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Blood Bank > ABO Blood Group System > Flashcards

ABO Blood Group System Flashcards

1
Q

Basic precursor substance

A

Paragloboside/Glycan

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2
Q

Described the theory for the inheritance of the ABO groups

A

Bernstein (1924)

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3
Q

Expression of ABO is through

A

Codominance expression

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4
Q

Inheritance pattern of group O phenotype

A

Autosomal recessive

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5
Q

Presence of two identical alleles

A

Homozygous genotype

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6
Q

Inheritance of different alleles

A

Heterozygous genotype

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7
Q

Sequence of DNA that is inherited

A

Genotype

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8
Q

Anything that is produced by the genotype

A

Phenotype

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9
Q

Glycosyltransferase coded by H gene

A

A-2-L-fucosyltransferase

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10
Q

Glycosyltransferase coded by A gene

A

A-3-N-acetylgalactosaminyltransferase

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11
Q

Glycosyltransferase coded by B gene

A

A-3-D-galactosyltransferase

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12
Q

Immunodominant sugar of H gene

A

L-fucose

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13
Q

Immunodominant sugar of A gene

A

N-acetyl-D-galactosamine

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14
Q

Immunodominant sugar of B gene

A

D-galactose

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15
Q

ABO antigens form as early as

A

37th day of fetal life

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16
Q

Full expression of ABO antigens occur at what age

A

2-4 years

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17
Q

Precursor chain of ABO antigens on RBCs

A

Type 2

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18
Q

Precursor chain of ABO antigens in secretions

A

Type 1

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19
Q

Linkage of ABO antigens on RBCs

A

Beta 1-4 linkage

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20
Q

Linkage of ABO antigens in secretions

A

Beta 1-3 linkage

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21
Q

ABH secretions can be found in

A

DUBSTAMP

Digestive juices
Urine
Bile
Saliva
Tears
Amniotic fluid
Milk
Pathogenic fluid

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22
Q

Excessive ABH substances in secretions can be observed in

A

PIC

Pseudomucious ovarian cyst
Intestinal obstruction
Carcinoma of stomach and pancreas

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23
Q

Determination secretor status is by

A

Hemagglutination Inhibition

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24
Q

Unbranched straight chains of H antigens

A

H1 and H2

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25
Q

Complex branched chains of H antigens

A

H3 and H4

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26
Q

Reactivity of anti-H antisera or anti-H lecti with ABO blood groups

A

O > A2 > B > A2B > A1 > A1B

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27
Q

Reacts with anti-A1, anti-A, and anti-AB

A

A1

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28
Q

Reacts with anti-A and anti-AB

A

A2

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29
Q

MF reaction with anti-A and anti-AB

A

A3

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30
Q

Reacts with anti-AB, no recation with anti-A

A

Ax

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31
Q

MF reaction with anti-A and anti-AB but with only few agglutinates (<10% of cells)

A

Aend

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32
Q

Weak/no reaction with anti-A and anti-AB

A

Am

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33
Q

No reaction with anti-A and anti-AB

A

Ael

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34
Q

No reaction with anti-A and anti-AB; observed in siblings; germline mutation of an A gene

A

Ay

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35
Q

Method used to confirm the presence of Am, Ael, and Ay antigens

A

Adsorption & Elution

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36
Q

Predominantly Aa and Ab and unconverted H3 and H4 antigen sites

A

A2 RBCs

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37
Q

Aa, Ab, Ac, and Ad determinants and no unconverted H3 and H4 antigen sites

A

A1 RBCs

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38
Q

Reacts with anti-B and anti-AB

A

B

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39
Q

MF reaction with anti-B and anti-AB; most frequent B subtype

A

B3

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40
Q

Weak reaction with anti-B and anti-AB

A

Bx

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41
Q

No/Weak reaction with anti-B and anti-AB

A

Bm

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42
Q

Converts Bm subgroup to B when incubated with

A

Uracil diphosphate

43
Q

No reaction with anti-B and anti-AB: extremely rare phenotype

A

Bel

44
Q

Method used to confirm the presence of Bm and Bel antigens

A

Adsorption & Elution

45
Q

Phenotype that results in the inability to form the H antigen subsequently the A or B antigens

A

Bombay phenotype

46
Q

Bombay phenotype was first reported by

A

Dr. Y. M. Bhende (1952) in Bombay (Mumbai), India

47
Q

Causes silenced H gene

A

Mutation in FUT 1 gene

48
Q

Causes silenced Se gene

A

Mutation in FUT2 gene

49
Q

Antibodies in the serum of Bombay phenotype

A

Anti-A, Anti-B, Anti-AB, and Anti-H

50
Q

Bombay phenotype blood group

A

Group O

51
Q

Absent or only trace amount of ABH antigens on RBCs with normal expression in secretion or body fluids

A

Parabombay phenotype

52
Q

Causes of Parabombay phenotype

A

1) Mutated FUT1 gene w/ or w/o an active FUT2 gene

2) Silenced FUT1 gene with an active FUT2 gene

53
Q

Naturally occurring Abs directed against the A and/or B antigens absent from and individual’s RBCs

A

ABO Abs

54
Q

ABO Abs are produced at_____but detected only at _____months of age

A

Birth, 4-6 months

55
Q

ABO Abs are cold reacting

A

Predominantly IgM

56
Q

ABO ABs react at what temp

A

Room temp or after IS phase

57
Q

ABO Abs activate complement at what temp and can cause what

A

37 degC, cause in vitro/in vivo hemolysis

58
Q

Plants or seed extracts that agglutinate human cells

A

Lectins

59
Q

Anti-A1 lectin

A

Dolichos biflorus

60
Q

Anti-B lectin

A

Bandeiraea simplicifolia/ Griffonia simplicifolia

61
Q

Anti-H lectin

A

Ulex europaeus

62
Q

Anti-N lectin

A

Vicia graminea

63
Q

Anti-M lectin

A

Iberis amara

64
Q

Anti-T, Th lectin

A

Arachis hypogaea

65
Q

Anti-Tn lectin

A

Salvia sclarea

66
Q

ABO Ags appear as early as ___ , peak at ___ , and decline at ___

A

37th day of fetal life, 2-4 years old, remain constant throughout life

67
Q

ABO Abs appear as early as ___ , peak at ___ , and decline at ___

A

Birth (detected only at 3-6 months), 5-10 years old, after 10 years

68
Q

Using antisera to detect Ags on px RBCs

A

Forward grouping

69
Q

Typing sera must be:

A

1) monoclonal

2) IgG

3) highly specific

70
Q

Typing sera preservative

A

Formalin/ sodium azide

71
Q

Antisera QC that ensures the reactivity of antisera

A

Positive control

72
Q

Antisera QC that ensures the specificity of the antisera

A

Negative control

73
Q

Uses reagent RBCs to detect ABO Abs in px serum

A

Reverse grouping

74
Q

Reagent for reverse grouping

A

4-5% human red cells (A1 and B cells)

75
Q

Universal RBC donor

A

Type O

76
Q

Universal plasma donor

A

Type AB

77
Q

Universal RBC recipient

A

Type AB

78
Q

Universal plasma recipient

A

Type O

79
Q

Grading with one solid agglutinate

A

4+

80
Q

Grading several large agglutinates, clear bg

A

3+

81
Q

Grading with medium agglutinates, clear bg

A

2+

82
Q

Grading with small agglutinates, turbid bg

A

1+

83
Q

Grading with tiny agglutinates, turbid bg

A

W+

84
Q

Grading with no agglutination or hemolysis

A

0

85
Q

Conditions that cause weaker rxns

A

1) leukemia (MF)

2) chromosome 9 translocation

3) hemolytic dses

4) hogkin’s lymphoma

5) hypogammaglobulinemia/immunodeficiency

86
Q

Conditions that cause pseudoantigens

A

1) acquired A phenomenon

2) acquired B phenomenon

87
Q

Conditions that cause acquired A phenomenon: “PT”

A

1) P. mirabilis infxn

2) T cell inactivation

88
Q

Conditions that cause acquired B phenomenon: “EPIC-C”

A

1) E.coli 086 infxn

2) P.vulgaris infxn

3) Intestinal obstruction

4) Carcinoma of colon & rectum

5) C.tetani infxn

89
Q

How to differentiate acquired B fom true B

A

Acquired B cells will not react with pH <6 or > 8.5

90
Q

Most common source of ABO discrepancy

A

Incorrect specimen/labelling/recording of results

91
Q

Failure to add reagents/sample

A

False neg

92
Q

Cell suspension too heavy

A

False pos

93
Q

Cell suspension too light

A

False neg

94
Q

Contaminated reagents/materials

A

False pos

95
Q

Problem: reverse grouping
Causes: weakly reacting/missing Abs

A

Group l discrepancies

96
Q

Causes of group l discrepancies: “NE-HAPA”

A

1) newborn
2) elderly
3) hypogammaglobulinemia
4) agammaglobulinemia
5) plasma transfusion/exchange therapy
6) ABO subgroups

97
Q

Problem: forward grouping
Causes: weakly reacting Ags/missing Ags

A

Group ll discrepancies

98
Q

Causes of group ll discrepancies: “AWP”

A

1) ABO subgroups
2) weakend expression of A and B Ags
3) pseudoantigens

99
Q

A rare group ll discrepancy wherein the reagent anti-A or anti-B is neutralized, leaving no unbound Ab to react with px cells

A

Blood Group Specific Soluble (BGSS) substances

100
Q

Problem: forward and reverse groupings
Causes: plasma/protein abnormalities

A

Group lll discrepancies

101
Q

Causes of goup lll discrepancies: “EEP-W”

A

1) elevated globulin levels
2) eleavated fibrinogen
3) plasma expanders
4) wharton’s jelly in cord blood samples

102
Q

Plasma expanders that may cause group lll discrepancies

A

1) dextran
2) polyvinylpyrrolidone

103
Q

Problem: forward and reverse groupings
Causes: miscellaneous problems

A

Group IV discrepancies

104
Q

Causes of group IV discrepancies: “CUUM-P”

A

1) cold reactive autoantibodies
2) unexpected ABO isoagglutinins
3) unexpected non-ABO alloantibodies
4) more than one ABO group RBCs (transfusion, BM or stem cell transplant)
5) polyagglutination

Blood Bank (4 decks)

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