Review Asthma? in Chapter 27 of the Huether and McCance text. Identify the pathophysiological mechanisms of chronic asthma and acute asthma exacerbation. Consider how these disorders are si
- Review “Asthma” in Chapter 27 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 construct 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 Exacerbating Acute and Chronic Asthma
Asthma alludes to a pulmonary condition that results into either a chronic or acute inflammation of the respiratory tubes coupled with a tightening of the smooth muscles of the respiratory tract. In some cases, episodes of bronchoconstriction will accompany it as well. Establishing the pathophysiological mechanism of each asthma is an important step in determining its exacerbation, diagnosis and prescribing treatment for the patient.
The pathophysiological exacerbation of chronic cancer is closely tied to the etiological aspect of persistent viruses and chlamydia. Viruses and other organisms play a huge part in providing the necessary conditions for asthma to thrive. The key mechanism in this exacerbation is the viral replication that results in the epithelial cells of the respiratory tract triggering cytokine release, inflammation and the eventual large mucus production. However, the viral and chlamydia has does not result into sporadic changes in the arterial blood patterns. The asthma attack takes time and so blood PaO2 of 100 mm Hg will only fall slightly to around 85 mm Hg followed by a slight rise in the PH to 7.45 from its initial 7.40 (Casale et al 2016). Despite these processes being necessary for clearance of the viral infection, they are still super-imposed over the already existing inflammatory condition in the airways that ignites symptomatology instead. Furthermore, it means that the immune system is slowed down hence making it unable to clear the viruses. As a result, there is infiltration of the pulmonary vein which exacerbates asthma inflammation.
Dehydration plays a very a far wider role in acute exacerbation of asthma. Studies show that asthma has a close relation with the water levels in the body with regard to airway epithelial cells. This will from time to time contribute to a fraction of epithelial and edema damage coupled with hyper-responsiveness. However, this does not only result should it be exercised-induced asthma. According to Walsh, Sills and Arnold (2017), during asthma attack through dehydration, the arterial blood patterns exhibit very sharp changes in the blood PH which could rise to as high as 7.60 while the blood PaO2 reduces to very low levels within a short time as low as 40 mm Hg coupled with a sharp rise in PaCO2.
Acute asthma can also be triggered by a period of emotional stress grief and sorrow are upheavals to asthma symptoms exacerbations. Interestingly, greater anxiety has been noted to be common to asthma patients than hepatitis B Patients. The level of oxygen in the blood reduces very fast as the patient’s loose instant breath while the CO2 levels climbs up along with the PH levels in almost the same proportion. For instance in a study including 230 patients, 45% scored high on depression rating taken as depressed (Gelb, Christenson & Nadel, 2016). However, the patients with depression had health related issues. Conversely, having intense emotions brings out asthma symptoms such as airway reactivity, decreased peak expiratory flow rate, increased respiratory resistance and shortness of breath.
Even though asthma is a predominantly multifactorial condition, it’s most pressing risk factor remains as the allergies. This involves the chronic asthma in particular. Having a family history of allergic reactions can speed asthma exacerbation. In this case, an immunological response to the allergy is a triggering factor in the symptomatology of asthma. The disruption of the normal epithelial cells leads to triggering of a response which explains the commonly occurring allergic responses to the inhalant antigens particularly among those individuals exposed to these agents.
Exposure to metal toxicity in the respiratory tract exacerbates chronic asthma. Zinc, cadmium, copper and aluminum results into both chronic obstructive lung disease and the acute self-limiting neutrophil alveolitis (Morris, 2016). With time, this develops into pulmonary fibrosis as well as damaging the functional impairment based on the potential of the agent to cause that damage. Metal raise the PH levels in the body as the CO2 content in the blood rises up as well with a reduction in the Oxygen content.
The factors mentioned above have widespread effects on the pathophysiological disorders present in asthma. First, viruses provide conditions for damaging of the epithelial cells in the body. This comes through triggering of the cytokine release that spearheads inflammation and large mucus production. Secondly, exposure to toxic metals leads into chronic lung disease and the self-limiting neutrophil that results into pulmonary fibrosis based on the damaging extent of the metal agent (Morris, 2016). Thirdly, the emotional stress and dehydration connotes to similar effects because they both predispose patients to sudden acute asthma exacerbation that involves decreased peak expiratory flow rate, increased respiratory resistance and shortness of breath.
Diagnosis of asthma follows a very specific approach as established by its exacerbation. For the case of allergy, an allergy test is performed by the doctor. During this period, medical history and breathing tests are performed establishing how well a patient’s lungs are working. Even though there is no cure for asthma, the allergist will recommend taking medications that avoids asthma triggers. Corticosteroids are taken daily. Dehydration test involves testing a patient’s water level in which if it is found out that he/she is lacking sufficient water, they are recommend to be taking more water to boost it. For case of metal toxicity, body fluids and solids are tested for any presence of toxic substances in the body including the blood stream. Based on this heavy detoxification is conducted. Lastly, cases of viruses and chlamydia can be tested through conducting epistemological tests in the body by a qualified doctor. Upon their establishment, antibiotics are administered to attack the virus and hence reduce the risk of asthma.
Acute asthma mind map
Diagnosis
Treatment
Acute asthma
Emotional stress
Therapy
Dehydration
Clinical presentation
Epistemology
Corticosteroids daily
Water addition
Anxiety
Briefing tests
Depression an
Pathophysiological
Disruption of epithelial cells
Pulmonary fibrosis
Chronic asthma mind map.
Detoxification
Viruses and chlamydia
Chronic asthma
Antibiotics
Treatment
Allergies
Lung infection
Disruption of epithelial cells
Working lungs
Mucus production
Inflammation
Medical history
Clinical presentation
Pathophysiology
Epistemology
Diagnosis
Metal toxicity
References
Casale, T. B., Tashkin, D. P., Lühmann, R., Engel, M., Moroni-Zentgraf, P., & Kerstjens, H. A. (2016). Therapy Demonstrates Reduced Risk of Severe Asthma Exacerbation and Asthma Worsening in Symptomatic Asthma, Independent of IgE or Blood Eosinophil Levels. Journal of Allergy and Clinical Immunology, 137(2), AB214.
Gelb, A. F., Christenson, S. A., & Nadel, J. A. (2016). Understanding the pathophysiology of the asthma–chronic obstructive pulmonary disease overlap syndrome. Current opinion in pulmonary medicine, 22(2), 100-105.
Morris, M. (2016). Drugs and Diseases: Pulmonology. Medscape. Retrieved from: emedicine.medscape.com/article/296301-overview
Walsh, C. G., Sills, M. R., & Arnold, D. H. (2017). Time-dependent severity change during treatment of pediatric patients hospitalized for acute asthma exacerbations. Annals of Allergy, Asthma & Immunology, 118(2), 226-227.
USW1.46926.202030 – NURS-6501N-47,Advanced Pathophysiology.2019 Winter Qtr 11/25-02/16-PT27
Assignment – Week 4
semiloore Akerele on Mon, Dec 23 2019, 2:50 AM 60% highest match Submission ID: 51f66acd-31c4-44cf-97bc-e15b2de0a79f
- wk4assgn Akerele S Patho.docx
Word Count: 1,202
Attachment ID: 2465234879
60%
Citations (14/14)
- 1 Another student's paper
Citation is highlighted. Click to remove highlighting
- 2 Another student's paper
Citation is highlighted. Click to remove highlighting
- 3 Another student's paper
Citation is highlighted. Click to remove highlighting
- 4 Another student's paper
Citation is highlighted. Click to remove highlighting
- 5 Another student's paper
Citation is highlighted. Click to remove highlighting
- 6 Another student's paper
Citation is highlighted. Click to remove highlighting
- 7 Another student's paper
Citation is highlighted. Click to remove highlighting
- 8 Another student's paper
Citation is highlighted. Click to remove highlighting
- 9 Another student's paper
Citation is highlighted. Click to remove highlighting
- 10 http://www.einthovenlaboratory.com/onderzoeken/the-link-between-venous-thrombosis-and-arterial-thrombosis/
Citation is highlighted. Click to remove highlighting
- 11 https://papyrus.bib.umontreal.ca/xmlui/handle/1866/5464
Citation is highlighted. Click to remove highlighting
- 12 https://coggle.it/diagram/WNP1ok0gXwABrEbg/t/-
Citation is highlighted. Click to remove highlighting
- 13 Another student's paper
Citation is highlighted. Click to remove highlighting
- 14 Another student's paper
Citation is highlighted. Click to remove highlighting
Running head: 1 DISORDERS OF THE VEINS AND ARTERIES 1 Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx DISORDERS OF THE VEINS AND ARTERIES 1 Source – Another student's paper DISORDERS OF THE VEINS AND ARTERIES 1 2 DISORDERS OF THE VEINS AND ARTERIES 6
Suspected Entry: 84% match Uploaded – wk4assgn Akerele S Patho.docx DISORDERS OF THE VEINS AND ARTERIES 6 Source – Another student's paper Disorders of the Veins and Arteries Disorders of the Veins and Arteries
Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx Disorders of the Veins and Arteries Source – Another student's paper Disorders of the Veins and Arteries Semiloore Akerele Walden University: NURS- 6501N December 22nd , 2019. 3 Disorder of the Veins and Arteries Two of the most common medical disease in adult population are Chronic Venous Insufficiency (CVI) and Deep Vein Thrombosis (DVT) that presents so many similarities.
Suspected Entry: 76% match Uploaded – wk4assgn Akerele S Patho.docx Disorder of the Veins and Arteries Two of the most common medical disease in adult population are Chronic Venous Insufficiency (CVI) and Deep Vein Thrombosis (DVT) that presents so many similarities Source – Another student's paper Disorder of the Veins and Arteries Chronic Venous Insufficiency (CVI) and Deep Vein Thrombosis (DVT) are two prevalent disorders that present with many similarities It is imperative as an advanced nurse practitioner to have a knowledge of the differences between these two disorders as well as their differences to prevent misdiagnosis. mistreatments, and possible complications that might arise during the course of the treatment of the disease. This paper is aimed at identifying the pathophysiology of CVI and DVT, difference between CVI and arterial thrombosis. 3 Also, the patient factor followed will highlight the effects of the female gender on the pathophysiology of these illnesses.
Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx Also, the patient factor followed will highlight the effects of the female gender on the pathophysiology of these illnesses Source – Another student's paper Also, the patient factor followed will highlight the effects of the female gender on the pathophysiology of these illnesses Also, a constructed mind map will accentuate the epidemiology, pathophysiology, clinical manifestations, diagnoses and treatment of Chronic Venous Insufficiency and Deep Vein Thrombosis.
Suspected Entry: 90% match Uploaded – wk4assgn Akerele S Patho.docx Also, a constructed mind map will accentuate the epidemiology, pathophysiology, clinical manifestations, diagnoses and treatment of Chronic Venous Insufficiency and Deep Vein Thrombosis Source – Another student's paper Lastly, a constructed mind map will highlight the epidemiology, pathophysiology, clinical manifestations, diagnoses and treatment of Chronic Venous Insufficiency and Deep Vein Thrombosis Pathophysiology of Chronic Venous Insufficiency According to Heuther and McCance (2017), Varicose vein and valvular insufficiency can progress to Chronic Venous Insufficiency (CVI). CVI is an inadequate venous return over a period of time which result in pool of blood within the vein which results into swollen, twisted and tangible vein. 4 Structurally, the veins are thin walled highly distensible vessels with valves to prevent backflow and pooling of blood.
Suspected Entry: 78% match Uploaded – wk4assgn Akerele S Patho.docx Structurally, the veins are thin walled highly distensible vessels with valves to prevent backflow and pooling of blood Source – Another student's paper Huether & McCance (2017) defines veins as “thin-walled, highly distensible vessels with valves to prevent backflow and pooling of blood” (p When one valve is damaged and there is an inadequate venous return, section of the vein is subjected to the pressure of a larger volume of blood under the influence of gravity which result int swelling of the surrounding tissue (Heuther & McCance, 2017). 2 Over the years, venous hypertension, circulatory stasis, and tissue hypoxia caused by sluggish circulation and unmet metabolic needs (waste collection and oxygen delivery) produce an inflammatory reaction in the vessels and tissues.
Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx Over the years, venous hypertension, circulatory stasis, and tissue hypoxia caused by sluggish circulation and unmet metabolic needs (waste collection and oxygen delivery) produce an inflammatory reaction in the vessels and tissues Source – Another student's paper Over the years, venous hypertension, circulatory stasis, and tissue hypoxia caused by sluggish circulation and unmet metabolic needs (waste collection and oxygen delivery) produce an inflammatory reaction in the vessels and tissues This process induces a fibrosclerotic remodeling of the skin which then causes ulceration.
Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx This process induces a fibrosclerotic remodeling of the skin which then causes ulceration Source – Another student's paper This process induces a fibrosclerotic remodeling of the skin which then causes ulceration (Huether & McCance, 2017).
Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx (Huether & McCance, 2017) Source – Another student's paper (Huether & McCance, 2017) 5 Pathophysiology of Deep Vein Thrombosis Deep Vein Thrombosis (DVT) essentially occurs in the lower extremities.
Suspected Entry: 80% match Uploaded – wk4assgn Akerele S Patho.docx Pathophysiology of Deep Vein Thrombosis Deep Vein Thrombosis (DVT) essentially occurs in the lower extremities Source – Another student's paper Deep Vein Thrombosis Deep vein thrombosis (DVT) are clots that essentially occur in the lower extremities 6 Three factors are known to promote DVT (the triad of Virchow):
Suspected Entry: 82% match Uploaded – wk4assgn Akerele S Patho.docx Three factors are known to promote DVT (the triad of Virchow) Source – Another student's paper Three factors promote DVT known as the Triad of Virchow which includes 2 venous stasis, venous injury, and hypercoagulable states.
Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx venous stasis, venous injury, and hypercoagulable states Source – Another student's paper venous stasis, venous injury, and hypercoagulable states DVT’s builds up when the inner lining the vessels are damaged/ impaired. 3 This impairment initiates the clotting cascade to heal the damaged epithelium.
Suspected Entry: 74% match Uploaded – wk4assgn Akerele S Patho.docx This impairment initiates the clotting cascade to heal the damaged epithelium Source – Another student's paper This damage initiates the clotting cascade to heal the injured epithelium 6 The accumulation of clotting factors and platelets lead to thrombus formation which usually occur at the venous valve.
Suspected Entry: 71% match Uploaded – wk4assgn Akerele S Patho.docx The accumulation of clotting factors and platelets lead to thrombus formation which usually occur at the venous valve Source – Another student's paper Accumulation of clotting factors and platelets leads to thrombus formation in the vein, often near a venous valve The growth of the thrombus leads to increase in blood pressure while blood flow diminishes. 2 Increased pressure in the vein behind the clot may produce edema in the extremity, and persistent venous obstruction can lead to Chronic Venous Insufficiency.
Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx Increased pressure in the vein behind the clot may produce edema in the extremity, and persistent venous obstruction can lead to Chronic Venous Insufficiency Source – Another student's paper Increased pressure in the vein behind the clot may produce edema in the extremity, and persistent venous obstruction can lead to Chronic Venous Insufficiency DVT can lead to a clot breaking off and go to the lungs which is called pulmonary embolism and can also result in embolic stroke or death. 2 (Hammer & McPhee, 2014).
Suspected Entry: 100% match Uploaded – wk4assgn Akerele S Patho.docx (Hammer & McPhee, 2014) Source – Another student's paper (Hammer & McPhee, 2014) 7 Differences between venous thrombosis and arterial thrombosis A thrombus can develop in either the arterial system or the venous system.
Suspected Entry: 83% match Uploaded – wk4assgn Akerele S Patho.docx Differences between venous thrombosis and arterial thrombosis A thrombus can develop in either the arterial system or the venous system Source – Another student's paper The Differences between Venous Thrombosis and Arterial Thrombosis A thrombus is composed of fibrin and blood cells and can develop in either the arterial or the venous system 8 The arterial thrombi form under the condition of high blood flow and rare composed mostly of platelet aggregates held together by fibrin stands.
Suspected Entry: 82% match Uploaded – wk4assgn Akerele S Patho.docx The arterial thrombi form under the condition of high blood flow and rare composed mostly of platelet aggregates held together by fibrin stands Source – Another student's paper Arterial thrombi form under conditions of high blood flow and are composed mostly of platelet aggregates held together by fibrin stands(Huether & McCance,2017) 9 Venous thrombi form under the conditions of low blood flow and are composed of red cells with larger amounts of fibrin and few (Heuther & McCance 2017).
Suspected Entry: 87% match Uploaded – wk4assgn Akerele S Patho.docx Venous thrombi form under the conditions of low blood flow and are composed of red cells with larger amounts of fibrin and few (Heuther & McCance 2017) Source – Another student's paper Venous thrombi form under conditions of low flow and are composed mostly of red cells with larger amounts of fibrin and few platelets (Huether & McCance, 2017) 10 Inflammation plays major role in the development of venous thrombosis while arterial thrombosis is influenced by the state of the coagulation system.
Suspected Entry: 78% match Uploaded – wk4assgn Akerele S Patho.docx Inflammation plays major role in the development of venous thrombosis while arterial thrombosis is influenced by the state of the coagulation system Source – http://www.einthovenlaboratory.com/onderzoeken/the-link-between-venous-thrombosis-and-arterial-thrombosis/ Increasing evidence indicates that inflammation does also play a role in the development of venous thrombosis, while arterial thrombosis is influenced by the state of the coagulation system Venous thrombotic risk is determined by flexible combination of both acquired and genetic risk factor while arterial thrombotic risk factors are either acquired or lifestyle related such as high blood pressure, smoking et.c.
Suspected Entry: 66% match Uploaded – wk4assgn Akerele S Patho.docx Venous thrombotic risk is determined by flexible combination of both acquired and genetic risk factor while arterial thrombotic risk factors are either acquired or lifestyle related such as high blood pressure, smoking et.c Source – http://www.einthovenlaboratory.com/onderzoeken/the-link-between-venous-thrombosis-and-arterial-thrombosis/ Arterial thrombotic risk factors are either acquired or lifestyle related such as high blood pressure, smoking, unfavorable lipid profile et cetera ( Rosendale, 2016). Patient Factors: Gender (Female) Both male and female are affected by DVT and CVI, but female is at higher risk because of the possibility of pregnancy and also birth control. Rosendale (216), stated that, many drugs put the women at risk of developing thrombus which are basically female hormones and oral contraceptives (Rosendaal, 2016). Also, women between the age of 16 and 50 who are pregnant or on birth control are at risk of CVI and DVT. Countrywide according to Goldman & Weiss (2016), about 15% and 25% of women and men respectively are affected by varicose veins, and an approximated 3% estimated to affect European countries populations, prevalence compared to that of diabetes (Goldman & Weiss, 2016). CVI and DVT can be diagnosed by physical examination. D- timers is also done before proceeding to other diagnosis method. Ultrasonography diagnosis can also be done together wit
Collepals.com Plagiarism Free Papers
Are you looking for custom essay writing service or even dissertation writing services? Just request for our write my paper service, and we'll match you with the best essay writer in your subject! With an exceptional team of professional academic experts in a wide range of subjects, we can guarantee you an unrivaled quality of custom-written papers.
Get ZERO PLAGIARISM, HUMAN WRITTEN ESSAYS
Why Hire Collepals.com writers to do your paper?
Quality- We are experienced and have access to ample research materials.
We write plagiarism Free Content
Confidential- We never share or sell your personal information to third parties.
Support-Chat with us today! We are always waiting to answer all your questions.
