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The medical perspective on burnout

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Kakiashvili T., Leszek J., Rutkowski K.
International Journal of Occupational Medicine and Environmental Health
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2013
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vol. 26
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issue 3
401-412
EN
Objective: The aim of this study was to review recent medical findings related to burnout, its diagnosis, treatment, characteristic pathophysiological features, and preventive measures. Materials and Methods: A systematic review of the scientific literature in PubMed/Medline was performed. The most recent and important findings were reported. Results: Burnout was found to be a risk factor for myocardial infarction and coronary heart disease. It was also related to reduced fibrinolytic capacity, decreased capacity to cope with stress and hypothalamic-pituitary-adrenal (HPA) axis hypoactivity. Severe burnout symptoms are associated with a lower level or smaller increase of the cortisol awakening response (CAR), higher dehydroepiandrosterone-sulphate (DHEAS) levels, lower cortisol/DHEAS ratios and stronger suppression as measured by the dexamethasone suppression test (DST). More and more literature works suggest that the evaluation of the HPA axis should be brought to the attention of primary care physicians. There is no universal agreement on specific treatment and diagnostic measures to evaluate the wide range of HPA axis disorders. The cost-effective evaluation of adrenal hormones via saliva samples by a primary care physician may significantly alter the course of therapy in numerous chronic disease patients. Psychiatric disorders may have similar symptoms, but they have distinctive hormonal profiles. Having burnout recognized as a medical condition would help in differentiating burnout from similar clinical syndromes, such as depression or anxiety, and provide appropriate treatment to burnout patients. Proper treatment is essential for a fast and full recovery. Conclusion: Chronic stress-related disorders often fall outside the category of a "true" disease and are often treated as depression or not treated at all. The evaluation of adrenal hormones via saliva samples helps to predict burnout. Burnout screening techniques, dietary and nutritional guidelines and lifestyle changes for supporting the HPA function need to be developed. The presented material includes hormonal, dietary, and pharmaceutical perspectives.
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Pathophysiology of thromboembolism in patients with COVID-19

88%
Vityala Y., Krishna A., Pandla D., Kanteti K. P., Sadhu J., Boddeti H., Kintali T., Khalid M. S.
European Journal of Clinical and Experimental Medicine
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2022
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issue 2
212-216
EN
Introduction and aim. A small number of critically ill patients with coronavirus disease (COVID-19) develop thromboembolism (arterial or venous), both micro- and macrovascular complications such as deep vein thrombosis, pulmonary embolism, and pulmonary arterial thrombosis. The objective of the study is to describe the pathophysiology of venous thromboembolism in patients with COVID-19. Material and methods. In this article a narrative review regarding pathophysiology of thromboembolism in patients with COVID-19. Analysis of the literature. The development of coagulopathy is a consequence of the intense inflammatory response associated with hypercoagulability, platelet activation, and endothelial dysfunction. The pathophysiology that relates pulmonary thromboembolism (PTE) with COVID-19 is associated with a hypercoagulable state. PTE is suspected in hospitalized patients presenting dyspnea, decreased oxygen requirement, hemodynamic instability, and dissociation between hemodynamic and respiratory changes. In COVID-19-associated coagulopathy, initially, patients present with elevated levels of fibrinogen and D-dimer, with minimal changes in prothrombin time and platelet count. The main risk factor for the development of pulmonary embolism is the increase in D-dimer that is associated with the development of PTE. The administration of iodine-based contrast agent to patients with COVID-19 would affect P-creatinine and renal function, where Ultrasound is viewed as cost-effective and highly portable, can be performed at the bedside. Conclusion. Acute respiratory distress syndrome severity in patients with COVID-19 can explain PTE as a consequence of an exaggerated immune response.
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