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[Immunohematology] Lec > [10] CHAPTER IV LESSON 2 > Flashcards

[10] CHAPTER IV LESSON 2 Flashcards

1
Q

A. MANAGEMENT OF THE FETUS

A
  1. Fetal Ultrasound
  2. Invasive Monitoring—Cordocentesis and Amniocentesis
  3. Intrauterine Transfusion
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2
Q

B. MANAGEMENT OF THE INFANT

A
  1. Cord Blood Testing
  2. Exchange Transfusion
  3. Simple Transfusions
  4. Phototherapy
  5. Intravenous Immune Globulin
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3
Q
  1. Cord Blood Testing
A

ABO Grouping

RhD Typing

Direct Antiglobulin Test

Elution

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4
Q

PREVENTION

A
  1. Selection of RBCs for Females
  2. Rh Immune Globulin
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5
Q
  1. Rh Immune Globulin
A

a. Dose and Administration

b. Maternal Weak D

c. Other considerations

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6
Q

At about (?), the clinical diagnosis of fetal anemia can be made using an ultrasound technique called

A

16 to 20 weeks’ gestation

fetal middle cerebral artery peak systolic velocity (MCA-PSV)

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7
Q

Readings are typically done every (?) to track the degree of fetal anemia; those that are greater than (?) multiples of the mean (MoM) are sensitive enough to predict significant fetal anemia in which intervention may be needed.

A

Fetal Ultrasound

2 weeks

1.5

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8
Q

Enhancement of blood flow, the umbilical vein is visualized at the level of the cord insertion into the placenta.

A

Invasive Monitoring—Cordocentesis and Amniocentesis

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9
Q

A spinal needle is inserted into the umbilical vein, and a sample of the fetal blood is obtained.

A

Invasive Monitoring—Cordocentesis and Amniocentesis

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10
Q

For risk stratification of fetal anemia, (?) to monitor amniotic fluid bilirubin levels has been replaced with MCA-PSV

A

Invasive Monitoring—Cordocentesis and Amniocentesis

amniocentesis

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11
Q

In the past, the concentration of (?) was used to estimate the extent of fetal hemolysis.

A

Invasive Monitoring—Cordocentesis and Amniocentesis

bilirubin pigment in the amniotic fluid

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12
Q

The amniotic fluid is tested by a (?) at 450 nm (the absorbance of bilirubin).

A

Invasive Monitoring—Cordocentesis and Amniocentesis

spectrophotometric scan optical density (∆OD)

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13
Q

The measurement is plotted on a graph (?) according to gestational age.

A

Invasive Monitoring—Cordocentesis and Amniocentesis

spectrophotometric scan optical density (∆OD)

Liley Curve Graph

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14
Q

An increasing or unchanging (?) as pregnancy proceeds predicts worsening of the hemolysis.

A

Invasive Monitoring—Cordocentesis and Amniocentesis

∆OD 450 nm

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15
Q

High values indicate severe and often life-threatening hemolysis (?) and require urgent intervention.

A

Invasive Monitoring—Cordocentesis and Amniocentesis

fetal hemoglobin less than 8 g/dL

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16
Q

is performed by accessing the fetal umbilical vein (cordocentesis) and injecting donor RBCs directly into the vein

A

Intrauterine transfusion

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17
Q

The goal is to maintain fetal hemoglobin above 10 g/dL.

A

Intrauterine Transfusion

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18
Q

Intrauterine Transfusion

Once initiated, the procedure is typically repeated every (?) until delivery to suppress fetal hematopoiesis.

A

2 to 4 weeks

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19
Q

The initial Intrauterine Transfusion is rarely performed after (?) gestation.

A

36 weeks’

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20
Q

Intervention in the form of intrauterine transfusion becomes necessary when one or more of the following conditions exists:

a. MCA-PSV indicates anemia (?).
b. [?] is noted on ultrasound examination.
c. Cordocentesis blood sample has hemoglobin level [?].
d. Amniotic fluid [?] results are high and/or increasing.

A

> 1.5 MoM

Fetal hydrops

less than 10 g/dL

∆OD 450 nm

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21
Q

Selection of RBC products for intrauterine transfusion

A

a. Group O
b. RhD-negative (or RhDpositive, depending on maternal blood group antibody)
c. Leukocyte reduced
d. Hemoglobin S negative
e. CMV-safe (CMV seronegative or leukocyte reduced)
f. Irradiated
g. Antigen-negative for maternal red blood cell antibody/antibodies
h. Hematocrit level greater than 70%

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22
Q

i. ABO antigens are not fully developed in newborn infants

A

ABO Grouping

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23
Q

ii. Infants do not have their own isohemagglutinins but may have those of the mother, so reverse grouping cannot be used to confirm the ABO group.

A

ABO Grouping

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24
Q

i. Rarely, the infant’s RBCs can be heavily antibodybound with (?), causing a false-negative Rh type, or what has been called (?)

A

RhD Typing

maternal anti-D

blocked Rh

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25
Q

ii. An eluate from these RBCs will reveal (?), and typing of the eluted RBCs will show reaction with (?).

A

RhD Typing

anti-D

anti-D

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26
Q

i. The most important serologic test for diagnosing HDFN is the [?] with (?).

A

Direct Antiglobulin Test

anti-IgG reagent

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27
Q

A positive test result indicates that there is antibody coating the infant’s RBCs

A

Direct Antiglobulin Test

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28
Q

however, the strength of the reaction does not correlate well with the severity of the HDFN.

A

Direct Antiglobulin Test

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29
Q

i. The preparation of an eluate may be helpful when the cause of HDFN is in question or suspected.

A

Elution

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30
Q

is the use of whole blood or equivalent to replace the neonate’s circulating blood and simultaneously remove maternal antibodies and bilirubin.

A

Exchange Transfusion

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31
Q

RBC units less than (?) from collection from the donor are selected to reduce the risk of (?).

A

Exchange Transfusion

7 to 10 days

hyperkalemia

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32
Q

After a (?) exchange transfusion, approximately (?) of the red blood cells have been replaced and (?) of the bilirubin has been removed.

A

Exchange Transfusion

two-volume

90%

50%

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33
Q

After the procedure, a platelet count should be performed to monitor for (?).

A

Exchange Transfusion

iatrogenic thrombocytopenia

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34
Q

The infant may receive small-volume or (?) RBC transfusions to correct anemia anytime from after birth to many weeks later.

A

Simple Transfusions

“top-off”

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35
Q

Many hospitals will keep (?) dedicated to an infant with HDFN and draw small aliquots from the parent RBC unit over time to decrease donor exposure over multiple transfusion episodes.

A

Simple Transfusions

1 unit

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36
Q

is used to metabolize the unconjugated bilirubin to isomers that are less lipophilic, less toxic to the brain, and able to be excreted through urine.

A

Phototherapy at 460 to 490 nm

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37
Q

is used to treat hyperbilirubinemia of the newborn caused by HDFN.

A

Intravenous immune globulin (IVIG)

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38
Q

competes with the mother’s antibodies for the Fc receptors on the macrophages in the infant’s spleen, reducing the amount of hemolysis.

A

Intravenous immune globulin (IVIG)

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39
Q

First pregnancy can be affected ABO

A

Yes

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40
Q

First pregnancy can be affected RhD

A

Rare

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41
Q

Disease predicted by titers ABO

A

No

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42
Q

Disease predicted by titers RhD

A

Yes

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43
Q

Causative antibody IgG ABO

A

Yes (AntiA,B)

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44
Q

Causative antibody IgG RhD

A

Yes (AntiD, etc)

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45
Q

Bilirubin level at birth ABO

A

Normal range

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46
Q

Bilirubin level at birth RhD

A

Elevated

47
Q

Intrauterine Transfusion needed ABO

A

None

48
Q

Intrauterine Transfusion needed RhD

A

Sometimes

49
Q

Anemia at birth ABO

A

No

50
Q

Anemia at birth RhD

A

Yes

51
Q

Phototherapy beneficial ABO

A

Yes

52
Q

Phototherapy beneficial RhD

A

Yes

53
Q

Exchange Transfusion Needed ABO

A

Rare

54
Q

Exchange Transfusion Needed RhD

A

Uncommon

55
Q

In some countries, minor blood group antigens are matched (or provided as (?)) for women of childbearing potential.

A

Selection of RBCs for Females

negative

56
Q

For instance, a number of countries use (?) RBC units for women younger than (?).

A

Selection of RBCs for Females

K-negative

45 to 50 years of age

57
Q

Other nations provide additional matching for antigens such as (?).

A

Selection of RBCs for Females

c and E

58
Q

In a large international review of women with infants with severe HDFN, a transfusion policy of (?) for RBC transfusion did not provide protection from HDFN.

A

Selection of RBCs for Females

prospective antigen matching

59
Q

This appears to be driven by the fact that (?) of maternal sensitization that went on to cause severe HDFN was due to previous pregnancy and not transfusion itself.

A

Selection of RBCs for Females

83%

60
Q

The mechanism of action is uncertain.

A

Rh Immune Globulin

61
Q

Evidence indicates it interferes with B-cell priming to make anti-D, although other modes of action may occur.

A

Rh Immune Globulin

62
Q

Administration of corresponding RBC antibody to prevent active immunization induced by the RBC antigen

A

Rh Immune Globulin

63
Q

Bind to and inactivate (?) before the mother’s immune system can respond by producing her own (?).

A

Rh Immune Globulin

fetal Rh antigens

anti-Rh Ab’s

64
Q

should be given to RhD-negative mothers.

A

Rh Immune Globulin

65
Q

The first dose is provided at (?) gestation, as recommended by the American College of Obstetricians and Gynecologists.

A

Rh Immune Globulin

28 weeks’

66
Q

Based on experiments conducted many years ago, it is recommended to give [?] within (?) after delivery.

A

Rh Immune Globulin

72 hours

67
Q

Even if more than 72 hours have elapsed, [?] should still be given, as it may be effective and is not contraindicated.

A

Rh Immune Globulin

68
Q

The mother should be (?), and the infant should be (?).

A

Rh Immune Globulin

D-negative

D-positive or D-variant

69
Q

If the type of the infant is unknown (e.g., if the infant is stillborn), [?] should also be administered.

A

Rh Immune Globulin

70
Q
  • contains sufficient anti-D to protect against 15 mL of packed RBCs or 30 mL of whole blood.
A

Regular dose vial in the United States

71
Q

This is equal to 300 µg of the World Health Organization (WHO) reference material.

A

Regular dose vial in the United States

72
Q
  • contains about 100ug, which appears to be adequate for postpartum prophylaxis.
A

Regular dose vial in the United Kingdom

73
Q
  • can be used for abortions and ectopic pregnancies before the 12th week of gestation.
A

Microdose (United States)

74
Q

are approved for use in the United States.

A

Intravenous preparations (IV) of RhIG

75
Q

These products also contain 300 µg in each vial and can be administered either intramuscularly or intravenously.

A

Intravenous preparations (IV) of RhIG

76
Q

A maternal sample should be obtained within 1 hour of delivery and screened using a test such as the

A

rosette technique for massive fetomaternal hemorrhage

77
Q

If positive, quantitation of the hemorrhage must be done by

A

Kleihauer-Betke or by flow cytometry assays

78
Q

is treated with citric acid and then stained with counterstain.

A

Kleihauer-Betke test

Maternal blood smear

79
Q

which is resistant to acid and will remain pink.

A

Kleihauer-Betke test

Fetal cells contain fetal hemoglobin (Hgb F)

80
Q

will appear as ghosts.

A

Kleihauer-Betke test

maternal cells

81
Q

Kleihauer-Betke test

After 2,000 cells are counted, the percentage of fetal cells is determined, and the volume of fetal hemorrhage is calculated using this formula:

A

Kleihauer-Betke test

82
Q

Kleihauer-Betke test

Rounding Rules:
a. If calculated dose to the right of the decimal point is [?], then round up to the next whole number and add one vial.
b. If calculated dose to the right of the decimal point is [?], then round down to the next whole number and add one vial.

A

> /= to 0.5

< 0.5

83
Q

Because one [?] dose covers [?] of whole blood, the calculated volume of fetomaternal hemorrhage is then divided by [?] to determine the number of required vials of RhIG.

A

300-µg

30 mL

30

84
Q

Because the [?] is an estimate, one vial is added to the calculated answer. When needed, the additional vials of RhIG should be administered within [?] of delivery or as soon as possible.

A

Kleihauer-Betke

72 hours

85
Q

In certain patients, serologic reagents do not accurately detect the RhD type.

A

Maternal Weak D

86
Q

The most common genetic backgrounds that account for this serologic typing problem are called

A

Maternal Weak D

weak D phenotypes.

87
Q

Recently, authors have encouraged the use of (?) for patients with a weak D phenotype to provide accurate and actionable results for RhD blood typing and RhIG administration.

A

Maternal Weak D

RhD genetic testing

88
Q

Further scientific study is needed to elucidate the clinical significance of different RhD genotypes in various ethnic backgrounds and the risk factors for RhIG failure.

A

Maternal Weak D

89
Q

RhIG is of no benefit once a person has been actively immunized and has formed

A

anti-D

90
Q

RhIG is not indicated for the mother if the infant is found to be.

A

Dnegative

91
Q

The blood type of fetuses in [?] usually cannot be determined; therefore, RhIG should be administered in these circumstances.

A

abortions, still-births, and ectopic pregnancies

92
Q

The following women are not candidates for RhIg:

A
  1. D negative women who have D negative babies
  2. D positive women
  3. D negative women known to be immunized to D
93
Q

RhIg must be given to D negative women under the following circumstances in which the baby’s D is unknown:

A
  1. After amniocentesis
  2. After miscarriage
  3. After abortion
  4. After ectopic pregnancy
  5. Vaginal bleeding at anytime during the pregnancy
  6. Cordocentesis
  7. Chorionic villus sampling
94
Q

HDFN is prevented, monitored, and treated with the help of tests performed in the laboratory. Understanding the physiology of HDFN is important in choosing the correct tests to perform and detecting [?]. Important points to remember when performing these tests are outlined.

A

early indicators of hemolytic disease

95
Q

Fetal red cells, carrying antigens inherited from the father, stimulate the mother to produce

A

IgG antibodies

96
Q

destroy fetal red cells.

A

Maternal IgG antibodies

97
Q

In utero, this destruction can cause [?], which can result in heart failure and possibly death.

A

severe anemia

98
Q

After delivery, red cell destruction continues with the increase of bilirubin, causing [?] and possible damage to the CNS (?).

A

jaundice

kernicterus

99
Q

is the most common type of HDFN and occurs most commonly in group O mothers who deliver group A or B babies.

A

ABO HDFN

100
Q

is the most severe type of HDFN

A

HDFN caused by anti-D

101
Q

it occurs in D-negative women with anti-D who deliver D-positive infants.

A

HDFN caused by anti-D

102
Q

can cause HDFN if the child inherits the antigen from the father and the red cell antigen is well developed on the fetal red cells.\

A

Any IgG antibody

103
Q

are most frequently reported after anti-D.

A

Anti-c and anti-K

104
Q

are performed on the mother before delivery

A

ABO/D phenotype and antibody screen

105
Q

D-negative mothers before delivery should receive

A

prenatal RhIG

106
Q

can be helpful in deciding when to perform diagnostic and invasive procedures.

A

Titration of the maternal antibody

107
Q

can aid in predicting the severity of HDFN.

A

(?) of the amniotic fluid and use of the [?]

Spectrophotometric analysis

Liley graph

108
Q

determines whether a D-negative mother should receive postpartum RhIG.

A

Cord blood testing

109
Q

RhIG dosage is determined by the [?] performed on the mother.

A

fetal screen (rosette) and Kleihauer-Betke test

110
Q

If HDFN is suspected, [?] should be performed; hemoglobin and bilirubin levels should also be closely monitored.

A

ABO and D phenotype and DAT

111
Q

Depending on the severity of HDFN, treatment can begin [?].

A

in utero or after delivery

112
Q

After delivery, [?] is used to correct anemia, remove sensitized red cells, and reduce levels of maternal antibody and bilirubin.

A

exchange transfusion

113
Q

Blood for exchange and intrauterine transfusion should be [?].

A

less than 7 days old, irradiated, CMV-reduced-risk, hemoglobin S–negative, and negative for the antigen corresponding to the maternal antibody

114
Q

[?] resuspended in AB plasma are used most often.

A

Group O, D-negative RBCs

[Immunohematology] Lec (35 decks)

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