Chapter 19 Hemostasis
Coagulation
1. What is the mechanism of coagulation?
2. What activates platelets to form the initial platelet plug at the site of vascular injury?
3. What is the role of activated platelets in the formation of a blood clot?
4. Where is tissue factor located? What is its role in coagulation at the site of vascular injury?
5. What physiologic event leads to the secretion of tissue plasminogen activator and eventually fibrinolysis?
6. How is fibrinolysis affected normally by surgery or massive trauma?
7. What is the potential clinical effect of systemic fibrinolysis? What can be used for the treatment of systemic fibrinolysis?
Common laboratory tests of hemostasis
8. Name some laboratory tests of platelet function.
9. How can a difficult blood draw result in an artificially low platelet count number?
10. Which test of platelet function is the single best predictor of functional platelet disorders?
11. How is a bleeding time test of platelet function performed?
12. What is a normal bleeding time?
13. What are some limitations of the bleeding time test of platelet function?
14. What function of platelets is evaluated by the platelet function analysis test?
15. What are some common causes of platelet dysfunction that can be detected by the platelet function analysis test?
16. What are platelet aggregation studies of platelet function?
17. What are a benefit and a drawback of platelet aggregation studies over other platelet function tests?
18. Name some laboratory tests of coagulation.
19. Low levels of which factors will result in a prolonged prothrombin time?
20. What is the international normalized ratio (INR)? What is it useful for?
21. Low levels of which factors will result in a prolonged partial thromboplastin time?
22. What drug therapy can be monitored by the partial thromboplastin time?
23. A low level of which factor will result in a prolonged prothrombin time and a normal partial thromboplastin time?
24. What is evaluated by the thrombin time test?
25. What is the relationship between the results of the thrombin time test and the results of the prothrombin time and partial thromboplastin time tests?
26. What is tested by the activated clotting time (ACT)? What is its clinical use?
27. What elements of blood clot formation, consolidation, and lysis are measured by thromboelastography?
28. Name some laboratory tests of fibrinolysis.
29. What is suggested by elevated levels of fibrinopeptide or fibrin monomer?
30. What is suggested by elevated levels of fibrin degradation products?
Disorders associated with altered hemostasis during surgery
32. In general, what laboratory values of platelet counts are associated with uncontrolled intraoperative bleeding?
33. In general, what percent of coagulation factors must be present to prevent uncontrolled intraoperative bleeding?
34. Name some diseases associated with an increased incidence of bleeding during surgery.
35. Name some diseases or conditions associated with an increased incidence of thrombosis during surgery.
36. Name some diseases that are associated with initiating disseminated intravascular coagulation during surgery.
37. What are some hereditary coagulation and platelet disorders? Which of these is the most common?
38. How are hereditary coagulation disorders treated?
39. Where is von Willebrand factor stored?
40. Name three important hemostatic functions of von Willebrand factor.
41. How does von Willebrand disease inhibit the formation of fibrin?
42. What are the clinical effects of von Willebrand disease?
43. How can von Willebrand disease be distinguished from factor VIII deficiency?
44. How many types of von Willebrand disease are there? What are they and how are they inherited?
45. What is the anesthetic management of a patient with von Willebrand disease when undergoing a surgical procedure?
46. What disease or condition is a contraindication to the administration of desmopressin acetate tablets (DDAVP)?
47. What are alternative perioperative treatment options of patients with von Willebrand disease if DDAVP is not available?
48. How does vitamin K support coagulation?
49. Which coagulation factors are vitamin K dependent?
50. How could a patient become vitamin K deficient without fasting?
51. Which coagulation factor is not synthesized in the liver? Where, instead, is this factor made?
52. Name three reasons for the increased risk of bleeding caused by severe liver disease.
53. What diseases or conditions are associated with acquired antibodies to coagulation factor VIII? What is the clinical relevance of this?
54. What are some causes of peripheral platelet destruction?
55. What are some causes of thrombocytopenia that can occur during pregnancy?
56. What percent of platelets are normally sequestered in the spleen? What happens during pathologic splenic sequestration of platelets?
57. Name some causes of an impaired quality of platelet function despite the adequate number of circulating platelets.
58. What are some intraoperative conditions that may facilitate bleeding?
59. At what body temperature can hypothermia begin to contribute to intraoperative bleeding?
Disorders favoring thrombosis
61. What are some inherited factor deficiencies that can lead to a hypercoagulable state?
63. What is antiphospholipid syndrome?
64. What percent of patients with systemic lupus erythematosus have circulating lupus anticoagulant? What is the clinical implication of this?
65. What laboratory analysis values for partial thromboplastin time and prothrombin time are associated with lupus anticoagulant?
66. What is the classic set of circumstances, sometimes referred to as Virchow triad, that predisposes patients to perioperative thrombosis?
67. What is disseminated intravascular coagulation (DIC)?
68. What coagulation test results would you expect in a patient with DIC?
69. Which conditions have similar laboratory findings as those of DIC? Which lab finding might help distinguish between DIC and these conditions?
Anticoagulants, thrombolytics, and antiplatelet drugs
71. What are some common clinical complications associated with perioperative thrombosis?
72. What categories of drugs are available to prevent and treat perioperative thrombotic complications?
73. What are some clinically used anticoagulants?
74. What is the mechanism of action of warfarin (Coumadin)?
75. Which of the coagulation factors has the shortest half-life? Why is knowledge of this factor’s plasma half-life important for warfarin therapy?
76. Why is it necessary to coadminister heparin in the early phases of warfarin treatment?
77. What laboratory test monitors warfarin therapy? Why is it necessary to monitor warfarin therapy and not therapy with oral direct thrombin inhibitors?
78. What are some advantages of unfractionated heparin therapy over low-molecular-weight heparin (LMWH) or pentasaccharide (fondaparinux) drugs?
79. Why does unfractionated heparin therapy need to be closely monitored?
80. Why is it necessary to monitor unfractionated heparin therapy and not therapy with LMWH or pentasaccharide drugs?
81. What laboratory test is used to monitor unfractionated heparin therapy?
82. What are some procedures in which heparin is administered to prevent blood clotting? What laboratory test value is the usual end point for heparin therapy in these procedures?
83. How is heparin anticoagulation during surgery reversed? What is the dose? What is its mechanism of action?
84. What are some potential negative effects of the administration of protamine to reverse the anticoagulation effects of heparin?
85. What are some potential disadvantages and/or side effects of the administration of heparin?
86. What is heparin-induced thrombocytopenia? How many types are there?
87. How is the diagnosis of heparin-induced thrombocytopenia (HIT) type 2 made? What is its incidence among patients who receive heparin therapy? What is the mortality rate of patients with HIT type 2?
88. What is the incidence of HIT type 2 among patients who receive heparin therapy? What is the mortality rate of patients with HIT type 2?
89. What is the management of heparin-induced thrombocytopenia once the diagnosis is made?
90. What is heparin resistance and what causes it?
91. How is heparin resistance treated?
92. How does heparin differ from both LMWH and pentasaccharide drugs regarding its effect on thrombin?
93. What is the mechanism of action of LMWH and pentasaccharide drugs for anticoagulation?
94. What are some advantages and disadvantages of LMWH and pentasaccharide drugs over heparin for anticoagulation therapy?
95. What are some direct thrombin inhibitor drugs that are in current clinical use?
96. What are the drawbacks of direct thrombin inhibitor drugs for intraoperative anticoagulation?
97. A patient with a recent history of HIT type 2 is scheduled for a semielective coronary artery bypass graft surgery. If the risk of bleeding associated with intraoperative direct thrombin inhibitor therapy is considered excessive, what other management options exist to meet the need for systemic anticoagulation for cardiopulmonary bypass?
98. What are some thrombolytic drugs currently used in clinical practice?
99. What is the mechanism of action of thrombolytic drugs?
100. How long is surgery contraindicated after thrombolytic therapy?
101. What are some classes of antiplatelet drugs currently used in clinical practice? What are some examples of drugs in each of these classes?
102. How is platelet function affected by aspirin, nonsteroidal antiinflammatory drugs, and COX-2 inhibitors?
103. How is platelet function affected by thienopyridine derivatives?
104. What is the duration of the effects of the thienopyridine derivatives clopidogrel and ticlopidine on platelets after their discontinuation?
105. How is platelet function affected by GPIIb/IIIa antagonists?
106. What is the duration of the effects of GPIIb/IIIa drugs after their discontinuation?
An approach to patients who are anticoagulated
107. When a patient on warfarin presents for surgery, what are the conflicting risks?
108. Which surgeries are generally associated with high risks of perioperative thrombosis?
109. Which baseline medical conditions place patients on chronic warfarin therapy at a high risk of perioperative thrombosis regardless of the type of surgery?
110. Which baseline medical conditions place patients on chronic warfarin therapy at an intermediate risk of perioperative thrombosis regardless of the type of surgery?
111. Which baseline medical conditions place patients on chronic warfarin therapy at a low risk of perioperative thrombosis regardless of the type of surgery?
112. Why is it important to stratify the risk of perioperative thrombosis for patients on chronic warfarin therapy?
113. In what way does the management of patients on chronic warfarin therapy at high risk for perioperative thrombosis differ from those at intermediate or low risk?
114. In a patient receiving perioperative heparin bridging therapy for warfarin treatment, when should the intravenous heparin infusion be stopped prior to surgery and when is it restarted?
115. In a patient receiving perioperative LMWH bridging therapy for warfarin treatment, when is the last dose of LMWH administered and when is it restarted?
116. In which patients should the administration of perioperative heparin likely be avoided?
117. How should a patient on chronic warfarin therapy who needs emergency surgery be managed?
118. Why should the administration of oral vitamin K be considered for the emergency patient on chronic warfarin therapy who is receiving fresh frozen plasma or prothrombin complex to reverse the effects of warfarin?
119. How should vitamin K be administered for emergency surgery in patients on chronic warfarin therapy? Why is this route preferred over the others?
An approach to patients receiving antiplatelet therapy
120. How long do patients with bare metal coronary stents require antiplatelet therapy?
121. How long do patients with drug-eluting coronary stents require antiplatelet therapy?
122. Why do patients with drug-eluting coronary stents require antiplatelet therapy much longer than patients with bare metal coronary stents?
123. How should patients with coronary stents that require antiplatelet therapy be managed in the perioperative period?
An intraoperative approach to uncontrolled bleeding
125. In the event of the massive transfusion of blood, and when laboratory testing is not available, at what volume of blood loss does the dilution of coagulation factors and platelets warrant the transfusion of fresh frozen plasma or platelets, respectively?
126. During ongoing blood loss, what laboratory value would indicate the need for the replacement of coagulation factors with fresh frozen plasma?
127. During ongoing blood loss, what laboratory value would indicate the need for the replacement of platelets with a transfusion of concentrated platelets?
128. During ongoing blood loss, what laboratory value of fibrinogen would indicate the need for a transfusion of cryoprecipitate?
129. What are some indications for the transfusion of cryoprecipitate?
130. What is the role of recombinant factor VIIa in perioperative hemorrhage?
131. List some adjuvant hemostatic agents and their mechanism of action.
132. What are some of the indications for DDAVP as an adjuvant hemostatic agent?
Answers*
Coagulation
1. The traditional thinking regarding the mechanism of coagulation was that there were two independent pathways, which could independently activate a common pathway leading to the generation of thrombin, which converts fibrinogen to fibrin. These two pathways were termed intravascular (intrinsic) and extravascular (extrinsic). It is now believed that this thinking is flawed; it appears the intrinsic pathway is not important in physiologic coagulation per se. Instead, the current understanding is that coagulation is a cell-based process that occurs on the surface of subendothelial cells and platelets, and that it involves elements of both the intrinsic and extrinsic systems. Specifically the extrinsic system generates a small amount of thrombin, which then activates parts of the intrinsic system. The extrinsic system also activates the intrinsic system directly via a recently discovered link between the two systems. This then leads to the overwhelming generation of thrombin (thrombin burst), which causes blood to clot. (349, Figure 22-1)
2. Platelets are activated at the site of vascular injury to form the initial platelet plug by adhering to collagen or von Willebrand factor. (349)
3. Platelets, once activated, degranulate and release large amounts of calcium and factors V and VIII. This activates a series of events that eventually leads to a cross-linked fibrin meshwork that traps activated platelets and red blood cells to form a blood clot. (349)
4. Tissue factor is located on subendothelial cells. Tissue factor located on the surface of perivascular subendothelial cells at the site of vascular injury binds with circulating factor VII to form a complex that leads to coagulation. (349)
5. The secretion of tissue plasminogen activator occurs when the endothelium is activated by injury. This results in the activation of plasminogen to plasmin, which degrades fibrin to soluble products such as D-dimers. This normally remains localized to areas of thrombus. (350)
6. In general, surgery and/or massive trauma results in an elevation of acute phase reactants that induces both a hypercoagulable state and inhibits the normal process of fibrinolysis. (350)
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