Disorders of Hemostasis. Essay Example

Q1: Explain using your knowledge of hypercoagulability why the trip to Australia contributed to Leona’s DVT. Why was Leona already at risk for thrombus development?

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The trip to Australia led to the development of thrombosis in Leona, who is already suffering from overweight and atherosclerosis. Atherosclerosis is a condition where plaque-like cholesterol, calcium, and other substances accumulate in blood vessels like the arteries. Since arteries carry blood used to move oxygen in the blood from the heart to the other body parts, it makes it difficult for the arteries to transport the oxygen to the body parts. On the other hand, hypercoagulation is a condition developed when there is a clot of blood formed in the blood vessels; hence the situation may increase blood clotting in the arteries. The problem can either be inherited or acquired. The cause of acquired hypercoagulation is an individual having cancer, obesity, surgery, immobility, recent trauma, pregnancy, and other more.

Therefore, it means that since Leona was overweight and had to travel for many hours, the travel time contributed to the development of thrombosis in her deep vein. Her obesity condition and immobility for a long time during the Australian flight contributed to the start of acquired hypercoagulation. The condition will lead to blood clots in the vein (venous thrombosis) and happens in a vein found deep in the leg muscles of the calf and the thigh. Due to Leona smoking cigarettes, she was in danger of developing a thrombus because smoking cigarettes has been connected with starting and exacerbating atherosclerotic. The long time used to travel without stretching, and obesity increased the danger of contracting thrombosis. The risk factors of thrombosis include; inactivity, family history of blood clots, obesity, and either heart, cancer, or previous venous thromboembolism, therefore, leaving Leona at danger of developing thrombosis (Andersson et al., 2018).

Q2: How does Leona’s atherosclerosis affect platelet function? Conversely, what is the effect of increased platelet activity on the development of atherosclerosis?

The blood cells processed in the bone marrow from the megakaryocytic cytoplasm are known as the platelets. The cells play a crucial part in the hemostatic process as they circulate in the blood and create the thrombus layer after a person has an endothelial injury. The underlying cause of arterial and coronary artery disease is atherosclerosis due to its process of inflammation, which is described by the piling up of lipids and lymphocytes in the large arteries' intimae. Therefore, bloodborne materials or the deposition lymphocytes and lipids cause the thickening and construction of the arteries walls, restricting the blood flow carrying the platelets whose major purpose is the formation of clots that happens on the body parts are injured. Hence disruption and plaque deposition starts gluing of the platelets, which is a union that is not normal of the membranous due to inflammation or an injury and aggregation on the surface exposed, leading to the initiation of clotting process that can end, causing the atherothrombotic process. Therefore, atherosclerosis affects or limits the platelets' function ability in the process of clotting after inflammation or an endothelial injury (Marx et al., 2019).

Further, the platelets' involvement in thrombus and hemostasis formation is connected to atherosclerotic vascular disease. They take part in conveying of molecules used for regulation in inflammatory reaction and intervention of atherosclerosis progression. Most of the secreted molecules related to platelet moderate the interconnection between the leukocytes and endothelium in the beginning phases of atherosclerosis in the vascular up taking of cholesterol. Free cholesterol creation originates from the endocytosed cholesterol, although they originate from the cell membranes. Some of the dead cells, leucocytes, and activated platelets may discharge free cholesterol, and if it is in big amounts, it may cause plague, thereby narrowing down of the arteries, which reduces the blood flow in the body organs and the body in general (Marx et al., 2019).

Q3: How do atherosclerosis and immobility promote changes in blood coagulation?

Blood coagulation helps the body avoid much blood following an endothelial injury because the body loses much blood, can experience shock, or even the victim can die. Therefore, atherosclerosis and the ability to move can actively act in aiding changes in blood coagulation, which includes protein and cellular elements. The inability to move limits muscles from tightening, which is vital in ensuring blood flow in the veins and mainly in the legs. Prolonged immobility, therefore, may cause blood pooling in the legs and may cause stiffness, discomfort, and lead to the legs swelling and may cause coagulation or blood clot, which is abnormal in the body. Immobility also leads to blood clotting in the body abnormally as it flows in the blood vessels, also recognized as deep vein thrombosis.

Conversely, atherosclerosis that incorporates the bloodborne materials or lymphocytes and deposition lipids gives rise to the thickening and constriction of the arteries walls hence reducing blood flow containing platelets. The major role of platelets is for clotting the body parts with injuries. Essentially, plaque disruption and deposition begin platelet adhesion, which is the membranous union that is not normal caused by an inflammation or injury, and aggregation on the body part exposed; thus, clotting cascade is begun, which causes the atherothrombotic process. Therefore, atherosclerosis affects or reduces the ability of the platelets to function as they perform the clotting duty after inflammation or endothelial injury (Marx et al., 2019)

Q4: When Leona was in hospital. She received heparin therapy. Explain why this course of action was taken to treat her DVT. Why was she not given heparin tablets to take back to the hotel with her?

Heparin is an anticoagulant or thinner of blood that typically avoids blood clots to be formed; hence it is utilized in treating and avoiding blood clots in the veins, lungs, and arteries. The primary purpose of heparin is not mainly thinning blood, but it avoids new blood clots from forming and the ones present spots from growing bigger. It does these by obstruction of the manufacturing of specific proteins required for the process of clotting. Thus, the health care department's heparin injection and therapy was the best thing to assist Leona because the injection has a liquid that is injected deeply under the skin or intravenously administered in the body as a dilute solution. The heparin injection will help Leona better because it moves quickly and fast in the body hence quick recovery. The heparin tablets would use more time to produce anticoagulation because it would take time before they are absorbed in the blood from the stomach; thus, they would not assist Leona hence the best option is the injection since it is direct to the blood. The heparin will help lower the number of clots and avoid any more clot formation by preventing some vital proteins (Dong et al., 2019). Thus, Leona's better option was not the tablets because they would delay the process of recovery and worsen the situation. The hospital took the best course for Leona for quick recovery.

References

Andersson, E. M., Fagerberg, B., Sallsten, G., Borné, Y., Hedblad, B., Engström, G., & Barregard, L. (2018). Partial mediation by cadmium exposure of the association between tobacco smoking and atherosclerotic plaques in the carotid artery. American journal of epidemiology, 187(4), 806-816. Retrieved from https://academic.oup.com/aje/article-abstract/187/4/806/4110405

Dong, Y., Wang, Y., Ma, R. L., Liu, M., Gao, J. Z., Su, W. Y., ... & Sun, J. J. (2019). Efficacy and safety of direct oral anticoagulants versus low-molecular-weight heparin in patients with cancer: a systematic review and meta-analysis. Journal of thrombosis and thrombolysis, 48(3), 400-412. Retrieved from https://link.springer.com/article/10.1007/s11239-019-01871-4

Marx, C., Novotny, J., Salbeck, D., Zellner, K. R., Nicolai, L., Pekayvaz, K., ... & Stocker, T. J. (2019). Eosinophil-platelet interactions promote atherosclerosis and stabilize thrombosis with eosinophil extracellular traps. Blood, The Journal of the American Society of Hematology, 134(21), 1859-1872. Retrieved from https://ashpublications.org/blood/article-abstract/134/21/1859/374963