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CP Reviewer 2 > Blood bank > Flashcards

Blood bank Flashcards

1
Q

Donation interval: One unit of whole blood.

A

8 weeks.

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2
Q

Donation interval: A double unit of whole blood by apheresis.

A

16 weeks.

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3
Q

Reasons for a 12-month deferral from donation (Part 1).

A 
Paying for sex.
Receiving blood products, tissue, etc.
Immune globulin for hepatitis B.
Syphilis or gonorrhea.
Mucous-membrane exposure to blood.
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4
Q

Reasons for a 12-month deferral from donation (Part 2).

A 
Tattoos, piercings, etc.
Residing with someone with viral hepatitis.
Unlisted vaccines.
Incarceration >72 hours.
Sex with someone with HIV.
Malaria-endemic area, travel to.
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5
Q

Reasons for a 3-year deferral from donation.

A

Residence in a malaria-endemic area.
Personal history of malaria.
Soriatane (acetretin).

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6
Q

Reasons for a 6-month deferral from donation.

A

Avodart (dutaseride).

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7
Q

Donor requirements: Body temperature.

A

No more than 37.5 degrees C.

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8
Q

Donor requirements: Blood pressure.

A

No more than 180 over no more than 100.

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9
Q

Donor requirements: Hemoglobin and hematocrit.

A

At least 12.5 g/dL or 38%.

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10
Q

Autologous donation: Requirements.

A

Physician’s order.

Hemoglobin at least 11 g/dL or Hct at least 33%.

No risk of bacteremia.

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11
Q

When, relative to surgery, is autologous blood collected?

A

At least 72 hours before the operation.

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12
Q

Introduction of unused autologous blood into the general inventory.

A

Not allowed.

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13
Q

Plasmapheresis: Minimum weight of donor.

A

50 kg.

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14
Q

Plasmapheresis: Donation interval for typical donors.

A

4 weeks.

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15
Q

Plasmapheresis: Donation interval for frequent donors.

A

No more than twice a week.

At least 2 days between donations.

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16
Q

Plasmapheresis: How much whole blood may be removed?

A

Up to 500 mL (600 mL if donor weighs at least 80 kg).

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17
Q

Platelet-pheresis: Donation interval.

A

No more than twice a week.

At least 2 days between donations.

No more than 24 times a year.

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18
Q

Platelet-pheresis: Required platelet count.

A

150,000/μL.

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19
Q

Introduction of blood from a hemochromatosis patient (therapeutic phlebotomy) into the general blood supply.

A

The patient can have no medical conditions that would disqualify any allogeneic donor.

The unit must be labeled with the patient’s condition.

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20
Q

What happens when testing of a unit of autologous blood yields abnormal results?

A

The patient and the patient’s physician must be notified.

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21
Q

How to prevent bacterial contamination of platelets during collection.

A

Use a diversion pouch to collect the first 30 mL of whole blood and the skin plug.

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22
Q

Volume of whole blood drawn for donation:

A. Maximum.
B. Time limit.

A

A. 10.5 mL/kg.

B. 15 minutes.

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23
Q

Typical volume of whole blood drawn for donation.

A

Depending on the system:

450 ± 45 mL

  • or -

500 mL ± 50 mL.

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24
Q

Definition of low-volume unit of whole blood.

A

Depending on the system:

300-404 mL or 333-449 mL.

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25
Q

Testing for weak D:

A. When?
B. How?

A

A. When there is no reaction of the donor’s red cells with the anti-D reagent.

B. Prolonged incubation and use of antihuman globulin.

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26
Q

How to label a unit found to have weak D.

A

As Rh positive.

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27
Q

Confirmatory blood grouping to be done at the blood bank upon receipt of new units of red cells.

A

ABO and Rh.

Confirmation of weak D is not required.

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28
Q

Screening for infectious diseases: Required tests.

A 
Anti-HBc.
HBsAg.
Anti-HCV.
HCV RNA.
Anti-HIV.
HIV RNA.
Anti-HTLV1 and anti-HTLV2.
RPR.
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29
Q

Screening for infectious diseases: Two agents for which testing is often done although not mandated.

A

West Nile virus.

Trypanosoma cruzi.

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30
Q

Screening for infectious diseases: Omission of testing requires ___ (4).

A

Approval of the medical director of the donor center.

Approval of the medical director of the transfusion service.

Labeling of the unit to indicate the omission.

Completion of testing as soon as possible.

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31
Q

Screening for infectious diseases: Directed apheresis donors and autologous donors.

A

Initially and every 30 days.

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32
Q

Obtaining a new pretransfusion sample in a known patient:

A. In whom is it required?
B. When is the sample taken?

A

A. In anyone who has been transfused or pregnant within the past 3 months.

B. No more than 72 hours before the transfusion.

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33
Q

After a transfusion, what must be retained for 7 days?

A

The pretransfusion blood sample.

A tube segment from the transfused unit.

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34
Q

Testing for weak D in a recipient.

A

Not required.

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35
Q

Antibody screen: Number of clinically significant antibodies that must be represented.

A

18.

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36
Q

Antibody screen: Phases of testing.

A

Immediate spin.

Incubation at 37 degrees.

Incubation with antihuman globulin.

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37
Q

Autocontrol:

A. Definition.
B. When used.

A

A. The incubation of the donor’s serum or plasma with the donor’s red cells.

B. With the antibody panel.

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38
Q

Why is it important to compare the results of pretransfusion testing with records of previous results (3)?

A

To avoid errors in patient identification.

To avoid sample mix-ups.

To be aware of previous antibodies, such as anti-Kidd, that can become undetectable.

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39
Q

Computer crossmatch: Requirements.

A

Negative antibody screen.

Validated computer system.

At least two previous determinations of ABO and Rh group.

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40
Q

Immediate-spin crossmatch vs. full crossmatch.

A

Full crossmatch
− Includes incubation with antihuman globulin.
− Required if clinically significant alloantibodies are detected in the immediate-spin phase.

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41
Q

Crossmatch in neonatal recipients: When not required.

A

When the neonate is <4 months old and there are no clinically significant maternal antibodies.

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42
Q

Giving Rh-positive platelets to an Rh-negative recipient.

A

Should be avoided if possible; otherwise, RhIg should be offered.

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43
Q

Rh-positive recipient <4 months old: First choice of RBCs.

A

O positive.

CMV negative.

Irradiated.

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44
Q

Rh-positive recipient <4 months old: Second choice of RBCs.

A

O negative.

CMV negative.

Irradiated.

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45
Q

Rh-negative recipient <4 months old: First choice of RBCs.

A

O negative.

CMV negative.

Irradiated.

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46
Q

Rh-negative recipient <4 months old: Second choice of RBCs.

A

Type specific.

CMV negative.

Irradiated.

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47
Q

Any recipient <4 months old: First and second choices of plasma.

A

First choice: AB.

Second choice: Type specific.

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48
Q

Any recipient >4 months old: First and second choices of plasma.

A

First choice: Type specific.

Second choice: AB.

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49
Q

Standard filter:

A. Size of pore.
B. Policy regarding reuse.

A

A. 170 μm.

B. May be reused for many times within 4 hours.

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50
Q

Standard filter: Use in leukocyte reduction.

A

Cannot be used for leukocyte reduction.

Can be omitted if a proper leukocyte-reduction filter is in place.

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51
Q

Fluids that may be infused in the same line as the red-cell unit.

A

Normal saline.

FDA-approved crystalloids.

No lactated Ringer’s solution, no dextrose solutions.

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52
Q

Transfusion:

A. Period of observation.
B. Infusion rate.

A

A. For the first 15 minutes of the transfusion.

B. 2 mL/minute.

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53
Q

Transfusion: When to take vital signs.

A

At 0 minutes, 15 minutes, and the completion of the transfusion.

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54
Q

Transfusion: Duration.

A

May last up to 4 hours but is usually completed within 90 minutes.

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55
Q

Causes of a positive autocontrol (3).

A

Autoantibody.

Antibody to previous transfused red cells.

Drug-induced positive DAT.

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56
Q

Antigens whose reactivity are enhanced by enzymes.

A

ABO, Lewis, I/i, P.

Rh.

Kidd.

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57
Q

Antigens whose reactivity is abolished by enzymes.

A

MNS.

Duffy.

Lutheran.

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58
Q

Titer at which cold-reacting IgM antibodies may be clinically significant.

A

1 : 1000.

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59
Q

Causes of a complex pattern of reactivity on an antibody panel (6).

A 
Multiple antibodies.
Antibody showing dosage.
Antibody to antigens of high incidence.
Antibody to antigens of low incidence.
Polyagglutination.
Antibody to a reagent.
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60
Q

High-titer, low-avidity antibodies: When to suspect their presence.

A

When there is a weak reaction with all cells of the antibody panel at the AHG phase.

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61
Q

High-titer, low-avidity antibodies: Specificities of clinically significant ones.

A

Yt-a.

Gy, Hy (members of the Dombrock system).

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62
Q

High-titer, low-avidity antibodies: Significance of “insignificant” ones.

A

They may mask significant alloantibodies.

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63
Q

Antibody to a reagent: When to suspect its presence.

A

When there is reactivity with all cells of the antibody panel.

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64
Q

Antibody to a reagent: How to circumvent it (4).

A

Use a different lot of reagent.

Use a different enhancement medium.

Wash the test cells.

If using a solid or gel medium, perform the tests in a test tube.

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65
Q

Antibody to a low-incidence antigen: When to suspect its presence.

A

When there is a reaction with one cell in the antibody panel.

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66
Q

T-activation: Examples of antigens subject to it.

A

T, Tk, Tn, Cad.

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67
Q

T-activation: Cause.

A

Bacterial neuraminidase exposes cryptic antigens on red cells.

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68
Q

T-activation: Specific causes.

A

Streptococcus pneumoniae: Atypical hemolytic-uremic syndrome.

Clostridium: Necrotizing enterocolitis.

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69
Q

T-activation: Detection (2).

A

Agglutination of affected red cells by adult serum but not by cord serum.

Arachis hypogaea.

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70
Q

T-activation: Clinical significance.

A

Transfusion of adult plasma (which contains natural anti-T antibodies) into affected infants can cause intravascular hemolysis.

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71
Q

T-activation: Treatment.

A

Give washed or plasma-poor blood products.

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72
Q

T-activation: Duration.

A

Resolves with the inciting infection.

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73
Q

Methods of elution.

A

Heat.

Acid.

Freeze-thaw method.

Digitonin.

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74
Q

Auto-adsorption:

A. Purpose.
B. Agent.

A

A. To remove autoantibodies from red cells so that any clinically significant alloantibodies can be detected.

B. ZZAP.

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75
Q

Auto-adsorption:

A. When it cannot be used.
B. Alternate technique.

A

A. In anyone who has been transfused or pregnant within the past 3 months.

B. Alloadsorption.

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76
Q

Hemagglutinin inhibition: Agent.

A

Neutralizing substance.

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77
Q

What neutralizes Sd-a?

A

The urine of guinea pigs.

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78
Q

What neutralizes the P antigen?

A

Pigeon eggs.

Hydatid-cyst fluid.

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79
Q

What neutralizes H substance?

A

Saliva.

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80
Q

What neutralizes Chido / Rodgers antigens?

A

Plasma.

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81
Q

What neutralizes Le-a substance?

A

Saliva.

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82
Q

Lectin: A1.

A

Dolichos biflorus.

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83
Q

Lectin: B.

A

Bandeirea simplicifolia.

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84
Q

Lectin: H.

A

Ulex europaeus.

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85
Q

Lectin: N.

A

Vicea graminea.

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86
Q

Antigen frequency: D.

A

85%.

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87
Q

Antigen frequency: C.

A

70%.

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88
Q

Antigen frequency: c.

A

80%.

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89
Q

Antigen frequency: Cw.

A

2%.

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90
Q

Antigen frequency: E.

A

30%.

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91
Q

Antigen frequency: e.

A

98%.

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92
Q

Antigen frequency: G.

A

84%.

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93
Q

Antigen frequency: f.

A

65%.

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94
Q

Antigen frequency: V.

A

1%.

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95
Q

Antigen frequency: K.

A

9%.

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96
Q

Antigen frequency: k.

A

99.8%.

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97
Q

Antigen frequency: Jk-a.

A

75%.

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98
Q

Antigen frequency: Jk-b.

A

75%.

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99
Q

Antigen frequency: Kp-a.

A

2%.

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100
Q

Antigen frequency: Js-a.

A

Whites: 0.1%.

Blacks: 20%.

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101
Q

Antigen frequency: Fy-a.

A

Whites: 65%.

Blacks: 10%.

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102
Q

Antigen frequency: Fy-b.

A

Whites: 83%.

Blacks: 20%.

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103
Q

Antigen frequency: M.

A

80%.

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104
Q

Antigen frequency: N.

A

72%.

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105
Q

Antigen frequency: S.

A

55%.

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106
Q

Antigen frequency: s.

A

90%.

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107
Q

Antigen frequency: U.

A

Whites: 99.9%.

Blacks: 99%.

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108
Q

Antigen frequency: P1.

A

80%.

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109
Q

Causes of a positive crossmatch: Negative antibody screen (4).

A

ABO mismatch.

Passively acquired ABO antibodies.

Anti-A₁.

Antibody to a low-incidence antigen.

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110
Q

Interpretation (3): 4+ reaction with anti-D reagent, 2+ reaction with D+ test cells.

A

Anti-LW.

Partial D.

Autoantibody with specificity for Rh.

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111
Q

B(A) phenotype:

A. Cause.
B. Recognition.

A

A. Production of a small amount of A substance on group B cells.

B. Forward phase: Weak reaction with anti-A reagent.
Reverse phase: As expected for group B.

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112
Q

Acquired-B phenotype:

A. Causes.
B. Recognition.

A

A. Persistent bacteremia, esp. bowel obstruction, bowel carcinoma, Gram-negative sepsis.

B. Forward phase: Weak reaction with anti-B reagent.
Reverse phase: As expected for group A.

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113
Q

Acquired-B phenotype: Confirmation (5).

A

Use a different manufacturer’s anti-B reagent.
Reacetylate the patient’s red cells.
Observe lack of reaction with acidified human anti-B.
Observe reaction with the patient’s own anti-B.
Observe absence of B substance in patient’s saliva.

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114
Q

Antibodies to A₁: Incidence (2).

A

A₂: 1-8%.

A₂B: 22-35%.

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115
Q

Antibodies to A₁: Clinical significance.

A

Usually none, unless reactive at 37 degrees.

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116
Q

Antibodies to A₁: Recognition.

A

Forward phase: As expected for group A or AB.

Reverse phase: Weak reaction with A test cells.

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117
Q

Interpretation: Weak reactivity with all cells in the panel at the AHG phase only.

A

Antibody to a high-titer, low-avidity antigen such as Chido / Rodgers.

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118
Q

Interpretation: Reactivity with all cells in the panel and the autocontrol, but only in the AHG phase.

A

Warm autoantibody.

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119
Q

Interpretation: Reactivity with all cells in the panel and the autocontrol in the immediate-spin phase.

A

Cold autoantibody.

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120
Q

Interpretation: Reactivity with all cells in the panel and the autocontrol at the immediate spin and at 37 degrees.

A

Cold autoantibody with a very broad thermal amplitude.

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121
Q

Effect of some hematolymphoid neoplasms on ABO testing.

A

Weakened expression of A or B antigen on red cells.

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122
Q

Effect of some gastric adenocarcinomas on ABO testing.

A

Excess free ABO antigens neutralize the anti-A and anti-B reagents, giving a false impression of group O.

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123
Q

Interpretation of a positive DAT:

A. With anti-IgG and anti-C3.
B. With IgG only.
C. With C3 only.

A

A, B. Probable warm autoantibody.

C. Probable cold autoantibody.

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124
Q

Positive DAT with anti-IgG: Next step.

A

Use elution or adsorption to look for any masked alloantibodies.

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125
Q

Causes of a positive DAT other than primary autoimmunity.

A

Neonatal: Passive transfer of antibodies, HDN, RhIg.
ABO-incompatible bone-marrow transplant.
Recent transfusion.
Drugs.
Antithymocyte globulin for transplant of solid organ.

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126
Q

When an autoantibody is suspected, what is the very next step?

A

To determine whether the patient is hemolyzing.

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127
Q

Warm autoantibodies: Significance of a positive anti-C3.

A

Its presence and strength correlate with the likelihood of hemolysis.

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128
Q

Warm autoantibodies: Guidance concerning transfusion.

A

Avoid if at all possible; otherwise, use techniques to unmask any clinically significant alloantibodies.

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129
Q

Benign cold autoantibodies: Thermal amplitude.

A

4-22 degrees, reacting best at 4 degrees.

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130
Q

Common types of benign cold agglutinin.

A

Anti-I in adults.

Anti-i in children.

Anti-H.

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131
Q

Benign vs. pathological cold agglutinins: Titers.

A

At 4 degrees C

Benign: 1 to 64.

Pathologic: 1 to 1000.

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132
Q

Primary cold autoimmune hemolytic anemia:

A. Synonym.
B. Typical patient.

A

A. Cold-agglutinin syndrome.

B. Elderly person with acrocyanosis and Raynaud’s phenomenon.

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133
Q

Primary cold autoimmune hemolytic anemia:

A. Type of hemolysis.
B. Type of antibody.

A

A. Intravascular, moderate.

B. IgM anti-I or anti-i.

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134
Q

Secondary cold autoimmune hemolytic anemia: Types (3).

A

Anti-I due to Mycoplasma pneumoniae.

Anti-i due to infectious mononucleosis.

Anti-I due to lymphoproliferative disorder.

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135
Q

Mixed autoantibodies: Classes.

A

Cold-reacting IgM and warm-reacting IgG.

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136
Q

Mixed autoantibodies: Specificity.

A

No consistent specificity.

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137
Q

Mixed autoantibodies: Clinical presentation.

A

Acute hemolytic anemia, sometimes associated with lupus.

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138
Q

Paroxysmal cold hemoglobinuria: Typical patient.

A

Child with viral infection or otitis media.

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139
Q

Paroxysmal cold hemoglobinuria: Clinical presentation.

A

Exposure to cold leads to hemolytic anemia with fever, chills, pain, jaundice, hemoglobinuria.

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140
Q

Paroxysmal cold hemoglobinuria: Degree of anemia.

A

Usually severe.

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141
Q

Paroxysmal cold hemoglobinuria: Treatment.

A

Keeping the patient warm and giving transfusions as needed.

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142
Q

Paroxysmal cold hemoglobinuria: Antibody and its specificity.

A

IgG anti-P.

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143
Q

Paroxysmal cold hemoglobinuria: DAT.

A

Positive with anti-C3 reagent only.

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144
Q

Paroxysmal cold hemoglobinuria: The Donath-Landsteiner test.

A

Blood incubated at 4 degrees and then at 37 degrees shows hemolysis.

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145
Q

How to keep cold autoantibodies from interfering with tests for alloantibodies (3).

A

Perform all tests at 37 degrees.

Use only monoclonal anti-IgG in the AHG phase.

Adsorption.

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146
Q

Mechanisms of drug-induced positive DAT.

A

Hapten.

Autoimmune induction.

Non-immune adsorption.

Drug-dependent antibody.

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147
Q

Hapten mechanism: Location of hemolysis.

A

Intravascular.

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148
Q

Hapten mechanism: Prototypical agent.

A

Penicillin.

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149
Q

Hapten mechanism: Diagnosis.

A

Incubation of serum and eluate with drug-treated and untreated red cells.

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150
Q

Drug-dependent-antibody mechanism: Location of hemolysis.

A

Extravascular.

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151
Q

Drug-dependent-antibody mechanism: Prototypical agents.

A

Piperacillin.

Cephalosporins.

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152
Q

Drug-dependent-antibody mechanism: DAT.

A

Positive with anti-C3 (complement-mediated hemolysis) and possibly with anti-IgG also.

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153
Q

Autoimmune induction: Effect of withdrawal of offending drug.

A

Autoimmunity persists but may subside with prolonged withdrawal of the drug.

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154
Q

Autoimmune induction: Prototypical agents.

A

Methyldopa.

Levodopa.

Procainamide.

Fludarabine.

2nd- and 3rd-generation cephalosporins.

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155
Q

Autoimmune induction: Diagnosis.

A

Autoantibody indistinguishable from those that of idiopathic WAIHA.

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156
Q

Non-immune adsorption: Mechanism.

A

A drug causes nonspecific binding of antibody onto red cells.

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157
Q

Non-immune adsorption: Prototypical agent.

A

Cephalothin (Keflin).

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158
Q

Non-immune adsorption: Diagnosis.

A

Positive antibody screen, positive DAT.

Negative eluate.

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159
Q

Transfusion in sickle-cell disease: Endpoint.

A

Reduction of concentration of HbS below

50% in adults.

30% in children.

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160
Q

Transfusion in sickle-cell disease: ASPEN syndrome.

A

Association of sickle-cell disease with priapism, exchange transfusion, and neurological events.

Occurs within 11 days after exchange transfusion.

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161
Q

Transfusion in sickle-cell disease: Specificities of most common antibodies.

A

K, C, E, Fy-a, Jk-b.

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162
Q

Transfusion in sickle-cell disease: Rate of alloimmunization per unit of phenotypically

A. Unmatched blood.
B. Matched blood.

A

A. 3%.

B. 0.5%.

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163
Q

Class I hemorrhage: Amount.

A

<15% of blood volume (750 mL).

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164
Q

Class II hemorrhage:

A. Amount.
B. Treatment.

A

A. 15-30% of blood volume.

B. Fluid resuscitation usually suffices.

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165
Q

Class III hemorrhage:

A. Amount.
B. Treatment.

A

A. 30-40% of blood volume.

B. Fluid resuscitation first; transfusion usually necessary.

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166
Q

Class IV hemorrhage:

A. Amount.
B. Treatment.

A

A. >40% of blood volume.

B. Fluid resuscitation first; transfusion necessary.

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167
Q

When to switch from fluid resuscitation to transfusion when treating a hemorrhage.

A

When 30 mL/kg (about 2 L) fluid have been given.

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168
Q

Emergency release of cells: Documentation.

A

Signed release by treating physician within 24 hours.

Unit labeled as not having undergone compatibility testing.

169
Q

RhIg therapy for recipients of Rh-incompatible blood products:

A. How soon to give RhIg.
B. How much to give.
C. How fast to give it.
D. When not to give it.

A

A. Within 72 hours.

B. 90 IU/mL of transfused Rh-positive blood.

C. In 3-5 minutes.

D. When Rh-positive blood constitutes >20% of the patient’s blood volume.

170
Q

Emergency release to one with known anti-C and/or anti-E.

A

Rh-negative blood should be released.

171
Q

Complications of massive transfusion (6).

A

Hypothermia.
Decreased pH.
Decreased release of oxygen from transfused cells.

Hyperkalemia.
Increased free hemoglobin.

Coagulopathy.

172
Q

Definitions of therapy Categories I-IV.

A

Category I: Standard as main therapy.

Category II: Accepted as adjunctive or supportive therapy.

Category III: May help, but evidence is lacking.

Category IV: No indication.

173
Q

Indications for apheresis: Category I (7).

A

TTP.
Guillain-Barré syndrome.
Goodpasture’s syndrome.
ANCA-positive RPGN.

Chr. inflammatory demyelinating polyneuropathy.
Hyperviscosity syndrome with IgM.
Severe or symptomatic cryoglobulinemia.

174
Q

Indications for apheresis: Category II (5).

A

Renal transplant: HLA sensitization or ABO incompatibility.

Catastrophic antiphospolipid syndrome.

MS with steroid-refractory CNS disease.
Rasmussen’s (chronic focal) encephalitis.
Lupus: Cerebritis or diffuse alveolar hemorrhage.

175
Q

Indication for apheresis: Category III.

A

Humoral rejection of cardiac transplant.

176
Q

Indications for apheresis: Category IV.

A

Diarrhea of the hemolytic-uremic syndrome.

ITP.

Lupus nephritis.

177
Q

Apheresis: Permissible replacement fluids.

A

Normal saline.

5% albumin.

Allogeneic plasma.

178
Q

Apheresis: Properties of drugs that may be readily removed by it.

A

Much binding to protein.

Low volume of distribution.

179
Q

Type of drug that should be discontinued before apheresis.

A

ACE inhibitor, 24 hours before.

180
Q

Blood for a neonatal/intrauterine transfusion must be ___ (5).

A

Group O.

Fresh (less than 5 days old) or washed.

Irradiated.

Without active maternal antibody.

CMV-negative or leukocyte-reduced (esp. in fetus and in small neonates).

181
Q

Neonatal/intrauterine transfusion: Dose of RBCs.

A

10-15 mL/kg.

182
Q

Neonatal/intrauterine transfusion: Dose of FFP.

A

10-15 mL/kg.

183
Q

Neonatal/intrauterine transfusion: Dose of platelets.

A

5-10 mL/kg.

184
Q

Neonatal/intrauterine transfusion: Dose of cryoprecipitate.

A

1-2 units per kg.

185
Q

Maternal ITP: Possible neonatal complications.

A

Severe thrombocytopenia.

Serious hemorrhage.

186
Q

Neonatal alloimmune thrombocytopenia: Antigen and its frequency.

A

HPA 1a, 98%.

187
Q

Neonatal alloimmune thrombocytopenia: Relevance to number of pregnancies.

A

Can occur in the first pregnancy.

Gets worse with each pregnancy.

188
Q

Neonatal alloimmune thrombocytopenia: Main complication and its incidence.

A

Intracranial hemorrhage; 20%.

189
Q

Neonatal alloimmune thrombocytopenia:

A. How soon can platelets be given?
B. What kind?
C. Can maternal platelets be given?

A

A. As early as 18 weeks of gestation.

B. Antigen negative.

C. Yes, if washed and irradiated.

190
Q

Neonatal alloimmune thrombocytopenia: Other treatments.

A

IVIg.

Corticosteroids.

191
Q

Neonatal alloimmune thrombocytopenia: Period of greatest risk of postnatal hemorrhage.

A

24-36 hours after delivery.

192
Q

Antibodies that can cross the placenta.

A

IgG1, IgG3, IgG4.

193
Q

Sensitization to the D antigen in an Rh-negative mother: Incidence.

A

About 15%.

194
Q

Sensitization to the D antigen in an Rh-negative mother: Relevance to ABO group.

A

Less likely if there is ABO incompatibility between mother and fetus.

195
Q

Rosette test for fetal-maternal hemorrhage:

A. Rôle of test.
B. Sensitivity.

A

A. Qualitative.

B. Detects as little as 10 mL of fetal blood.

196
Q

Rosette test for fetal-maternal hemorrhage:

A. Response to a negative result.
B. Response to a positive result.

A

A. If there is clinical suspicion of fetal-maternal hemorrhage, then give 300 μg RhIg.

B. Proceed to a quantitative test.

197
Q

Kleihauer-Betke test: Principle.

A

HbF resists elution by acid; fetal cells will appear bright red.

198
Q

Titer of maternal anti-D:

A. Critical value.
B. What to do about it.

A

A. 1 : 16.

B. Test amniotic fluid for bilirubin and/or use noninvasive transvaginal Doppler ultrasound to measure blood flow through the fetal middle cerebral artery.

199
Q

Preventive dose of RhIg in routine cases:

A. When to give.
B. How much to give.

A

A. At 28 weeks of gestation and at term.

B. 300 μg.

200
Q

Preventive dose of RhIg in the event of a fetal-maternal hemorrhage: How much to give.

A

300 μm plus the amount corresponding to amount of the hemorrhage.

201
Q

Situations in which RhIg is not indicated.

A

D-positive mother.

D-negative mother who has already made anti-D antibodies.

202
Q

A 90-kg mother with a Kleihauer-Betke result of 2%: How many vials of RhIg should she receive?

A

90 kg × 0.7 = 6.3 L (blood volume).

  1. 3 × 2 (percent) / 3 = 4.2.
  2. 2 + 1 = 5.2.

Round to nearest whole number: 5 vials.

203
Q

Routes of administration of RhIg.

A

Intramuscular: No more than 5 vials at a time.

Intravascular: Continuous infusion.

204
Q

Hemolytic disease of the newborn, ABO mediated:

A. Severity.
B. Antibody.
C. Relevance to number of pregnancies.

A

A. Mild.

B. IgG anti-A,B.

C. May affect the first pregnancy.

205
Q

Hemolytic disease of the newborn: Most common antigens implicated in severe disease.

A

K, C.

206
Q

Hemolytic disease of the newborn due to anti-K:

A. Why so severe?
B. Critical titer of maternal antibody.

A

A. Because the K antigen is found on red-cell precursors.

B. 1 : 8.

207
Q

Hemolytic disease of the newborn: Screening tests performed upon admission to the labor-and-delivery unit (3).

A

Maternal antibody screen.

ABO and Rh of cord blood.

DAT of cord blood.

208
Q

Hemolytic disease of the newborn: Response to a positive DAT.

A

Maternal antibody screen . . .

  • Positive: Use red-cell panel to determine specificity of alloantibody.
  • Negative: Exclude ABO incompatibility, previous RhIg, maternal antibody to fetal antigen of low incidence.
209
Q

RBCs and whole blood: Shelf life in AS solutions.

A

42 days.

210
Q

RBCs and whole blood: Shelf life in CPD or CP2A.

A

21 days.

211
Q

RBCs and whole blood: Shelf life in CPDA-1.

A

35 days.

212
Q

RBCs and whole blood: Storage temperature.

A

1 to 6 degrees.

213
Q

RBCs: Required hematocrit.

A

No more than 80%.

214
Q

Apheresis RBCs: Required hemoglobin.

A

At least 50 g.

215
Q

RBCs: Conditions of freezing.

A

10 years at -65 degrees.

216
Q

RBCs, thawed: Conditions of storage.

A

24 hours at 1 to 6 degrees.

217
Q

Washed RBCs: Conditions of storage.

A

24 hours at 1 to 6 degrees.

218
Q

Leukocyte-reduced RBCs: Special QC requirements.

A

No more than 5 million WBCs in 95% of units.

Preservation of at least 85% of red cells.

Apheresis: Preservation of at least 50 g hemoglobin.

219
Q

Irradiated RBCs: Shelf life.

A

28 days or the original expiration date, whichever is sooner.

220
Q

RBCs: Temperature during transportation.

A

1 to 10 degrees.

221
Q

RBCs: Shelf life after “spiking” (2).

A

24 hours at 1-6 degrees.

4 hours at room temperature.

222
Q

RBCs: Usual volume and iron concentration.

A

350 mL; 1 mg/mL.

223
Q

Platelets: Conditions of storage.

A

5 days at 20-24 degrees, with gentle agitation.

224
Q

Platelets pooled in an open system: Conditions of storage.

A

4 hours at 20-24 degrees.

225
Q

Platelets: Required quantity (2).

A

Random donor: 5.5 × 10¹⁰ in 90% of units.

Apheresis: 3.0 × 10¹¹ in 90% of units.

226
Q

Platelets: Required pH.

A

At least 6.2 in 90% of units.

227
Q

Leukocyte-reduced platelets:

A. Required quantity of platelets per unit.
B. Maximum allowable WBCs.

A

A. Random donor: 5.5 × 10¹⁰ in 75% of units; no more than 830,000 WBCs in 95% of units.

B. Apheresis: 3.0 × 10¹¹ in 75% of units; no more than 5 million WBCs in 95% of units.

228
Q

Granulocytes: Conditions of storage.

A

24 hours at 20-24 degrees; no agitation.

229
Q

Granulocytes: Required quantity per unit.

A

1 × 10¹⁰ in 95% of units.

230
Q

Plasma: Conditions of freezing.

A

1 year at -18 degrees.

7 years at -65 degrees.

231
Q

Plasma, thawed: Conditions of storage.

A

24 hours at 1 to 6 degrees.

232
Q

Cryoprecipitate: Conditions of freezing.

A

1 year at -18 degrees.

233
Q

Cryoprecipitate, thawed and unpooled: Conditions of storage.

A

6 hours at 20-24 degrees.

234
Q

Cryoprecipitate, thawed and pooled: Conditions of storage.

A

4 hours at 20 to 24 degrees.

235
Q

Cryoprecipitate: Required contents.

A

Fibrinogen, at least 150 mg, in all units.

Factor VIII, at least 80 IU, in all units.

236
Q

RBCs: Amount of anticoagulant-preservative per unit.

A

About 60 mL.

237
Q

Contents of CPDA preservative.

A

Citrate.

Phosphate.

Dextrose.

Adenine.

238
Q

Contents of additive solutions.

A

Buffers.

Adenine.

NaCl.

Dextrose.

239
Q

Platelets: Who needs crossmatched units (2)?

A

Neonates.

Recipients of many transfusions.

240
Q

Which additives contain mannitol?

A

AS-1, AS-5.

241
Q

RBCs: Biochemical changes that occur during storage.

A

Decreased pH.
Decreased ATP.
Decreased DPG.

Increased potassium.
Increased free hemoglobin.

242
Q

RBCs: How long may a unit remain unrefrigerated?

A

Up to 30 minutes.

243
Q

RBCs: How long can they wait to be frozen?

A

With additive solution: No later than the expiration date of the unit.

Without additive solution: No later than 6 days after collection.

244
Q

Leukocyte reduction of frozen RBCs.

A

Not necessary.

245
Q

RBCs: Pediatric dose required to raise the hemoglobin by 1 g/dL.

A

About 4 mL/kg.

246
Q

RBCs: Relative contraindications.

A

Autoimmune hemolytic anemia.

Hyperhemolytic syndrome in sickle-cell disease.

247
Q

Platelets: How long can they go without agitation?

A

Up to 24 hours.

248
Q

Platelets:

A. Volume of a single-donor unit.
B. Fibrinogen content of the same.

A

A. About 50 mL.

B. About 80 mg.

249
Q

Platelets:

A. Volume of an apheresis unit.
B. Fibrinogen content of the same.

A

A. About 100 mL.

B. About 150 mg.

250
Q

Thresholds for transfusion of platelets:

A. Healthy non-bleeding patient.
B. Bleeding patient with extracranial hemorrhage.

A

A. 10,000/μL.

B. 50,000/μL.

251
Q

Thresholds for transfusion of platelets: Intracranial hemorrhage.

A

100,000/μL.

252
Q

Thresholds for transfusion of platelets:

A. Neurosurgical patient.
B. Other surgical patients.

A

A. 100,000/μL.

B. 50,000/μL.

253
Q

Platelets: Use in renal failure.

A

DDAVP or cryoprecipitate should be tried first.

254
Q

Platelets: Relative contraindication.

A

ITP.

255
Q

Platelets: Absolute contraindications (2).

A

TTP.

Heparin-induced thrombocytopenia.

256
Q

Platelets: Expected increase in count following transfusion of 1 apheresis unit.

A

About 30,000/μL.

257
Q

Platelets:

A. When to use a filter.
B. When to crossmatch.

A

A. Always.

B. When the unit is grossly bloody.

258
Q

Platelets: Rh matching.

A

Recommended.

259
Q

Platelets: Shelf life of pooled unit.

A. Open system.
B. Closed system.

A

A. 4 hours at 20-24 degrees.

B. 5 days or expiration date of oldest random-donor unit; 20-24 degrees.

260
Q

“Thawed plasma”:

A. Definition.
B. Shelf life.

A

A. Plasma that has been kept refrigerated for 24 hours.

B. 5 days at room temperature.

261
Q

FP24:

A. Definition.
B. Uses.

A

A. Plasma that has been frozen between 8 and 24 hours after collection.

B. As for FFP except not in the treatment of DIC.

262
Q

FFP: Prescribed temperature of thawing.

A

30-37 degrees.

263
Q

Plasma:

A. Volume.
B. Contents.

A

A. About 200 mL.

B. Fibrinogen, about 200 mg; coagulation factors, about 1 IU/mL of each.

264
Q

Plasma: PTT, PT, and INR values that often lead to transfusion.

A

PTT, PT: About 1.5 × normal.

INR: About twice normal.

265
Q

Plasma: Indication other than correction of coagulopathy.

A

Treatment of deficiency of C1 esterase inhibitor.

266
Q

Plasma: Use in reversal of anticoagulation.

A

Heparin: Not indicated.

Warfarin: As a last resort.

267
Q

Dose of plasma:

A. Adults.
B. Neonates.

A

10-15 mL/kg for both.

268
Q

Plasma: Timing of transfusion relative to an invasive procedure.

A

No more than 2 hours before incision.

269
Q

Plasma: Expected effect on activities of coagulation factors.

A

About a 20% increase in each one.

270
Q

Plasma: Rh matching.

A

Not important.

271
Q

Cryoprecipitate: How made.

A

Plasma is thawed to 1 to 6 degrees and then centrifuged.

The precipitate is placed in the freezer at -18 degrees within 1 hour.

272
Q

Cryoprecipitate: Volume.

A

15 mL.

273
Q

Cryoprecipitate: Contents.

A

Fibrinogen.

Factor VIII.

Factor XIII.

vWF.

274
Q

Cryoprecipitate: What it does not contain.

A

Factor V.

275
Q

Cryoprecipitate: Effect on plasma fibrinogen.

A

An increase of 7 mg/dL per unit (70 mg/dL per pool of 10 units).

276
Q

Cryoprecipitate: Indications (4).

A

Replacement of fibrinogen or factor XIII.

Treatment of von Willebrand’s disease.

Treatment of bleeding in uremic patients.

As fibrin glue.

277
Q

Factor VII concentrate: Indications (2).

A

Treatment of inherited deficiency of factor VII.

Treatment of suspected inhibitor of factor VIII or factor IX.

278
Q

Humate-P: Indications.

A

Treatment of

− Factor VIII deficiency.
− Von Willebrand’s disease.

279
Q

Factor VIII: Half-life and intravascular recovery.

A

12 hours; nearly 100%.

280
Q

Factor IX: Half-life and intravascular recovery.

A

24 hours; about 50%.

281
Q

Irradiation of blood products: Required dose.

A

25 Gy to the center of the product.

At least 15 Gy to the periphery.

282
Q

Irradiation of blood products: Purpose.

A

Prevention of transfusion-associated GVHD.

283
Q

Irradiation of blood products: Who needs it?

A 
Blood received from blood relatives.
Bone-marrow or stem-cell transplant.
T-cell defects, congenital.
Aplastic anemia.
Purine analogs for chemotherapy.
Immunosuppression and lymphoma.
Neonates, fetuses.
Granulocyte transfusion.
284
Q

Leukocyte-reduction of blood products: Indications (4).

A

Prevention of

− HLA alloimmunization.
− Febrile non-hemolytic transfusion reaction.
− CMV transmission.
− Transfusion-related immune modulation.

285
Q

Washing of blood products: Indications (2).

A

Prevention of allergic transfusion reactions, esp. in IgA-deficient recipients.

Removal of incompatible plasma from cellular products to be given to neonates.

286
Q

Type 1 and type 2 precursor carbohydrates: Locations.

A

Type 1: Secretions.

Type 2: Red cells.

287
Q

Origin of H antigen.

A

Secretions: Action of product of Se gene (FUT2) on type 1 chains.

Red cells: Action of product of H gene (FUT1) on type 2 chains.

288
Q

Origin of Lewis antigens.

A

Le-a: Action of product of Le gene (FUT3) on unmodified type 1 chain.

Le-b: Action of FUT3 on type 1 H antigen.

289
Q

Relevance of Lewis antigens to microbiology.

A

H. pylori and Norwalk virus attach via Le-b.

290
Q

Relevance of Lewis antigens to tumor biology.

A

CA 19-9 is Le-a.

291
Q

Origin of A antigen.

A

Action of product of A gene (N-acetylgalactosamine transferase) on type 1 and 2 chains.

292
Q

Origin of B antigen.

A

Action of product of B gene (galactosyltransferase) on type 1 and 2 chains.

293
Q

I and i antigens: Differences.

A

I: Branched type 1 and 2 chains; found in adults.

i: Simple chains; found in neonates.

294
Q

Causes of postnatal expression of i antigen.

A

Congenital dyserythropoietic anemia, type 2.

Diamond-Blackfan anemia.

High turnover of cells.

295
Q

A₁ and A₂:

A. Difference.
B. Distribution.

A

A. A₁ cells have much more A antigen.

B. A₁: 80% of group A.

296
Q

A₁ and A₂: Distinction in the blood bank (3).

A

A₁: Stronger reaction with Dolichos biflorus and with anti-A₁ made by individuals of group B.

A₂: Stronger reaction with Ulex europaeus.

297
Q

Anti-A₁:

A. Frequency.
B. Clinical significance.

A

A. A₂: 5%; A₂B: 35%.

B. Usually none.

298
Q

Bombay vs. para-Bombay.

A

Bombay type: No H gene, no Se gene.

Para-Bombay type: No Se gene.

299
Q

ABO distribution: Whites.

A

O: 45%.

A: 40%.

B: 10%.

AB: 5%.

300
Q

ABO distribution: Blacks.

A

O: 50%.

A: 25%.

B: 20%.

AB: 5%.

301
Q

ABO distribution: Hispanics.

A

O: 55%.

A: 30%.

B: 10%.

AB: 5%.

302
Q

D-positivity: Distribution.

A

Whites: 82%.

Blacks, Hispanics: 92%.

303
Q

H antigen: Amount on cells by ABO type.

A

O > A₂ > B > A₂B > A₁ > A₁B.

304
Q

Gene frequency: Se.

A

80%.

305
Q

How do Lewis antigens end up on red cells?

A

Through passive adsorption.

306
Q

Causes of the phenotype Le(a-b-).

A

Neonatal state.

Pregancy.

Absence of Le gene.

307
Q

Distribution of Lewis phenotype in whites.

A

Le(a+b-): 22%.

Le(a-b+): 72%.

Le(a-b-): 6%.

308
Q

Distribution of Lewis phenotype in blacks.

A

Le(a+b-): 22%.

Le(a-b+): 55%.

Le(a-b-): 23%.

309
Q

Predict the Lewis phenotype:

A. Le/Se.
B. Le/se.
C. le/Se.
D. le/se.

A

A. Le(a-b+); Le-b > Le-a, ABH in secretions.

B. Le(a+b-); Le-a in secretions.

C. Le(a-b-); ABH in secretions.

D. Le(a-b-); nothing in secretions.

310
Q

ABO antigens:

A. When first detectable.
B. When adult levels are reached.

A

A. At 3-6 months.

B. At about 2 years.

311
Q

Major vs. minor ABO incompatibility.

A

Major: Incompatible red cells.

Minor: Incompatible plasma.

312
Q

Most common specificity of Lewis antibodies.

A

Le-a.

313
Q

Why Lewis antigens rarely cause hemolytic transfusion reactions (2).

A

The transfused cells take on the Lewis phenotype of the recipient.

Lewis antibodies get neutralized by circulating free Lewis antigen.

314
Q

Why Lewis antigens do not cause hemolytic disease of the newborn (2).

A

Fetuses have no Lewis antigens.

The typical Lewis antibody is IgM and thus cannot cross the placenta.

315
Q

I and i antigens: Microbiological associations.

A

I: Mycoplasma pneumoniae.

i: Infectious mononucleosis.

316
Q

Groups to which the following antigens belong: P, P-k, P1.

A

P and Pk: GLOB.

P1: The only member of the P system.

317
Q

P antigen: Associations.

A

Paroxysmal cold hemoglobinuria.

Parvovirus B19.

318
Q

P phenotypes: Expressed antigens.

A

P1 phenotype: P and P1, but not P-k.

p phenotype: No P antigens.

319
Q

Antibodies made by those with the p phenotype:

A. Names.
B. Associations.

A

A. Anti-PP1P-k, anti-Tj-a.

B. Acute hemolytic transfusion reaction, spontaneous abortion.

320
Q

Agglutinators of the P antigen.

A

Pigeon eggs.

Hydatid-cyst fluid.

321
Q

Rh genes: Chromosome.

A

1.

322
Q

Rh antigens: Structure.

A

Transmembrane proteins with many extracellular domains.

323
Q

Most common Rh-negative genotype.

A

r/r (dce/dce).

324
Q

Wiener’s notations: Rh-positive.

A

R₀: Dce.

R₁: DCe.

R₂: DcE.

Rz: DCE.

325
Q

Wiener’s notation: Rh-negative.

A

r: dce.

r’: dCe.

r’’: dcE.

r-y: dCE.

326
Q

Most common Rh combinations in

A. Whites.
B. Blacks.

A

A. R₁ > r > R₂ > R₀.

B. R₀ > r > R₁ > R₂.

327
Q

Rh-null state: Other affected antigens.

A

LW.

Fy5.

S, s, U.

328
Q

Rh-null state: Hematological manifestations.

A

Stomatocytosis, mild anemia.

329
Q

Rh-null state: Transfusion.

A

Requires Rh-null blood.

330
Q

Weak-D individuals:

A. What happens when they receive D-positive blood?

B. What happens when they give blood to a D-negative person?

A

A. No antibody is made.

B. Sensitization can occur.

331
Q

Weak-D state:

A. Traditional definition.
B. Current reality.

A

A. D-positivity becomes apparent only in the AHG phase.

B. Monoclonal anti-D reagents tend to react with anti-D cells in the IS phase.

332
Q

Weak-D state: Causes.

A

Most common: Mutation in the RHD gene imparts weakened expression.

Another cause: Presence of Ce on the other chromosome.

333
Q

What happens when a partial-D individual

A. Receives D-positive blood?
B. Gives blood to a D-negative person?

A

Sensitization can occur in either case.

334
Q

Partial-D state: How recognized.

A

A D-positive person is found to be making anti-D antibodies.

335
Q

Rh antigens: Rate of sensitization after emergent transfusion.

A

About 20-30%.

336
Q

Rh antibodies that often occur together; why?

A

Anti-c and anti-E.

Because the most common Rh combination is R₁ (DCe), and the most common E-positive combination is R₂ (DcE).

337
Q

Why is important to remember that a patient with anti-E will often has anti-c as well?

A

Because anti-c can be undetectable but can still cause delayed HTR.

338
Q

Anti-G:

A. Definition.
B. Significance.

A

A. Antibody to the G antigen, which is present whenever there is D or C.

B. Anti-G can be confused with anti-D. This could cause a D-negative mother to miss getting RhIg in the mistaken belief that she already has anti-D.

339
Q

Anti-f:

A. Definition.
B. Significance.

A

A. Antibody to the combination ce.

B. Can cause mild HTR and mild HDN.

340
Q

Kidd phenotypes: Whites.

A

Jk(a+b-): 25%.

Jk(a-b+): 25%.

Jk(a+b+): 50%.

341
Q

Kidd phenotypes: Blacks.

A

Jk(a+b-): 50%.

Jk(a-b+): 10%.

Jk(a+b+): 40%.

342
Q

Kidd antibodies: Associated reactions.

A

Delayed HTR: Often severe, intravascular.

Acute HTR: Severe.

HDN: Mild.

343
Q

Duffy antigens: Microbiological association.

A

Point of entry of P. vivax.

344
Q

Duffy antibodies: More significant.

A

Anti-Fy-a.

345
Q

Duffy antibodies: Reactions (2).

A

Delayed HTR: Severe, usually extravascular.

HDN: Mild.

346
Q

Frequency of Fy(a-b-) in black populations.

A

68% in the United States; higher in Africa.

347
Q

M and N antigens: Location.

A

On glycophorin A.

348
Q

M and N antigens: Distribution.

A

M+N-: 25%.

M-N+: 25%.

M+N+: 50%.

349
Q

S, s, and U antigens: Location.

A

On glycophorin B.

350
Q

S, s, and U antigens: Frequency.

A

S: 55%.

s: 90%.

U: 99%.

351
Q

Anti-N: Significance.

A

Occurs only in those who lack glycophorin B, which contains an N-like domain (‘N’).

352
Q

Anti-Nf.

A

Antibody to an N antigen that has been modified by exposure to formalin, as in hemodialysis.

353
Q

Kell antigens: Frequency of

A. K.
B. Kp-a.
C. Js-a.

A

A. 9%.

B. 2%.

C. 0.1% in whites, 20% in blacks.

354
Q

Kell antigens: Frequency of

A. k.
B. Kp-b.
C. Js-b.

A

All: >99%.

355
Q

Age at one may donate blood products.

A

17 (in some states, at age 16 with parental consent).

356
Q

Kell-null phenotype: Expression of antigens.

A

No Kell antigens.

Overexpression of non-Kell antigen Kx.

357
Q

McLeod phenotype: Expression of antigens.

A

No Kx.

Weakened expression of Kell antigens.

358
Q

McLeod phenotype: Hematological manifestations.

A

Acanthocytosis.

Frequent association with chronic granulomatous disease.

359
Q

McLeod phenotype: Other clinical associations.

A

Retinitis pigmentosa.

Muscular dystrophy of late onset.

360
Q

McLeod phenotype: Transfusion.

A

Requires McLeod-type blood.

361
Q

Absence of Diego antigen: Hematological associations (3).

A

Hereditary elliptocytosis.

Hereditary spherocytosis.

Acanthocytosis.

362
Q

Absence of Gerbich antigen: Hematological association.

A

Hereditary elliptocytosis.

363
Q

Antibodies that give a mixed-field reaction.

A

Anti-Lutheran.

Anti-Sd.

364
Q

Agents that diminish the expression of Kell antigens.

A

ZZAP.

2-mercaptoethanol.

Dithiothreitol.

365
Q

Lutheran antigens: Frequency.

A

Lu-a: 7%.

Lu-b: 99%.

366
Q

MHC III proteins:

A. Location of genes.
B. Examples (4).

A

A. 6p21.3.

B. Complement proteins, CYP21 (21-hydroxylase), HFE, TNF.

367
Q

HLA class I: Structure of antigens.

A

A single transmembrane polypeptide chain that is noncovalently bound to β₂-microglobulin.

368
Q

HLA class I: Expression of antigens on red cells.

A

Most are found only on young cells; Bg antigens are found on all red cells.

369
Q

HLA class I: Expression of antigens on platelets.

A

Present.

370
Q

HLA class II: Structure of antigen.

A

Two polypeptide chains, α and β, that share a sequence with light-chain immunoglobulins.

371
Q

HLA Class II: Expression of antigens on red cells and platelets.

A

Absent.

372
Q

How to estimate the probability of a HLA-matched sibling.

A

P = 1 - 0.75^n,

where n is the number of siblings.

373
Q

Transfusion reactions: What to do when the posttransfusion serum sample is drawn late and no hemolysis can be seen.

A

Inspect for icterus; if present, the serum bilirubin will remain elevated for 24-36 hours after the reaction.

374
Q

Transfusion reactions: Steps of investigation.

A

Clerical check.

Inspection of serum sample for hemolysis / icterus.

Recheck of ABO group.

DAT.

375
Q

Transfusion reactions: Whom to notify in case of death or serious morbidity.

A

FDA: Within 24 hours by telephone, within 7 days in writing.

Donor center: Immediately by telephone, to be followed by written notification.

376
Q

Transfusion-related infection: Whom to notify (3).

A

Donor center.

All recipients of products from that donor.

Patient’s physician.

377
Q

Transfusion reactions: Most common type.

A

Febrile, non-hemolytic.

378
Q

Febrile, non-hemolytic transfusion reaction:

A. Cause.
B. Prevention.

A

A. Cytokines released by leukocytes within the bag.

B. Leukocyte reduction.

379
Q

Allergic transfusion reaction:

A. Cause.
B. Prevention (3).

A

A. IgE-mediated reaction to foreign plasma proteins.

B. Washing of blood products; premedication with antihistamines; giving IgA-deficient blood products.

380
Q

Extravascular hemolysis: Clinical presentation.

A

Usually asymptomatic but may present with pallor, anemia, hyperbilirubinemia.

381
Q

Delayed serologic transfusion reaction: Definition.

A

A transfusion reaction in which there is a new alloantibody but neither hemolysis nor symptoms.

382
Q

Delayed hemolytic transfusion reaction: Laboratory findings.

A

Positive DAT (mixed-field) reaction.

Microspherocytosis.

Hyperbilirubinemia.

383
Q

Delayed hemolytic transfusion reaction: Implicated antibodies.

A

Intravascular: Anti-Kidd.

Extravascular: Anti-Duffy, anti-c, anti-E, anti-Kell.

384
Q

Delayed hemolytic transfusion reaction:

A. Time of presentation.
B. Treatment.

A

A. 5-14 days after the transfusion.

B. Usually none is required.

385
Q

Transfusion-related sepsis: Incidence and mortality

A. For platelets units.
B. For red-cell units.

A

A. 1 in 25,000; 25%.

B, 1 in 250,000; 70%.

386
Q

Transfusion-related sepsis: Causative organisms.

A. In platelet units.
B. In red-cell units.

A

A. Staphylococci.

B. Yersinia enterocolitica.

387
Q

Transfusion-related sepsis: Laboratory findings.

A

Gram stain of blood product may be positive.

There may be free hemoglobin in urine and/or serum, but the DAT is negative.

388
Q

Approximate probability of transfusion-related transmission of

A. HIV.
B. HCV.
C. HTLV-1.

A

A,B. 1 in 2 million.

C. 1 in 3 million.

389
Q

Approximate probability of transfusion-related transmission of HBV.

A

1 in 200,000.

390
Q

Transfusion-related GVHD: Clinical manifestations (4).

A

Rash.

Enterocolitis.

Hepatitis (elevated liver enzymes).

Marrow suppression.

391
Q

Transfusion-related GVHD: Prevention.

A

Irradiation of blood products.

392
Q

Leading cause of transfusion-related fatality.

A

Transfusion-related acute lung injury.

393
Q

Transfusion-related acute lung injury:

A. Incidence.
B. Mortality.

A

A. 1 in 5000.

B. 5-10%.

394
Q

Transfusion-related acute lung injury: Proposed diagnostic criteria (4).

A

Onset within 6 hours after transfusion.

Hypoxemia.

Bilateral pulmonary infiltrates.

No other explanation for symptoms.

395
Q

Transfusion-related acute lung injury: Proposed mechanism.

A

Antibodies against HLA or other antigens cause clumping of granulocytes within the pulmonary microvasculature.

396
Q

Transfusion-related acute lung injury: Clinical finding other than respiratory distress.

A

Fever.

397
Q

Transfusion-related acute lung injury: Risk factors

A. In the patient.
B. In the donor.

A

A. Chemotherapy, cardiac bypass.

B. Multiparity.

398
Q

Transfusion-related acute lung injury: How to distinguish from circulatory overload.

A

In circulatory overload, there is

− A rapid response to diuretics.
− An increased PCW pressure.
− An increased BNP.

399
Q

Transfusion-related acute lung injury: How to distinguish from anaphylaxis (3).

A

In anaphylaxis, there is

− A rapid response to epinephrine.
− Wheezing and edema of the upper airways.
− Usually no pulmonary infiltrate.

400
Q

Transfusion-related acute lung injury: Period of recovery.

A

Up to 72 hours.

401
Q

Posttransfusion purpura: Time of onset.

A

2-14 days after the transfusion.

402
Q

Posttransfusion purpura: Typical victim.

A

Multipara.

403
Q

Posttransfusion purpura: Mechanism.

A

Production of antibodies to HPA-1a leads to destruction of the transfused platelets and the native platelets.

404
Q

Posttransfusion purpura: Period of recovery without treatment.

A

About 3 weeks.

405
Q

Posttransfusion purpura: Treatment.

A

IVIg.

406
Q

Platelet refractoriness: Causes.

A

Primary: Alloantibodies to HLA.

Secondary (more common): Infection, splenomegaly, DIC, amphotericin B.

407
Q

Platelet refractoriness: Formula for corrected count increment (CCI).

A

Observed increase in platelet count × body surface area / number of transfused platelets.*

*in multiples of 10¹¹.

408
Q

Platelet refractoriness: CCI associated with

A. Normal response.
B. Refractoriness.

A

A. >7500.

B. <5000.

409
Q

Platelet refractoriness: Prevention (3).

A

Limit platelet transfusions.

Give only apheresis platelets.

Leukocyte reduction.

410
Q

Testing of blood products for HCV (3).

A

Anti-HCV.

RIBA (if anti-HCV) is positive.

HCV RNA.

411
Q

Testing of blood products for HBV (3).

A

Anti-HBc.

HBsAg.

HBV DNA (optional).

412
Q

Testing of blood products for HIV.

A

Anti-HIV-1 and -2.

HIV RNA.

413
Q

Testing of blood products for HTLV.

A

Anti-HTLV-1 and -2.

414
Q

Prevention of transfusion-transmitted West Nile virus (2).

A

Nucleic-acid testing during outbreaks.

Exclusion of potential donors who have compatible symptoms.

415
Q

Transfusion-associated imbalances of potassium.

A

Increased free potassium in blood products more often causes hyperkalemia, but hypokalemia can result from transcellular shifts.

416
Q

Transfusion-associated hypothermia: Significance.

A

May exacerbate the effects of hypocalcemia and hyperkalemia.

417
Q

Whole-body iron content at which overload can develop.

A

500 mg/kg.

418
Q

Transfusion-related immune modification: Definition.

A

Immunosuppression due to transfusion of cellular products.

CP Reviewer 2 (8 decks)

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