Deep Vein Thrombosis (DVT)
Instructions:
Leona is 52 years old and smokes. She is also overweight and has atherosclerosis. When she was given a 2-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 3 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.
1. 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?
2. How does Leona’s atherosclerosis affect platelet function? Conversely, what is the effect of increased platelet activity on the development of atherosclerosis?
3. How do atherosclerosis and immobility promote changes in blood coagulation?
4. When Leona was in the 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?
Solution.
Deep Vein Thrombosis (DVT)
Question 1
When a healthy person is injured, platelets in the body stick
together to form a clot that prevents excess bleeding in a process called
coagulation (Smalberg et al, 2011). Normal coagulation is vital for the body
because it prevents anemia. However, when blood clots without the presence of
an injury, it is termed as hypercoagulable and its incidence is high on people
with hereditary disorders or acquired conditions. People are born with
hereditary disorders but acquired hypercoagulable conditions are mainly caused
by lifestyle choices such as smoking, extended immobility and leading an
inactive life. Leona’s DVT was an acquired condition because immobilization
also known as the “economy class syndrome” triggered the hypercoagulability
(Smalberg et al, 2011). Given that Leona was overweight, a smoker and known to
have a cardiovascular condition; she was at risk of thrombus development. All
the three factors cause the hardening of arterial walls hence compromising
blood circulation and causing the formation of clots.
Question 2
Hardening
of the arteries (atherosclerosis) caused by formation of plague on arterial
walls leads to blockage of blood flow. When the plague formed cracks, it causes
high platelet activation because of more strained blood flow (Porth, 2014). On
the other hand, during the process of vascular inflammation, certain 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.
Question 3
Atherosclerosis
promotes blood coagulation by damaging endothelia causing more platelet
adherence in the arteries whereas immobility reduces fibrinolysis needed to
improve blood circulation by dissolving clots (Porth, 2014).
Question 4
Heparin reduces the high activity of platelets in an anticoagulation process. For initial treatment of DVT, heparin therapy through intravenous fusion is the treatment of choice as opposed to heparin tablets. Intravenous heparin is more effective in preventing thrombus growth that may progress to pulmonic embolism, in such a case where the anticoagulant response is unpredictable (Porth, 2014).
References
Porth, C. (2014). Essentials of pathophysiology: Concept of altered states. Philadelphia: Wolters Kluwer.
Smalberg, J. H. Kruip, M., L.A. Janssen, Rijken, D C. Leebeek, W.G. and Moniek P.M. de Maat (2011). Hypercoagulability and Hypo-fibrinolysis and Risk of Deep Vein Thrombosis and Splanchnic Vein Thrombosis Arteriosclerosis, Thrombosis, and Vascular Biology 31, 485-493
