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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5565_Библиотеки_им_академика_М_И_Перельмана.pdf
THERAPEUTIC APHERESIS 181
A. 5%
B. 15%
C. 25%
D. 50%
E. 75%
B. To estimate the actual volume assume 70 mL/kg of blood/body mass. The hema-
tocrit in a spinning bowl apheresis device is approximately 80%. Therefore, extra-
corporeal volume = (bowl volume × 0.8)/patient hematocrit.
________________________________ ________________________________
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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.
A. Typical line-related risks are bleeding and infection, while there are numerous
procedure-related risks predominantly due to fluid shifts or blood component loss.
Usually citrate is used as an anticoagulant and is cleared by the liver. Because
citrate chelates calcium, elevated citrate levels pose the risk of hypocalcemia.
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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.
A. The mainstay of therapy for Goodpasture syndrome is plasmapheresis and immu-
nosuppression. It is thought that suppression prevents rebound postpheresis anti-
body production.
182 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
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Question 7: What is the predominantly intravascular pathological immunoglobulin
in Waldenstrom macroglobulinemia?
A. IgA
B. IgD
C. IgG
D. IgM
E. IgF
D. Because IgM is predominantly intravascular, the hyperviscosity of Waldenstrom
macroglobulinemia is effectively treated with plasma exchange. However, care
must be taken to treat the underlying condition in order to prevent relapses.
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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%
E. Aggressive plasma exchange has reduced the fatality rate from 90% to approxi-
mately 20% (notwithstanding a significant proportion of survivors who experience
recurrent bouts of TTP). Given the high fatality rate, the index of suspicion for TTP
should be high and plasma exchange considered early in the course.
________________________________ _______________________________
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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.
B. ADAMTS13 is a metalloprotease that cleaves von Willebrand factor multimers. A
deficiency of ADAMTS13 (most often through autoantibody formation) leads to
THERAPEUTIC APHERESIS 183
increased circulating unusually large von Willebrand factor multimers. In addition
to supplying replacement ADAMTS13, therapeutic exchange may facilitate TTP
treatment by removing the autoanti-ADAMTS13. There is no evidence that thera-
peutic exchange prevents the formation of antibodies.
________________________________ ________________________________
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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.
A. Patients with AML tend to be at greater risk for stroke due to leukostasis than with
the other diseases listed.
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SUGGESTED READING
General
Grima KM. Therapeutic apheresis in hematological and oncological diseases. J Clin
Apheresis 2000;15:28-52.
Koo AP. Therapeutic apheresis in autoimmune and rheumatic diseases. J Clin
Apheresis 2000;15:18-27.
McLeod BC, Szczepiorkowski ZM, Weinstein R, Winters JL, eds. Apheresis: Princi-
ples and practice. 3rd ed. Bethesda, MD: AABB, 2010.
Owen HG, Brecher ME. Atypical reactions associated with use of angiotensin-con-
verting enzyme inhibitors and apheresis. Transfusion 1994;34:891-4.
Szczepiorkowski ZM, Winters JL, Bandarenko N, et al. Guidelines on the use of
therapeutic apheresis in clinical practice—evidence-based approach from the
Apheresis Applications Committee of the American Society for Apheresis. J Clin
Apher 2010;25:83-177.
Weinstein R. Therapeutic apheresis in neurologic disorders. J Clin Apheresis 2000;
15:74-128.
Winters JL, Gottschall JL, eds. Therapeutic apheresis: A physician’s handbook. 3rd
ed. Bethesda, MD: AABB, 2011.
184 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
Winters JL, Pineda AA, McLeod BC, Grima KM. Therapeutic apheresis in renal and
metabolic diseases. J Clin Apheresis 2000;15:53-73.
Guillain-Barré Syndrome
Hughes RAC, Wijdicks EFM, Barohn R, et al, for the Quality Standards Subcommit-
tee of the American Academy of Neurology. Practice parameter: Immunotherapy for
Guillain-Barré syndrome. Neurology 2003;61:736-40.
Van der Meche FGA, Schmitz PIM. A randomized trial comparing intravenous
immune globulin and plasma ex-change in Guillain-Barré syndrome. N Engl J Med
1992;326:1123-9.
Myasthenia Gravis
Kothari MJ. Myasthenia gravis. J Am Osteopath Assoc 2004;104:377-84.
Romi F, Gilhus NE, Aarli JI. Myasthenia gravis: Clinical, immunological, and thera-
peutic advances. Acta Neurol Scand 2005;111:134-41.
Goodpasture Syndrome
Kaplan AA. Therapeutic apheresis for renal disorders. Ther Apher 1999;1:25-30.
Winters JL, Pineda AA, McLeod BC, Grima KM. Therapeutic apheresis in renal and
metabolic diseases. J Clin Apheresis 2000;15:53-73.
Dysproteinemia
Drew MJ. Plasmapheresis in the dysproteinemias. Ther Apher 2002;6:45-52.
Gertz MA, Anagnostopoulos A, Anderson K, et al. Treatment recommendations in
Waldenstrom’s macroglobulinemia: Consensus panel recommendations from the
Second International Workshop on Waldenstrom’s Macroglobulinemia. Semin
Oncol 2003;30:121-6.
Kyle RA, Treon SP, Alexanian R, et al. Prognostic markers and criteria to initiate
therapy in Waldenstrom’s macroglobulinemia: Consensus panel recommendations
from the Second International Workshop on Waldenstrom’s Macroglobulinemia.
Semin Oncol 2003;30:116-20.
Phatak DR. Serum hyperviscosity in Waldenstrom’s macroglobulinemia. Transfusion
2003;43:989.
Siami GA, Siami FS. Plasmapheresis and paraproteinemia: Cryoglobulininduced dis-
eases, monoclonal gammopathy, Waldenstrom’s macroglobulinemia, hyperviscos-
ity syndrome, light chain disease, and amyloidosis. Ther Apher 1999;3:8-19.
THERAPEUTIC APHERESIS 185
Thrombotic Thrombocytopenic Purpura
Ahmed A, Aggarwal A, Sharma D, et al. Rituximab for treatment of refractory/relaps-
ing thrombotic thrombocytopenic purpura (TTP). Am J Hematol 2004;77:171-6.
Brecher ME. How I approach a thrombotic thrombocytopenic purpura patient.
Transfusion 2006;46:687-9.
Cohen JA, Brecher ME, Bandarenko N. Cellular source of serum lactate dehydroge-
nase elevation in patients with thrombotic thrombocytopenic purpura. J Clin Apher-
esis 1998;13:16-19.
Darabi K, Berg AH. Rituximab can be combined with daily plasma exchange to
achieve effective B-cell depletion and clinical improvement in acute autoimmune
TTP. Am J Clin Pathol 2006;125:592-7.
Ellis J, Theodossiou C, Schwarzenberger P. Treatment of thrombotic thrombocytope-
nic purpura with the cryosupernatant fraction of plasma: A case report and review of
the literature. Am J Med Sci 1999;318:190-3.
Fontana S, Hovinga JAK, Lammle B, Taleghani BM. Treatment of thrombotic throm-
bocytopenic purpura. Vox Sang 2005;90:245-54.
Furlan M, Lammle B. Deficiency of von Willebrand factor-cleaving protease in
familial and acquired thrombotic thrombocytopenic purpura. Baillieres Clin Hae-
matol 1998;11:509-14.
Furlan M, Robles R, Galbusera M, et al. Von Willebrand factor-cleaving protease in
thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome. N Engl
J Med 1998;339:1578-84.
Furlan M, Robles R, Morselli B, et al. Recovery and half-life of von Willebrand fac-
tor-cleaving protease after plasma therapy in patients with thrombotic thrombocyto-
penic purpura. Thromb Haemost 1999;81:8-13.
George JN. Thrombotic thrombocytopenic purpura. N Engl J Med 2006;354:1927-
35.
Mannucci PM. Thrombotic thrombocytopenic purpura: A simpler diagnosis at last?
Thromb Haemost 1999;82:1380-1.
Moake JL. Moschcowitz, multimers, and metalloprotease. N Engl J Med 1998;339:
1629-31.
Raife TJ, Friedman KD, Dwyre DM. The pathogenicity of von Willebrand factor in
thrombotic thrombocytopenic purpura: Reconsideration of treatment with cryopoor
plasma. Transfusion 2006;46:74-9.
Rock G, Anderson D, Clark W, et al, for the Canadian Apheresis Group and the
Canadian Association of Apheresis Nurses. Does cryosupernatant plasma improve
outcome in thrombotic thrombocytopenic purpura? No answer yet. Br J Haematol
2005;129:79-86.
186 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
Rock GA, Shumak KH, Buskard NA, et al. Comparison of plasma exchange with
plasma infusion in the treatment of thrombotic thrombocytopenic purpura. Cana-
dian Apheresis Study Group. N Engl J Med 1991;325:393-7.
Tsai H-M, Lian E C-Y. Antibodies to von Willebrand factor-cleaving protease in
acute thrombotic thrombocytopenic purpura. N Engl J Med 1998;339:1585-94.
Leukostasis
Lichtman MA, Rowe JM. Hyperleukocytic leukemias: Rheological, clinical, and
therapeutic considerations. Blood 1982;60:279-83.
In: Leonard G, Licata M.
Practical Self-Assessment for Transfusion Medicine Professionals
Bethesda, MD: AABB Press, 2012
15
Managing a Hospital Transfusion Service
QUESTIONS
Question 1: To which of the following must a transfusion-related mortality be
reported?
A. AABB.
B. Food and Drug Administration.
C. ICCBBA.
D. College of American Pathologists.
E. American Society of Clinical Pathology.
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Question 2: What does MSBOS stand for?
A. Material safety blood operating system.
B. Maximum safety in blood ordering system.
C. Maximum surgical blood order schedule.
D. Minimal stipulations for blood ordering safety.
E. Morphologic standards in blood ordering safety.
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Question 3: What is the best description of a maximum surgical blood order sched-
ule?
A. A list of the absolute maximum allowable blood usage for a procedure.
B. An ordering list for the blood bank for routine blood component purchase.
C. The dates and times surgeons are allowed to order blood components.
D. A list of the number of RBC units that the blood bank will crossmatch for a spe-
cific surgical procedure.
E. None of the above.
188 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
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Question 4: Which of the following statements is true regarding the transfusion of
Rh-positive cellular blood components to Rh-negative recipients?
A. The blood bank should inform the patient’s physician of the exposure and the
possible risk of Rh alloimmunization.
B. The blood bank is required to report the event to the FDA.
C. The blood bank should notify the patient or patient’s guardian.
D. The unit and attached tubing should be returned to the blood center where the
unit was drawn.
E. All of the above.
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Question 5: Which of the following is NOT part of root-cause analysis?
A. Collection of data regarding the error or incident.
B. Interview of key personnel involved in the error or incident.
C. Charting causes of the error or incident.
D. Identification of root causes of the error or incident.
E. Punitive corrective measures against individuals involved in the error or inci-
dent.
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Question 6: Within what period should transfusion-related deaths be reported to the
FDA in writing?
A. 1 day.
B. 1 week.
C. 1 month.
D. 6 months.
E. Up to 1 year.
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Question 7: How often should standard operating procedures (SOPs) be reviewed?
A. Weekly.
B. Monthly.
C. Quarterly.
D. Yearly.
E. Only when revised.
MANAGING A HOSPITAL TRANSFUSION SERVICE 189
_____________________________ _____________________________
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Question 8: Which of the following terms refers to identifying and notifying recipi-
ents of blood components collected from donors who subsequently tested positive
for transfusion-transmitted infectious diseases?
A. Testament.
B. Retrospective review.
C. Look-forward.
D. Look-back.
E. Post-donation information.
_____________________________ _____________________________
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Question 9: How often should a blood usage committee meet?
A. Weekly.
B. Monthly.
C. Quarterly.
D. Yearly.
E. Only as needed.
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Question 10: When should audits for transfusion appropriateness be conducted?
A. Concurrently.
B. Retrospectively.
C. They can be performed either concurrently or retrospectively.
D. Neither concurrently nor retrospectively.
E. As needed.
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Question 11: Which of the following statements is true about informed consent?
A. The most important aspect is proper documentation of the patient’s signature.
B.
The consent must be separate from the general consent for invasive procedures.
C. Consent is a process that includes informing the patient of the risks/benefits of,
the alternatives to, and the consequences of not having the transfusion.
D. Informed consent is generally used only with Jehovah’s Witness patients.
E. All of the above.
190 PRACTICAL SELF-ASSESSMENT FOR TRANSFUSION MEDICINE PROFESSIONALS
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Question 12: What’s the best description of a staffing plan?
A. A list of all available staff.
B. A means to optimize productivity while maintaining sufficient staff to allow for
peak demands and temporary vacancies.
C. A schedule for hiring created by the blood bank director and given to the hos-
pital administration.
D. A diagram of the nearest exits for staff to exit the blood bank in the event of an
emergency.
E. All of the above.
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Question 13: Which of the following is an example of an indirect cost?
A. Reagents.
B. Disposables.
C. Wages.
D. Outsourcing.
E. Utilities.
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Question 14: What is the typical interval between inspections for accreditation of
transfusion services?
A. 6 months.
B. 1 year.
C. 2 years.
D. 5 years.
E. 10 years.
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ANSWERS
Question 1: To which of the following must a transfusion-related mortality be
reported?
A. AABB.