Blood bank Flashcards
1
Q
Donation interval: One unit of whole blood.
A
8 weeks.
2
Q
Donation interval: A double unit of whole blood by apheresis.
A
16 weeks.
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.
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.
5
Q
Reasons for a 3-year deferral from donation.
A
Residence in a malaria-endemic area.
Personal history of malaria.
Soriatane (acetretin).
6
Q
Reasons for a 6-month deferral from donation.
A
Avodart (dutaseride).
7
Q
Donor requirements: Body temperature.
A
No more than 37.5 degrees C.
8
Q
Donor requirements: Blood pressure.
A
No more than 180 over no more than 100.
9
Q
Donor requirements: Hemoglobin and hematocrit.
A
At least 12.5 g/dL or 38%.
10
Q
Autologous donation: Requirements.
A
Physician’s order.
Hemoglobin at least 11 g/dL or Hct at least 33%.
No risk of bacteremia.
11
Q
When, relative to surgery, is autologous blood collected?
A
At least 72 hours before the operation.
12
Q
Introduction of unused autologous blood into the general inventory.
A
Not allowed.
13
Q
Plasmapheresis: Minimum weight of donor.
A
50 kg.
14
Q
Plasmapheresis: Donation interval for typical donors.
A
4 weeks.
15
Q
Plasmapheresis: Donation interval for frequent donors.
A
No more than twice a week.
At least 2 days between donations.
16
Q
Plasmapheresis: How much whole blood may be removed?
A
Up to 500 mL (600 mL if donor weighs at least 80 kg).
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.
18
Q
Platelet-pheresis: Required platelet count.
A
150,000/μL.
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.
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.
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.
22
Q
Volume of whole blood drawn for donation:
A. Maximum.
B. Time limit.
A
A. 10.5 mL/kg.
B. 15 minutes.
23
Q
Typical volume of whole blood drawn for donation.
A
Depending on the system:
450 ± 45 mL
- or -
500 mL ± 50 mL.
24
Q
Definition of low-volume unit of whole blood.
A
Depending on the system:
300-404 mL or 333-449 mL.
25
Testing for weak D:
A. When?
B. How?
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.
26
How to label a unit found to have weak D.
As Rh positive.
27
Confirmatory blood grouping to be done at the blood bank upon receipt of new units of red cells.
ABO and Rh.
Confirmation of weak D is not required.
28
Screening for infectious diseases: Required tests.
```
Anti-HBc.
HBsAg.
Anti-HCV.
HCV RNA.
Anti-HIV.
HIV RNA.
Anti-HTLV1 and anti-HTLV2.
RPR.
```
29
Screening for infectious diseases: Two agents for which testing is often done although not mandated.
West Nile virus.
| Trypanosoma cruzi.
30
Screening for infectious diseases: Omission of testing requires ___ (4).
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.
31
Screening for infectious diseases: Directed apheresis donors and autologous donors.
Initially and every 30 days.
32
Obtaining a new pretransfusion sample in a known patient:
A. In whom is it required?
B. When is the sample taken?
A. In anyone who has been transfused or pregnant within the past 3 months.
B. No more than 72 hours before the transfusion.
33
After a transfusion, what must be retained for 7 days?
The pretransfusion blood sample.
A tube segment from the transfused unit.
34
Testing for weak D in a recipient.
Not required.
35
Antibody screen: Number of clinically significant antibodies that must be represented.
18.
36
Antibody screen: Phases of testing.
Immediate spin.
Incubation at 37 degrees.
Incubation with antihuman globulin.
37
Autocontrol:
A. Definition.
B. When used.
A. The incubation of the donor's serum or plasma with the donor's red cells.
B. With the antibody panel.
38
Why is it important to compare the results of pretransfusion testing with records of previous results (3)?
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.
39
Computer crossmatch: Requirements.
Negative antibody screen.
Validated computer system.
At least two previous determinations of ABO and Rh group.
40
Immediate-spin crossmatch vs. full crossmatch.
Full crossmatch
− Includes incubation with antihuman globulin.
− Required if clinically significant alloantibodies are detected in the immediate-spin phase.
41
Crossmatch in neonatal recipients: When not required.
When the neonate is <4 months old and there are no clinically significant maternal antibodies.
42
Giving Rh-positive platelets to an Rh-negative recipient.
Should be avoided if possible; otherwise, RhIg should be offered.
43
Rh-positive recipient <4 months old: First choice of RBCs.
O positive.
CMV negative.
Irradiated.
44
Rh-positive recipient <4 months old: Second choice of RBCs.
O negative.
CMV negative.
Irradiated.
45
Rh-negative recipient <4 months old: First choice of RBCs.
O negative.
CMV negative.
Irradiated.
46
Rh-negative recipient <4 months old: Second choice of RBCs.
Type specific.
CMV negative.
Irradiated.
47
Any recipient <4 months old: First and second choices of plasma.
First choice: AB.
Second choice: Type specific.
48
Any recipient >4 months old: First and second choices of plasma.
First choice: Type specific.
Second choice: AB.
49
Standard filter:
A. Size of pore.
B. Policy regarding reuse.
A. 170 μm.
B. May be reused for many times within 4 hours.
50
Standard filter: Use in leukocyte reduction.
Cannot be used for leukocyte reduction.
Can be omitted if a proper leukocyte-reduction filter is in place.
51
Fluids that may be infused in the same line as the red-cell unit.
Normal saline.
FDA-approved crystalloids.
No lactated Ringer's solution, no dextrose solutions.
52
Transfusion:
A. Period of observation.
B. Infusion rate.
A. For the first 15 minutes of the transfusion.
B. 2 mL/minute.
53
Transfusion: When to take vital signs.
At 0 minutes, 15 minutes, and the completion of the transfusion.
54
Transfusion: Duration.
May last up to 4 hours but is usually completed within 90 minutes.
55
Causes of a positive autocontrol (3).
Autoantibody.
Antibody to previous transfused red cells.
Drug-induced positive DAT.
56
Antigens whose reactivity are enhanced by enzymes.
ABO, Lewis, I/i, P.
Rh.
Kidd.
57
Antigens whose reactivity is abolished by enzymes.
MNS.
Duffy.
Lutheran.
58
Titer at which cold-reacting IgM antibodies may be clinically significant.
1 : 1000.
59
Causes of a complex pattern of reactivity on an antibody panel (6).
```
Multiple antibodies.
Antibody showing dosage.
Antibody to antigens of high incidence.
Antibody to antigens of low incidence.
Polyagglutination.
Antibody to a reagent.
```
60
High-titer, low-avidity antibodies: When to suspect their presence.
When there is a weak reaction with all cells of the antibody panel at the AHG phase.
61
High-titer, low-avidity antibodies: Specificities of clinically significant ones.
Yt-a.
Gy, Hy (members of the Dombrock system).
62
High-titer, low-avidity antibodies: Significance of "insignificant" ones.
They may mask significant alloantibodies.
63
Antibody to a reagent: When to suspect its presence.
When there is reactivity with all cells of the antibody panel.
64
Antibody to a reagent: How to circumvent it (4).
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.
65
Antibody to a low-incidence antigen: When to suspect its presence.
When there is a reaction with one cell in the antibody panel.
66
T-activation: Examples of antigens subject to it.
T, Tk, Tn, Cad.
67
T-activation: Cause.
Bacterial neuraminidase exposes cryptic antigens on red cells.
68
T-activation: Specific causes.
Streptococcus pneumoniae: Atypical hemolytic-uremic syndrome.
Clostridium: Necrotizing enterocolitis.
69
T-activation: Detection (2).
Agglutination of affected red cells by adult serum but not by cord serum.
Arachis hypogaea.
70
T-activation: Clinical significance.
Transfusion of adult plasma (which contains natural anti-T antibodies) into affected infants can cause intravascular hemolysis.
71
T-activation: Treatment.
Give washed or plasma-poor blood products.
72
T-activation: Duration.
Resolves with the inciting infection.
73
Methods of elution.
Heat.
Acid.
Freeze-thaw method.
Digitonin.
74
Auto-adsorption:
A. Purpose.
B. Agent.
A. To remove autoantibodies from red cells so that any clinically significant alloantibodies can be detected.
B. ZZAP.
75
Auto-adsorption:
A. When it cannot be used.
B. Alternate technique.
A. In anyone who has been transfused or pregnant within the past 3 months.
B. Alloadsorption.
76
Hemagglutinin inhibition: Agent.
Neutralizing substance.
77
What neutralizes Sd-a?
The urine of guinea pigs.
78
What neutralizes the P antigen?
Pigeon eggs.
Hydatid-cyst fluid.
79
What neutralizes H substance?
Saliva.
80
What neutralizes Chido / Rodgers antigens?
Plasma.
81
What neutralizes Le-a substance?
Saliva.
82
Lectin: A1.
Dolichos biflorus.
83
Lectin: B.
Bandeirea simplicifolia.
84
Lectin: H.
Ulex europaeus.
85
Lectin: N.
Vicea graminea.
86
Antigen frequency: D.
85%.
87
Antigen frequency: C.
70%.
88
Antigen frequency: c.
80%.
89
Antigen frequency: Cw.
2%.
90
Antigen frequency: E.
30%.
91
Antigen frequency: e.
98%.
92
Antigen frequency: G.
84%.
93
Antigen frequency: f.
65%.
94
Antigen frequency: V.
1%.
95
Antigen frequency: K.
9%.
96
Antigen frequency: k.
99.8%.
97
Antigen frequency: Jk-a.
75%.
98
Antigen frequency: Jk-b.
75%.
99
Antigen frequency: Kp-a.
2%.
100
Antigen frequency: Js-a.
Whites: 0.1%.
Blacks: 20%.
101
Antigen frequency: Fy-a.
Whites: 65%.
Blacks: 10%.
102
Antigen frequency: Fy-b.
Whites: 83%.
Blacks: 20%.
103
Antigen frequency: M.
80%.
104
Antigen frequency: N.
72%.
105
Antigen frequency: S.
55%.
106
Antigen frequency: s.
90%.
107
Antigen frequency: U.
Whites: 99.9%.
Blacks: 99%.
108
Antigen frequency: P1.
80%.
109
Causes of a positive crossmatch: Negative antibody screen (4).
ABO mismatch.
Passively acquired ABO antibodies.
Anti-A₁.
Antibody to a low-incidence antigen.
110
Interpretation (3): 4+ reaction with anti-D reagent, 2+ reaction with D+ test cells.
Anti-LW.
Partial D.
Autoantibody with specificity for Rh.
111
B(A) phenotype:
A. Cause.
B. Recognition.
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.
112
Acquired-B phenotype:
A. Causes.
B. Recognition.
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.
113
Acquired-B phenotype: Confirmation (5).
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.
114
Antibodies to A₁: Incidence (2).
A₂: 1-8%.
A₂B: 22-35%.
115
Antibodies to A₁: Clinical significance.
Usually none, unless reactive at 37 degrees.
116
Antibodies to A₁: Recognition.
Forward phase: As expected for group A or AB.
Reverse phase: Weak reaction with A test cells.
117
Interpretation: Weak reactivity with all cells in the panel at the AHG phase only.
Antibody to a high-titer, low-avidity antigen such as Chido / Rodgers.
118
Interpretation: Reactivity with all cells in the panel and the autocontrol, but only in the AHG phase.
Warm autoantibody.
119
Interpretation: Reactivity with all cells in the panel and the autocontrol in the immediate-spin phase.
Cold autoantibody.
120
Interpretation: Reactivity with all cells in the panel and the autocontrol at the immediate spin and at 37 degrees.
Cold autoantibody with a very broad thermal amplitude.
121
Effect of some hematolymphoid neoplasms on ABO testing.
Weakened expression of A or B antigen on red cells.
122
Effect of some gastric adenocarcinomas on ABO testing.
Excess free ABO antigens neutralize the anti-A and anti-B reagents, giving a false impression of group O.
123
Interpretation of a positive DAT:
A. With anti-IgG and anti-C3.
B. With IgG only.
C. With C3 only.
A, B. Probable warm autoantibody.
C. Probable cold autoantibody.
124
Positive DAT with anti-IgG: Next step.
Use elution or adsorption to look for any masked alloantibodies.
125
Causes of a positive DAT other than primary autoimmunity.
Neonatal: Passive transfer of antibodies, HDN, RhIg.
ABO-incompatible bone-marrow transplant.
Recent transfusion.
Drugs.
Antithymocyte globulin for transplant of solid organ.
126
When an autoantibody is suspected, what is the very next step?
To determine whether the patient is hemolyzing.
127
Warm autoantibodies: Significance of a positive anti-C3.
Its presence and strength correlate with the likelihood of hemolysis.
128
Warm autoantibodies: Guidance concerning transfusion.
Avoid if at all possible; otherwise, use techniques to unmask any clinically significant alloantibodies.
129
Benign cold autoantibodies: Thermal amplitude.
4-22 degrees, reacting best at 4 degrees.
130
Common types of benign cold agglutinin.
Anti-I in adults.
Anti-i in children.
Anti-H.
131
Benign vs. pathological cold agglutinins: Titers.
At 4 degrees C
Benign: 1 to 64.
Pathologic: 1 to 1000.
132
Primary cold autoimmune hemolytic anemia:
A. Synonym.
B. Typical patient.
A. Cold-agglutinin syndrome.
B. Elderly person with acrocyanosis and Raynaud's phenomenon.
133
Primary cold autoimmune hemolytic anemia:
A. Type of hemolysis.
B. Type of antibody.
A. Intravascular, moderate.
B. IgM anti-I or anti-i.
134
Secondary cold autoimmune hemolytic anemia: Types (3).
Anti-I due to Mycoplasma pneumoniae.
Anti-i due to infectious mononucleosis.
Anti-I due to lymphoproliferative disorder.
135
Mixed autoantibodies: Classes.
Cold-reacting IgM and warm-reacting IgG.
136
Mixed autoantibodies: Specificity.
No consistent specificity.
137
Mixed autoantibodies: Clinical presentation.
Acute hemolytic anemia, sometimes associated with lupus.
138
Paroxysmal cold hemoglobinuria: Typical patient.
Child with viral infection or otitis media.
139
Paroxysmal cold hemoglobinuria: Clinical presentation.
Exposure to cold leads to hemolytic anemia with fever, chills, pain, jaundice, hemoglobinuria.
140
Paroxysmal cold hemoglobinuria: Degree of anemia.
Usually severe.
141
Paroxysmal cold hemoglobinuria: Treatment.
Keeping the patient warm and giving transfusions as needed.
142
Paroxysmal cold hemoglobinuria: Antibody and its specificity.
IgG anti-P.
143
Paroxysmal cold hemoglobinuria: DAT.
Positive with anti-C3 reagent only.
144
Paroxysmal cold hemoglobinuria: The Donath-Landsteiner test.
Blood incubated at 4 degrees and then at 37 degrees shows hemolysis.
145
How to keep cold autoantibodies from interfering with tests for alloantibodies (3).
Perform all tests at 37 degrees.
Use only monoclonal anti-IgG in the AHG phase.
Adsorption.
146
Mechanisms of drug-induced positive DAT.
Hapten.
Autoimmune induction.
Non-immune adsorption.
Drug-dependent antibody.
147
Hapten mechanism: Location of hemolysis.
Intravascular.
148
Hapten mechanism: Prototypical agent.
Penicillin.
149
Hapten mechanism: Diagnosis.
Incubation of serum and eluate with drug-treated and untreated red cells.
150
Drug-dependent-antibody mechanism: Location of hemolysis.
Extravascular.
151
Drug-dependent-antibody mechanism: Prototypical agents.
Piperacillin.
Cephalosporins.
152
Drug-dependent-antibody mechanism: DAT.
Positive with anti-C3 (complement-mediated hemolysis) and possibly with anti-IgG also.
153
Autoimmune induction: Effect of withdrawal of offending drug.
Autoimmunity persists but may subside with prolonged withdrawal of the drug.
154
Autoimmune induction: Prototypical agents.
Methyldopa.
Levodopa.
Procainamide.
Fludarabine.
2nd- and 3rd-generation cephalosporins.
155
Autoimmune induction: Diagnosis.
Autoantibody indistinguishable from those that of idiopathic WAIHA.
156
Non-immune adsorption: Mechanism.
A drug causes nonspecific binding of antibody onto red cells.
157
Non-immune adsorption: Prototypical agent.
Cephalothin (Keflin).
158
Non-immune adsorption: Diagnosis.
Positive antibody screen, positive DAT.
Negative eluate.
159
Transfusion in sickle-cell disease: Endpoint.
Reduction of concentration of HbS below
50% in adults.
30% in children.
160
Transfusion in sickle-cell disease: ASPEN syndrome.
Association of sickle-cell disease with priapism, exchange transfusion, and neurological events.
Occurs within 11 days after exchange transfusion.
161
Transfusion in sickle-cell disease: Specificities of most common antibodies.
K, C, E, Fy-a, Jk-b.
162
Transfusion in sickle-cell disease: Rate of alloimmunization per unit of phenotypically
A. Unmatched blood.
B. Matched blood.
A. 3%.
B. 0.5%.
163
Class I hemorrhage: Amount.
<15% of blood volume (750 mL).
164
Class II hemorrhage:
A. Amount.
B. Treatment.
A. 15-30% of blood volume.
B. Fluid resuscitation usually suffices.
165
Class III hemorrhage:
A. Amount.
B. Treatment.
A. 30-40% of blood volume.
B. Fluid resuscitation first; transfusion usually necessary.
166
Class IV hemorrhage:
A. Amount.
B. Treatment.
A. >40% of blood volume.
B. Fluid resuscitation first; transfusion necessary.
167
When to switch from fluid resuscitation to transfusion when treating a hemorrhage.
When 30 mL/kg (about 2 L) fluid have been given.
168
Emergency release of cells: Documentation.
Signed release by treating physician within 24 hours.
Unit labeled as not having undergone compatibility testing.
169
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. 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
Emergency release to one with known anti-C and/or anti-E.
Rh-negative blood should be released.
171
Complications of massive transfusion (6).
Hypothermia.
Decreased pH.
Decreased release of oxygen from transfused cells.
Hyperkalemia.
Increased free hemoglobin.
Coagulopathy.
172
Definitions of therapy Categories I-IV.
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
Indications for apheresis: Category I (7).
TTP.
Guillain-Barré syndrome.
Goodpasture's syndrome.
ANCA-positive RPGN.
Chr. inflammatory demyelinating polyneuropathy.
Hyperviscosity syndrome with IgM.
Severe or symptomatic cryoglobulinemia.
174
Indications for apheresis: Category II (5).
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
Indication for apheresis: Category III.
Humoral rejection of cardiac transplant.
176
Indications for apheresis: Category IV.
Diarrhea of the hemolytic-uremic syndrome.
ITP.
Lupus nephritis.
177
Apheresis: Permissible replacement fluids.
Normal saline.
5% albumin.
Allogeneic plasma.
178
Apheresis: Properties of drugs that may be readily removed by it.
Much binding to protein.
Low volume of distribution.
179
Type of drug that should be discontinued before apheresis.
ACE inhibitor, 24 hours before.
180
Blood for a neonatal/intrauterine transfusion must be ___ (5).
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
Neonatal/intrauterine transfusion: Dose of RBCs.
10-15 mL/kg.
182
Neonatal/intrauterine transfusion: Dose of FFP.
10-15 mL/kg.
183
Neonatal/intrauterine transfusion: Dose of platelets.
5-10 mL/kg.
184
Neonatal/intrauterine transfusion: Dose of cryoprecipitate.
1-2 units per kg.
185
Maternal ITP: Possible neonatal complications.
Severe thrombocytopenia.
Serious hemorrhage.
186
Neonatal alloimmune thrombocytopenia: Antigen and its frequency.
HPA 1a, 98%.
187
Neonatal alloimmune thrombocytopenia: Relevance to number of pregnancies.
Can occur in the first pregnancy.
Gets worse with each pregnancy.
188
Neonatal alloimmune thrombocytopenia: Main complication and its incidence.
Intracranial hemorrhage; 20%.
189
Neonatal alloimmune thrombocytopenia:
A. How soon can platelets be given?
B. What kind?
C. Can maternal platelets be given?
A. As early as 18 weeks of gestation.
B. Antigen negative.
C. Yes, if washed and irradiated.
190
Neonatal alloimmune thrombocytopenia: Other treatments.
IVIg.
Corticosteroids.
191
Neonatal alloimmune thrombocytopenia: Period of greatest risk of postnatal hemorrhage.
24-36 hours after delivery.
192
Antibodies that can cross the placenta.
IgG1, IgG3, IgG4.
193
Sensitization to the D antigen in an Rh-negative mother: Incidence.
About 15%.
194
Sensitization to the D antigen in an Rh-negative mother: Relevance to ABO group.
Less likely if there is ABO incompatibility between mother and fetus.
195
Rosette test for fetal-maternal hemorrhage:
A. Rôle of test.
B. Sensitivity.
A. Qualitative.
B. Detects as little as 10 mL of fetal blood.
196
Rosette test for fetal-maternal hemorrhage:
A. Response to a negative result.
B. Response to a positive result.
A. If there is clinical suspicion of fetal-maternal hemorrhage, then give 300 μg RhIg.
B. Proceed to a quantitative test.
197
Kleihauer-Betke test: Principle.
HbF resists elution by acid; fetal cells will appear bright red.
198
Titer of maternal anti-D:
A. Critical value.
B. What to do about it.
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
Preventive dose of RhIg in routine cases:
A. When to give.
B. How much to give.
A. At 28 weeks of gestation and at term.
B. 300 μg.
200
Preventive dose of RhIg in the event of a fetal-maternal hemorrhage: How much to give.
300 μm plus the amount corresponding to amount of the hemorrhage.
201
Situations in which RhIg is not indicated.
D-positive mother.
D-negative mother who has already made anti-D antibodies.
202
A 90-kg mother with a Kleihauer-Betke result of 2%: How many vials of RhIg should she receive?
90 kg × 0.7 = 6.3 L (blood volume).
6. 3 × 2 (percent) / 3 = 4.2.
4. 2 + 1 = 5.2.
Round to nearest whole number: 5 vials.
203
Routes of administration of RhIg.
Intramuscular: No more than 5 vials at a time.
Intravascular: Continuous infusion.
204
Hemolytic disease of the newborn, ABO mediated:
A. Severity.
B. Antibody.
C. Relevance to number of pregnancies.
A. Mild.
B. IgG anti-A,B.
C. May affect the first pregnancy.
205
Hemolytic disease of the newborn: Most common antigens implicated in severe disease.
K, C.
206
Hemolytic disease of the newborn due to anti-K:
A. Why so severe?
B. Critical titer of maternal antibody.
A. Because the K antigen is found on red-cell precursors.
B. 1 : 8.
207
Hemolytic disease of the newborn: Screening tests performed upon admission to the labor-and-delivery unit (3).
Maternal antibody screen.
ABO and Rh of cord blood.
DAT of cord blood.
208
Hemolytic disease of the newborn: Response to a positive DAT.
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
RBCs and whole blood: Shelf life in AS solutions.
42 days.
210
RBCs and whole blood: Shelf life in CPD or CP2A.
21 days.
211
RBCs and whole blood: Shelf life in CPDA-1.
35 days.
212
RBCs and whole blood: Storage temperature.
1 to 6 degrees.
213
RBCs: Required hematocrit.
No more than 80%.
214
Apheresis RBCs: Required hemoglobin.
At least 50 g.
215
RBCs: Conditions of freezing.
10 years at -65 degrees.
216
RBCs, thawed: Conditions of storage.
24 hours at 1 to 6 degrees.
217
Washed RBCs: Conditions of storage.
24 hours at 1 to 6 degrees.
218
Leukocyte-reduced RBCs: Special QC requirements.
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
Irradiated RBCs: Shelf life.
28 days or the original expiration date, whichever is sooner.
220
RBCs: Temperature during transportation.
1 to 10 degrees.
221
RBCs: Shelf life after "spiking" (2).
24 hours at 1-6 degrees.
4 hours at room temperature.
222
RBCs: Usual volume and iron concentration.
350 mL; 1 mg/mL.
223
Platelets: Conditions of storage.
5 days at 20-24 degrees, with gentle agitation.
224
Platelets pooled in an open system: Conditions of storage.
4 hours at 20-24 degrees.
225
Platelets: Required quantity (2).
Random donor: 5.5 × 10¹⁰ in 90% of units.
Apheresis: 3.0 × 10¹¹ in 90% of units.
226
Platelets: Required pH.
At least 6.2 in 90% of units.
227
Leukocyte-reduced platelets:
A. Required quantity of platelets per unit.
B. Maximum allowable WBCs.
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
Granulocytes: Conditions of storage.
24 hours at 20-24 degrees; no agitation.
229
Granulocytes: Required quantity per unit.
1 × 10¹⁰ in 95% of units.
230
Plasma: Conditions of freezing.
1 year at -18 degrees.
7 years at -65 degrees.
231
Plasma, thawed: Conditions of storage.
24 hours at 1 to 6 degrees.
232
Cryoprecipitate: Conditions of freezing.
1 year at -18 degrees.
233
Cryoprecipitate, thawed and unpooled: Conditions of storage.
6 hours at 20-24 degrees.
234
Cryoprecipitate, thawed and pooled: Conditions of storage.
4 hours at 20 to 24 degrees.
235
Cryoprecipitate: Required contents.
Fibrinogen, at least 150 mg, in all units.
Factor VIII, at least 80 IU, in all units.
236
RBCs: Amount of anticoagulant-preservative per unit.
About 60 mL.
237
Contents of CPDA preservative.
Citrate.
Phosphate.
Dextrose.
Adenine.
238
Contents of additive solutions.
Buffers.
Adenine.
NaCl.
Dextrose.
239
Platelets: Who needs crossmatched units (2)?
Neonates.
Recipients of many transfusions.
240
Which additives contain mannitol?
AS-1, AS-5.
241
RBCs: Biochemical changes that occur during storage.
Decreased pH.
Decreased ATP.
Decreased DPG.
Increased potassium.
Increased free hemoglobin.
242
RBCs: How long may a unit remain unrefrigerated?
Up to 30 minutes.
243
RBCs: How long can they wait to be frozen?
With additive solution: No later than the expiration date of the unit.
Without additive solution: No later than 6 days after collection.
244
Leukocyte reduction of frozen RBCs.
Not necessary.
245
RBCs: Pediatric dose required to raise the hemoglobin by 1 g/dL.
About 4 mL/kg.
246
RBCs: Relative contraindications.
Autoimmune hemolytic anemia.
Hyperhemolytic syndrome in sickle-cell disease.
247
Platelets: How long can they go without agitation?
Up to 24 hours.
248
Platelets:
A. Volume of a single-donor unit.
B. Fibrinogen content of the same.
A. About 50 mL.
B. About 80 mg.
249
Platelets:
A. Volume of an apheresis unit.
B. Fibrinogen content of the same.
A. About 100 mL.
B. About 150 mg.
250
Thresholds for transfusion of platelets:
A. Healthy non-bleeding patient.
B. Bleeding patient with extracranial hemorrhage.
A. 10,000/μL.
B. 50,000/μL.
251
Thresholds for transfusion of platelets: Intracranial hemorrhage.
100,000/μL.
252
Thresholds for transfusion of platelets:
A. Neurosurgical patient.
B. Other surgical patients.
A. 100,000/μL.
B. 50,000/μL.
253
Platelets: Use in renal failure.
DDAVP or cryoprecipitate should be tried first.
254
Platelets: Relative contraindication.
ITP.
255
Platelets: Absolute contraindications (2).
TTP.
Heparin-induced thrombocytopenia.
256
Platelets: Expected increase in count following transfusion of 1 apheresis unit.
About 30,000/μL.
257
Platelets:
A. When to use a filter.
B. When to crossmatch.
A. Always.
B. When the unit is grossly bloody.
258
Platelets: Rh matching.
Recommended.
259
Platelets: Shelf life of pooled unit.
A. Open system.
B. Closed system.
A. 4 hours at 20-24 degrees.
B. 5 days or expiration date of oldest random-donor unit; 20-24 degrees.
260
"Thawed plasma":
A. Definition.
B. Shelf life.
A. Plasma that has been kept refrigerated for 24 hours.
B. 5 days at room temperature.
261
FP24:
A. Definition.
B. Uses.
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
FFP: Prescribed temperature of thawing.
30-37 degrees.
263
Plasma:
A. Volume.
B. Contents.
A. About 200 mL.
B. Fibrinogen, about 200 mg; coagulation factors, about 1 IU/mL of each.
264
Plasma: PTT, PT, and INR values that often lead to transfusion.
PTT, PT: About 1.5 × normal.
INR: About twice normal.
265
Plasma: Indication other than correction of coagulopathy.
Treatment of deficiency of C1 esterase inhibitor.
266
Plasma: Use in reversal of anticoagulation.
Heparin: Not indicated.
Warfarin: As a last resort.
267
Dose of plasma:
A. Adults.
B. Neonates.
10-15 mL/kg for both.
268
Plasma: Timing of transfusion relative to an invasive procedure.
No more than 2 hours before incision.
269
Plasma: Expected effect on activities of coagulation factors.
About a 20% increase in each one.
270
Plasma: Rh matching.
Not important.
271
Cryoprecipitate: How made.
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
Cryoprecipitate: Volume.
15 mL.
273
Cryoprecipitate: Contents.
Fibrinogen.
Factor VIII.
Factor XIII.
vWF.
274
Cryoprecipitate: What it does not contain.
Factor V.
275
Cryoprecipitate: Effect on plasma fibrinogen.
An increase of 7 mg/dL per unit (70 mg/dL per pool of 10 units).
276
Cryoprecipitate: Indications (4).
Replacement of fibrinogen or factor XIII.
Treatment of von Willebrand's disease.
Treatment of bleeding in uremic patients.
As fibrin glue.
277
Factor VII concentrate: Indications (2).
Treatment of inherited deficiency of factor VII.
Treatment of suspected inhibitor of factor VIII or factor IX.
278
Humate-P: Indications.
Treatment of
− Factor VIII deficiency.
− Von Willebrand's disease.
279
Factor VIII: Half-life and intravascular recovery.
12 hours; nearly 100%.
280
Factor IX: Half-life and intravascular recovery.
24 hours; about 50%.
281
Irradiation of blood products: Required dose.
25 Gy to the center of the product.
At least 15 Gy to the periphery.
282
Irradiation of blood products: Purpose.
Prevention of transfusion-associated GVHD.
283
Irradiation of blood products: Who needs it?
```
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
Leukocyte-reduction of blood products: Indications (4).
Prevention of
− HLA alloimmunization.
− Febrile non-hemolytic transfusion reaction.
− CMV transmission.
− Transfusion-related immune modulation.
285
Washing of blood products: Indications (2).
Prevention of allergic transfusion reactions, esp. in IgA-deficient recipients.
Removal of incompatible plasma from cellular products to be given to neonates.
286
Type 1 and type 2 precursor carbohydrates: Locations.
Type 1: Secretions.
Type 2: Red cells.
287
Origin of H antigen.
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
Origin of Lewis antigens.
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
Relevance of Lewis antigens to microbiology.
H. pylori and Norwalk virus attach via Le-b.
290
Relevance of Lewis antigens to tumor biology.
CA 19-9 is Le-a.
291
Origin of A antigen.
Action of product of A gene (N-acetylgalactosamine transferase) on type 1 and 2 chains.
292
Origin of B antigen.
Action of product of B gene (galactosyltransferase) on type 1 and 2 chains.
293
I and i antigens: Differences.
I: Branched type 1 and 2 chains; found in adults.
i: Simple chains; found in neonates.
294
Causes of postnatal expression of i antigen.
Congenital dyserythropoietic anemia, type 2.
Diamond-Blackfan anemia.
High turnover of cells.
295
A₁ and A₂:
A. Difference.
B. Distribution.
A. A₁ cells have much more A antigen.
B. A₁: 80% of group A.
296
A₁ and A₂: Distinction in the blood bank (3).
A₁: Stronger reaction with Dolichos biflorus and with anti-A₁ made by individuals of group B.
A₂: Stronger reaction with Ulex europaeus.
297
Anti-A₁:
A. Frequency.
B. Clinical significance.
A. A₂: 5%; A₂B: 35%.
B. Usually none.
298
Bombay vs. para-Bombay.
Bombay type: No H gene, no Se gene.
Para-Bombay type: No Se gene.
299
ABO distribution: Whites.
O: 45%.
A: 40%.
B: 10%.
AB: 5%.
300
ABO distribution: Blacks.
O: 50%.
A: 25%.
B: 20%.
AB: 5%.
301
ABO distribution: Hispanics.
O: 55%.
A: 30%.
B: 10%.
AB: 5%.
302
D-positivity: Distribution.
Whites: 82%.
Blacks, Hispanics: 92%.
303
H antigen: Amount on cells by ABO type.
O > A₂ > B > A₂B > A₁ > A₁B.
304
Gene frequency: Se.
80%.
305
How do Lewis antigens end up on red cells?
Through passive adsorption.
306
Causes of the phenotype Le(a-b-).
Neonatal state.
Pregancy.
Absence of Le gene.
307
Distribution of Lewis phenotype in whites.
Le(a+b-): 22%.
Le(a-b+): 72%.
Le(a-b-): 6%.
308
Distribution of Lewis phenotype in blacks.
Le(a+b-): 22%.
Le(a-b+): 55%.
Le(a-b-): 23%.
309
Predict the Lewis phenotype:
A. Le/Se.
B. Le/se.
C. le/Se.
D. le/se.
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
ABO antigens:
A. When first detectable.
B. When adult levels are reached.
A. At 3-6 months.
B. At about 2 years.
311
Major vs. minor ABO incompatibility.
Major: Incompatible red cells.
Minor: Incompatible plasma.
312
Most common specificity of Lewis antibodies.
Le-a.
313
Why Lewis antigens rarely cause hemolytic transfusion reactions (2).
The transfused cells take on the Lewis phenotype of the recipient.
Lewis antibodies get neutralized by circulating free Lewis antigen.
314
Why Lewis antigens do not cause hemolytic disease of the newborn (2).
Fetuses have no Lewis antigens.
The typical Lewis antibody is IgM and thus cannot cross the placenta.
315
I and i antigens: Microbiological associations.
I: Mycoplasma pneumoniae.
i: Infectious mononucleosis.
316
Groups to which the following antigens belong: P, P-k, P1.
P and Pk: GLOB.
P1: The only member of the P system.
317
P antigen: Associations.
Paroxysmal cold hemoglobinuria.
Parvovirus B19.
318
P phenotypes: Expressed antigens.
P1 phenotype: P and P1, but not P-k.
p phenotype: No P antigens.
319
Antibodies made by those with the p phenotype:
A. Names.
B. Associations.
A. Anti-PP1P-k, anti-Tj-a.
B. Acute hemolytic transfusion reaction, spontaneous abortion.
320
Agglutinators of the P antigen.
Pigeon eggs.
Hydatid-cyst fluid.
321
Rh genes: Chromosome.
1.
322
Rh antigens: Structure.
Transmembrane proteins with many extracellular domains.
323
Most common Rh-negative genotype.
r/r (dce/dce).
324
Wiener's notations: Rh-positive.
R₀: Dce.
R₁: DCe.
R₂: DcE.
Rz: DCE.
325
Wiener's notation: Rh-negative.
r: dce.
r': dCe.
r'': dcE.
r-y: dCE.
326
Most common Rh combinations in
A. Whites.
B. Blacks.
A. R₁ > r > R₂ > R₀.
B. R₀ > r > R₁ > R₂.
327
Rh-null state: Other affected antigens.
LW.
Fy5.
S, s, U.
328
Rh-null state: Hematological manifestations.
Stomatocytosis, mild anemia.
329
Rh-null state: Transfusion.
Requires Rh-null blood.
330
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. No antibody is made.
B. Sensitization can occur.
331
Weak-D state:
A. Traditional definition.
B. Current reality.
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
Weak-D state: Causes.
Most common: Mutation in the RHD gene imparts weakened expression.
Another cause: Presence of Ce on the other chromosome.
333
What happens when a partial-D individual
A. Receives D-positive blood?
B. Gives blood to a D-negative person?
Sensitization can occur in either case.
334
Partial-D state: How recognized.
A D-positive person is found to be making anti-D antibodies.
335
Rh antigens: Rate of sensitization after emergent transfusion.
About 20-30%.
336
Rh antibodies that often occur together; why?
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
Why is important to remember that a patient with anti-E will often has anti-c as well?
Because anti-c can be undetectable but can still cause delayed HTR.
338
Anti-G:
A. Definition.
B. Significance.
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
Anti-f:
A. Definition.
B. Significance.
A. Antibody to the combination ce.
B. Can cause mild HTR and mild HDN.
340
Kidd phenotypes: Whites.
Jk(a+b-): 25%.
Jk(a-b+): 25%.
Jk(a+b+): 50%.
341
Kidd phenotypes: Blacks.
Jk(a+b-): 50%.
Jk(a-b+): 10%.
Jk(a+b+): 40%.
342
Kidd antibodies: Associated reactions.
Delayed HTR: Often severe, intravascular.
Acute HTR: Severe.
HDN: Mild.
343
Duffy antigens: Microbiological association.
Point of entry of P. vivax.
344
Duffy antibodies: More significant.
Anti-Fy-a.
345
Duffy antibodies: Reactions (2).
Delayed HTR: Severe, usually extravascular.
HDN: Mild.
346
Frequency of Fy(a-b-) in black populations.
68% in the United States; higher in Africa.
347
M and N antigens: Location.
On glycophorin A.
348
M and N antigens: Distribution.
M+N-: 25%.
M-N+: 25%.
M+N+: 50%.
349
S, s, and U antigens: Location.
On glycophorin B.
350
S, s, and U antigens: Frequency.
S: 55%.
s: 90%.
U: 99%.
351
Anti-N: Significance.
Occurs only in those who lack glycophorin B, which contains an N-like domain ('N').
352
Anti-Nf.
Antibody to an N antigen that has been modified by exposure to formalin, as in hemodialysis.
353
Kell antigens: Frequency of
A. K.
B. Kp-a.
C. Js-a.
A. 9%.
B. 2%.
C. 0.1% in whites, 20% in blacks.
354
Kell antigens: Frequency of
A. k.
B. Kp-b.
C. Js-b.
All: >99%.
355
Age at one may donate blood products.
17 (in some states, at age 16 with parental consent).
356
Kell-null phenotype: Expression of antigens.
No Kell antigens.
Overexpression of non-Kell antigen Kx.
357
McLeod phenotype: Expression of antigens.
No Kx.
Weakened expression of Kell antigens.
358
McLeod phenotype: Hematological manifestations.
Acanthocytosis.
Frequent association with chronic granulomatous disease.
359
McLeod phenotype: Other clinical associations.
Retinitis pigmentosa.
Muscular dystrophy of late onset.
360
McLeod phenotype: Transfusion.
Requires McLeod-type blood.
361
Absence of Diego antigen: Hematological associations (3).
Hereditary elliptocytosis.
Hereditary spherocytosis.
Acanthocytosis.
362
Absence of Gerbich antigen: Hematological association.
Hereditary elliptocytosis.
363
Antibodies that give a mixed-field reaction.
Anti-Lutheran.
Anti-Sd.
364
Agents that diminish the expression of Kell antigens.
ZZAP.
2-mercaptoethanol.
Dithiothreitol.
365
Lutheran antigens: Frequency.
Lu-a: 7%.
Lu-b: 99%.
366
MHC III proteins:
A. Location of genes.
B. Examples (4).
A. 6p21.3.
B. Complement proteins, CYP21 (21-hydroxylase), HFE, TNF.
367
HLA class I: Structure of antigens.
A single transmembrane polypeptide chain that is noncovalently bound to β₂-microglobulin.
368
HLA class I: Expression of antigens on red cells.
Most are found only on young cells; Bg antigens are found on all red cells.
369
HLA class I: Expression of antigens on platelets.
Present.
370
HLA class II: Structure of antigen.
Two polypeptide chains, α and β, that share a sequence with light-chain immunoglobulins.
371
HLA Class II: Expression of antigens on red cells and platelets.
Absent.
372
How to estimate the probability of a HLA-matched sibling.
P = 1 - 0.75^n,
where n is the number of siblings.
373
Transfusion reactions: What to do when the posttransfusion serum sample is drawn late and no hemolysis can be seen.
Inspect for icterus; if present, the serum bilirubin will remain elevated for 24-36 hours after the reaction.
374
Transfusion reactions: Steps of investigation.
Clerical check.
Inspection of serum sample for hemolysis / icterus.
Recheck of ABO group.
DAT.
375
Transfusion reactions: Whom to notify in case of death or serious morbidity.
FDA: Within 24 hours by telephone, within 7 days in writing.
Donor center: Immediately by telephone, to be followed by written notification.
376
Transfusion-related infection: Whom to notify (3).
Donor center.
All recipients of products from that donor.
Patient's physician.
377
Transfusion reactions: Most common type.
Febrile, non-hemolytic.
378
Febrile, non-hemolytic transfusion reaction:
A. Cause.
B. Prevention.
A. Cytokines released by leukocytes within the bag.
B. Leukocyte reduction.
379
Allergic transfusion reaction:
A. Cause.
B. Prevention (3).
A. IgE-mediated reaction to foreign plasma proteins.
B. Washing of blood products; premedication with antihistamines; giving IgA-deficient blood products.
380
Extravascular hemolysis: Clinical presentation.
Usually asymptomatic but may present with pallor, anemia, hyperbilirubinemia.
381
Delayed serologic transfusion reaction: Definition.
A transfusion reaction in which there is a new alloantibody but neither hemolysis nor symptoms.
382
Delayed hemolytic transfusion reaction: Laboratory findings.
Positive DAT (mixed-field) reaction.
Microspherocytosis.
Hyperbilirubinemia.
383
Delayed hemolytic transfusion reaction: Implicated antibodies.
Intravascular: Anti-Kidd.
Extravascular: Anti-Duffy, anti-c, anti-E, anti-Kell.
384
Delayed hemolytic transfusion reaction:
A. Time of presentation.
B. Treatment.
A. 5-14 days after the transfusion.
B. Usually none is required.
385
Transfusion-related sepsis: Incidence and mortality
A. For platelets units.
B. For red-cell units.
A. 1 in 25,000; 25%.
B, 1 in 250,000; 70%.
386
Transfusion-related sepsis: Causative organisms.
A. In platelet units.
B. In red-cell units.
A. Staphylococci.
B. Yersinia enterocolitica.
387
Transfusion-related sepsis: Laboratory findings.
Gram stain of blood product may be positive.
There may be free hemoglobin in urine and/or serum, but the DAT is negative.
388
Approximate probability of transfusion-related transmission of
A. HIV.
B. HCV.
C. HTLV-1.
A,B. 1 in 2 million.
C. 1 in 3 million.
389
Approximate probability of transfusion-related transmission of HBV.
1 in 200,000.
390
Transfusion-related GVHD: Clinical manifestations (4).
Rash.
Enterocolitis.
Hepatitis (elevated liver enzymes).
Marrow suppression.
391
Transfusion-related GVHD: Prevention.
Irradiation of blood products.
392
Leading cause of transfusion-related fatality.
Transfusion-related acute lung injury.
393
Transfusion-related acute lung injury:
A. Incidence.
B. Mortality.
A. 1 in 5000.
B. 5-10%.
394
Transfusion-related acute lung injury: Proposed diagnostic criteria (4).
Onset within 6 hours after transfusion.
Hypoxemia.
Bilateral pulmonary infiltrates.
No other explanation for symptoms.
395
Transfusion-related acute lung injury: Proposed mechanism.
Antibodies against HLA or other antigens cause clumping of granulocytes within the pulmonary microvasculature.
396
Transfusion-related acute lung injury: Clinical finding other than respiratory distress.
Fever.
397
Transfusion-related acute lung injury: Risk factors
A. In the patient.
B. In the donor.
A. Chemotherapy, cardiac bypass.
B. Multiparity.
398
Transfusion-related acute lung injury: How to distinguish from circulatory overload.
In circulatory overload, there is
− A rapid response to diuretics.
− An increased PCW pressure.
− An increased BNP.
399
Transfusion-related acute lung injury: How to distinguish from anaphylaxis (3).
In anaphylaxis, there is
− A rapid response to epinephrine.
− Wheezing and edema of the upper airways.
− Usually no pulmonary infiltrate.
400
Transfusion-related acute lung injury: Period of recovery.
Up to 72 hours.
401
Posttransfusion purpura: Time of onset.
2-14 days after the transfusion.
402
Posttransfusion purpura: Typical victim.
Multipara.
403
Posttransfusion purpura: Mechanism.
Production of antibodies to HPA-1a leads to destruction of the transfused platelets and the native platelets.
404
Posttransfusion purpura: Period of recovery without treatment.
About 3 weeks.
405
Posttransfusion purpura: Treatment.
IVIg.
406
Platelet refractoriness: Causes.
Primary: Alloantibodies to HLA.
Secondary (more common): Infection, splenomegaly, DIC, amphotericin B.
407
Platelet refractoriness: Formula for corrected count increment (CCI).
Observed increase in platelet count × body surface area / number of transfused platelets.*
*in multiples of 10¹¹.
408
Platelet refractoriness: CCI associated with
A. Normal response.
B. Refractoriness.
A. >7500.
B. <5000.
409
Platelet refractoriness: Prevention (3).
Limit platelet transfusions.
Give only apheresis platelets.
Leukocyte reduction.
410
Testing of blood products for HCV (3).
Anti-HCV.
RIBA (if anti-HCV) is positive.
HCV RNA.
411
Testing of blood products for HBV (3).
Anti-HBc.
HBsAg.
HBV DNA (optional).
412
Testing of blood products for HIV.
Anti-HIV-1 and -2.
HIV RNA.
413
Testing of blood products for HTLV.
Anti-HTLV-1 and -2.
414
Prevention of transfusion-transmitted West Nile virus (2).
Nucleic-acid testing during outbreaks.
Exclusion of potential donors who have compatible symptoms.
415
Transfusion-associated imbalances of potassium.
Increased free potassium in blood products more often causes hyperkalemia, but hypokalemia can result from transcellular shifts.
416
Transfusion-associated hypothermia: Significance.
May exacerbate the effects of hypocalcemia and hyperkalemia.
417
Whole-body iron content at which overload can develop.
500 mg/kg.
418
Transfusion-related immune modification: Definition.
Immunosuppression due to transfusion of cellular products.
