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Exploring the Causes of Shortness of Breath: Respiratory vs. Non-Respiratory Complications by Native Assignment Help
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Shortness of breathing is a common phenomenon in the lives of human beings and there are various reasons behind this phenomenon. The reason can be derived from respiratory complications or non-respiratory complications. For the disintegration of the working procedure of the lung and other breathing organelles, breathlessness can be felt by the patient. On the other hand, complications in cardiac functioning or “Atherosclerosis” can also be the reason behind the shortness of breath. In that condition, the patient too feels the complications in pulling in or releasing the air. The patients can have “Chronic Obstructive Pulmonary Disorder” (COPD) which is “Respiratory” in origin and can cause problems in breathing in and out. On the contrary, a simple pregnancy can also cause breathlessness and that can also happen in the case of obesity.
This question on the respiratory and non-respiratory reasons behind shortness of breath is highly relevant and important as the compilation in the respiratory system of human beings is increasing for the increasing pollution and the quality of lifestyle of the people.
This essay is going to compare and contrast the respiratory and non-respiratory reasons behind the shortness of breath of human beings. For that agenda, the essay contains 4 areas of discussion including the related tissue and the remodelling of the selected disease. Innate or adaptive immunity components that are functioning for each of the diseases, the differential diagnosis for each of the diseases and the opportunities for better treatment options are also included. The essay highlights the comparison and contrast between the respiratory and non-respiratory reasons behind the shortness of breath among humans which is one of the major symptoms of respiratory diseases.
Thesis statement:Shortness of breath is one of the major symptoms of respiratory disease.
SOB is a phenomenon which can felt by the people when people are involved in strenuous exercise. However when it observe in normal condition, it can be considered as an indication of disease. Patients suffering from “Chronic Obstructive Pulmonary Disorder” (COPD) can have complexity in breathing for the obstructive airflow. The most common cause of COPD is smoking and deaths due to COPD are increasing around the whole world. 2 types of COPD can be seen among the patients and they are “Chronic bronchitis and Emphysema” (Jindal, 2018). In the case of chronic bronchitis, the inflammation of the bronchi can be seen which is in the air pathway towards the lungs (Heusch et al. 2018). On the other hand, Emphysema is damage to the alveoli that is remaining inside the lungs (Eapen et al. 2021). In the case of Emphysema, the walls of the damaged air sacs get stretched out and the size of the lungs gets bigger which makes it harder to breathe for the patients.
In most cases, “Chronic Obstructive Pulmonary Disorder” is caused by smoking. On the other hand, people that are in long-term exposure to harmful pollutants can also catch the symptoms of COPD (Higham et al. 2019). Some people can even get COPD from long-term exposure to lung irritant substances in the working place such as dust, fumes, acids or some chemicals. In the initiation of this phenomenon, shortness of breathing includes and tiring easily are other symptoms of COPD. Later the patient can develop a cough which can include phlegm, mucus and blood.
The disease COPD is characterised by healthcare professionals by the increasing rate of macrophages, neutrophils, and T-lymphocytes (CD8>CD4) in the lungs of the affected person. The tracer of the increased neutrophil sand can be seen in the induced sputum and the bronchoalveolar fluid. In this case, the airways of the patients get inflamed and thickened. In the case of the remodelling of the airways in COPD, structural alteration of the small and large airways for subepithelial fibrosis is seen in this condition (Di et al. 2021). On the other hand, the mass of the smooth muscle is also increased in this condition which can also be considered as the remodelling of the airways (Tohirova and Shernazarov, 2022). COPD patients also show the symptoms such as glandular hypertrophy and neovascularization which is the remodelling of the breathing structure (Karakioulaki et al. 2020). The remodelling of the airways of COPD patients can determine or highlight the deterioration or disintegration of the lung health of the patients. Based on that case, the narrowing of the lumina and the thickening of the bronchial walls can be seen.
On the other hand, breathing problems can also happen to Atherosclerosis in patients. Atherosclerosis is the build-up of fat tissues along with cholesterol and other substances in the walls of the artery. This build-up of cholesterol and fats can be the remodelling of the heart which is called plaque (Li et al. 2019). These plaques cause the blockage of blood flow from or to the heart which can also cause the narrowing of the arteries and blood vessels. These plaques can even burst which can further cause clots inside the blood vessels (Kytömaa et al. 2019). This symptom can cause shortness of breath for the lack of blood flow into other parts of the body into the heart. The reasons behind this problem are the lack of physical activity, eating much more saturated fats, high blood pressure, and triglyceride levels. In the case of atherosclerosis, the remodelling of the heart and the blood vessels can be seen. The remodelling of the coronary arteries initiated in the endothelium increases the atherosclerotic plaque that can cause ischemia and infarction which further provokes myocardial remodelling (Fang et al. 2021). Shortness of breath is a common symptom in the case of atherosclerosis and fatigue can be felt.
“Chronic Obstructive pulmonary disease (COPD)” is a progressive and chronic lung inflammatory disease that can cause limitations in the continuous flow of air. “Macrophages, dendritic cells, neutrophils”, and “CD8+ T-lymphocytes” are the essential inflammatory cells implicated in COPD (Nurwidya et al. 2018). Cigarette smoking which is connected to COPD disease starts the innate immune cells by activating the “pattern recognition receptors” in order to release the “Danger Signal” (Pietrangelo, 2021). This danger signal responds like the “toll-like receptors”, initiating the exhibition of cytokines that can include innate inflammation. Impaired immune function contributes to the development of COPD and the disease progression is further exacerbated by infections to impaired immune response. The impaired immune procedure has a contribution in the maturation of COPD and disease advancement is further aggravated by diseases due to damaged immune reactions.
On the contrary, Atherosclerosis is a chronic provocative disease that can incorporate both innate and adaptive immunity functions which can adjudicate the initiation, advancement and foremost thrombotic difficulties of atherosclerosis (Miteva et al. 2018). In the initiation of this disorder, endothelial dysfunction happens which is further triggered by the accumulation of cholesterol carrying low-density lipoproteins (LDL) (Martel, 2021). In this case, the inflammatory response is further triggered. The “damage-associated molecular patterns (DAMP)” change and the “NLRP3 Inflammasome” is activated. In addition, the “innate and adaptive immune cells” are included in the atherogenesis process (Packard et al. 2019). This response can regulate the entry of the monocytes into the intima and their differentiation process into macrophages. After that this can also turn into Foam cells which is followed by an “adaptive immune response” with “Helper T (Th) cells” and the “Th2, Th17, CD8+ T cells, B cells, T regulatory Cells (Treg),” and “natural killer cells(NKT)”. Effectively, dysregulated lipid metabolism and inciting processes together contribute to the construction of atherosclerotic plaque in the arterial wall.
Generally, COPD is misdiagnosed by healthcare practitioners in the healthcare sector and until the disease is advanced the occurrence of COPD is not diagnosed. The signs and symptoms of patients with slight respiratory problems can be checked and family and medical history are checked with assessing their exposure to lung irritants (Shah et al. 2020). The tests that are given to the patients in order to test for COPD are a Pulmonary function test, CT scan, laboratory tests, and chest X-rays.
On the other hand, Atherosclerosis can be diagnosed by blood tests, Celectrocardiograns (ECG or EKG), exercise stress tests, and other imaging tests (Wang et al. 2020).
The lung or pulmonary function test is the test that can measure the amount of air that is inhaled or exhaled and whether the lungs of the patient can deliver enough oxygen to the blood. The respiratory physiology is analysed along with the gas exchange mechanism with measurement of lung homeostasis. The gas exchange happens in the pulmonary alveoli and there are 300 million alveoli in the lungs. With the “Spirometer”, the breathing of the patients is measured that can give rise to a graphical representation.
Through the spirometric graph, the forced expiratory volume in 1 second or FEV1 is measured along with the FVC (Forced Vital Capacity) ratio.
On the other hand, the airflow is measured using a simple mathematical formula-
F=?P/R
In this case, the change of pressure is measured with the altitude, weather and lung elasticity which can be the alveolar pressure. On the other hand, the change of the resistance is also measured through the narrowing of the lung airways. Moreover, the airways resistance and the radius of the airways are measured with respect to the total volume of the airways (Pietrangelo, 2021). Based on that, the equation and relation can be suggested for the resistance in the airways. The volume of the airways when elevated, the radius is also high, and then the resistance will be low. Therefore the resistance in the airways is inversely proportional to the radius and the volume of the airways.
The maximum inspiration and maximal forceful expiration are measured along with the “Peak Expiratory Flow Rate”. In that case, the peak flow metre is also included in the diagnosis process of COPD (Di et al. 2021). In modern times, the parameters that are considered while measuring the airflow in the lung are posture, age, sex and location, clothing that is worn by the patients, lung tissue elasticity, muscle strength and pain or comfort. The problems in the skeletal structure or Kyphosis are also kept in mind while diagnosing COPD.
In contemporary times, atherosclerosis is diagnosed with further promising tests that can surely detect or identify the problems that are happening in the blood vessels. Among the tests, the most important tests are echocardiogram, angiogram, and coronary calcium scan which can highlight the probability of atherosclerosis in patients (Wang et al. 2020). Detailed pictures of the heart walls, arterial walls and blood vessel layers are taken out to detect the issue.
Conclusion
From the above discussion, it can be concluded that breathlessness can be a symptom of different respiratory and non-respiratory diseases. COPD is the basic cause that many people face in this generation because smoking habits mainly hold the symptoms of breathlessness. It can be seen that people are mostly engaged with their smoking habits and 1 in 5 smokers can have a chance to catch COPD. In that case, the breathing can be very much struggling for the obstruction in the airflow. Moreover, people can die from the disease. On the other hand, the cause of atherosclerosis can also include shortness of breath among people who are having high-fat content in their bodies.
In that case, the fat and cholesterol bits are stuck inside the blood vessels and the heart's inner layering which can be considered plaque. This also hinders the free flow of blood and that can cause trouble in breathing and taking air inside. On that note, both health issues can cause the triggering of the innate and adaptive immune response which can activate the T cells and B cells and other regulatory cells. In the healthcare sector, the diagnosis of these two different disorders is assessed differently by professionals. Therefore the diagnosis process can be different from each other and the treatment can also be different from each other. There are better opportunities for treatment and diagnosis in the healthcare sectors in the contemporary period. Therefore, SOB can be a potential indication of COPD which may create a life threatening situation. However, further diagnosis is recommended which can confirm the respiratory disease in this case and doctor can prescribe the medication and treatment for health improvement and consequence reduction.
References
Journals
Di, T., Yang, Y., Fu, C., Zhang, Z., Qin, C., Sai, X., Liu, J., Hu, C., Zheng, M., Wu, Y. and Bian, T., 2021. Let?7 mediated airway remodelling in chronic obstructive pulmonary disease via the regulation of IL?6. European journal of clinical investigation, 51(4), p.e13425.
Eapen, M.S., Lu, W., Hackett, T.L., Singhera, G.K., Mahmood, M.Q., Hardikar, A., Ward, C., Walters, E.H. and Sohal, S.S., 2021. Increased myofibroblasts in the small airways, and relationship to remodelling and functional changes in smokers and COPD patients: potential role of epithelial–mesenchymal transition. ERJ open research, 7(2).
Fang, M., Ishigami, J., Echouffo-Tcheugui, J.B., Lutsey, P.L., Pankow, J.S. and Selvin, E., 2021. Diabetes and the risk of hospitalisation for infection: the Atherosclerosis Risk in Communities (ARIC) study. Diabetologia, 64(11), pp.2458-2465.
Heusch G, Libby P, Gersh B, Yellon D, Böhm M, Lopaschuk G, Opie L. 2018. Cardiovascular remodelling in coronary artery disease and heart failure. Lancet. 383(9932):1933-43.
Higham, A., Quinn, A.M., Cançado, J.E.D. and Singh, D., 2019. The pathology of small airways disease in COPD: historical aspects and future directions. Respiratory research, 20(1), pp.1-11.
Jindal SK. 2018. Remodeling in asthma and COPD-recent concepts. Lung India.;33(1):1-2.
Karakioulaki, M., Papakonstantinou, E. and Stolz, D., 2020. Extracellular matrix remodelling in COPD. European Respiratory Review, 29(158).
Kytömaa, S., Hegde, S., Claggett, B., Udell, J.A., Rosamond, W., Temte, J., Nichol, K., Wright, J.D., Solomon, S.D. and Vardeny, O., 2019. Association of influenza-like illness activity with hospitalizations for heart failure: the atherosclerosis risk in communities study. JAMA cardiology, 4(4), pp.363-369.
Li, X., Joehanes, R., Hoeschele, I., Rich, S.S., Rotter, J.I., Levy, D., Liu, Y., Redline, S. and Sofer, T., 2019. Association between sleep disordered breathing and epigenetic age acceleration: evidence from the Multi-Ethnic Study of Atherosclerosis. EBioMedicine, 50, pp.387-394.
Miteva, K; Rosalinda, M., Raffaele, C.D., Linthout, V., Sophie, 2018. Innate and adaptive immunity in atherosclerosis. Vascular Pharmacology, 65(2), S1537189117304640
Nurwidya F, Damayanti T, Yunus F. 2018.The Role of Innate and Adaptive Immune Cells in the Immunopathogenesis of Chronic Obstructive Pulmonary Disease. Tuberc Respir Dis (Seoul). 79(1):5-13.
Packard RR, Lichtman AH, Libby P. 2019. Innate and adaptive immunity in atherosclerosis. Semin Immunopathol. 31(1):5-22.
Shah, N.A., Reid, M., Kizer, J.R., Sharma, R.K., Shah, R.V., Kundel, V., Ambale-Venkatesh, B., Fayad, Z.A., Shea, S.J., Kaplan, R.C. and Lima, J.A., 2020. Sleep-disordered breathing and left ventricular scar on cardiac magnetic resonance: results of the Multi-Ethnic Study of Atherosclerosis. Journal of Clinical Sleep Medicine, 16(6), pp.855-862.
Tohirova, J. and Shernazarov, F., 2022. Atherosclerosis: causes, symptoms, diagnosis, treatment and prevention. Science and innovation, 1(D5), pp.7-12.
Wang, J., Chen, X., Liao, J., Zhou, L., Han, H., Tao, J. and Lu, Z., 2020. Non breathing-related sleep fragmentation and imaging markers in patients with atherosclerotic cerebral small vessel disease (CSVD): a cross-sectional case-control study. BMC neurology, 20(1), pp.1-8.
Won, C.H., Reid, M., Sofer, T., Azarbarzin, A., Purcell, S., White, D., Wellman, A., Sands, S. and Redline, S., 2020. Sex differences in obstructive sleep apnea phenotypes, the multi-ethnic study of atherosclerosis. Sleep, 43(5), p.zsz274.
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