Her risk factors for VTE are her 72 years of age, diagnose of cholangiocarcinoma, her recent post proximal bile duct open laparotomy, extended right hepatectomy with portal vein resection and reconstruction, radical bile duct resection, hepaticojejunostomy and cholecystectomy surgery, gemcitabine therapy, pain and leg swelling x 2 weeks, 15-pound weight gain, difficulty with breathing, feeling weak, debilitated and multiple falls; also her previous history of thrombosis. Her history of 3+ pitting edema in the bilateral lower extremities and her recent abdominal ultrasound revealing occlusive portal vein thrombosis also is a risk factor for Mrs. X’s VTE.
2. What are …show more content…
the age-dependent physiologic changes which occur in the coagulation cascade that make a geriatric patient more prone to develop a venous thromboembolism (VTE)?
Some of the age-dependent physiological changes which can occur in the coagulation cascade that makes geriatric patient more prone to develop a venous thromboembolism could be the fact that elderly patients have more comobidities, multiple drugs and the slow metabolization of the drugs that they are on. (Robert & Reghini, 2010)
3. What is protein S? What is the function of Protein S and how is it altered during inflammatory states? What does this mean for the risk of thrombosis?
Protein S is considered a protein that inhibits coagulation and compels vitamin K for its production and works in conjunction with Protein C. Protein S function is to inhibit the actions of factor V and Factor VIII, which are also clotting proteins. During inflammatory states, a protein S plasma concentration increases. Increase protein S increases the risk of thrombosis. (Wypasek & Undas 2013).
4. Traditional treatment of a venous thromboembolism is heparin or enoxaparin and warfarin initiated at the same time. Why is therapy overlapped? Hint- the complete answer is not solely related to the immediate anticoagulant effects achieved using of heparin or enoxaparin.
Treatment therapy of heparin or enoxaparin and warfarin is overlapped to prevent the risk of thrombotic events which can occur when starting warfarin and this is triggered by too much factor II that anticoagulant may not be able to resist.
Overlapping heparin or enoxaparin therapy is especially important in patients who have a much more risk factor to thrombotic events such as patient with protein C or S deficiency and also patient who metabolizes Coumadin more rapidly than the average person. (Heit et. al. 2011)
5. What are the indications which would trigger the need to evaluate a person for the presence of a hereditary thrombophilia?
A person presenting with DVT or pulmonary embolism, family history of thrombophilia are some of the indication that would trigger the need to evaluate for the presence of hereditary thrombophilia. (Schwartz & Rote, 2014)
Does Mrs. X need to be further evaluated for a hereditary thrombophilia? Why or why not?
Mrs. X definitely needs to be further evaluated for thrombophilia because she has a family history of cancer which she currently has; she has a history of thrombocytopenia and iron deficiency …show more content…
anemia.
6.
Why does she have ascites and splenomegaly?
Mrs. X Ascites and splenomegaly are from the worsening cholangiocarcinoma and her recent surgical history. Mrs. X may need to be reevaluated for hepatocarcinoma given that her brother died from this at the age of
60.
7. What two things are likely causing Mrs. X’s thrombocytopenia?
Two things that are likely causing Mrs. X’s thrombocytopenia are her chemotherapy treatment of gemcitabine therapy, her recent surgery for proximal bile duct open laparotomy, extended right hepatectomy with portal vein resection and reconstruction, radical bile duct resection, hepaticojejunostomy and cholecystectomy; another likely cause could be the splenomegaly. (Schwartz & Rote, 2014)
8. What is causing her leukopenia?
Mrs. X’s leukopenia could be caused by her chemotherapy drug gemcitabine. (Schwartz & Rote, 2014)