NR 507 Week 2: Discussion Part Two
Chamberlain University NR 507 Week 2: Discussion Part Two– Step-By-Step Guide
This guide will demonstrate how to complete the Chamberlain University NR 507 Week 2: Discussion Part Two assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NR 507 Week 2: Discussion Part Two
Whether one passes or fails an academic assignment such as the Chamberlain University NR 507 Week 2: Discussion Part Two depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NR 507 Week 2: Discussion Part Two
The introduction for the Chamberlain University NR 507 Week 2: Discussion Part Two is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
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How to Write the Body for NR 507 Week 2: Discussion Part Two
After the introduction, move into the main part of the NR 507 Week 2: Discussion Part Two assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NR 507 Week 2: Discussion Part Two
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NR 507 Week 2: Discussion Part Two
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Sample Answer for NR 507 Week 2: Discussion Part Two
What is the etiology of bronchitis?
There are two kinds of Bronchitis: Acute Bronchitis, that is caused by “Infections or lung irritants,” and Chronic Bronchitis, that is caused by “repeatedly breathing in fumes that irritate and damage lung and airway tissues” (National Heart, Lung, and Blood Institute, 2018). This could be like smoking or inhaling second-hand smoke. The etiology of bronchitis is the same that causes upper respiratory infections. The names of the viruses that cause bronchitis are coronavirus, rhinovirus, respiratory syncytial virus, and adenovirus. Most cases of bronchitis come from a virus instead of bacteria. Current smoking is associated with a more goblet cell hyperplasia and number, and chronic bronchitis is associated with more goblet cells, independent of the presence of airflow obstruction. This provides clinical and pathologic correlation for smokers with and without COPD (Kim et al., 2015).
Describe in detail the pathophysiological process of bronchitis.
The pathophysiological process of bronchitis is very simple. The symptoms of acute bronchitis are due to acute inflammation of the bronchial wall, which causes increased mucus production along with edema of the bronchus (National Heart, Lung, and Blood Institute, 2018). This leads to the productive cough that is the hallmark of a lower respiratory tract infection. While the infection may clear in several days, repair of the bronchial wall may take several weeks. During the period of repair, patients will continue to cough. Pulmonary function studies of patients with acute bronchitis demonstrate bronchial obstruction similar to that in asthma. As the symptoms of acute bronchitis subside, pulmonary function returns to normal. Most patients will cough for less than 2 weeks with the illness. If a patient coughs longer than 1 month then the term is post bronchitis syndrome (National Heart, Lung, and Blood Institute, 2018). The bronchial walls are trying to repair after the clearance of the infection.
- Identify hallmark signs identified from the physical exam and symptoms.
The hallmark sign and symptoms are duration of cough less than 30 days, productive cough, no history of chronic respiratory illness, and fever. Production of mucus (sputum), which can be clear, white, and yellowish-gray or green in color can occur in acute bronchitis. Acute bronchitis is caused by a virus. Cough from the irritated and inflamed bronchial epithelium and increased mucus production (McCance, Huether, Brashers and Rote, 2013).
Describe the pathophysiology of complications of bronchitis.
As with most diseases, complications can arise from bronchitis. Around one person in 20 with bronchitis may develop a secondary infection in the lungs leading to pneumonia. The infection is commonly bacterial although the initial infection that caused the bronchitis may be viral. The infection affects the tiny air sacs known as alveoli in the lungs (National Heart, Lung, and Blood Institute, 2018). Although a single episode of bronchitis usually isn’t cause for concern, it can lead to pneumonia in some people. Repeated bouts of bronchitis, however, may mean that you have chronic obstructive pulmonary disease, or COPD. Chronic bronchitis can lead to long term COPD with progressively diminishing lung reserves and breathing difficulties. COPD further raises the risk of occasional flare ups and increased risk of recurrent and frequent chest infections. When you breathe, air moves in your trachea through two tubes called bronchi. The bronchi branch out into smaller tubes called bronchioles. At the ends of the bronchioles are little air sacs called alveoli. And at the end of alveoli are capillaries, which are tiny blood vessels. Oxygen moves around in the lungs to the bloodstream through the capillaries. Carbon dioxide moves from the blood into the capillaries and then into the lungs and exhaled. The fibers in the walls of the lungs can become damage (Kim et al, 2015). They are not able to expand and make them less elastic when you exhale.
What teaching related to her diagnosis would you provide?
I would educate Tammy about second-hand exposure to smoke. This could make her bronchitis even worse if exposed. Tammy would most likely be prescribed an inhaler that would open up her bronchioles, helping her breath better. Most people should drink at least 8 eight-ounce cups of water a day. You may need to drink more liquids when you have acute bronchitis. Liquids help keep your air passages moist and help you cough up mucus. I would encourage Tammy to get plenty of rest to help fight the infection. Tammy could use a cool mist humidifier to decrease her cough and make it easier for her to breath (National Heart, Lung, and Blood Institute, 2018).
References
Kim, V., Oros, M., Durra, H., Kelsen, S., Aksoy, M., Cornwell, WD., et al. (2015) Chronic Bronchitis and Current Smoking Are Associated with More Goblet Cells in Moderate to Severe COPD and Smokers without Airflow Obstruction. PLoS ONE 10(2). Doi: https://doi.org/10.1371/journal.pone.0116108
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby.
National Heart, Lung, and Blood Institute. (2018). Bronchitis. National Institute of Health. Retrieved from https://www.nhlbi.nih.gov/health-topics/bronchitis
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Sample Answer 2 for NR 507 Week 2: Discussion Part Two
I read enjoyed reading your informative post and especially like your educational area. I think too many people do not realize the value of water and hydration. You covered this area very well. Having had bronchitis, I remember being exhausted and the cure all was homemade chicken noodle soup. The old wise tales were very interesting and perhaps there was truth. And of course, there was guaifenesin, a mucoactive drug, to which the doctor stated that it would loosen the mucus to make the cough more productive. Albrecht, Dicpinigaitis & Guenin (2017) stated that the dosing range is 200 to 400 mg every 4 hours and can be taken to six times daily. There are both immediate release formulas as well as those that are extended release and is tolerable for most pediatric and adult patients. Teaching would also include to make sure that if this patient had any children or grandchildren. Again, I really enjoyed your post.
I found an interesting research article that I wanted to share about the use of bronchodilators. After thinking about the topic, for those with asthma, there has to be mention about bronchodilator drugs, Sarioglu, Bilen, Sackes & Gencer (2015) discussed bronchodilator drugs and antibiotics and went into detail about carbonic anhydrase (CA). Carbonic anhydrase (CA) is an enzyme controlling the acid-base balance and Sarioglu, Bilen Sacke & Gencer (2015) added that this enzyme also has a role in electrolyte secretion in tissues. In a study that looked at CA I and II activities, Sarioglu, Bilen Sacke & Gencer (2015) acknowledged that there is strong evidence that there are adverse effects when utilizing antibiotics and bronchodilator drugs because of the carbonic anhydrase inhibition. Again, this has captured my attention because we as clinicians have to look at the patient medications with a fine tooth comb in the prevention of adverse reactions.
Reference:
Albrecht, H. H., Dicpinigaitis, P. V., & Guenin, E. P. (2017). Role of
guaifenesin in the management of chronic bronchitis and upper
respiratory tract infections. Multidisciplinary Respiratory Medicine, 121.
doi:10.1186/s40248-017-0113-4
Sarioglu, N., Bilen, C., Sackes, Z., & Gencer, N. (2015). The effects of
bronchodilator drugs and antibiotics used for respiratory infection on
human erythrocyte carbonic anhydrase I and II isozymes. Archives Of
Physiology & Biochemistry, 121(2), 56-61.
doi:10.3109/13813455.2015.1011068
Sample Answer 3 for NR 507 Week 2: Discussion Part Two
Very informative post ladies it seems like antibiotics are thrown around like candy at a parade nowadays. The concern that the overuse of antibiotics can cause resistance to drugs and potentiate a drug-resistant organism is a reality (Dempsey at al., 2014). The need for follow up after the use of antibiotics and this disease process is important to ascertain that the patient did indeed take all the medicine and has resolved all her respiratory issues. We must also be concerned with any side effects from the antibiotic such as diarrhea, rash, nausea, vomiting or any number of reactions what could hinder the resolution of this disease process. The need for education prior to the patient leaving the office setting is important that they understand when to call if there are complications and the importance of following up afterwards.
A sputum culture would also be a possibility since she is coughing up copious amounts of foul smelling green sputum so we can be assured the antibiotic prescribed will be effective. Treating the cause of this infection will aid in preventing lung scaring and prevent continued damage to the lungs from recurrent infections. Education on potential smoking cessation of tobacco should she smoke is appropriate. Finding out what her living conditions are can have a direct impact on her health, for instance cockroach allergens are similar to dust mites as their fecal material leaves behind fragments of their body and becomes airborne (American Lung Association, 2016). These allergens can trigger asthma, which is especially seen in preschool children. Although Tammy is an adult we did not get a history of her health in this scenario. So the goal would be to do the investigative work and discover if there are any pre-existing conditions. Setting health related goals for this patient with her input would be of benefit to help her reach her maximum health status and possibly eliminate any potential hazards in the future.
Reference:
American Lung Association.(2016). Cockroaches. Retrieved from http://www.lung.org/our-initiatives/healthy-air/indoor/indoor-air-pollutants/cockroaches.html?referrer=https://www.google.com/
Sample Answer 4 for NR 507 Week 2: Discussion Part Two
Thank you for your very thorough and informative post. I have a family member that has chronic bronchitis. He usually presents with a very dry barking cough and it lasts for weeks. He usually gets it every year. He does not smoke but worked in an automobile factory while going to college many years ago. It usually starts with a cold. Exposure to second-hand smoke and many other irritants in and around the factory is more than likely the cause. He was prescribed antibiotics a few years ago but they did nothing for him.
Kinkade and Long (2016) explain how the use of antibiotics for bronchitis is not appropriate in most cases. It is important to rule out pneumonia or other bacterial infections first. Bronchitis is usually caused by viral infections in 90% of all cases. A study, between 1996-2010, of antibiotic use found that antibiotics were prescribed in 71% of visits relating to acute bronchitis. Overuse of antibiotics causes antimicrobial resistance and extensive health care costs. Antibiotic use can also cause severe diarrhea, allergic reactions, nausea, headache, and vaginitis.
Biomarkers may help practitioners determine if there is a bacterial infection. C-Reactive protein levels above 50 mcg/ml can help in identifying pneumonia. A chest x-ray can also help to rule out pneumonia. Symptoms of bronchitis can be treated with over-the-counter medications, and some prescribed medications, such as cough medication or inhalers. It is important to differentiate between viral and bacterial infections to avoid unecessary use of antibiotics.
Reference
Kinkade, S., & Long, N. (2016, October 1). Acute bronchitis. American Family Physician, 94(7), 560-565. www.aafp.org/afp
NR 507 Week 3 Case Study
Pathophysiology and Clinical Findings
Question One
The patient’s spirometry results are consistent with obstructive pulmonary disease, as evidenced by the low forced expiratory volume in 1 second that ranges typically above 80%. The COPD diagnosis was considered since patient A.C. has presented with complaints of dry cough in the morning, dyspnea, sputum production, and history of exposure to tobacco smoke. However, the forced spirometry will demonstrate the presence of non-fully reversible airflow limitation using post-bronchodilator FEV1/FVC < 0.70 is compulsory to confirm the COPD diagnosis. A.C most likely pulmonary diagnosis is COPD based on the spirometry findings. The predicted results revealed that the Absolute FEV1/FVC ratio was 81%. Following the test, the pre-bronchodilator and post-bronchodilator predictions were 69% and 64%, which are less than 70% of the predicted value.
Question Two
Chronic obstructive pulmonary disease is a heterogeneous condition characterized by a wide range of chronic respiratory symptoms, which can be linked to airway abnormalities and alveoli that can cause persistent and airflow obstruction (Venkatesan, 2023). Emphysema can be characterized by the destruction of alveoli walls owing to the imbalance of proteinase–antiproteinase enzymatic activities (Leap et al., 2021). In healthy lung tissues, the protective antiproteinase counteracts the protein-degrading enzymes secreted by white blood cells. Under rare circumstances, a genetic condition, alpha-1 antitrypsin deficiency, could play a function in causing COPD. Persons living with the condition tend to have low alpha-1 antitrypsin, a protein produced in the liver. Chronic inflammation can be caused by chronic exposure to lung irritants, or long-term cigarette smoking recurrently recruits white blood cells into the alveoli (Dunphy et al., 2023). The burning of cigarettes produces a mixture of gases and chemicals that reach the alveoli and peripheral airways, where particles can easily collide with the surfaces and cause damage (Higham, et al., 2019). Counter to the atopic asthma processes, the COPD lymphocytic infiltration constitutes mainly of CD8+ T cells instead of CD4+ T-helper cells. Neutrophils and monocyte-/macrophage-derived proteins progressively destroy the alveolar walls and overcomes anti-proteinase defenses resulting in overdistended, hyperinflated, and weak elastic alveoli. As a result, there is air trapping, an increase in residual lung volume, low expiratory flow, and carbon dioxide retention.
Persons may experience hypercapnia but maintain adequate oxygenation in the early stages of the disease process. The desensitization of the central respiratory receptors to PCO2 occurs with long-term hypercapnia leading to the loss of normal respiratory stimulus to breathe independently and reliance on low oxygen levels to activate breathing. Chronic bronchitis is the more common pathological mechanism involved in COPD. Airflow obstruction is caused by bronchiole edema, mucus-producing goblet cell hyperplasia, and bronchiole smooth muscle hypertrophy (Dunphy et al., 2023). Chronic bronchitis is presented as long-term coughing or recurrent sputum production. Persons with cyanosis and hypoxia develop problems with ventilatory obstruction and suboptimal blood oxygen. Whereas, in chronic bronchitis, long-term hypoxia can lead to pulmonary vasoconstriction and pulmonary hypertension. The increased pulmonary resistance against the right ventricle leads to pulmonale or right ventricular failure. Chronic hypoxia stimulates renal erythropoietin that triggers and prolongs red blood cell synthesis in the bone marrow, increasing hemoglobin concentration and hematocrit. Acute exacerbations of chronic bronchitis are characteristic of COPD evidenced by Increased purulent sputum and worsened shortness of breath.
Question Three
The patient has presented with chief complaints of fatigue and increasing dyspnea on exertion for the last three months, but he did not seek medical help. In addition, he has been experiencing Dry, nonproductive cough in the morning. The patient has smoking history of 35 years. However, he has considerably reduced to one cigarette daily after the initiation of cardiac intervention.
Question Four
The chest ray exam has indicated signs of hyperinflation as both lungs are hyper-inflated and flattening of the diaphragm. The second objective finding is the presence of bilateral wheezing where there is forced exhalation and prolonging of expiratory phase. The vital signs reveal that respiratory rate and oxygen saturation is 22 and 93%. The patient has a history of cardiology consultation, rehabilitation, and successful angioplasty. Finally, the spirometry results reveal pre-bronchodilator and post-bronchodilator predictions for the FEV1/FVC ratio were 69% and 64%, which are less than 70% of the predicted value.
Management of COPD
Question One
The spirometric cut points have been proposed for simplicity in Table 2.5 of the GOLD standards. The spirometry results reveal that pre-bronchodilator and post-bronchodilator predictions for the FEV1 were 64% and 64%. The current classification is stage 2 moderate as stated in the GOLD criteria, where the FEV1 values are greater than 50 percent and lower than 80 percent (Global Initiative for Chronic Obstructive Lung Disease, 2023). After analyzing the patient CA’s well-managed symptoms, spirometry results, and assessment that reveals pulmonary decline is minimized, he can be considered stable.
Question Two
Pharmacological therapy is used to lessen symptoms, severity, and frequency of exacerbations and improve health status. The medication classes used to treat COPD are shown in Table 3.3. The choice in each medication class depends on the availability, cost, and clinical responses balanced against side effects. The clinician should individualize the treatment regimen since the relationship between symptom severity, airflow obstruction, and exacerbations differ between patients. The recommended medication classes are bronchodilators and antimuscarinic drugs. Examples of short-acting beta-agonists are Albuterol and long-acting beta-agonists are Formoterol. Examples of short-acting antimuscarinics, ipratropium and long-acting muscarinic antagonists are tiotropium and aclidinium.
Question Three
The available empirical data suggests that numerous pharmacological treatment options can reduce the mortality. The inhaled bronchodilators will be used to increase the FEV1 values and alter the other variables in the spirometric tests. The mechanism of action is alteration of the airway’s smooth muscle tone as well as improvements in expiratory flows, which can be reflected in the airways widening as opposed to changes in lungs elastic recoil. In addition, the bronchodilators can also lessen dynamic hyperinflation presented during resting periods and exercise and improvement in performance (Global Initiative for Chronic Obstructive Lung Disease, 2023). Specifically, the principal mechanism action of the beta2-agonist drugs is the relaxation of airways’ smooth muscles by the stimulation of beta2-adrenergic receptors to boost cyclic AMP and generate functional antagonism and bronchoconstriction. The short-acting beta2-agonists improve FEV1, and symptoms and effects usually wear off within four to six hours, while long-acting beta2-agonists improve FEV1, lung volumes, dyspnea, exacerbation rates, no hospitalizations, and health status. Secondly, the antimuscarinic medication class aids in blocking the bronchoconstrictor acetylcholine effect on the M3 muscarinic receptors within the airway smooth muscles. The short-acting antimuscarinic drugs block the inhibitory neuronal receptors M2 that trigger vagal- induced bronchoconstriction. At the same time, the long-acting muscarinic antagonists bind to M3 muscarinic receptors, which has faster dissociation from M2 muscarinic receptors, which prolongs the duration of bronchodilator effects.
Question Four
The available empirical data suggests that numerous non-pharmacological treatment options can reduce the mortality. The recommended non-pharmacological therapies for patient AC is smoking cessation and pulmonary rehabilitation. First, smoking cessation is considered the single most effective non-pharmacological treatment option to reduce the progression of COPD. The Lung Health Study conducted a randomized clinical trial including asymptomatic or mildly symptomatic COPD patients who were treated with a ten-week smoking cessation program and followed up for 14.50 years, where there was a reduction in overall mortality rate in the smoking cessation intervention group than regular care group (Global Initiative for Chronic Obstructive Lung Disease, 2023). Hence, the patient should be asked about the progress in all visits. Secondly, pulmonary rehabilitation is comprehensive intervention, which is based on thorough assessment followed by the delivery of patient-tailored therapies including exercise training, patient education, self-management interventions aiming at behavior changes. The program is designed to improve the psychological and physical condition of people and promote the long-term adherence to health-enhancing behaviors. The core components of the pulmonary rehabilitation will improve exercise capacity, prevent symptoms, and increase quality of life. Finally, participation in an outpatient pulmonary rehabilitation program will assist in improving the shortness of breath and overall health status.
References
Dunphy L. M. H. Winland-Brown J. E. Porter B. O. & Thomas D. J. (2023). Primary care: The art and science of advanced practice nursing – an interprofessional approach. F.A. Davis Company.
Global Initiative for Chronic Obstructive Lung Disease, Inc. (2023). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. https://goldcopd.org/wp-content/uploads/2023/01/GOLD-2023-ver-1.2-7Jan2023_WMV.pdf
Higham, A., Quinn, A. M., Cançado, J. E. D., & Singh, D. (2019). The pathology of small airways disease in COPD: historical aspects and future directions. Respiratory research, 20(1), 1-11. https://doi.org/10.1186/s12931-019-1017-y
Leap, J., Arshad, O., Cheema, T., & Balaan, M. (2021). Pathophysiology of COPD. Critical Care Nursing Quarterly, 44(1), 2-8. https://doi.org/10.1097/CNQ.0000000000000334
Venkatesan, P. (2023). GOLD COPD report: 2023 update. The Lancet Respiratory Medicine, 11(1), 18 https://doi.org/10.1016/S2213-2600(22)00494-5