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Running Head Insert Shortened Title 50 Characters Or Fewer1insert

1 INSERT SHORTENED TITLE (50 CHARACTERS OR FEWER) 2 Title of Paper Student Name Colorado State University – Global Campus Title of Paper Academic essays should begin with an introduction . The introduction will provide readers with the context necessary for understanding your argument and the body of your paper. When composing the introduction, think about what context or background information the reader would benefit from knowing. Once your context is established, transition from that context into your thesis statement . The thesis statement generally comes at the end of your introduction and usually consists of a few sentences that sum up the argument for your paper overall.

Thesis statements should also provide a roadmap for the reader so that they can navigate through the ideas present in the rest of your paper. Level 1 Header Headers are useful for organizing your paper. Level 1 headers are used with broad or general topics in your paper. Depending on the topic, length, and genre of your assignment, you might use only Level 1 headers. Level 1 headers should be bolded and centered.

The longer and more complex your argument is, the more you might benefit from using Level 2 and Level 3 headers. Level 4 and Level 5 headers exist, but they should only be used in manuscripts with many topics and subtopics. Generally, if you choose to use subsections (Level 2–5 headers) in your paper, you should have at least two subsections for each level of header. For more information on how to use headings in your paper, visit the APA Style Blog . Level 2 Header Body paragraphs should follow the MEAL structure .

This structure will help your ideas build on one another in order to support your thesis statement and to develop your argument over the course of your essay. Each body paragraph should consist of a claim, which also functions as the topic sentence or the main idea of a paragraph. The claim should then be followed by evidence. Evidence is typically source material that you either paraphrase or quote directly. Remember, APA style guidelines prefer paraphrasing to directly quoting a source.

Evidence should provide support for your main idea in the form of examples, statistics, facts, anecdotes, etc. Next, your paragraph should include analysis. Analysis is your explanation of the preceding evidence and its significance. In other words, you should not let the evidence speak for itself. Through analysis, you can show the reader exactly how you interpret the evidence, how it supports your claim for the paragraph, and how it supports your thesis statement.

Finally, each body paragraph should end with a sentence that functions as a conclusion for the paragraph. This sentence can rephrase the claim for the paragraph, tie back to the thesis statement, or transition to the idea you present in the next paragraph. Level 2 Header Whenever you use a source, it must be cited both in text and in the references. However, there are two types of sources that should only be cited in text and do not need to be included on the References page: (a) Sources that do not produce recoverable data and cannot be located by the reader, such as personal communications , and (b) Religious texts and classical works, such as the Bible, the Qur’an, and Greek or Roman works. Both your in-text citations and references should follow APA style.

In academic writing that follows APA style, it is important to paraphrase source material whenever possible, as opposed to quoting the source directly. When paraphrasing source material, you can use page numbers to point the reader to a specific portion of the source, but this is optional. When paraphrasing, you should follow the paraphrased material with an in-text citation that contains the author’s last name and the source’s year of publication (Author, Year) or use a signal phrase to introduce the paraphrased material with the author and year (ex: “According to Eriksson (2015)...â€). When quoting source material directly, a page number (p. ) or page range (pp. ) is always required. If the source does not include page numbers, use a paragraph number (para. ) instead.

When citing in text, parenthetical citations should appear as close to the source material as possible. The author’s name should never be separate from the year of publication. In-text citations point readers to the References page, which is a list of all the sources used in your assignment. When formatting the References page, start a new page. Then, type and center the word References at the top, but do not use any additional formatting (e.g., bold, underline, italics, quotation marks, etc.).

Alphabetize the references according to the first author’s last name or by the name of the organization if there is no individual author for a text. All references should have a hanging indent: The first line of each reference should be flush with the left margin, and subsequent lines should be indented. Finally, each reference should follow APA style, and the proper formatting will change depending on the type of source. Conclusion The last section or paragraph of your paper should be the conclusion . A conclusion should reiterate the major points of your argument.

To do this, think about developing your thesis by adding more detail or by retracing the steps of your argument. You can recap major sections for the reader. You can also summarize the primary supporting points or evidence you discussed in the paper. The conclusion should not introduce any new information in order to avoid confusing the reader. To end the paper, think about what you want your reader to do with all the information you just presented.

Explain what logical next steps might be taken in order to learn more about this topic. Use the conclusion to establish the significance and importance of your work, motivate others to build on what you’ve done in this paper, and encourage the reader to explore new ideas or reach other conclusions. References Centers for Disease Control and Prevention. (n.d). Coping with a traumatic event. Retrieved from Chaitin, J., & Steinberg, S. (2013).

“I can almost remember it nowâ€: Between personal and collective memories of massive social trauma. Journal of Adult Development, 21 (1), 30–42. Eriksson, M. (2015). Managing collective trauma on social media: The role of Twitter after the 2011 Norway attacks. Media, Culture & Society, 38 (3), 365–380.

Kaplan, E. M. (2005). Trauma culture: The politics of terror and loss in media and literature . Piscataway, NJ: Rutgers University Press. Meek, A. (2011).

Trauma and media . National Institute of Mental Health. (2017). Post-traumatic stress disorder (PTSD). Retrieved from DQ-1 The goals of COPD therapy include slowing the progression, initiating a smoking cessation plan, and ensuring the patient is up-to-date on vaccinations including influenza and pneumococcal (Global Initiative for Chronic Obstructive Lung Disease [GOLD], 2020). Evidently, patients who received the influenza vaccine showed a significant reduction of exacerbations compared to those who received a placebo, and COPD patients vaccinated had decreased risks of ischemic heart disease (GOLD, 2020).

To reduce symptoms of COPD, pharmacological therapy can be utilized, but treatment depends on the severity of symptoms and exacerbations. Short-acting beta-agonists (SABAs) are the first-line treatment in asthma and are commonly used for mild COPD. According to the GOLD guidelines (2020), regular single-dose and PRN use of SABA or short-acting muscarinic antagonists (SAMA) can improve FEV1 and COPD symptoms, and a combination of both have a better outcome than either medication alone. SABA should be utilized as PRN only as frequent usage can potentially lead to paradoxical bronchospasm and worsening the quality of life. In more moderate cases of COPD, LABAs and LAMAs can improve FEV1, reduce exacerbation rates, and improve quality of life (GOLD, 2020).

Levalbuterol is a beta2-receptor agonist that binds to beta-2 adrenergic receptors in bronchial smooth muscle leading to the activation of adenylate cyclase and increasing cyclic-3’,5’-adenosine monophosphate (cAMP) levels (Hsu & Bajaj, 2019). The increase levels of cAMP activate protein kinase A inhibits the phosphorylation of myosin and lower intracellular calcium concentrations; thus, resulting in smooth muscle relaxation and promoting bronchodilatory effects (Hsu & Bajaj, 2019). The increase levels of cAMP activate protein kinase A inhibits the phosphorylation of myosin and lower intracellular calcium concentrations; thus, resulting in smooth muscle relaxation and promoting bronchodilatory effects (Hsu & Bajaj, 2019). The increase levels of cAMP activate protein kinase A inhibits the phosphorylation of myosin and lower intracellular calcium concentrations; thus, resulting in smooth muscle relaxation and promoting bronchodilatory effects (Hsu & Bajaj, 2019). Levalbuterol may cause ECG changes, such as prolongation of the QT interval and ST-segment depression, increasing the risk of arrhythmias. Additionally, beta-2 agonists decrease serum potassium and promote glycogenolysis increasing serum glucose (Levalbuterol, 2019). Other adverse effects of levalbuterol include headache, viral infection, rhinitis, pharyngitis, tremor, nervousness, and asthma. It’s important to consider monitoring FEV1 changes, heart rate, blood pressure, and, in certain patients, serum glucose and potassium. To avoid additive cardiovascular effects, drugs that should be used with caution include atomoxetine, cannabinoid-containing products, haloperidol, linezolid, monoamine oxidase inhibitors, and tricyclic antidepressants (Levalbuterol, 2019).

In addition, drugs to avoid during levalbuterol use include beta-blockers as they block beta-adrenergic agonists diminishing the bronchodilatory effect and loop and thiazide diuretics as they may enhance hypokalemic effects (Levalbuterol, 2019). References Global Initiative for Chronic Obstructive Lung Disease. (2020). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved from Hsu, E., Bajaj, T. (2019). Beta 2 agonists.

StatPearls Publishing. Retrieved from Levalbuterol. (2019). Retrieved from DQ-2 In 2007, and expert panel was commissioned by the National Asthma Education and Prevention Program (NAEPP) to develop guidelines for classifying asthma, establishing goals for treating it, and providing a stepwise approach for medication selection (Miller, 2016, p. 913). The panel classified asthma into four groups based on its severity.

Those groups are mild intermittent asthma, mild persistent asthma, moderate persistent asthma, and severe persistent asthma. These groups take into account the patients’ need for medication to relieve their symptoms, their nighttime symptoms, and their lung function (Miller, 2016, p. 915). The panel set the goals for therapy to include reducing the patients’ impairment, reducing their risk for recurrent exacerbations, and preventing the loss of lung function. Drug selection is, of course, dependent upon the classification of asthma that the patient falls into.

An albuterol inhaler is a short acting inhaled beta-2 adrenergic agonist used in the treatment of mild intermittent asthma. It works by relaxing smooth muscle in the airways and allowing airflow to increase in the lungs. More specifically, it increases the levels of cyclic adenosine monophosphate (cAMP) through the stimulation of beta-2 adrenergic receptors in the smooth muscle, resulting in bronchodilation, which reduces airway resistance (Edmunds et al., 2014, p. 208). The inhaled formulation of albuterol generally exerts its effects locally and after inhalation, it is absorbed over several hours from the respiratory tract.

It is the drug of choice for the fast relief of symptoms in asthmatic patients and is primarily used on an as needed basis. It is also used to prevent exercise-induced asthma (Edmunds et al., 2014, p. 208). Some common side effects include palpitations, tachycardia, increased blood pressure, cough, dry throat, chest tightness, GI distress, headache, dizziness, vertigo, and hypersensitivity. Serious adverse effects include arrhythmias, dyspnea, and hypokalemia (Edmunds et al., 2014, p.

219). Because albuterol is a sympathomimetic, its effects are increased when combined with other sympathomimetics. When taken with beta-adrenergic blocking agents, albuterol’s bronchodilating effects are decreased. Its effectiveness is also decreased when taken with insulin or oral hypoglycemic agents. When prescribing this medication, one thing to consider is the patient’s cardiovascular history.

Albuterol may cause adverse cardiovascular effects in some patients, especially those with coronary insufficiency, cardiac arrhythmias, and hypertension (Edmunds et al., 2014, p. 216). References: Edmunds, M. W., Mayhew, M. S., & Setter, S.

M. (2014). Asthma and chronic obstructive pulmonary disease medications. In Pharmacology for the primary care provider (4th ed., pp. ). Mosby. Miller, B.

J. (2016). Asthma and chronic obstructive pulmonary disease. In T. M. Woo & M.

V. Robinson, Pharmacotherapeutics for advanced practice nurse prescribers (4th ed., pp. ). F A Davis Company. DQ-3 Anticholinergics antagonize the parasympathetic effects of acetylcholine, which is a parasympathetic neurotransmitter in the airways that is involved in the pathophysiology of obstructive airway diseases, such as asthma. Tiotropium bromide (Spiriva) is an anticholinergic medication that reduces the acetylcholine-induced inflammatory response by inhibiting the release of chemokines and the recruitment of inflammatory cells.

These long-acting muscarinic antagonists (LAMA) give clinicians and patients an additional tool to manage asthma as add-on therapy to inhaled corticosteroids (ICS) and a long-acting beta-adrenoceptor agonist (LABA) (Bonini & Scichilone, 2017). Dosage is 2.5 mcg inhaled orally for once daily maintenance in patients ages 6 years and older. Common side effects include dry mouth, runny nose, tachycardia, upper respiratory tract infection, shortness of breath and headache. Severe side effects may include angioedema, blurred vision, hypertension, worsening bronchospasm, and QT prolongation (Gosens & Gross, 2018). It should also cautiously be used in patients with moderate to severe renal impairment.

Tiotropium is contraindicated in patients with hypersensitivity to ipratropium and to milk protein. Due to this drug’s anticholinergic properties, it is known to worsen conditions such as narrow-angle glaucoma, benign prostatic hyperplasia, and bladder neck obstruction. Drug interactions with tiotropium include benztropine mesylate, dimenhydrinate, donepezil, tacrine, scopolamine, and dicyclomine. Cannabinoid containing products may enhance the tachycardic effect of tiotropium (Chari & McIvor, 2018). Bonini and Scichilone (2017) provide evidence from several clinical trials in adult and pediatric populations showing that tiotropium is well tolerated and significantly improves symptoms as an add-on treatment.

The first study showed that tiotropium added on to ICS and LABA therapy in adult patients with poorly controlled symptomatic asthma resulted in an improvement of up to 154 mL in peak FEV1, with a 21 percent risk reduction for severe asthma exacerbation. The second study showed that tiotropium had a comparable safety profile to placebo in adolescents and children, as well as demonstrated it as a well-tolerated treatment improving lung function and asthma control regardless of severity. Overall, these data show that tiotropium is efficacious and has a favorable safety profile across a range of asthma severity in adults, adolescents, and children. References Bonini, M., & Scichilone, N. (2017). Tiotropium in asthma: back to the future of anticholinergic treatment.

Clinical & Molecular Allergy, 15, 1–11. Chari, V. M., & McIvor, R. A. (2018). Tiotropium for the Treatment of Asthma: Patient Selection and Perspectives.

Canadian respiratory journal , 2018 , . Gosens, R., & Gross, N. (2018). The mode of action of anticholinergics in asthma. The European respiratory journal , 52 (4), . Need help to reply three post.

DO NOT JUST REPEAT SAME INFORMATION, DO NOT JUST SAY I AGREE OR THINGS LIKE THAT. YOU NEED TO ADD NEW INFORMATION TO DISCUSSION. YOU MUST FOLLOW THE GUIDELINES for responses stated above. Each reply should be at least 200 words, include one scholarly reference within the last five years, and follow APA style. Your response should not contain placeholder text, but provide a comprehensive, analytical reply that adds insight to the discussion.

Paper For Above instruction

Chronic Obstructive Pulmonary Disease (COPD) and asthma are complex respiratory conditions that require tailored therapeutic approaches. Understanding various pharmacological agents and their mechanisms is critical for effective management and improving patient outcomes. This paper explores the pharmacotherapy of COPD and asthma, emphasizing recent guidelines, drug mechanisms, adverse effects, and clinical considerations, integrating current scholarly research to enhance understanding.

Introduction

The management of COPD and asthma encompasses a range of pharmacological interventions aimed at alleviating symptoms, preventing exacerbations, and improving quality of life. With evolving clinical guidelines, especially those by the GOLD and GINA, healthcare providers are better equipped to customize therapy based on disease severity and patient-specific factors. This paper reviews key medications such as beta-agonists, anticholinergics, and inhaled corticosteroids, emphasizing latest evidence to support their use and safety profiles.

Pharmacological Management of COPD

The primary goals in COPD treatment include slowing disease progression, reducing exacerbations, and preventing complications like cardiovascular comorbidities (GOLD, 2020). Vaccination against influenza and pneumococcus remains cornerstone preventive measures, with evidence indicating a significant reduction in exacerbation frequency and cardiovascular risks among vaccinated patients (GOLD, 2020). For symptom control, bronchodilators like SABAs, LABAs, SAMAs, and LAMAs form the pharmacological backbone.

Levalbuterol, a selective beta-2 receptor agonist, operates by increasing intracellular cAMP, leading to smooth muscle relaxation—a process supported by recent research highlighting its safety profile when used judiciously (Hsu