Concepts of Cardiovascular and Respiratory Disorders Essay
The level of cholesterol plays an indispensable role in the cardiovascular disease process. For instance, hyperlipidemia increases the risk of the development of atherosclerotic cardiovascular disease. HDL (high-density lipoprotein) cholesterol is considered “good” cholesterol because it mops up cholesterol from the bloodstream and peripheral tissues to the liver where it is metabolized (Barter & Genest, 2019). Cholesterol is ordinarily stored in foam cells of atherosclerotic plaques. Consequently, HDL cholesterol has anti-atherogenic and anti-inflammatory properties as it diminishes the size of the plaque and its bracketed inflammation. According to Barter and Genest (2019), HDL cholesterol is considered low when it is less than 40 mg/dl and high while it is desirable when it is 60 mg/dl or more.
How does inflammation contribute to the development of atherosclerosis?
Inflammation plays a central role in the development and progression of atherosclerosis (McCance & Huether, 2019). According to McCance and Huether (2019), atherosclerosis is a disease of chronic inflammation distinguished by a dysfunctional interplay between lipids and the immune system. Inflammation is present at all stages of atherosclerosis. Endothelial injury leads to endothelial dysfunction. Endothelial cell dysfunction results in the expression of adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), which result in monocyte adhesion and emigration into the intima. Subsequent macrophage and T-cell activation results in increased cytokine production that spearheads smooth muscle cell proliferation and matrix synthesis (Jebari-Benslaiman et al., 2022). Additionally, macrophages oxidize LDL cholesterol. Oxidized LDL cholesterol is toxic to the intima and enhances endothelial cell injury causing a vicious cycle of endothelial cell injury and subsequent inflammation.
Given the history of the patient explain what contributed to the development of a deep venous thrombosis (DVT)
DVT originates from an interplay between venous stasis, endothelial damage, and hypercoagulability (McCance & Huether, 2019). Endothelial injury stimulates an inflammatory response as well as the activation of the coagulation system. On the other hand, venous stasis brings platelets into contact with the endothelium, prevents the dilution of activated clotting factors, and retards the inflow of clot-inhibiting factors. This Virchow’s triad interrelates in various degrees to stimulate cytokine production and leucocyte adhesion that facilitate thrombus formation (Zhang et al., 2019). Consequently, factors predisposing to venous stasis, endothelial damage, and hypercoagulability increase the risk of developing DVT. The patient has risk factors for venous stasis, such as advanced age, immobility, and obesity. Additionally, the patient had a hypercoagulable state significantly contributed by the surgery of the hip (Zhang et al., 2019). Finally, trauma due to surgery is the principal cause of endothelial injury. The ultimate result is the formation of a clot in the deep venous system whose propagation depends entirely on the balance between thrombolytic and coagulation pathways.
There is a clear relationship between emphysema and COPD, explain the pathophysiology of emphysema and the relationship to COPD
Emphysema is a condition characterized by permanent dilatation distal to the terminal bronchiole without fibrosis. It is ordinarily due to alveolar wall destruction. Irritants, particularly cigarette smoking, stimulate an inflammatory process that results in protease-antiprotease as well as oxidant-antioxidant imbalances. Proteases, particularly elastase, destroy elastic fibers leading to loss of elastic recoil and alveolar collapse (Brandsma et al., 2020). Additionally, oxidants found in cigarette smoke and reactive oxygen species produced by activated neutrophils and macrophages leading to the depletion of local antioxidants such as glutathione and superoxide dismutase with subsequent oxidative damage. Ultimately, the destruction of the air sacs results leading to airflow obstruction. Since these changes are incompletely reversible, COPD results (Brandsma et al., 2020).
Barter, P., & Genest, J. (2019). HDL and ASCVD risk stratification – A debate. Atherosclerosis, 283, 7–12. https://doi.org/10.1016/j.atherosclerosis.2019.01.001
Brandsma, C.-A., Van den Berge, M., Hackett, T.-L., Brusselle, G., & Timens, W. (2020). Recent advances in chronic obstructive pulmonary disease pathogenesis: from disease mechanisms to precision medicine. The Journal of Pathology, 250(5), 624–635. https://doi.org/10.1002/path.5364
Jebari-Benslaiman, S., Galicia-García, U., Larrea-Sebal, A., Olaetxea, J. R., Alloza, I., Vandenbroeck, K., Benito-Vicente, A., & Martín, C. (2022). Pathophysiology of atherosclerosis. International Journal of Molecular Sciences, 23(6), 3346. https://doi.org/10.3390/ijms23063346
McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby.
Zhang, W., Huai, Y., Wang, W., Xue, K., Chen, L., Chen, C., & Qian, A. (2019). A Retrospective cohort study on the risk factors of deep vein thrombosis (DVT) for patients with a traumatic fracture at Honghui Hospital. BMJ Open, 9(3), e024247. https://doi.org/10.1136/bmjopen-2018-024247
Â· In this exercise, you will complete essay-type questions in Knowledge Check to gauge your understanding of this moduleâ€™s content.
Â· Like the discussion question assigned, there are some points to make substantively, do need to cite in KC at least one primary current reference. but each answer is worth 20 points. I would expect about 1 paragraph per answer (a paragraph would include 6-10 sentences).