Blood Cells and the Hematopoietic System
Leona is 52-years old and smokes. She is also overweight and has atherosclerosis. When she was given a 2-week vacation from work, she packed up her bags and flew from Minnesota to Sydney, Australia, for the trip she always wanted to take. Unfortunately, just 3 days after she arrived, she was hospitalized when her left calf became inflamed, causing her considerable pain. The physician attending to her told her she developed a deep vein thrombosis.
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?
How does Leona’s atherosclerosis affect platelet function? Conversely, what is the effect of increased platelet activity on the development of atherosclerosis?
How do atherosclerosis and immobility promote changes in blood coagulation?
When Leona was in the 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?
How the Trip to Australia Contributed to Leona’s DVT and Why She Already at Risk for Thrombus Development?
Hypercoagulability increases the tendency for the blood to thrombose. Venous thromboembolism (VTE) manifests as deep venous thrombosis (DVT). VTE’s pathophysiological mechanism can be described using Virchow’s triad of vascular endothelial lesions, venous stasis, and hypercoagulability. The trip to Australia contributed to the development of DVT for Leona due to reduced mobility and pressurization of the cabin. Prolonged sitting of about 4 to 6 hours without movement of the calf muscles promotes venous stasis leading to accumulation of platelets and other activated clotting factors. Statis also causes reduced chemical interactions between the coagulation inhibitors, increasing the formation of a thrombus (Cazaubon, 2015). Air travel is linked to a hypoxic environment due to decreased cabin pressure. The environment is associated with decreased oxygen partial pressure leading to saturation. The altitude provokes hypobaric hypoxia, a risk factor for sustaining endothelial injury (Onida & Davies, 2020). Leona was already at risk of developing thrombus since she is overweight and she smokes. Smoking leads to increased fibrin formation, which is a source of hypercoagulability (Al-Nasser, 2020). Atherosclerosis also puts Leona at risk of developing DVT. Atherosclerosis is a condition characterized by narrowing and hardening of the arteries due to arteries being clogged with fatty substances known as plaque. It results in restricted blood flow, increasing the risk of the formation of blood clots. Hypercoagulability and statis with no endothelial injury results in VTE.
How Atherosclerosis Affect Platelet Function and Effects of Increased Platelet Activity on the Development of Atherosclerosis
Atherosclerosis increases platelet adherence by interfering with blood flow and damaging the endothelium vessel. Platelets do not activate or adhere to non-activated endothelium. Early stages of atherosclerosis are characterized by inflammations that lead to activation of the endothelium layer, stimulating the attachment of the platelets. Platelets also become more sensitive to factors that promote aggregation and adhesiveness. The increased platelet activity increases the release of mediators that are retained within the granules. The mediators stimulate cell adhesion, coagulation and proteolysis, synthesis of chemokines, proliferation and survival, and proinflammatory cytokines, enhancing the inflammatory process that promotes plaque development. A significant number of secretory molecules related to platelet mediates the interaction between the endothelium and leukocytes in the early stages of arteriosclerosis. They also contribute to atherosclerosis by mediating the uptake of cholesterol to the vascular wall (Nording, Baron, & Langer, 2020).
How Atherosclerosis and Immobility Promote Changes in Blood Coagulation
Both atherosclerosis and immobility increase coagulability. Atherosclerosis increases coagulation by increasing platelet functions through adherence and aggregation. Early stages of atherosclerosis are characterized by inflammations that activate the endothelium resulting in the adhesion of the platelets, and they are aggregated to the site leading to the formation of a platelet plug (LaPelusa & Dave, 2019). Atherosclerosis is also characterized by the formation of a plague that becomes brittle or inflamed, resulting in rupturing that triggers the formation of a clot. Constriction and relaxation of muscles that take place when walking facilitate compression of the deep veins that pump the blood upwards. The vein has valves that prevent blood from flowing back. Immobility increases the risk of clot formation by slowing blood circulation, increasing the risk of a blood pool. The formation of a static pool of blood creates an ideal environment for blood clotting. Mobility also increases the release of the blood clot dissolver, known as tissue-type plasminogen activator. Mobility can facilitate the dissolving of blood clots.
Why Leona was Given Heparin Therapy and Why She was not Given Heparin Tablets to take back to the Hotel with her
Heparin is a blood thinner used in preventing and treating blood clots, including venous thrombosis. Heparin belongs to a class category of drugs known as anticoagulants. The drug works by disrupting blood clot formation in the veins. It prevents clot formation and prevents enlargement of the already formed clots. The drug is available in two forms, including an injectable solution injected under the skin while the other solution is injected intravenously and can only be conducted by the doctor at the hospital. Heparin disrupts clot formation by binding to antithrombin leading to an aggressive change that results in the inactivation of thrombin, factor Xa and other involved clotting factors. It suppresses the formation of fibrin and inactivation of clotting factors (Streiff, Agnelli, Connors, Crowther, Eichinger, Lopes, & Ansell, 2016). Leona was not given heparin tablets to take back to the hotel. They cannot be absorbed from the gastrointestinal system. Patients are usually issued with oral warfarin treatment by the time they are discharged from the hospital. There has been a forthcoming thrombin inhibitor known as ximelagatran intended to replace warfarin, and although the studies conducted were promising, there are still concerns about hepatotoxicity when the drug is used for an extended period. The current use of warfarin also has serious drawbacks that involve food-drug and drug-drug interactions resulting in a narrow therapeutic index. Frequent monitoring of patients is required, which is inconvenient for patients that take the drug chronically.