Case Study 1: Disorders of Hemostasis

The chosen case study deals with disorders of hemostasis and it involves Leona, a 52-year-old who developed deep venous thrombosis after a long flight. The patient flew from Minnesota to Sydney and after three days she was hospitalized with an inflamed left calf. DVT is a disorder that results from the coagulation of blood in veins, especially in the thighs, pelvis, and lower leg (Kruger et al., 2019). The disorder can trigger disability and cause serious complications if left untreated.

DVT can be caused by several factors including smoking, long periods of immobility, atherosclerosis, and certain chronic diseases. This discussion focuses on the reasons why Leona was at risk for DVT, the mechanisms of thrombus formation, and why specific treatment approaches were used to manage her condition.

Leona’s Trip and the Risk for Thrombus Development

Leona’s trip to Australia contributed to the development of DVT because of prolonged immobility. Immobility is known to cause reduced blood flow to the legs and stasis which then causes blood clot formation (Chang, 2022). Venous stasis is associated with pooling of blood in the lower legs and this increases the risk for clot formation. Hypercoagulability is a state where blood has an increased tendency to clot as influenced by various factors. For instance, blood stasis causes the accumulation of clotting factors and platelets preventing their reaction with inhibitors.

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Leona was already at risk for thrombus formation because of various modifiable risk factors. The first reason for her increased risk was that she is a smoker which affects blood flow. Smoking tobacco is observed to cause hemoglobin binding and this reduces red blood cell flow leading to the thickening of blood (Kruger et al., 2019). In addition, smoking increases blood viscosity and induces a hypercoagulable state by altering the balance of coagulation factors. The second reason for the increased risk of thrombus formation is atherosclerosis.

This condition involves the buildup of plaques in the arteries, which can lead to reduced blood flow and contribute to hypercoagulability (Kruger et al., 2019). It also indicates an underlying endothelial dysfunction, which can predispose to clot formation. Leona is also an obese individual which contributes to thrombus formation due to increased pressure in the legs. Increased pressure in the legs causes reduced blood flow and chronic inflammation associated with this condition is a risk factor for hypercoagulability.

Atherosclerosis and Increased Platelet Activity

The effect of atherosclerosis on platelet function can be observed when plaques form within the walls of blood vessels. The build-up of plaques causes damage to endothelial walls leading to activation of platelets. During this process, there is the release of chemicals like thromboxane A2 and ADP that further enhance platelet aggregation (Chang, 2022). Atherosclerosis causes damage to the endothelia walls which exposes collagen and crucial clotting factors like Von Willebrand factor. These factors allow or promote the adhesion of platelets to the damaged walls.

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Increased aggregation of platelets is another mechanism through which atherosclerosis affects platelet activity (Chang, 2022). Platelet aggregation occurs with the release of intraplatelet materials that impede the flow of blood. There is also a mechanism that involves high-density lipoproteins which activates platelet activity. Lastly, atherosclerosis is observed to increase oxidative stress within the blood vessels and oxidized low-density lipoproteins can cause enhanced platelet adhesion and aggregation.

Increased platelet activity can contribute to atherosclerosis through mechanisms that involve endothelial inflammation. For instance, increased inflammatory responses within the arterial walls attract chemokines and cytokines that impair endothelial functioning. Activated platelets upon endothelial injury promote the release of inflammatory mediators like platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-β) which promote inflammation and progression of atherosclerosis (Stark & Massberg, 2021).

Another mechanism will involve the proliferation and migration of smooth muscle cells upon activation of platelets. The vascular smooth muscle cells migrate to the intima of the artery contributing to plaque growth and thickening of the arterial walls. Lastly, platelet activation can lead to the formation of aggregates with leukocytes, particularly monocytes (Stark & Massberg, 2021). These aggregates adhere to the endothelium and transmigrate into the arterial wall, contributing to the formation and progression of atherosclerotic lesions.

Atherosclerosis and Immobility

Atherosclerosis contributes to changes in blood coagulation through several mechanisms. The first mechanism involves endothelial dysfunction following injury. The endothelium normally has anticoagulant properties. In atherosclerosis, the endothelium becomes damaged and loses its anticoagulant function, leading to increased thrombogenicity. Exposed subendothelial collagen and tissue factor (TF) promote platelet adhesion and activation, initiating the coagulation cascade (Chang, 2022). For example, atherosclerosis activates platelets which cause conformation changes in glycoprotein IIIa which enhances thrombocyte aggregation.

Another mechanism is through inflammation as a result of atherosclerosis. Inflammatory cytokines like interleukin-6 (IL-6) stimulate the liver to produce more coagulation factors, such as fibrinogen, and decrease the production of natural anticoagulants, such as protein C and antithrombin (Stark & Massberg, 2021). The rupture of atherosclerotic plaque can also cause changes in blood coagulation by exposing highly thrombogenic materials like collagen, tissue factor, and lipid-rich substances.

Immobility causes changes in blood coagulation through mechanisms like venous stasis and reduced fibrinolysis (Chang, 2022). Lack of movement reduces the muscle contractions that normally help propel blood through the veins, leading to venous stasis. Stagnant blood flow increases the risk of clot formation as it facilitates the interaction of clotting factors and platelets. Venous stasis can lead to localized hypoxia which causes damage at the cellular level. Inflammatory responses triggered by this damage activate the coagulation cascade leading to changes in blood coagulation (Stark & Massberg, 2021).

Immobility can also impair the fibrinolytic system which is responsible for breaking down clots. Impaired clot breakdown can further lead to inflammation, thrombus persistence, and growth. There is also a combined effect of immobility and atherosclerosis which enhances platelet activation and aggregation. Immobility makes the activated platelets interact more freely with coagulation factors in stagnant blood, promoting clot formation.

Heparin Therapy

Heparin therapy was used to treat Leona’s DVT because it is the standard therapy (Ortel et al., 2020). This drug is indicated for the management of conditions like DVT, pulmonary embolism, and events like atria fibrillation. The drug works by binding to antithrombin which causes surface changes that inactivate thrombin. The binding to antithrombin blocks several different factors of the clotting cascade, but two are predominant: thrombin (Factor IIa) and Factor Xa (Ortel et al., 2020). This mechanism leads to the prevention of clot formation and prolonging the clotting time of blood. Heparin was also administered to ensure that complications like pulmonary embolism could be prevented.

Leona was not given heparin tablets to take back to the hotel with her because heparin does not exist in tablet form. Heparin is not available in tablet form because of issues with bioavailability and monitoring. For instance, the drug is a negatively charged molecule that is poorly absorbed through the gastrointestinal tract (Ortel et al., 2020). Oral administration would not provide the therapeutic levels needed for anticoagulation. The initial phase of DVT management requires monitoring that can only be done in a hospital setup.

References

Chang, J. C. (2022). Pathogenesis of two faces of DVT: New identity of venous thromboembolism as combined micro-macrothrombosis via unifying mechanism based on “Two-Path Unifying Theory” of hemostasis and “Two-Activation Theory of the Endothelium”. Life, 12(2), 220.

https://doi.org/10.3390/life12020220

Kruger, P. C., Eikelboom, J. W., Douketis, J. D., & Hankey, G. J. (2019). Deep vein thrombosis: Update on diagnosis and management. Medical Journal of Australia, 210(11), 516-524. https://doi.org/10.5694/mja2.50201

Ortel, T. L., Neumann, I., Ageno, W., Beyth, R., Clark, N. P., Cuker, A., … & Zhang, Y. (2020). American Society of Hematology 2020 guidelines for management of venous thromboembolism: Treatment of deep vein thrombosis and pulmonary embolism. Blood Advances, 4(19), 4693-4738.

https://doi.org/10.1182/bloodadvances.2020001830

Stark, K., & Massberg, S. (2021). Interplay between inflammation and thrombosis in cardiovascular pathology. Nature Reviews Cardiology, 18(9), 666-682. https://doi.org/10.1038/s41569-021-00552-1