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Case Study 7 Disorders of Hemostasis
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?
Running Head: DEEP VEIN THROMBOSIS 1
DEEP VEIN THROMBOSIS 6
PATHOPHYSIOLOGY CASE STUDY
Leona was overweight and she was suffering from atherosclerosis even before she travelled. Her trip to Australia led to the developments of thrombosis. Atherosclerosis refers to the condition where cholesterol, calcium and fats (also referred to as plaque) build inside the arteries (Badimon, et.al, 2012). Arteries are the vessels in the body that transport oxygenated blood from the heart to the other parts of the body. Therefore constriction of the blood vessels that arises from plaque deposit limits the transportation and flow of oxygenated blood in the body. Hyper-coagulation is an acquired or inherited condition and in most cases arises due to cancer, pregnancy, trauma, obesity, prolonged rest or immobility. Given that Leona was overweight, the prolonged immobility over the course of her flight played a role in the development of deep vein thrombosis. Leona had acquired hyper-coagulation because she was overweight, and coupled with the long flight, clots developed in her leg (Rissanen, 2014). These two conditions resulted in the formation of blood clots in the vein (venous thrombosis) that occur in the deep vein which runs from the thigh muscles to the calf of the leg. Leona was a cigarette smoker and this exposed her to a high risk of thrombus development as it initiates the exacerbation of the process of atherosclerosis (Diana, 2013). Being overweight, a smoker and immobile increased the possibility of development of deep vein thrombosis. Other factors that exposed Leona to the development of DVT include inactivity and previous venous thromboembolism.
Platelets are cells that are found in the blood and their origination is the megakaryocytic cytoplasm which is located in the bone marrow. The cells circulate in the body as the blood moves playing a homeostatic role and also assisting in the formation of the thrombus layer following an endothelial injury (Badimon, et.al, 2012). Arterial diseases and coronary diseases are often as a result of atherosclerosis. Lymphocytes and lipids accumulate in the large arteries leading to inflammation. This lymphocyte and lipids deposition leads to the thickening of the arterial walls and the constrictions of the arteries. This limits the movement of platelets (in the blood) whose main role is to aid n clotting of blood when one is injured. The deposition of plaque and disruption of the flow of platelets causes the platelets to “stick” to each other through membranous union upon injury. This activation of the clotting cascade causes atherothrombosis, Atherosclerosis therefore limits the platelet functionality with regards to blood clotting after injury or after an endothelial lining (Davis, 2015). The platelets are not only involved in homeostatic functions and formation of thrombus but they are also involved in transporting regulatory molecules when an inflammation occurs in mediation of the progress of atherosclerosis.
When an individual is travelling on a plane for long periods, they are relatively immobile. Stasis causes platelets and activated clotting factors to accumulate. Immobility also leads to a decrease in the chemical interactions with the inhibitors of coagulation. Ultimately this increases the risk of formation of thrombus, In Leona’s case, her weight and habit of smoking were increased risk factors for thrombus formation. Atherosclerosis disrupts blood flow and it also damages the endothelium thereby increasing the adherence of the platelets (Rissanen, 2014). The platelets are also increasingly sensitive to factors that lead to aggregation and adhesiveness. The adhering platelets lodge growth factors that enhance the proliferation of the smooth muscles in the wall of the arteries. As a result, the aggregation of the platelets contribute to the formation and progression of atherosclerosis. These two conditions increase the possibility of cogulability. Atherosclerosis causes an increase in the functions of the platelets through adherence and aggregation. In contrast, immobility causes hypercoagulability as it causes a spike in the procoagulation factors. Blood clots form after the crack of the fibrous cap in the atherosclerotic plaque thereby reducing the amount of blood that is flowing through that specific blood vessel.
Clots can dislodge and travel from their point of formation. This may lead to a reduction of blood flow in organs such as the lungs, heart and brain. A blood clot that has dislodged is referred to as an embolus. Approximately 80% of heart attacks occur as a result of the formation of an undesirable clot that blocks the flow of blood in arteries that supply the heart with blood. Immobility of the limbs also raises the possibility of clot occurrence because it slows down the process of blood circulation thereby increasing the likelihood of pooling (Badimon, et.al, 2012). When a pool of blood is static, this is an ideal environment for the formation of a clot. According to reports obtained from the World Health Organization, the risks of developing deep vein thrombosis double when one travels in a plane. However, the risk of DVT formation is still very minimal considering that only one 1 in 6,000 people can develop DVT from remaining completely immobile during a flight.
Heparin is an anti-coagulant drug that prevents formation of blood clots. It is also referred to as a blood thinner as it serves the purpose of thinning blood to ensure that it flows more easily through constricted vessels. It is used to prevent formation and treat blood clots that have lodged in the lungs, veins or in the arteries. Heparin also prevents the formation of new clots and it also limits the already formed clots from enlarging. It is able to do this by inhibiting the production of proteins that have to be formed in order for the clot to be formed (Ziegelstein, 2016). In the absence of these proteins, blood clots cannot be formed. Heparin injections or therapy that are administered by a health institution are the right way to contain Leona’s condition. The injection delivers an intravenous solution deep into the veins. The intravenous injection gets straight to the veins and therefore it will aid Leona in felling batter much faster. Tablets would have also delayed the anticoagulation process in Leona’s case. However, if the therapist chose to use Heparin tablets, which would have been administered orally, it would have taken a longer time for the drug to be absorbed into the blood system. Since the Heparin injection is administered in liquid form, it is easy for it to get absorbed into the blood and it is also easier for it to flow through the entire body. The effects of the Heparin would therefore be felt all over the body thereby reducing the size of the already formed clots and preventing the formation of other clots. The tablets would not be the best option to contain Leona’s situation as it would only derail the recovery process. Leona’s condition had escalated from bad to worse and it therefore needed to be contain as fast as possible.
Badimon, L., Padró, T., & Vilahur, G. (2012). Atherosclerosis, platelets and thrombosis in acute ischaemic heart disease. European Heart Journal , 60-74.
Diana, J. N. (2013). Tobacco Smoking and Atherosclerosis: Pathogenesis and Cellular Mechanisms.
Rissanen, P., et al,(2014). Weight change and blood coagulability and fibrinolysis in healthy obese women. Int J Obes Relat Metab Disord, 25(2):212-218,
Davis, J.W., et al,(2015) Effects of tobacco and non-tobacco cigarette smoking on endothelium and platelets. Clinical Pharmacological Therapy, 37(5):529-533
Ziegelstein, R.C., et al, (2016). Platelet function in patients with major depression. Intern Med J, 39(1):38-43
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