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

Question

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.

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?

Answer 1

When travelling by plane, particularly for long periods, the individual is relatively immobile. Stasis leads to an accumulation of activated clotting factors and platelets. Immobility also decreases chemical interactions with coagulation inhibitors. The end result is an increased risk for thrombus formation. In Leona's situation, her weight and smoking habit were additional risk factors for the condition.

Atherosclerosis disturbs the flow of blood and damages vessel endothelium causing an increase in platelet adherence. There is also an increased sensitivity by platelets to factors that cause adhesiveness and aggregation.
Adhering platelets release growth factors that enhance smooth muscle proliferation in the vessel wall. Consequently, platelet aggregation is able to contribute to the development and progression of atherosclerosis.

Both conditions increase coagulability. Atherosclerosis increases platelet function by encouraging aggregation and adherence. Immobility, in contrast, contributes to hypercoagulability by increasing procoagulation factors.

Heparin effectively encourages the inactivation of clotting factors, thereby inhibiting fibrin formation. Heparin cannot be absorbed through the gastrointestinal system and can only be administered by injection or IV infusion.