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[Immunohematology] Lec > [9] CHAPTER IV LESSON 1 > Flashcards

[9] CHAPTER IV LESSON 1 Flashcards

1
Q

is the destruction of red blood cells (rbcs) of a fetus and neonate by antibodies produced by the mother.

A

Hemolytic disease of the fetus and newborn (hdfn)

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2
Q

: secondary to previous pregnancy or transfusion

A

Maternal antibody formation

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3
Q

Hemolytic disease of the fetus and newborn (hdfn)
Also known as

A

erythroblastosis fetalis

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4
Q

the initial diagnosis of maternal rbc alloimmunization is

A

serologic

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5
Q

After detection, the [?] of hdfn have been improved with advances in technology.

A

risk stratification and management

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6
Q

[?] have greatly increased the success of accurately diagnosing and adequately treating this disease.

A

Ultrasonography, doppler assessment of middle cerebral artery peak systolic velocity, cordocentesis, fetal dna analysis from amniotic fluid or maternal plasma, and intravascular intrauterine transfusion

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7
Q

reported a transfusion reaction from transfusing a husband’s blood to a postpartum woman.

A

Levine and Stetson

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8
Q

They postulated that the mother had been immunized to the father’s antigen through fetomaternal hemorrhage (FMH).

A

Levine and Stetson

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9
Q

The antigen was later identified as

A

RhD.

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10
Q

Maternal RBC alloimmunization can be caused by

A

previous pregnancy or previous transfusion.

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11
Q

Some authors suggest significant impact of [?] on development of future HDFN.

A

previous transfusion

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12
Q

Maternal RBC alloimmunization Causes:

A
  1. Rh BGS – anti-D
  2. ABO BGS – anti-A , anti-B
  3. Other antibodies – other Rh antibodies, Kell BGS
  4. Rarer antibodies – Duffy BGS, MNS BGS
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13
Q
  1. Rh BGS –
A

anti-D

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14
Q
  1. ABO BGS –
A

anti-A , anti-B

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15
Q
  1. Other antibodies –
A

other Rh antibodies, Kell BGS

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16
Q
  1. Rarer antibodies –
A

Duffy BGS, MNS BGS

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17
Q

Most common cause of HDFN

A

HDFN Caused By ABO

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18
Q

Maternal ABO antibodies that are IgG can cross the placenta and attach to the

A

ABO antigens of the fetal RBCs.

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19
Q

[?] are most likely to form high-titered IgG antiABO antibodies, ABO HDFN is nearly always limited to [?] with potent [?].

A

Group O individuals

A or B infants of group O mothers

anti-A,B antibodies

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20
Q

can occur in the first pregnancy and in any, but not necessarily all, subsequent pregnancies because it does not depend on previous foreign RBC stimulation.

A

ABO HDFN

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21
Q

Microspherocytes and increased RBC fragility are characteristic.

A

HDFN Caused By ABO

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22
Q

Like other forms of HDFN, the severity of the disease is independent of the presence of a positive DAT result or demonstrable anti-A, antiB, or anti-A,B in the eluate of the infant’s RBCs.

A

HDFN Caused By ABO

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23
Q

ABO HDFN causes a bilirubin peak at [?], which is later than with HDFN caused by other antibody specificities.

A

1 to 3 days

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24
Q

Phototherapy is usually sufficient for slowly rising bilirubin levels.

A

HDFN Caused By ABO

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25
Q

HDFN PATHOGENESIS

A
  1. HDFN Caused By ABO
  2. HDFN Caused by RBC Alloimmunization
  3. HEMOLYSIS, ANEMIA, AND ERYTHROPOIESIS
  4. BILIRUBIN
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26
Q

HDFN Caused by RBC Alloimmunization FACTORS:

A

A. Fetomaternal Hemorrhage

B. Maternal Factors

C. RBC Antibody Specificity

D. Influence of ABO Group

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27
Q

Previous pregnancy with [?] is the leading cause of maternal alloimmunization.

A

Fetomaternal Hemorrhage

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28
Q

Transplacental hemorrhage of fetal RBCs into the maternal circulation occurs in most women, but it is usually a very small amount (0.5 mL in 93% of women)

A

Fetomaternal Hemorrhage

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29
Q

Interventions such as amniocentesis and chorionic villus sampling and trauma to the abdomen can increase the risk of

A

Fetomaternal Hemorrhage

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30
Q

At delivery, the incidence is more than 50%; this is the time the placenta separates from the uterus, and fetal RBCs can enter the maternal circulation.

A

Fetomaternal Hemorrhage

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31
Q

Immunoglobulin class and subclass of the maternal antibody affects the severity of the HDFN.

A

Maternal Factors

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32
Q

Of the immunoglobulin classes (i.e., IgG, IgM, IgA, IgE, and IgD), only IgG is transported across the placenta.

A
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33
Q

The active transport of IgG begins in the [?] and continues until birth.

A

Maternal Factors

second trimester

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34
Q

Of all the RBC antigens, (?) is the most antigenic.

A

RBC Antibody Specificity

RhD

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35
Q

The common antigens in the Rh system (C, E, and c) are also potent immunogens and have been associated with moderate to severe cases of HDFN.

A

RBC Antibody Specificity

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36
Q

Of the non–Rh system antibodies,(?) is considered the most clinically significant in its ability to cause HDFN.

A

RBC Antibody Specificity

anti-Kell

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37
Q

When the mother is ABO-incompatible with the fetus (major incompatibility), the incidence of detectable fetomaternal hemorrhage is decreased.

A

Influence of ABO Group

38
Q

This apparent protection from RhD immunization is likely due to the clearing and/or hemolysis of ABO-incompatible (?)in the mother’s circulation before the RhD antigen can be recognized by her immune system.

A

Influence of ABO Group

RhD-positive fetal RBCs

39
Q

Common
Antibodies Identified in Prenatal Specimens That Can Cause HDFN

A

Anti-D
Anti-D + C
Anti-D + E
Anti-C
Anti-E
Anti-c
Anti-K

40
Q

Rare
Antibodies Identified in Prenatal Specimens That Can Cause HDFN

A

Anti-Fya
Anti-s
Anti-M
Anti-N
Anti-S
Anti-Jka

41
Q

Never
Antibodies Identified in Prenatal Specimens That Can Cause HDFN

A

Anti-Lea
Anti-Leb
Anti-I
Anti-IH
Anti-P1
Anti-e

42
Q

The maternal antibody crosses the placenta and binds to the

A

fetal antigen-positive cells

43
Q

occurs when maternal IgG attaches to specific antigens of the fetal RBCs.

A

Hemolysis

44
Q

The antibody-coated cells are removed from the circulation by the [?] of the fetal spleen.

A

macrophages

45
Q
  • Destruction of fetal RBCs and the resulting anemia stimulate the fetal bone marrow to produce RBCs at an accelerated rate, even to the point that immature RBCs (erythroblasts) are released into the circulation.
A

Erythroblastosis fetalis

46
Q

When the bone marrow fails to produce enough RBCs to keep up with the rate of RBC destruction, erythropoiesis outside the bone marrow is increased in the hematopoietic tissues of the [?].

A

fetal spleen and liver

47
Q

These organs become enlarged (hepatosplenomegaly), resulting in [?].

A

portal hypertension and hepatocellular damage

48
Q

Severe anemia and hypoproteinemia caused by decreased hepatic production of plasma proteins leads to the development of highoutput cardiac failure with generalized edema, effusions, and ascites, a condition known as [?].

A

hydrops fetalis

49
Q

The process of RBC destruction continues after birth as long as [?] persists in the newborn infant’s circulation.

A

maternal antibody

50
Q

There are three different phases of anemia caused by HDFN:

A

i. early (within 7 days of birth) due to antibody-mediated hemolysis;
ii. late hemolytic anemia (2 weeks or more after birth) due to continued hemolysis, the expanding intravascular compartment, and natural decline of hemoglobin levels; and
iii. late hyporegenerative anemia due to marrow suppression as a result of transfusions and IUT, antibody destruction of RBC precursors, and deficiency of erythropoietin

51
Q

due to antibody-mediated hemolysis;

A

i. early (within 7 days of birth)

52
Q

due to continued hemolysis, the expanding intravascular compartment, and natural decline of hemoglobin levels; and

A

ii. late hemolytic anemia (2 weeks or more after birth)

53
Q

due to marrow suppression as a result of transfusions and IUT, antibody destruction of RBC precursors, and deficiency of erythropoietin

A

iii. late hyporegenerative anemia

54
Q

RBC destruction releases hemoglobin, which is metabolized to [?] in different metabolic stages.

A

bilirubin

55
Q

During pregnancy, the [?] made by the fetus is transported across the placenta and conjugated by the maternal liver and safely excreted.

A

indirect bilirubin

56
Q

After birth, the immature infant liver cannot yet metabolize bilirubin efficiently, and this leads to the [?].

A

accumulation of unconjugated bilirubin and neonatal jaundice

57
Q

When a newborn infant is affected by HDFN, the levels of indirect bilirubin are higher due to the [?].

A

pathological RBC destruction

58
Q

With moderate to severe hemolysis of HDFN, the unconjugated, or indirect, bilirubin can reach levels toxic to the infant’s brain (generally, [?]), and if left untreated can cause [?] or permanent damage to the brain.

A

more than 18 to 20 mg/dL

kernicterus

59
Q

Levels of [?] in the fetal circulation and amniotic fluid may be elevated- does not cause clinical disease in the newborn.

A

total bilirubin

60
Q

After birth, accumulation of [?] can become a severe problem.

A

metabolic by-products of RBC destruction

61
Q

BILIRUBIN PATHOGENESIS
1. Fetomaternal [?]
2. Fetomaternal [?]
3. Maternal antibodies formed against [?]
4. During subsequent pregnancy, placental passage of [?]
5. Maternal antibody attaches to [?]
6. Fetal RBC [?]

A

incompatibility

hemorrhage

paternally derived antigens

maternal IgG antibodies

fetal RBC

hemolysis

62
Q

Effect of maternal antibody on the fetus:

A
  1. Hemolysis
  2. Erythroblastosis fetalis
  3. Hepatosplenomagaly
  4. Hydrops fetalis
63
Q

The rate of RBC destruction depends on antibody titer and specificity and on the number of antigenic sites on the fetal RBCs

A
  1. Hemolysis
64
Q

Destruction of fetal RBCs and the resulting anemia stimulate the fetal bone marrow to produce RBCs at an accelerated rate.

A
  1. Erythroblastosis fetalis
65
Q

Resulting in portal hypertension and hepatocellular damage

A
  1. Hepatosplenomagaly
66
Q

Severe anemia and hypoproteinemia leads to the development of high-output cardiac failure with generalized edema, effusions, and ascites.

A
  1. Hydrops fetalis
67
Q

is best done after birth.

A

Detection of ABO HDFN

68
Q

No single serologic test is diagnostic for

A

a. Postnatal Diagnosis

ABO HDFN.

69
Q

When a newborn develops jaundice within (?) after birth, various causes of jaundice need to be investigated.

A

a. Postnatal Diagnosis

12 to 48 hours

70
Q

is the most important diagnostic test.

A

a. Postnatal Diagnosis

DAT on the cord or neonatal RBCs

71
Q

on all delivered infants is highly recommended.

A

a. Postnatal Diagnosis

Collecting cord blood samples

72
Q

The sample should be collected by venipuncture to avoid contamination with maternal blood and Wharton’s jelly and should be anticoagulated for storage.

A

a. Postnatal Diagnosis

73
Q

If the neonatal infant develops jaundice, (?) can be carried out and the results can be assessed.

A

a. Postnatal Diagnosis

ABO, RhD, and DAT testing

74
Q

The recommended practice is to perform the type and antibody detection test at the first prenatal visit, preferably during the first trimester.

A

HDFN Caused by RBC Alloimmunization

75
Q

At that time, a maternal history must be taken to understand if there is a history of HDFN, the previous pregnancy outcomes, and whether there is a history of prior transfusions.

A

HDFN Caused by RBC Alloimmunization

76
Q

The prenatal specimen must be typed for

A

a. ABO, RhD and Antibody Screen

ABO and RhD.

77
Q

The antibody detection method, or (?), must be able to detect clinically significant IgG alloantibodies that are reactive at 37°C and in the antiglobulin phase.

A

a. ABO, RhD and Antibody Screen

indirect antihuman globulin test (IAT)

78
Q

If the antibody screen is nonreactive, repeat testing is recommended before RhIG therapy in RhD-negative prenatal patients and in the third trimester if the patient has been transfused or has a history of unexpected antibodies.

A

a. ABO, RhD and Antibody Screen

79
Q

To establish the immunoglobulin class, the serum can be treated with a sulfhydryl reagent, such as (?), and then retested with appropriate controls.

A

b. Antibody Identification

dithiothreitol or 2mercaptoethanol

80
Q

The J-chain of IgM antibodies will be destroyed by this treatment; IgG antibodies will remain reactive.

A

b. Antibody Identification

Sulfhydryl reagents

81
Q

If the antibody specificity is determined to be clinically significant and the antibody is IgG, further testing is required.

A

b. Antibody Identification

82
Q

Other than anti-D, the most common and most significant antibodies are anti-K, anti-E, anti-c, anti-C, and anti-Fya.

A

b. Antibody Identification

83
Q

The relative concentration of all antibodies capable of crossing the placenta and causing HDFN is determined by

A

c. Antibody Titers

antibody titration

84
Q

The patient serum or plasma is serially diluted and tested against appropriate RBCs to determine the highest dilution at which a reaction occurs.

A

c. Antibody Titers

85
Q

The method must include the indirect antiglobulin phase using antiIgG reagent.

A

c. Antibody Titers

86
Q

The result is expressed as either the reciprocal of the titration endpoint or as a titer score.

A

c. Antibody Titers

87
Q

The recommended method is the [?], with 60-minute incubation at 37°C and the use of anti-IgG reagent.

A

c. Antibody Titers

saline antiglobulin tube test

88
Q

For the recommended method, 16 is considered the critical titer.

A

c. Antibody Titers

89
Q

If the initial titer is 16 or higher, a second titer should be done at about (?).

A

c. Antibody Titers

18 to 20 weeks’ gestation

90
Q

A specimen of the father’s blood should be obtained and tested for the presence and zygosity (predicted copy number of the gene) of the corresponding blood group antigen to predict fetal risk of being affected by HDFN.

A

d. Paternal Phenotype and Genotype

91
Q

If the mother has anti-D and the father is RhD-positive, the paternal genotype determined by DNA methods is the only way to definitively determine how many copies of the RHD gene an RhD-positive person carries.

A

d. Paternal Phenotype and Genotype

92
Q

is the recommended test for RhD-positive fathers when the mother has anti-D antibody.

A

d. Paternal Phenotype and Genotype

RHD zygosity genotype testing

[Immunohematology] Lec (35 decks)

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