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The ABO and Rh Blood Group Systems Flashcards

1
Q

Who discovered the ABO Blood Group Systems?

A

Karl Landsteiner

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2
Q

At what age do antibodies appear?

A

3- 6 months

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3
Q

At what age do naturally occurring antibodies peak?

A

10 years old

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4
Q

What did Landsteiner demonstrate regarding a person’s serum and blood cells?

A

A person’s serums contained naturally occurring antibodies against an antigen absent from their own RBCs.

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5
Q

What is the reason for ABO incompatible organ transplantation?

A

ABO antigens are expressed in many other tissues. These antigens are a barrier against organ transplantation.

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6
Q

If the ABO antigen is present on the cells then______?

A

The corresponding antibody will be present inthe serum. If the ABO antibody is on the serum than the corresponding antigen will be absent on the RBC.

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7
Q

What is the result of ABO incompatible blood transfusion?

A

Acute intravascular hemolysis, renal failure and can be fatal.

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8
Q

ABO typing reagents are manufactured from ?

A

Monoclonal antibodies

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9
Q

What color are the anti-A and anti-B reagents?

A

Anti-A = Blue Anti-B = Yellow

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10
Q

What statement best describes the ABO antibody-antigen relationship?

A

There is always an inverse reciprocal relationship between the forward and reverse type. Thus one serves as a check on the other.

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11
Q

Forward typing identifies?

A

Antigen

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12
Q

Reverse typing identifies?

A

Antibodies

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13
Q

What are the major antigens of the ABO system?

A

A, B, and H (O)

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14
Q

What ABO Phenotype is most common to Hispanic and African Americans?

A

O - AA 50% and Hispanic 56%

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15
Q

The A Blood group is most common to?

A

Caucasians

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16
Q

The B Blood group is most common to?

A

A. Americans 20% and Asians 25%

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17
Q

The AB blood group is lease common to?

A

Hispanics

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18
Q

What are the major antibodies of the ABO system?

A

Anti-A (IgM), Anti-B (IgM), Anti-A,B (IgG), and Anti-H (IgG)

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19
Q

Why is the blood type of newborns and infants not considered valid?

A

Antibody production production appears months after birth (3-6m) Some may be maternal IgG

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20
Q

What statement best describes naturally occurring antibodies?

A

Produced without any exposure to RBCs.

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21
Q

The ABO genes are located on which chromosome?

A

Chromosome 9

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22
Q

Which genes are co-dominant and both expressed?

A

A and B

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23
Q

What is an Amorph?

A

No detectable antigen is produced with the O gene

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24
Q

What blood group is amorphous?

A

O

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25
Q

T/F: ABO Antigens result from the interactions of the genes at 3 separate loci (ABO, Hh, and Se)

A

True

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26
Q

What do the ABO genes code for and what does it do?

A

A specific Glycosyltransferase enzyme that adds a sugar to the basic precursor substance.

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27
Q

Identify the precursor chains that RBC antigens are constructed on? What is this precursor material called?

A

oligosaccharide chains of a type 2 precursor substance called a paragloboside / glycan. These chains are attached through the RBC membrane onto ceramide proteins.

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28
Q

Identify the difference between type 1 and type 2 chains?

A

Type 2 chains are found in body fluids

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29
Q

Where is the H-gene located? What are its alleles?

A

Chromosome 19, H and H

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30
Q

Identify the enzyme produced by the H-gene and what it does?

A

alpha-2-L-fucosyltransferase which transfers fucose to the end of the type II precursor chain.

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31
Q

The amount of H antigen on red cells is based on agglutination and is represented as?

A

O>A2>B>A2B>A1>A1B

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32
Q

Identify the blood group with the least H antigen?

A

A1B

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33
Q

Identify the enzyme coded for by the A gene?

What sugar is transferred by this enzyme?

A
  • N-acetylgalactoseaminyltrasferase
  • N-acetyl-D-Galactoseamine
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34
Q

Identify the enzyme coded for by the B gene?

What sugar is transferred?

A

D-galasyltransferase

D-galactose

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35
Q

What Lectin do O blood group react strongly with?

A

Ulex europaeus

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36
Q

What percentage of the US population are secretors?

A

80%

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37
Q

What enzyme does the Se gene code for?

A

alpha-2-L fucosyltransferase which modifies type I chains

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38
Q

What is the most common A subgroup?

A

A1

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39
Q

Why does the A1 subgroup have the least H antigen?

A

It has a higher concentration of the transferase enzyme that converts the H chains into A antigens.

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40
Q

What subgroup has the strongest reation with Anti-A1 at cold temperatures but is alsoi clinically significant at 37oC

A

A1

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41
Q

Identify the second most common A subgroup which represents how many group A and AB people?

A

A2​; 19.9% (20%)

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42
Q

1-8% of A2 people with for which naturally occuring antibody?

A

Anti-A1

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43
Q

What percentage of group A2B will for naturally occuring Anti-A1?

A

22-35%

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44
Q

This subgroup represents approximately 1:1000 of group A and AB people?

A

A3

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45
Q

Which subgroups have mixed field aggutination?

46
Q

Which Lectin is specific to A1?

A

Dolichus biflorus

47
Q

How are A1 and A2 phenotypes determined?

A

Dolichus biflorus

48
Q

What reagent is known as Anti-A1 Lectin?

A

Dolichus biflorus

49
Q

What statement best decribes the Bombay phenotype?

  • Do not inherit a H gene
  • Cannot make the H transferases to convert type II chains
  • Does not add Fucose
  • All of the above

What inheritance pattern is this phenotype?

A
  • All of the above
  • Homozygous recessive
50
Q

Which antibodies does the Bombay phenotype have?

A
  • Anti-A
  • Anti-B
  • Anti-A,B
  • Anti-H
51
Q

T/F anti-H in the bombay phenotype is potent and often reacts strongly at 37oC?

52
Q

What blood group does not react with the lectin Ulex europas?

  • A1B
  • A2B
  • Oh
  • B
A

Oh (Bombay) and A2B

53
Q

What statement best describes an ABO discrepancy?

A

The forward and reverse typing do not agree

54
Q

Most ABO descrepancies are the result of what?

A

Technical error

55
Q

If after a technical review the discrepancy persists, what step should be taken next?

A

Aqcuire essential info regarding patient info such as age, history, medication, Ig levels.

56
Q

What blood type may be agminstered while a dsicepancy has not yet been resolved?

A

O-compatible

57
Q

What are the four Non-technical ABO discrepancies?

A
  1. Group I Antibodies
  2. Group II Antigens
  3. Group III Protein
  4. Group IV Miscellaneous
58
Q

Describe what a Group I discrepancy is?

A

discrepancy between forward and reverse due to weakly reacting or missing antibodies.

59
Q

Identify the patients Group I discrepancies are common amoung? (6)

A
  • Elderly
  • Newborns
  • Immunodeficient
  • Hypergammaglobulinemia
  • Leukemia or lymphomas
  • immunosuppresive drug thereapy
60
Q

Describe chimerism?

A

the prescence of two cell populations

61
Q

What are some causes of chimerism? (4)

A
  • Transfusion
  • Bone marrow transplant
  • Exchange transfusions
  • Fetal-maternal bleeding
62
Q

How are group I discrepancies resolved?

A
  • Incubate 15-30 mins at room temp.
  • Spin and read
  • If necessary incubate at 4oC
63
Q

Describe group II discrepancies?

A

Unexpected reactions in forward grouping due to weak reacting or missing antigens?

64
Q

What are causes of group II descrepancies?

A
  • A and B subgroups
  • Leukemia*
  • Hodgkin’s Lymphoma
  • Acquired B Phenomenom
65
Q

How are group II discrepancies resolved?

A
  • Incubate 15-30 mins at room temp.
  • Spin and read
  • If necessary incubate at 4oC
66
Q

What control must always be tested with concurrently with reverse typing to resolve discrepancies?

A
  • Auto-control
  • O cell control
67
Q

Describe group III descrepancies?

A

descrepancies in forward and reverse grouping due to caused by protien or plasma abnormalities

68
Q

Identify causes of group III descrepancies?

A
  • Multiple Myeloma
  • Hodgkin’s Lymphoma*
  • Plasma expanders (i.e. Detran and Polyvinylpyrrolidone (PVP))
  • Chord blood cells contaminated by Wharton’s Jelly
69
Q

How are group III descrepancies resolved?

A

Wash patients cell several times with saline

70
Q

What are group IV descrepancies?

A

descrepancies between forward and reverse groupings from miscellaneous causes.

71
Q

Identify causes of group IV desrepancies?

A
  • Polyaggtination (T-antigen)
  • Cold reactive antibodies (allo and auto)
  • Warm autoantibodies
  • unexpected ABO isoagglutins
  • antibodies against the anti sera
72
Q

How are group IV descrepancies resolved? (5)

A
  • Test patient cells with lectin if Tactivation susupected
  • warm blood to 37oC
  • Autoantobody absorbed out
  • Elutions
  • check patient history
73
Q

Who identified the Rh system?

A

Landsteiner and Weiner in 1940

74
Q

How many antigens make up the Rh system?

A

5

  • D
  • C
  • c
  • E
  • e

*d is abscent

75
Q

What is the most complex human blood group system?

76
Q

how many specificities make up the Rh system?

77
Q

What percentage are categorized as D positive?

78
Q

Which theory proposed that the Rh locus contained 3 ditinct genes?

A

Fisher-race

79
Q

What is the basis of the Weiner theory?

A

One gene for Rh, which produced 3 factors

80
Q

What are the Fisher-Race Haplotypes?

A
  1. DCe
  2. DcE
  3. Dce
  4. DCE
  5. dCe
  6. dcE
  7. dce
  8. dCE
    9.
81
Q

What Rh Fisher-Race haplotype is most common to caucasians?

82
Q

Identify the Fisher-Race haplotype most common to Asians?

A

DCe (R1) (70%)

83
Q

What Rh Fisher-Race haplotype is most common to A.Americans?

84
Q

What Rh Fisher-Race haplotype is the least common across all ethnicities?

85
Q

Identiy the Rosenfield nomenclature?

A
  • D = 1
  • C = 2
  • E = 3
  • c = 4
  • e = 5
86
Q

For red cells that type D+ C+ E = c+ e+ what is the Rosenfield designation?

A

Rh: 1, 2, -3, 4, 5

87
Q

Which nomenclarture systen has no genetic basis?

A

Rosenfield

88
Q

How are Rh alleles inherited?

A

Codominant

89
Q

On what chromosome is the Rh loci?

A

Chromosome 1

90
Q

What genes are on the Rh loci? What do they determine the prescence of?

A
  • RHD - prescence or abscence of D
  • RHCE - production of C or c and E or e
91
Q

What gene does a D-negative individual inherit?

A

One RHCE gene from each parent

92
Q

Which gene is called a Coexpressor?

93
Q

What chromosome is the RHAG (Rh-associated glycoprotein located)?

A

Chromosome 6

94
Q

The lack of RHAG gene is responsible for which Rh type?

95
Q

The RhD and RhCE protiens are made up of how many amino acids and traverse RBC membranes how many times?

96
Q

What are the 3 Rh negative mutations arising from?

A
  • White - RHD deletion
  • Black - Unusual RHD (pseudogene)
  • Asian - Altered RHD gene making them type negative
97
Q

What are the 4 genetic mechanisms of weak D?

A
  • Genetic weak
  • Position effect
  • Partial D
  • Del (Rhnull)
98
Q

Describe Genetic Weak D?

What ethnicity is this common to?

A

Inheritance of genes that code for weak expression of D antigen. D antigen is normal but few in number.

Black

99
Q

Decribe Position effect?

A

C is Trans to RHD

RHD is in the trans position on the chromosome carrying C.

Antigen is normal, expression is weakened

100
Q

Describe Partial D?

A
  • Unique RHD gene produces D antigen with missing eitopes.
  • Produce anti-D to the eptiopes they lack when transfused with normal D-positive RBCs
101
Q

Rh antibodies react strongly at which phases of testing?

A
  • 37oC incubatio w LISS
  • AHG
102
Q

T/F: Rh antibodies bind complement?

A

False, it is very rare

103
Q

Which Rh antibodies show dosage?

A

Anti-E

Anti-D rarely shows dosage

104
Q

What antigen is the most immunogenic outside the ABO blood group system?

105
Q

Most Rh antibodies are which immunoglobulin? When are they produced?

A

IgG (IgG1, IgG2, IgG3, IgG4)
After exposure to foreign RBCs

106
Q

Which Rh IgG subclasses are the most clinically significant?

A

IgG1 and IgG3

107
Q

HDFN caused by Rh antibodies is often severe, how is this prevented?

A

Rh-immune globulin, a purified preperation of IgG antiD is given to D-negative women during preganancy and after delivery of D-posiive baby

108
Q

What is Amorph Rhnull?

A
  • Mutations in RHCE and Deletion on RHD
  • RHAG is normal
109
Q

Describe Rhnull syndrome?

A

not express and Rh antigens or severely reduced Rh antigen expression

110
Q

Describe Rhmod?

A

Partial supression of Rh gene expression caused by mutations in RHAG

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