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Blood Bank > ABO Blood group system (and H) > Flashcards

ABO Blood group system (and H) Flashcards

1
Q

Who first described the ABO system?

A

-Karl Landsteiner
-collected samples from himself and 5 other associates
-separated cells and serum and mixed each cell sample with each serum
-he was the first individual to inadvertently perform forward and reverse grouping
-he discovered the A, B, and O blood groups
-this is the only blood group system in which individuals have antibodies in their serum to antigens absent from their RBCs

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2
Q

What happens if you fail to determine an accurate ABO group?

A

-mortality and morbidity
-transfusion of incompatible blood may result in an immediate lysis of donor RBCs producing a severe if not fatal reaction

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3
Q

What is the leading cause of death in hemolytic transfusion reactions today?

A

-transfusion of the wrong ABO group

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4
Q

What is the ABO group frequencies of B +

A

8.5%

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5
Q

What is the ABO group frequencies of B-

A

1.5%

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6
Q

What is the ABO group frequencies of A-

A

6.3%

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7
Q

What is the ABO group frequencies of O-

A

6.6%

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8
Q

What is the ABO group frequencies of AB+?

A

3.4%

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9
Q

What is the ABO group frequencies of AB-

A

.6%
-most rare

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10
Q

What is the ABO group frequencies of A+

A

35.7%

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11
Q

What is the ABO group frequencies of O+?

A

37.4%
-most common

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12
Q

ABO frequencies for white people

A

O - 45
A - 40
B - 11
AB - 4
*most common is O and A

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13
Q

ABO frequencies for black people

A

O - 50
A - 26
B - 20
AB - 4
*most common is O

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14
Q

ABO frequencies for Hispanic people

A

O - 56
A - 31
B - 10
AB - 3
* most common is O

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15
Q

ABO frequencies for Asian people

A

O - 40
A - 28
B - 25
AB - 7
*Most common is O

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16
Q

Forward grouping

A

-use known commercial antisera (anti-A, anti-B)
-use the patient’s red cells
-detect antigens on the patient’s red cells
AKA: Front type

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17
Q

Reverse grouping

A

-use known reagent RBCs (A1 cells and B cells)
-use the patient’s serum
-detects ABO antibodies in the patient’s serum
AKA: Back type

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18
Q

ABO grouping

A

-most frequently performed test in the blood bank
-front and back typing is done on all patients
-inverse reciprocal relationship between front and back type (serve as a check for each other)

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19
Q

Group A: antigens, antibodies

A

Antibodies in plasma: Anti-B
Antigens in red blood cells: A antigen

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20
Q

Group B: antigens, antibodies

A

Antibodies in plasma: Anti-A
Antigens in red blood cells: B antigen

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21
Q

Group AB: antigens, antibodies

A

Antibodies in plasma: None
Antigens in red blood cells: A and B antigens

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22
Q

Group O: antigens, antibodies

A

Antibodies in plasma: Anti-A, Anti-B
Antigens in red blood cells: None
-O phenotype is an autosomal recessive trait because 2 non-functional genes are inherited

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23
Q

Naturally occurring antibodies

A

-it has been postulated that bacteria/pollen are chemically similar to A and B antigens
-bacterial/pollen is widespread, and we are constantly exposed
–exposure serves as a source of stimulants of Anti-A and Anti-B
-antibody production in most other blood groups requires the introduction of foreign RBCs (via transfusion or pregnancy)

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24
Q

What does naturally occurring mean

A

-produced without any exposure to RBCs

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25
Q

ABO antibodies

A

-naturally occurring
-individuals normally produce antibodies directed against the A/B antigens absent from their RBCs
-predominantly IgM
-activate complement
-react at RT and colder
-produce strong direct agglutination reactions during ABO testing
-production begins at 3-6 months old, peaks at 5-10 years, and diminishes when elderly

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26
Q

Can you detect antibodies in babies just birthed?

A

-Even though the production of antibodies is initiated at birth, the titers are too low to detect until around 4 months
-this is why front types are only performed on babies

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27
Q

What happens to elderly people and their antibodies?

A

-elderly people might have lower levels of Anti-A and Anti-B and therefore their back type (reverse grouping) may be weak or missing, resulting in ABO discrepancy

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28
Q

What class is Anti-A and Anti-B predominantly?

A

-IgM but may have IgG component

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29
Q

What antibodies do group O individuals have?

A

-they produce Anti-A, Anti-B, and Anti-A, B
-Anti-A.B is not a mix of Anti-A and Anti-B
-it has a separate cross-reacting antibody
-it is IgG in nature
**This can be a problem for a group O mom having an A or B baby, which can cause hemolytic newborn disease. Often the cord samples for babies of type O mom are tested for possible ABO HDFN

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30
Q

When is the Anti-A, B reagent used?

A

-routinely used in ABO confirmation of blood donors, it is more economical to use one reagent instead of two when verifying group O RBCs

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31
Q

Reagent Anti-A

A

-Monoclonal
-highly specific
-IgM
-clear blue reagent
-expect 3-4+ rxn

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32
Q

Reagent Anti-B

A

-monoclonal
-highly specific
-IgM
-clear yellow reagent (contains acriflavine dye)
-expect 3-4+ rxn

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33
Q

Reagent Anti-A.B

A

-more effective at detecting weak A/B antigens
-not as necessary since monoclonal Anti-A and Anti-B antisera were developed
-This reagent is more sensitive and can detect weaker expressions
-not routinely used for patient ABO grouping
-used for ABO confirmation of donor blood
-more economical, cheaper to use one reagent

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34
Q

Bernstein- Inheritance of ABO blood groups

A

-1924
-inherit one ABO gene from each parent
-these two genes determine which ABO antigens are on the RBC membrane
-Inheritance follows Mendelian genetics
-codominant expression

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35
Q

Which chromosome is the A, B, and O gene located on?

A

9

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36
Q

Is the O gene an amorph?

A

-Yes, no antigens are produced

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37
Q

Autosomal codominant inheritance

A

-blood group genes are not carried on sex genes, hence autosomal and not sex-linked. Whenever the gene is inherited the antigen is expressed on the RBCs, thus its codominant

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38
Q

Phenotype

A

-saying someone is group O or A

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39
Q

Genotype

A
  • AA/OO/AO etc is referring to genotype
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40
Q

Can you determine genotype serologically?

A

-no you cannot, family studies or molecular assays are necessary to determine the exact genotype
-you can for O because it is an autosomal recessive and results from inheriting 2 O genes (OO)
-you can for AB because codominant, so A came from one parent and B from another

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41
Q

What are the 3 different genes that form the ABH antigen?

A

-ABO
-Hh
-Se

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42
Q

What is the precursor material A, B, and H antigens are made from?

A

-paragloboside or glycan

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43
Q

A, B, and H antigens

A

-ABH genes do NOT code for antigens, they produce (code for) glycosyltransferases (enzymes)
-these enzymes add sugars to precursor substances

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44
Q

Which antigen is found in the greatest concentration of a group O individual

A

H antigen

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45
Q

How come the H antigen may not be detected in group A1 individuals?

A
  • The A1 gene is so good at converting H antigens into A
    -the more A, the less H antigen available
    -the H antigen on A1 and A1B RBCs are so well hidden that occasionally anti-H is found in the serum
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46
Q

What is anti-H?

A

-a naturally occurring IgM cold agglutinin that reacts best below room temp
-IgM can react at temperatures up at 37 C but will react better at cold

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47
Q

What is the precursor on which A and B antigens are made of?

A

H antigen

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48
Q

Are Hh and Se genes a part of the ABO system?

A

NO
-but their inheritance does influence A and B antigen expression (Chromosome 19)

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49
Q

Hh genes form ABO antigens where?

A

RBCs

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50
Q

Se gene form ABO antigens where?

A

Secretions
-you need to inherit this to form ABO antigens in secretions

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51
Q

Type 1 and Type 2

A

-type 1 and 2 refer to linkages found between the terminal sugars of D-galactose and N-acetylglucosamine

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52
Q

Type 1

A

-precursor substance in secretions
B1 –> 3 Linkage
-number 1 carbon of D-galactose –> number 3 carbon of N-acetylglucosamine

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53
Q

Type 2

A

-precursor substance on RBCs
-B1 –> 4 linkage
-the terminal galactose on the precursor substance is attached to the N-acetylglucosamine in a beta 1 –> 4 linkage

54
Q

ABH antigen expression

A

-ABH antigen develops early in fetal life
-Newborn RBCs have 25-50% number of antigenic sites found on adult RBCs (newborns have weaker front-type reactions)
-A and B antigen expression is fully developed by 2-4 years of age
-ABH antigen phenotypic expression can vary with race, genetic interaction, disease states

55
Q

H gene

A

-Group O individuals inherit at least one H gene (genotype = HH or Hh) and 2 O genes
-H gene produces enzyme a-2-L-fucosyltransferase
-Transfer sugars (L-fucose) to an oligosaccharide chain on terminal galactose of type 2 chain
-produce the H antigen
-O gene does NOT make catalytically active transferase
-H substance is unmodified in group O

56
Q

Immunodominant sugars

A

-the sugars that occupy terminal positions on this precursor chain confer blood group specificity
ex: L-fucose confers H specificity, blood group O has the highest concentration of H antigens
-need L-fucose (H substance) for other sugars to attach in response to A and B genes

57
Q

Bombay phenotype (Oh)

A

-lacks normal expression of ABH antigens, so do not react with anti-A, anti-B, or anti-H
-FUT1 (H gene) is silenced
-genotype is hh (extremely rare), is an autosomal recessive trait, and 99.99% of the population have H gene
-Does not produce a-2-L-fucosyltransferase
-L-fucose is NOT added to type 2 chains and H substance is not expressed on RBCs
-individuals may inherit ABO genes, but not express them because no H antigen to build upon
-ABH substance also absent from saliva, FUT2 (Se gene) is also silenced

58
Q

What will a Bombay phenotype show as?

A

-As group O, but true O RBCs react with anti-H lectin and Bombay does not (because no H antigen)

59
Q

Who can a Bombay patient receive blood from?

A

-A Bombay person can only receive blood from another Bombay because anti-H can be potent and react at 37 C
-normal group O RBCs have many H antigens and Bombays anti-H would cause immediate lysis

60
Q

The A gene codes for what enzyme?

A

a-3-N-acetylgalactosaminyltransferase

61
Q

What does a-3-N-acetylgalactosaminyltransferase do?

A

transfer N-acetyl-D-galactosamine (GalNAc) sugar to the H substance

62
Q

What is GalNAc sugar responsible for?

A

-A specificity

63
Q

A gene

A

-has more transferase than B gene, thus producing more antigen sites
-810,000 to 1,170,000 A antigen sites on adult A1 RBC

64
Q

The B gene codes for what enzyme?

A

a-3-D-galactosyltransferase

65
Q

What is the job of a-3-D-galactosyltransferase?

A

-transfers D-galactose (Gal) sugar to the H substance

66
Q

What sugar is responsible for B specificity?

A

D-galactose

67
Q

When both A and B genes are inherited, which one competes more efficiently?

A

-the B enzyme seems to compete more efficiently for the H substance than the A enzyme
-so on an AB person’s RBC there are approximately 600,000 A antigens and 720,000 B antigens

68
Q

What are the three immunodominant sugars?

A

Fucose - Group H
N-acetyl-D-galactosamine - Group A
Galactose - Group B

*** As more A or B antigen is made, less H antigen remains

69
Q

H antigen amount

A

O >A2>B>A2B>A1>A1B

70
Q

ABH soluble antigens

A

-found in all body secretions
-presence depends on ABO genes inherited AND inheritance of secretor genes (Sese)
-solubles are only on glycoproteins

71
Q

Secretors

A

SeSe or Sese
-80% of the US population are secretors

72
Q

Non-secretors

A

sese

73
Q

What does the Se gene code for?

A

a-2-L-fucosyltransferase

74
Q

What does a-2-L-fucosyltransferase do?

A

-modifies type 1 precursor substance in secretions to form H substance
-that H substance can then be modified to express A or B substance if the corresponding ABO gene is present

75
Q

Where can RBC antigens be found on?

A

-glycolipids, glycoproteins, and glycosphingolipids

76
Q

secretor studies

A

-80% of the population has the Se gene
-these people secrete water-soluble blood group substances in their saliva and body fluids
Group A = secrete A substance and some H
Group B = secrete B substance and some H
Group O = secretes H only
Group AB = secretes A and B substances and a little H

77
Q

Agglutination inhibition

A

-is used to determine the secretor status
-the presence of agglutination = negative test
-no agglutination = positive test
* for valid tests the control needs to agglutinate

*2 steps to this process
1. antibody neutralization
2. agglutination inhibition

78
Q

Antibody neutralization

A

-saliva is mixed with commercial antisera and incubated
-if the patient is a secretor, soluble blood group antigens in the saliva will react with the antibodies in the commercial antisera

79
Q

Agglutination inhibition

A

-commercial RBCs of appropriate blood groups are added to the test mixture
-if the patient is a secretor, there is no free antibody left for the commercial RBCs to react with
-thus if a patient is a secretor there will be NO agglutination

80
Q

ABO subgroups

A

-subgroups show weaker variable serologic reactivity with polyclonal anti-A, anti-B, and anti-A, B reagents
-due to decreased # of antigen sites
-not as often seen now due to the use of monoclonal reagents

81
Q

A subgroups

A

-more common than B subgroups
-99% of group A people are A1 or A2

82
Q

What is the percentage of A1?

A

80%

83
Q

What is the percentage of A2 or other A subgroups?

A

20%

84
Q

What are the immunodominant sugars on the A1 and A2?

A

-N-acetyl-D-galactosamine

85
Q

A1 gene

A

-higher concentrations of a-3-N-acetylgalactosaminyltransferase than A2
-A1 enzyme is 5-10 times more active than A2
-A1 is more effective at converting H antigen to A antigen
-A1 cells have 1,000,000 A antigens

86
Q

A2 gene

A

-A2 individuals have increased levels of H antigen, second only to group O
-A2 cells have 250,000 A antigens

87
Q

Weaker A subgroups

A

-subgroups weaker than A2 are rare, usually found through ABO discrepancies
-Subdivide individuals into A3, Ax, Aend, Am, Ay, Ael, etc
* secretor studies
*adsorption-elution tests
*molecular testing
-have less antigen, varying degrees of agglutination with anti- A, B variability in detectability of H antigen (anti-H)
-A3 RBC characteristically demonstrates a mixed-field pattern of agglutinations with anti-A
-if a weak A subgroup is suspected make sure the patient doesn’t have a disease that makes altered ABH antigens

88
Q

Potential problems: Weaker A subgroups

A

-if an Ax donor is mistyped as O type and transfused to O recipient, the recipient’s anti-A, B will agglutination/ lyse Ax RBCs –> rapid intravascular hemolysis

89
Q

A3 RBCs

A

-looks mixed field with anti-A and anti-A, B
-antigen sites: 35,000
-Anti -A1 may be present in the serum of A3 people and A substance is detected in saliva if secretor

90
Q

Ax RBCs

A

-not agglutinated by anti-A, but do agglutinate with anti-A, B
-Antigen sites: 4,000
-almost always produced anti-A1, but only H substance in saliva if secretor
-anti-A can be adsorbed and eluted from Ax cells without difficulty

91
Q

Anti-A1

A
  • 1-8% of A2 individuals make anti-A1 in their serum
  • 22-35% of A2B individuals make anti-A1
  • reagent anti-A agglutinates both A1 and A2 RBCs
    -usually first detected in the BackType, anti-A1 will react with the A1 cells used in the reverse typing
    -naturally occurring IgM cold reacting antibody and is unlikely to cause transfusion reaction b/c it only usually reacts below body temp
    -Both A1 and A2 strongly react with Anti-A in routine testing, but A1 can be distinguished through A1 lectin
92
Q

Anti-A1 lectin

A

name: dolichos biflorus
- use this to differentiate A1 and A2
-Anti A1 lectin will agglutinate A1 but NOT A2 cells

93
Q

Lectins

A

-lectin are seed extracts that agglutinate human cells with some degree of specificity

94
Q

Dolichos biflorus

A

-agglutinates A1 cells

95
Q

Bandeiraea simplicifolia

A

agglutinates B cells

96
Q

Ulex europaeus

A

-agglutinates O cells (is anti-H lectin)
-since the A2 phenotype reflects the inefficient conversion of H antigen to A antigen, A2 shows increased reactivity with anti-H lectin

97
Q

Adsorption/eluate studies for identification of A subgroups

A

-commercial anti-A is adsorbed onto red cells believed to be A subgroup
-eluate is prepared from the RBCs and then tested for anti-A
-if anti-A is recovered, presenced of A antigens is confirmed

98
Q

Subgroups of A

A

Aint, A3, Ax, Am, Aend, Ael, etc.

99
Q

B subgroup

A

-very rare
-like A subgroups, result from alternate alleles at the B gene locus
-usually have variations in reaction strength with anti-B and anti-A, B
-Includes B3, Bx, Bm, and Bel
-can do adsorption/eluate studies with anti-B
-presence/absence of ABO isoagglutinin in serum
-may initial front type as group O

100
Q

B3

A

-mixed field with anti-B and A,B (like A3), and B substances in secretions
* the most frequent B subgroup

101
Q

Bx

A

weak agglutination with anti-B and anti-A, B, readily adsorb and eluate anti-B
-secretors have lots of H substance and some B substance that is hard to detect

102
Q

Bm

A

-doesn’t agglutinate anti-A or anti-A, B

103
Q

How can disease states alter RBC antigens?

A

-can weaken reactions
-can acquire pseudoantigens (these would be seen during forward grouping)
-can cause forward grouping issues

104
Q

Weaker front-type reactions

A

-depressed antigen strength
-can look like mixed field
-can be due to leukemia, chromosome 9 translocations, thalassemia (stress hematopoiesis), Hodgkin’s disease
-antigen strength increases when in remission
-antigen strength increases when in remission

105
Q

Weaker- Back type reactions

A

-isoagglutinin (anti-A, anti-B, anti-A, B) may be weak/absent
-chronic lymphocytic leukemia (CLL)
*leukemia with hypogammaglobulinemia

-malignant lymphomas (non-Hodgkin’s)
*decreases in gamma globulin fraction

-agammaglobulinemia

106
Q

Acquired B phenomenon

A

-due to increased permeability of the intestinal wall (due to obstruction, colon/rectal cancer)
-allows passage of bacterial polysaccharides from E.coli serotype O86 into the patient’s circulation
-the patient’s group A RBCs adsorb the B-like polysaccharide and react with some anti-B reagents
-their forward grouping may appear as AB but with a weaker reaction with the anti-B antisera
-their reverse type would like group A

107
Q

What does bacterial deacetylase do?

A

-works on the A antigen by converting N-acetylgalactosamine (the terminal sugar for A antigen) to N-galactosamine (very similar to the terminal sugar for the B antigen- D galactose)

108
Q

When should you suspect acquired B phenomenon?

A

Acquired B is a transient serologic discrepancy seen in group A individuals. Acquired B should be suspected when a historical group A patient now has weak B expression in the front type (anti-B = 2+ or less)

109
Q

How would you resolve a patient with acquired B?

A

-retype using a different monoclonal anti-B or acidified human anti-B, acidified human anti-B will not react with the acquired B antigen

110
Q

What two mechanisms have been postulated for acquired B?

A
  1. In vivo: bacterial enzyme de-acetylase modifies the terminal a-N-acetyl-D-galactosamine into a D-galactosamine which looks like a D-galactose (B-antigen) and can react with anti-B
  2. In vitro: blood group B activity can be conferred onto A/O RBCs adsorbing B-active bacterial polysaccharides
111
Q

Undetectable ABO antigens

A

-can occur with carcinoma of the stomach or pancreas
-patient’s RBCs are unchanged, serum contains increased concentrations of blood-group specific soluble substances (BGSS)

*may neutralize antisera used in forward grouping

112
Q

ABO discrepancies

A

-forward and reverse grouping disagree
-must be resolved prior to transfusion
-can be due to problems with patient RBCs (forward group) or patient serum (reverse group)
-can be due to technical errors, labeling, missing reagents, contamination, etc.
-4 groups of discrepancies
*should always add serum and antiserum first then red cells, should always record results to prevent transcription error

113
Q

Group 1 discrepancies

A

-unexpected reactions in BACK TYPE due to weak/missing antibodies
-most common discrepancy group

114
Q

Who is affected by group 1 discrepancies?

A
  1. newborns/elderly (have lower antibodies levels)
  2. immunosuppression (ex: agammaglobulinemia)
  3. BMTs
  4. Dilution
  5. Subgroups (ABO)
    *patients with malignant lymphomas/CLL
    *patients who have been diluted by FFP transfusions
115
Q

How to resolve Group 1 discrepancies?

A

-get patient history
-increase serum to cell ratio
-increase the incubation time
-decrease temperature
* incubate at 4C with auto control and group O control cells (additional cells needed because decreased temp increases chance of detecting cold agglutinin reactivity)

116
Q

Group 2 discrepancies

A

-least frequent discrepancy
-unexpected reactions in FRONT TYPE due to weak/antigens
-blood group specific soluble (BGSS) substances
-chimerism

117
Q

How to resolve Group 2 discrepancies?

A

-increase incubation time by up to 30 minutes
-can decrease the temperature to 4C and run with auto control and group O cells

*If acquired B:
secretor studies: if the patient is a secretor, only A substance will be present
-can also treat cells with acetic anhydride-acquired B cells lose reactivity

118
Q

Who is affected by group 2 discrepancies?

A

*subgroups of A/B
*leukemias
*acquired B phenomenon

119
Q

BGSS Substances

A

-can occur due to carcinoma of the stomach/pancreas
*excess amounts of BGSS substances are present in plasma
*neutralize reagent anti-A or anti-B
*leaves no unbound antibody to react with patient cells
*cause a false negative or weak reaction in front type
-resolve by washing patient cells several times with saline

120
Q

chimerism

A

-presence of 2 cell populations in 1 person
-true chimerism is very rare and occurs in twins
-blood exchange occurs in utero
*2 cell population emerge
*both recognize as self, so the body doesn’t make anti-A or anti-B
-if no history of twins, could be due to dispermy (2 sperm + 1 egg) and maybe mosaic

121
Q

Artificial chimerism

A

-is more frequent than true chimerism and can be due to non-ABO matched blood transfusions, BMTs, exchange transfusions, FMH

122
Q

Group 3 discrepancies

A

-caused by protein or plasma abnormalities (in vitro problems like rouleaux)

123
Q

Who causes group 3 discrepancies?

A

-waldenstrom’s macroglobulinemia
-multiple myeloma
-some advanced Hodgkins lymphomas
-increased levels of fibrinogen
-plasma expanders (dextran)
-wharton’s jelly (cord blood only)

124
Q

Rouleaux

A

-RBCs stacked like coins

125
Q

How to resolve group 3 discrepancies?

A

-resolve rouleaux with saline replacement
*remove patient serum and replace with equal volume saline
*true agglutination remains

-Resolve Wharton’s jelly by washing cord cells up to 6 times with saline

126
Q

Group 4 discrepancies

A

-cold reactive autoantibodies
*RBCs so heavily coated that they spontaneously agglutinate

-mixed field
*more than one ABO group type RBCs circulating (ex: non-ABO identical RBC transfusion, BMT, stem cell transplant, ABO subgroup (A3))

-unexpected ABO isoagglutination or non-ABO alloantibody

-acriflavine antibody

127
Q

How to resolve group 4 discrepancies? due to cold autoantibodies

A

-if due to cold autoantibody-incubate patient RBCs at 37C and wash with 37C saline 3 times (get valid front type)
-can also treat RBCs with DTT to break up IgM agglutination
-can pre-warm
-can perform auto adsorption (get valid back type)

128
Q

How to resolve group 4 discrepancies? due to unexpected ABO isoagglutinin

A

-may be due to anti-A1
-identify anti-A1 using 3 examples of A1 cells, A2 cells, B cells, O cells, and auto control
-pattern determines the specificity
-test patient RBCs with dolichos biflorus (Anti-A1 lectin-agglutinates A1 cells)

129
Q

How to resolve group 4 discrepancies? due to unexpected alloantibodies

A

ex: anti-M
-perform antibody identification process
-find reagent A1 and B cells negative for antigen to correct reverse typing

130
Q

acriflavine antibody

A

-forms a complex that attaches to patients’ RBCs and causes agglutination in the forward type
-resolve by washing the patient’s cells with saline 3 times

131
Q

What is acriflavine?

A

-is the yellow dye in some anti-B antisera reagents, when someone has an antibody to this dye, it forms an acriflavine-anti acriflavine complex that attaches to patient RBCs and causes agglutination in the front type

Blood Bank (4 decks)

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