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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5565_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Table of Contents
- •Preface
- •About the Authors
- •1. Blood Component Preparation
- •2. Blood Component Storage
- •3. Pretransfusion Compatibility Testing
- •5. Polypeptide Blood Group Systems
- •6. Administration of Blood Components
- •7. Adverse Effects of Transfusion
- •8 Indications for Transfusion
- •9. Autologous Blood
- •11. Special Transfusion Situations
- •12. Transfusion Emergencies
- •14. Therapeutic Apheresis
- •15. Managing a Hospital Transfusion Service

PLASMA DERIVATIVES AND RECOMBINANT PLASMA PROTEINS 171
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Mohr AM, Holcomb JB, Dutton RP, Duranteau J. Recombinant activated factor VIIa
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Brueckmann M, Wizenmann J, Hoffmann U, et al. Clinical and laboratory effects of
recombinant human activated protein C in the treatment of a patient with sepsis-
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resets thrombin generation in patients with severe sepsis—a case control study. Crit
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vated protein C. Curr Opin Crit Care 2006;12:426-30.

172 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
Hoffmann JN, Vollmar B, Laschke MW, et al. Microcirculatory alterations in isch-
emia-reperfusion injury and sepsis: Effects of activated protein C and thrombin inhi-
bition. Crit Care 2005;9(Suppl 4):S33-7.
Antithrombin
Ansell J. Long-term anticoagulation: The prospects for alternatives to warfarin.
Semin Vasc Surg 2005;18:134-8.
Carr ME, Angchaisuksiri P, Carr SL, Martin EJ. Effect of non-heparin thrombin antag-
onists on thrombin generation, platelet function, and clot structure in whole blood.
Cell Biochem Biophys 2003;39:89-99.
De Santis M, Cavaliere AF, Straface G, et al. Inherited and acquired thrombophilia:
Pregnancy outcome and treatment. Reprod Toxicol 2006;22:227-33.
Fiessinger JN, Huisman MV, Davidson BL, et al. Ximelagatran vs low-molecular-
weight heparin and warfarin for the treatment of deep vein thrombosis: A random-
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Gurm HS, Bhatt DL. Thrombin, an ideal target for pharmacological inhibition: A
review of direct thrombin inhibitors. Am Heart J 2005;149(1 Suppl):S43-53.
Hrebickova L, Nawarskas JJ, Anderson JR. Ximelagatran: A new oral anticoagulant.
Heart Dis 2003;5:397-408.
Huisman MV, Bounameaux H. Treating patients with venous thromboembolism:
Initial strategies and long-term secondary prevention. Semin Vasc Med 2005;18:
276-84.
Keeling D, Davidson S, Watson H. The management of heparin-induced thrombo-
cytopenia. Br J Haematol 2006;133:259-69.
Mousa SA. Role of current and emerging antithrombotics in thrombosis and cancer.
Drugs Today (Barc) 2006;42:331-50.
Nelson SM, Greer IA. Thrombophilia and the risk for venous thromboembolism dur-
ing pregnancy, delivery, and puerperium. Obstet Gynecol Clin North Am 2006;33:
413-27.
Schulman S. The role of ximelagatran in the treatment of venous thromboembolism.
Pathophysiol Haemost Thromb 2005;34(Suppl 1):18-24.
Schwienhorst A. Direct thrombin inhibitors—a survey of recent developments. Cell
Mol Life Sci 2006;63:2773-91.
Steinmetzer T, Sturzebecher J. Progress in the development of synthetic thrombin
inhibitors as new orally active anticoagulants. Curr Med Chem 2004;17:2297-321.

PLASMA DERIVATIVES AND RECOMBINANT PLASMA PROTEINS 173
Immune Globulin
Bussel JB, Eldor A, Kelton JG, et al. IGIV-C, a novel intravenous immunoglobulin:
Evaluation of safety, efficacy, mechanisms of action, and impact on quality of life.
Thromb Haemost 2004;91:771-8.
Jolles S, Sewell WAC, Misbah SA. Clinical uses of intravenous immunoglobulin.
Clin Exp Immunol 2005;142:1-11.
Kirmse J. Subcutaneous administration of immunoglobulin. J Infus Nurs 2006;29:
S15-S20.
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Martin TD. IGIV: Contents, properties, and methods of industrial production—
evolving closer to a more physiologic product. Internat Immunopharm 2006;6:517-
22.
Mundy CA. Intravenous immunoglobulin in the management of hemolytic disease
of the newborn. Neonatal Netw 2005;24:17-24.
Orange JS, Hossny EM, Weiler CR, et al. Use of intravenous immunoglobulin in
human disease: A review of evidence by members of the Primary Immunodeficiency
Committee of the American Academy of Allergy, Asthma and Immunology. J Allergy
Clin Immunol 2006;117:S525-53.
Penalver JF, Jimenez-Yuste V, Almagro M, et al. Rituximab in the management of
chronic immune thrombocytopenic purpura: An effective and safe therapeutic alter-
native in refractory patients. Ann Hematol 2006;85:400-6.
Siegel J. The product: All intravenous immunoglobulins are not equivalent. Pharma-
cotherapy 2005;25(11 Pt 2):78S-84S.
Trejo SR, Hotta JA, Lebing W, et al. Evaluation of virus and prion reduction in a new
intravenous immunoglobulin manufacturing process. Vox Sang 2003;84:176-87.
Weiler CR. Immunoglobulin therapy: History, indications, and routes of administra-
tion. Internat J Derm 2004;43:163-6.
Hyperimmune Globulin
Bregenholt S, Haurum J. Pathogen-specific recombinant human polyclonal antibod-
ies: Biodefence applications. Expert Opin Biol Ther 2004;4:387-96.
Casadevall A. Passive antibody administration (immediate immunity) as a specific
defense against biological weapons. Emerg Infect Dis 2002;8:833-41.
Stowell CP. Therapy with immunoglobulin. Applications for monoclonal antibodies.
J Infus Nurs 2006;29(Suppl 3):S29-S44.

174 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
Rh Immune Globulin
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immunoglobulin versus low-dose intravenous immunoglobulin in the treatment of
childhood chronic idiopathic thrombocytopenic purpura. Acta Haematol 2006;115:
46-52.
Beliard R. Monoclonal anti-D antibodies to prevent alloimmunization: Lessons from
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D immune globulin in an adult with immune thrombocytopenic purpura. Am J
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Obstet Gynaecol Can 2003;25:765-73.
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75 g/kg is as effective as intravenous immune globulin at rapidly raising the platelet
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Fibrin Sealant
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Med 2005;26:154-66.

PLASMA DERIVATIVES AND RECOMBINANT PLASMA PROTEINS 175
Sandhaus RA. Alpha-1 antitrypsin deficiency-6: New and emerging treatments for
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Hematopoietic Growth Factors
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Haematol 2006;134:453-66.

176 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
Kaushansky K. The molecular mechanisms that control thrombopoiesis. J Clin Invest
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In: Leonard G, Licata M.
Practical Self-Assessment for Transfusion Medicine Professionals
Bethesda, MD: AABB Press, 2012
14
Therapeutic Apheresis
QUESTIONS
Question 1: Which of the following fluids is an appropriate replacement fluid?
A. Normal (0.9%) saline.
B. Cryoprecipitate.
C. Lactated Ringer’s solution.
D. Albumin and saline combined.
E. Human plasma.
________________________________ ________________________________
夝
Question 2: In which setting would plasma be a better choice as a replacement fluid
than albumin or saline?
A. Thrombotic thrombocytopenic purpura.
B. Posttranfusion purpura.
C. Myasthenia gravis.
D. Hyperviscosity.
E. Polycythemia vera.
________________________________ ________________________________
夝
Question 3: Which of the following drugs can cause profound hypotension during
apheresis?
A. Statins.
B. Beta-blockers.
C. Antihistamines.
D. ACE inhibitors.
E. Angiotensin II receptor blocker.

178 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
________________________________ _______________________________
夝
Question 4: What is the maximum permissible extracorporeal blood volume?
A. 5%
B. 15%
C. 25%
D. 50%
E. 75%
________________________________ _______________________________
夝
Question 5: Risks associated with apheresis can be divided into three major catego-
ries: Line-related, procedure-related, and __________-related.
A. Anticoagulant.
B. Machine.
C. Patient.
D. Medication.
E. None of the above.
________________________________ _______________________________
夝
Question 6: Which of the following is the rationale for combining plasma exchange
with immunosuppressive therapy in conditions such as Goodpasture syndrome?
A. Avoid rebound antibody production.
B. Keep serum levels of complement low.
C. Minimize host response to donor replacement plasma.
D. Clear antibody complexes through the kidney.
E. None of the above.
________________________________ _______________________________
夝
Question 7: What is the predominantly intravascular pathological immunoglobulin
in Waldenstrom macroglobulinemia?
A. IgA
B. IgD
C. IgG
D. IgM
E. IgF

THERAPEUTIC APHERESIS 179
________________________________ ________________________________
夝
Question 8: What was the fatality rate of thrombotic thrombocytopenic purpura
before the advent of plasma exchange?
A. <5%
B. 10%
C. 20%
D. 50%
E. 90%
________________________________ ________________________________
夝
Question 9: In the case of TTP, what is the role of plasma exchange?
A. Provides unusually large vWF multimers.
B. Replaces ADAMTS13, a protease that cleaves large vWF multimers and is defi-
cient in TTP patients.
C. Prevents formation of inhibitory autoanti-ADAMTS13.
D. Removes senescent platelets.
E. Removal of ammonia, which is responsible for the neurologic changes.
________________________________ ________________________________
夝
Question 10: In which of the following diseases is therapeutic leukapheresis most
commonly employed?
A. Acute myelogenous leukemia.
B. Chronic myelogenous leukemia.
C. B-cell acute lymphocytic leukemia.
D. Chronic lymphocytic leukemia.
E. T-cell acute lymphocytic leukemia.
________________________________ ________________________________
夝
ANSWERS
Question 1: Which of the following fluids is an appropriate replacement fluid?
A. Normal (0.9%) saline.
B. Cryoprecipitate.

180 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
C. Lactated Ringer’s solution.
D. Albumin and saline combined.
E. Human plasma.
D. In all cases the fluid must be FDA-approved for use with blood components.
Saline rapidly equilibrates between intra- and extravascular spaces, requiring
approximately three times the volume to be replaced. The best choice is 50/50 mix
of 5% albumin and normal saline. Cryo-reduced plasma has been used, but not typ-
ically the precipitate. Plasma carries the risks of exposure to infectious agents.
________________________________ _______________________________
夝
Question 2: In which setting would plasma be a better choice as a replacement fluid
than albumin or saline?
A. Thrombotic thrombocytopenic purpura.
B. Posttranfusion purpura.
C. Myasthenia gravis.
D. Hyperviscosity.
E. Polycythemia vera.
A. TTP treatment with plasma exchange presumably restores the deficient
ADAMTS13.
________________________________ _______________________________
夝
Question 3: Which of the following drugs can cause profound hypotension during
apheresis?
A. Statins.
B. Beta-blockers.
C. Antihistamines.
D. ACE inhibitors.
E. Angiotensin II receptor blocker.
D. In addition to inhibiting conversion of angiotensin I to angiotensin II, ACE inhibi-
tors also interfere with the breakdown of bradykinin. This can result in profound
hypotension. ACE inhibitors should be withheld for at least 24 hours prior to apher-
esis procedures. Angiotensin II receptor blocker does not have that effect.
________________________________ _______________________________
夝
Question 4: What is the maximum permissible extracorporeal blood volume?
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