1. d. Blood products are irradiated to disable the T cell lymphocytes, which are the major cells causing transfusion-associated graft versus host disease (TAGVHD). Patients who require irradiated blood include low birth weight newborns, infants requiring in utero red cell exchange, congenital immunodeficiency, patients receiving granulocytes transfusions, patients with Hodgkin lymphoma, and patients who are receiving intensive immunosuppressive chemotherapy. There are no reports of TAGVHD in HIV-infected patients.

2. e. All blood products which contain viable lymphocytes need to be irradiated. There are no viable lymphocytes in fresh frozen plasma (FFP). Lymphocytes become nonfunctional when frozen and thawed. However, fresh plasma contains viable cells.

3. d. The FDA requires irradiation exposure to be a minimum of 15 G at the periphery of the irradiated field and 25 G at the center.

4. e. Most of irradiators have a Cesium or Cobalt as a source for irradiation. The intensity and dose of irradiation depends on the half life of the source and not on the time of exposure. Recently intensive X-ray has been used for the source to irradiate the lymphocytes.

5. d. The irradiation source (cesium) is shielded with lead; any person including pregnant women may use the irradiator.

6. e. AABB and FDA are the usual inspection agencies for Blood Banks. Recently Congress passed a bill allowing the NRC the right to inspect the security for any institute use radioactive sources.

7. b. The ABO antigens are carbohydrate antigen which can be attached to proteins, sphingolipid, or lipid carrier molecules. The basic structure of ABH antigen is a linear oligosaccharide chain composed of three monosaccharides, adding fucose will form H (O) antigens, further adding N-acetylgalactosamine or galactose to form group A or B antigen. So, group A has N-acetylgalactosamine and group B has galactose moiety.

8. b. The ABO blood groups are carbohydrate antigens while IgM is the immunoglobin isotype produced as anti-ABO antibody.

9. e. ABO antibodies are mostly IgM which do not cross the blood/placenta barrier.

10. b. N-acetylgalactosidase can split or remove N-acetylgalactosamine from group A antigen and convert A to O antigen. This technique was used to artificially produce O blood type which is then transfused to patients with no side effects. However, preparing this product is not cost-effective for wide use.

11. c. Galactosidase can break down or remove the galactose from B antigen and convert B to O.

12. c. Type O plasma contains anti-A and anti-B antibodies. O plasma with high titer of anti-A and anti-B antibodies can cause hemolytic transfusion reaction (HTR).

13. e. Patients with type A2 may have low level of clinically insignificant anti-A antibody. A2 type patient may receive either A1 or O red cells.

14. c. This is a case of micro angiopathy hemolytic anemia (thrombotic thrombocytopenic purpura [TTP]) which causes destruction of red cells. Lactate dehydrogenase (LD) is usually elevated in any destruction process in the body.

15. b. There are many causes that could cause thrombocytopenia accompanied with low hemoglobin and normal coagulation. Although TTP is the key disorder in the differential diagnosis, malignant hypertension must also be included. With normal blood pressure and normal coagulation, TTP is the most logical diagnosis.

16. d. In TTP, the main pathology is the presence of high molecular weight (MW) von Willebrand factor (vWF) with formation of microthrombi. The apheresis will remove the high MW vWF and in more than 50% of patients will remove the ADAMTS13 inhibitors (autoantibodies).

17. d. Plasma is the preferred replacement fluid in TTP with dual functions; pheresis removes high MW vWF, removes ADAMTS13 inhibitor, and increases ADAMTS13 level.

18. c. These symptoms are due to citrate toxicity secondary to decrease in ionized calcium.

19. e. Calcium gluconate may be given; the best route is intravenously. Oral calcium salt is acceptable but not effective in many patients.

20. d. Angiotensin-converting enzyme inhibitor may interact with the polymers of the plastic bags and activate the kallikrein system and produce severe hypotension.

21. c. Antibody against a high frequency antigen may produce positive reactions in all tested red cells; however, the DAT test is always negative in these cases.

22. c. Citrate toxicity is the most common side effect of plasmapheresis due to low plasma ionized calcium.

23. d. Plasma is the most common replacement fluid for TTP. FFP, 24-plasma, and thawed plasma can all be used. Plasma will remove high MW von Willebrand factor and ADAMTS13 inhibitor, and will increase the ADAMSTS13 level.

24. d. Calcium citrate is not part of the additive in red cell preservative solutions. Sodium citrate is added as anticoagulant, phosphate salts function as buffer, dextrose, and mannitol as source of carbohydrate for energy production, and adenine as source for ATP.

25. d. The shelf life is 42 days for all new red cell preservative solutions including AS-1, AS-3.

26. d. During red cell storage, both ATP and 2,3 diphosoglycerate are decreased by red cells metabolism, pH is decreased due to H ion production, and plasma hemoglobin and potassium ions are elevated due to red cell hemolysis.

27. b. During red cells storage the red cells and the 2,3-diphosoglycerate concentration are reduced. The very low 2,3 DPG will shift the Hb-O association curve to the left.

28. d. Cryoprecipitated antihemophilic factor (AHF) is enriched with fibrogen, von Willebrand factor, factor VIII and factor XIII. Factor VII is present in low concentration in cryoprecipitate AHF.

29. d. Cryoprecipitate AHF is rich in fibrinogen, von Willebrand factor, factor VIII, and factor XIII.

30. b. Thawed Cryoprecipitate AHF will expire in 4 hours in an open system or pooled; 6 hours if thawed and not pooled.

31. b. Apheresis granulocyte function is time-dependent. Phagocytic functions deteriorate with time and a unit becomes unuseful after 24 hours and may be discarded.

32. e. Anti-Ko antibodies are known to suppress fetal bone marrow, causing intrauterine and postpartum severe anemic.

33. d. Duffy antigens are receptors for plasmodium vivax. In Africa, most of population are Duffy negative due elimination of infected Duffy positive population.

34. e. Anti-Kidd antibodies are high-affinity and highavidity antibodies. Roughly, 72% of whites are Jk(a+,b+) and their antibodies can cause moderate to severe hemolytic transfusion reaction.

35. e. The Lewis antigens are not developed in newborn and are not intrinsic to red cells but rather adsorbed from the plasma onto the red cell membranes and become expressed on glycosphingolipid type I chain. Lewis antibodies do not usually cause hemolysis.

36. d. Low platelets and low ADAMT13 are the most reliable findings in TTP. In addition, elevated LDH, low hematocrit, and presence of ADAMTS13 inhibitors are present in most cases of TTP.

37. e. The binding of high molecular weight von Willebrand factor to the platelet and forming platelet thrombus is the main pathology in TTP.

38. d. All plasma preparation may be used for apheresis of TTP including only male plasma which is collected only from male donors to prevent TRALI. Plasma will increase the level of ADAMTS13. Several studies showed that human serum albumin is not suitable replacement fluid for TTP treatment.

39. b. The exact cause for the severity of TAGVHD is not known. However, several publications supported the notion that the bone marrow hemopoietic trilineage cells may be the target for TAGVHD.

40. c. TAGVHD may develop in patients with cellular immunodeficiency (especially deficiency of T cells) and those receiving high doses of potent immunosuppressors. Patients with IgA deficiency have an intact immune system with deficiency of IgA production and will not develop transfusion-associated graft versus host disease. These patients do not require irradiated blood products.

41. c. The leukoreduction filter is not sufficient to remove all of the lymphocytes which can cause TAGFHD. Leukocyte-reduced blood products have efficient lymphocytes to cause TAGVHD. All other choices may also lead to TAGVHD except irradiation, which prevents proliferation of the donor lymphocytes.

42. a. Donor T lymphocyte population is the cellular component responsible for TAGVHD. Lymphocyte number is implicated.

43. c. Transfusion-related acute lung injury (TRALI) may be caused by agglutinating patient granulocytes with donor anti-HLA or white cell antibodies in the small pulmonary arterioles and capillaries. All the mentioned agents could cause the TRALI except donor lymphocyte antibodies. No study has shown that anti-lymphocyte antibodies are responsible for TRALI.

44. a. Platelets carry ABO group and HLA class I antigens but not HLA class II antigens. HLA class II antigens are expressed on antigen presenting cells including B lymphocytes, monocytes/macrophages, dendritic cells, and activated T lymphocytes.

45. d. ITP is treated with intravenous immunoglobulin (IVIG), immunosuppressors, or splenectomy. In 2008, the FDA approved recombinant platelets growth factor for treatment of ITP.

46. a. Anti-HPA-1a is the most common antiplatelet antibodies in ITP.

47. d. Anti D antibody may be used to treat D positive patients and not D negative patients. Anti-D will bind to Rh D positive red cells; the coated cells will attract phagocytic cells and prevent the attack on platelets coated with antibody.

48. b. All of these conditions are indications for transfusion except non-bleeding patients with platelet count 20,000/µl or more. Several studies showed that 10,000/µl platelets have a reasonable haemostatic efficacy in non-bleeding patients.

49. e. All mentioned criteria are accepted for blood duties except tattoo done 1 month ago. For donor with recent tattoo, 12 months or more must relapsed before accepting the donor. There is no age limit for blood donation.

50. c. All the mentioned criteria cause donor deferral except receiving recombinant growth factor. Donors who in the past received animal source growth factor are permanently deferred.

51. e. Post transfusion purpura is a rare thrombocytopenia secondary to blood transfusion occurring 1 week to 9 days after red cell transfusion. It is characterized by abrupt onset of severe thrombocytopenia. Most patients have been previously transfused or pregnant. Fatal intracranial hemorrhage may occur. The mechanism of patient’s platelets destruction by what appears to be platelets alloantibody is controversial. Treatment with IVIG or plasmapheresis is often helpful.

52. c. Screening for Cytomegalovirus by PCR is not a routine test for donor screening. It is not done routinely but upon request for patients whose immune system is suppressed such as in congenital immune deficiency, intrauterine blood exchange, or in those receiving highdose immunosuppression.

53. c. Single unit of cryoprecipitated AHF may be, if not transfused immediately, stored for 6 hours at 20-24°C.

54. c. Pooled cryoprecipitated AHF expires within 4 hours if kept at room temperature or 6 hours for a single unit.

55. c. Dolichos biflorus is a lectin which agglutinates A1 but not A2 red cells and may be used to differentiate between them.

56. c. Lectins are glycoproteins that may be bound to specific monosaccharides; either free monosaccharides or as part of glycoproteins.

57. d. Posttransfusion purpura is a rare post-red cell transfusion complication. It is characterized by severe thrombocytopenia occurring within an average 9 days (range of 1-24 days) after red cell transfusion. Most affected patients have been pregnant or transfused.