The atherosclerosis effect on platelet function
Leona is 52 years old and smokes. She is also overweight and has atherosclerosis. When she was given a two-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 three 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 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?
The Disorder of Hemostasis
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The Disorder of Hemostasis
The Atherosclerosis Effect on Platelet Function
Hemostasis disorders are typically categorized as either hemorrhagic or thrombotic. Irrespective of the nature and underlying cause, the diagnostic approach to patients with hemostasis disturbances is multifaceted and involves an accurate collection of clinical history taking and physical examination. Hemostasis can be defined as the mechanism leading to the cessation of bleeding from a blood vessel, and it involves multiple interlinked steps (Lippi & Favaloro, 2018). The cascade culminates in the formation of a plug that closes up the damaged site of the blood vessel controlling the bleeding. Primary hemostasis is when one’s body forms a temporary plug to seal an injury. Platelets circulating in one’s blood stick to damaged tissue and activate. The activation means they can recruit more platelets to form a platelet plug to stop blood loss from the damaged area. The clinical signs of primary hemostatic disorders include petechial, prolonged bleeding at injury sites and mucosal hemorrhage (Chang, 2018). Blood clots are frequently treated with medication identified as blood thinners which slows down the ability of our bodies to form clots. Life-threatening clots are sometimes treated with surgical removal or medicines that help dissolve clots. This essay will explore. The purpose of the essay is to describe the development of deep vein thrombosis in Leona, a 52-year-old woman with atherosclerosis, explore factors contributing to Leona’s DVT, look at the effects of atherosclerosis on platelet function, and lastly, look at the use of heparin therapy on the treatment of Leona’s DVT.
Why the Trip to Australia Contributed to Leona’s DVT
A flight from Minnesota to Sydney lasts about 19,5 hours, and when individuals travel by plane, especially during long periods, they remain relatively immobile, which is not the best state for those with CVS diseases. Normal coagulation is essential for the body because it prevents anemia. If a healthy person is injured, platelets in the body stick together to form a clot that prevents excess bleeding in coagulation (Yazdani et al., 2021). When blood clots without the presence of an injury, it can be explained as hypercoagulable, and its incidence is high in people with hereditary disorders or acquired conditions. People are born with hereditary disorders, but hypercoagulable conditions are mainly caused by lifestyle choices such as smoking and extended immobility, leading to an inactive life. Leona’s DVT seems to be an acquired condition as immobilization, also called the economy class syndrome, triggered hypercoagulability. Explained that Leona was a smoker, overweight, and known to have a cardiovascular condition; she was at risk of thrombus development. Such factors cause the hardening of arterial walls, compromising blood circulation and causing the formation of clots.
Leona’s Atherosclerosis Affects Platelet Function
Cardiovascular diseases are the leading cause of mortality worldwide. The hardening of arteries caused by plaque formation on arterial walls leads to blockage of blood flow, and when the formed plague cracks, it causes high platelet activation because of more strained blood flow. During the process of vascular inflammation, specific molecules stored on the granular platelets as well as the surface of platelets, are known to combine with inflammatory cells that develop and advance atherosclerosis (Bakogiannis et al., 2019). Platelets contribute to the progression of atherosclerosis by the deposition of chemokine and the recruitment of leukocytes. Remnant nuclear functions of platelets, such as the ability to translate and modify mRNA promoting inflammation and endothelial polarization. The primary function of platelets in terms of atherosclerosis is leukocyte recruitment through the direct interactions between receptors and ligands. Additionally, it might be augmented through released factors like chemokines. Dendritic cells (DCs) play the role of a specific leukocyte subtype. DC is a classical antigen that presents the cells of individuals’ bodies. Platelets interact with DCs, which function in atherosclerosis development, has recently been emphasized in numerous studies.
Atherosclerosis and Immobility in Promoting Changes in Blood Coagulation
The pay- off of atherosclerosis and immobility is slightly contradictory. Immobility causes increased pro-coagulation and therefore contributes to hypercoagulability. Atherosclerosis can improve platelet function through the encouragement of adherence and aggregation. Atherosclerosis progression assumes the active participation of platelets attached to intact endothelium (Carresi et al., 2021). Additionally, platelets are essential in thrombus formation on atherosclerotic plaque rupture. The thrombegenic substrates’ exposure to circulating platelets challenges the recruitment of the last to the vessel’s injured wall in specific series of events, and they include the arrest of platelets on the exposed sub endothelium, the additional platelet’s recruitment and activation utilizing the local release of primary platelet agonists, and platelet aggregates stabilization. During plaque rupture site, thrombus formation starts with the interaction of platelets with the exposure to blood extracellular matrix components, including non-collagenic adhesion proteins and fibrillary collagen (Bresteau, 2019). The rheological condition significantly influences such kinds of adhesive interactions. In addition, during the formation of a thrombus, platelets eject substances into the blood plasma that cause the development of the whole complex of changes in the vessel wall distinctive for atherosclerosis.
The Use of Heparin Therapy in the Treatment of Leona’s DVT
Heparin is one of the most efficient treatments encouraging the clotting factors inactivation and, hence, fibrin formation inhibiting. The gastrointestinal system never absorbs it, and it is appropriate to administer it only by iv infusion or injection, and at the same time, a certain number of a patient can receive treatment from home (Liu et al., 2022). If Leona’s doctor insisted that she stay at the hospital, it would be evident that she had an extensive blood clot and might have needed more treatment and invasive testing. This medication was likely to involve heparin therapy, the elevation of the affected leg, and wearing compression stockings, and this therapy aims to stop the clot’s growth and prevent the clot’s breaking off in the patient’s vein and the movement in the lungs and minimizes the risk of other blood clot formation. Heparin is a blood thinner and one of the most commonly used anticoagulants in cases of DVT, and it does not break up the existing clot, but it is efficient in preventing it from growing and reducing the risk of developing new blood clots, hence, the doctor might have preferred to keep the patient at the hospital for at least a few initial days of such therapy to ensure no threat to her life.
Conclusion
Hemostasis can be defined as the mechanism leading to the cessation of bleeding from a blood vessel, and it involves multiple interlinked steps the clinical signs of primary hemostatic disorders include petechial, prolonged bleeding at injury sites and mucosal hemorrhage. Leona’s DVT seems to be an acquired condition as immobilization, also called the economy class syndrome, triggered hypercoagulability. The hardening of arteries caused by plaque formation on arterial walls leads to blockage of blood flow, and when the formed plague cracks, it causes high platelet activation because of more strained blood flow. Immobility causes increased pro-coagulation and contributes to hypercoagulability, while atherosclerosis can improve platelet function by encouraging adherence and aggregation. Heparin is one of the most efficient treatments encouraging the clotting factors inactivation and, hence, fibrin formation inhibiting. The gastrointestinal system never absorbs it. It is appropriate to administer it only by iv infusion or injection; at the same time, a certain number of patients can receive treatment from home.
References
Bakogiannis, C., Sachse, M., Stamatelopoulos, K., & Stellos, K. (2019). Platelet-derived chemokines in inflammation and atherosclerosis. Cytokine, 122, 154157. https://doi.org/10.1016/j.cyto.2017.09.013
Bresteau, E. (2019). Adhesive Clathrin Structures Support 3D Haptotaxis Through Local Force Transmission (Doctoral dissertation, Université Paris Saclay (COmUE)).
Carresi, C., Mollace, R., Macrì, R., Scicchitano, M., Bosco, F., Scarano, F., … & Mollace, V. (2021). Oxidative stress triggers defective autophagy in endothelial cells: role in atherothrombosis development. Antioxidants, 10(3), 387. https://doi.org/10.3390/antiox10030387
Chang, J. C. (2018). Hemostasis based on a novel ‘two-path unifying theory’and classification of hemostatic disorders. Blood Coagulation & Fibrinolysis, 29(7), 573-584.
Lippi, G., & Favaloro, E. J. (2018). Hemostasis practice: state-of-the-art. J Lab Precis Med, 3(6), 67. http://dx.doi.org/10.21037/jlpm.2018.07.07
Liu, Y., Han, Q., Li, G., Lin, H., Liu, F., Li, Q., & Deng, G. (2022). Anticoagulation polyvinyl chloride extracorporeal circulation catheters for heparin-free treatment. Journal of Materials Chemistry B, 10(40), 8302-8314. https://doi.org/10.1039/D2TB01584F
Yazdani, A., Deng, Y., Li, H., Javadi, E., Li, Z., Jamali, S., … & Em Karniadakis, G. (2021). Integrating blood cell mechanics, platelet adhesive dynamics and coagulation cascade for modelling thrombus formation in normal and diabetic blood. Journal of the Royal Society Interface, 18(175), 20200834. https://doi.org/10.1098/rsif.2020.0834
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