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.
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.
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.
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