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.

 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 stu