require the individual to be treated with bronchodilator therapy. Also, this treatment with anti-inflammatory drugs may play a major role in reversing some of the symptoms (Herbert, Kumar & Shadie, 2013).

The pathophysiology of asthma is characterized by bronchoconstriction as well as other changes in the airways. Bronchoconstriction is, however, one of the leading physiological conditions that may lead to the constriction of the airways thereby interfering with the airflow. With regard to the acute exacerbations, one of the main happenings is that the bronchial smooth muscles tend to constrict quickly in response to the exposure to a particular allergen (Franzese, 2015).  This is due to the IgE- Dependent Production of Mediators from the Mast cells. Such mediators include histamine, prostaglandins, leukotriene as well as striptease. The treatment, in this case, can be done through the administration of drugs such as aspirin and nonsteroidal anti-inflammatory drugs. Other stimuli such as cold weather and irritants may also lead to the obstruction of the airways whose intensity related to the underlying infection (Franzese, 2015). Nevertheless, stress may also lay a major role in the development of asthma exacerbations through a mechanism that has not yet been discussed.

As asthma continues to be more persistent and the inflammation progresses, other factors may lead to the obstruction of the airflow. One of the factors that have been associated with airway obstruction is airway edema as well as over-secretion of mucus in the ma result in the structural changes in the airways such a hyperplasia of the airways smooth muscles. Similarly, the hype responsiveness of the airway due to a wide variety of stimuli. The treatment I this case may be through the administration of anti-inflammatory drugs.

The changes in the arterial blood gas patterns during an exacerbation

In the course of an asthma attack, several shifts in the arterial blood gasses may be observed as the attack progresses from a mild attack to more moderate and finally to severe disease. For instance, at the beginning of the attack, the PaO2 of 100 mm Hg falls to approximately 60mm Hg (Franzese, 2015).  On the other hand, the normal PaCO2 of 40 mm Hg also reduces to 30 mm Hg.  On the contrary, the Ph may rise from the normal 7.40 rises to approximately 7.50. As the disease worsens, a particular state is reached when the lungs cannot be able to exhale the excess carbon dioxide (Franzese, 2015). This causes the PaCO2 to change the Couse, and therefore they begin rising. The pH, on the contrary, may start to fall but the PaO2 instead of increasing continues to fall. As the attack worsens, it is evident that the ph. Level and the PaCO2 will tend to go back to their normal values. Under extreme circumstances, the levels of PaCO2 may rise steadily to reach about 50 mm Hg while the ph. may fall to reach 7.30 while at the same time the PaO2 progressively falls to approximately 20 mm Hg (Herbert, Kumar & Shadie, 2013).

Airway Inflammation Impacts on the Pathophysiology of Both Disorders

In acute asthma, the symptomatic asthma attack may be caused by several factors some of which are known and others which are unknown. For instance, the attack may be initiated by the exposure to the allergens, pollutants and in some cases viruses.  Once inhaled, the allergens may stimulate a response. The inflammatory response may lead to several effects some of which may be the induction of an inflammatory response (Carroll, & Grogan, 2015). The main characteristic that is associated with an acute asthma attack includes the dyspnea, wheezing, coughing and shortness of breath. In most cases, there are the symptoms that are taken into consideration during the diagnosis of asthma. The symptoms of acute asthma do not persist for longer that one or two days. The treatment of the acute asthma is mainly some of the quick relief medications. Some of the most effective medications include short-acting β2 agonists (Carroll, & Grogan, 2015).

Unlike in acute asthma, in chronic asthma, the inflammation is experienced in the entire mucosal immune system. All the airways, in this case, are involved in the attack (Carroll, & Grogan, 2015). The inflammation in cases of a chronic asthma attack is complex with severe symptoms. More so most of the cells such as the eosinophils, the macrophages as we; as the epithelial cells and smooth bronchial cells may become activated. The utmost results are that there is excessive secretion of mucus, vascular leakage as well as smooth muscle contraction. Furthermore, bronchial hyperresponsiveness may be observed accompanied by severe epithelial shedding (Carroll, & Grogan, 2015). The diagnosis may be based on the development and the severity of the symptoms. The treatment, in this case, will require the administration of oral glucocorticoids. Other medications that have been proven to be effective in the treatment of the condition includes the medications such as long-acting β2 agonists, leukotriene modifiers, cromoglycate, cromoglycate, and nedocromil (Sandrock & Norris, 2015). The mechanisms of such drugs include the inhibitory effect on the immune and inflammatory responses mainly through the modulation of the transcription factors (Carroll, & Grogan, 2015). The utmost effects are that there is a substantial reduction in the number of cytokines that are mainly involved in the recruitment and the survival of most of the inflammatory cells including the eosinophil, lymphocytes, and basophils. Therefore the inhaled corticosteroids in most cases have been effectively used to reduce the occurrence of the exacerbations (Carroll, & Grogan, 2015).

Mind Maps for Chronic Asthma and Acute Asthma Exacerbation

Chronic asthma

Acute Asthma

Pathophysiological Mechanisms of Chronic Asthma References

Bal, S. M., Ravanetti, L., Dijkhuis, A., & Lutter, R. (2013). Influenza exacerbations in an acute and chronic house dust mite ‘asthma’model. Journal of Inflammation, 10(1), 1.

Carroll, K. H., & Grogan, S. P. (2015). Are antibiotics effective in acute flares of chronic asthma?. Evidence Based Practice 18 ():.

Franzese, C. (2015, September). Management of acute asthma exacerbations. In the International forum of allergy & rhinology (Vol. 5, No. S1, pp. S51-S56).

Herbert, C., Kumar, R. K., & Shadie, A. M. (2013). Environmental Particulates As A Trigger For Acute Exacerbations Of Allergic Asthma. In B33. ASTHMA MEDIATORS AND BIOMARKERS (pp. A2628-A2628). American Thoracic Society.

Longmans, R. J., Gemperli, A., Cohen, J., Rubinstein, S. M., Sterk, P. J., Reddel, H. K., … & Ter Riet, G. (2014). Comparative effectiveness of long term drug treatment strategies to prevent asthma exacerbations: network meta-analysis.

Sandrock, C. E., & Norris, A. (2015). Infection in severe asthma exacerbations and critical asthma syndrome. Clinical reviews in allergy & immunology, 48(1), 104-113.

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