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BLOODBANK > ABO BLOOD GROUP SYSTEM > Flashcards

ABO BLOOD GROUP SYSTEM Flashcards

1
Q

● most important system in transfusion and transplantation therapy

A

ABO BLOOD GROUP SYSTEM

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2
Q

only blood group system in which individuals have antibodies in their serum to antigens that are absent from their RBC

A

ABO BLOOD GROUP SYSTEM

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3
Q

discovered ABO blood group system in 1901

A

Karl Landsteiner

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4
Q

the first one to perform the forward and reverse blood
typing.

A

Karl Landsteiner

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5
Q

genetic makeup of an individual

A

Genotype

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6
Q

​physically manifested/physical characteristics of an
individual

A

Phenotype

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7
Q

two subgroups of A

A

A1 (80%) and A2 (20%)

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8
Q

WHAT IS YOUR GENOTYPE if you are O

A

O

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9
Q

Genotype: if B

A

BB / BO

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10
Q

T or F: A1 is more dominant than A2

A

True

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11
Q

T or F: A and B genes are codominantly expressed

A

True

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12
Q

T or F: A and B genes are more dominant than O gene

A

True. When you combine O with A and B, O will not be
expressed. Only A and B genes will be expressed phenotypically

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13
Q

ABO genes are located on what chromosome?

A

Chromosome 9

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14
Q

used to show the codominant manner of
inheritance of the ABO blood group system

A

Punnett square

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15
Q

Are inherited in a codominant manner following simple Mendelian genetics laws

A

ABO GENES

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16
Q

A, B, and H Antigens are expressed on

A

Surface of RBC

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17
Q

H gene

Glycosyltransferase:
Immunodominant sugar:

A

Glycosyltransferase: L- fucosyltransferase
Immunodominant sugar: L-fucose

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18
Q

A gene

Glycosyltransferase:
Immunodominant sugar:

A

Glycosyltransferase: N-acetylgalactosaminyl-transferase
Immunodominant sugar: N-acetyl-D-galactosamine

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19
Q

B gene

Glycosyltransferase:
Immunodominant sugar:

A

Glycosyltransferase: D-galactosyltransferase
Immunodominant sugar: D-galactose

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20
Q

attachment of immunodominant sugars
occurs on the RBC membrane and it is dependent on ABH genes inherited.

A

37th day of fetal life

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21
Q

These antigens are not fully expressed until about

A

2-4 years of age

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22
Q

Compositions of the paragloboside:

A

○ Glucose
○ Galactose
○ N-acetylgalactosamine sugar
○ Terminal galactose
Sugars in type O individuals

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23
Q

Antigens under ABO are found on the

A

RBC membrane

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24
Q

ABO antibodies are predominantly and react at what temperature?

A

Igm, react at room temperature/ambient/cold

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25
Q

using known sources of commercial antisera (anti-A, anti-B) to detect antigens on an individual’s RBCs.

A

Forward grouping

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26
Q

defined as detecting ABO antibodies in the patient’s serum by using known reagent RBCs, namely A1 and B cells.

A

Reverse grouping

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27
Q

can be performed using the slide method or the tube
method.

A

Forward grouping

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28
Q

also known as serum typing or back typing.

A

Reverse grouping

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29
Q

Anti-A (blue): dye

Anti-B (yellow): dye

A

Anti-A (blue): TRYPAN BLUE

Anti-B (yellow): ACRIFLAVINE

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30
Q

T/F:

I. Always drop the clear solution first then followed by the colored solution or RBCs.

II. If the antisera is dropped first, it is because they do not want you to contaminate the antisera.

A

Both true

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31
Q

Regulates the formation of H antigen and subsequently, of A and B antigens in secretory cells

A

Sese system (secretor)

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32
Q

Are regulatory genes that will control the formation
of H antigens in the secretions in the erythrocytes.

A

Zz and Se genes

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33
Q

TorF:

You can’t used saliva as a back-up specimen for blood typing in case there are ABO discrepancies.

A

False

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34
Q

In red cells, epithelium tissues, BM, other cells
Glycolipids
Glucose Type 2
1 ​→ 4 linkage
FUT1 (Zz gene)

A

ABH Antigens

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35
Q

In all body secretions Glycoproteins
N-acetylgalactosamine Type 1
1 ​→ 3 linkage FUT2 (Se gene)

A

ABH SOLUBLE SUBSTANCES

36
Q

Anti-H​ is derived from ​

A

Ulex europaeus​ (lectin)

37
Q

Anti-A1 lectin is derived from

A

​Dolichos biflorus

38
Q

has more antigenic sites for H antigen thus giving (+) reaction with anti-H lectin; no A1 antigen

A

A2 cells

39
Q

H antigen sites occupied by both A and A1

A

A1 cell

40
Q

B lectin is derived from

A

Bandeiraea simplicifolia

41
Q

Reactivity of anti-H antisera or anti-H lectin with ABO blood
groups from least to greatest amount of H antigen

A

A1B>A1>A2B>B>A2>O

42
Q

are most often recognized through an ABO discrepancy (unex- pected reactions in the forward and reverse grouping).

A

Weak A SUBGROUPS

43
Q

Weak A phenotypes can be serologically differentiated using the following techniques:

A

• Forward grouping of A and H antigens with anti-A, anti-A,B, and anti-H
• Reverse grouping of ABO isoagglutinins and the presence of anti-A1
• Adsorption-elution tests with anti-A
• Saliva studies to detect the presence of A and H substances

44
Q

Weak A subgroups can be distinguished as

A

A3, Ax, Aend, Am, Ay, and Ael

45
Q

characteristically demonstrate a mixed-field pattern of agglutination with anti-A and most anti-A,B reagents

A

A3 RBC

46
Q

characteristically are not agglutinated by anti-A reagent but do agglutinate with most examples of anti-A,B

A

Ax RBC

47
Q

characteristically demonstrate very weak mixed-field agglutination with some anti-A and anti-A,B reagents.

A

Aend RBC

48
Q

characteristically not agglutinated, or are agglutinated only weakly, by anti-A or anti-A,B reagents.34 A strongly positive adsorption or elution of anti-A confirms the presence of A antigen sites.

A

Am RBC

49
Q

are not agglutinated by anti-A or anti-A,B reagents. Adsorption and elution of anti-A is the method used to confirm the presence of A antigens.

A

Ay RBC

50
Q

typically are unagglutinated by anti-A or anti-A,B reagents; however, adsorption and elution can be used to demonstrate the presence of the A antigen.

A

Ael RBC

51
Q

usually recognized by variations in reaction strength using anti-B and anti-A,B.

A

Weak B subgroups

52
Q

Serologic techniques can be used to characterize B sub- groups in the following categories:

A

B3, Bx, Bm, and Bel

53
Q

results from the inheri- tance of a rare gene at the ABO locus and is characterized by a mixed-field pattern of agglutination with anti-B and anti-A,B antisera.

A

B3 phenotype

54
Q

demonstrate weak agglutination with anti-B and anti-A,B antisera

A

Bx RBCs

55
Q

characteristically unagglutinated by anti-B or anti-A,B antisera. The Bm RBCs easily adsorb and elute anti-B.

A

Bm RBCs

56
Q

are unagglutinated by anti-B or anti-A,B anti- sera. This extremely rare phenotype must be determined by adsorption and elution of anti-B. No B glycosyltransferase has been identified in the serum or RBC membrane of individuals. Is inherited as a unique mutation in exon 7 of the B gene at the ABO locus.

A

Bel RBC

57
Q

Bombay phenotype was first reported

A

Bhende in 1952 in Bombay, India

58
Q

• hh genotype
• No H antigens formed; therefore, no A or B antigens formed
• Phenotypes as blood group O
• Anti-A, anti-B, anti-A,B, and anti-H present in the serum

A

The Bombay Phenotype (Oh)

59
Q

Bombay phenotype (Oh) do not react with what lectin

A

Anti-H lectin

60
Q

Bombay serum contains

A

anti-A, anti-B, anti-A,B, and anti-H

61
Q

occur when unexpected reactions are ob- tained in the forward and/or reverse grouping.

These can be due to problems with the patient’s serum (reverse grouping), problems with the patient’s RBCs (forward grouping), or problems with both the serum and cells.

A

ABO Discrepancies

62
Q

Technical errors can also cause ABO discrepancies. Examples include:

A

blood sample and test tube labeling errors, failure to add reagents, or the addition of incorrect reagents or sample.

63
Q

Resolution if there is an ABO Discrepancies

A
  • repeat testing of the same sample using a saline suspension of RBCs
  • all results must be recorded, but interpretation of the ABO type must be delayed until the discrepancy is resolved.
  • RBC and serum grouping reactions are very strong (3+ to 4+) and the weaker reactions typically represent the discrepancy.
64
Q

associated with unexpected reac- tions in the reverse grouping due to weakly reacting or missing antibodies.

These discrepancies are more common than those in the other groups listed.

A

Group 1 Discrepancies

65
Q

Common populations with discrepancies in this group are:

A

• Newborns
• Elderly patients
• Patients with a leukemia (e.g., chronic lymphocytic leukemia) or lymphoma (e.g., malignant lymphoma) demonstrating hypogammaglobulinemia
• Patients using immunosuppressive drugs
• Patientswithcongenitaloracquiredagammaglobulinemia or immunodeficiency diseases
• Patients with bone marrow or hematopoietic progenitor stem cell (HPC) transplants
• Patients whose existing ABO antibodies may have been diluted by plasma transfusion or exchange transfusion
• ABO subgroups

66
Q

Resolution of Common Group I Discrepancies

A

enhance the weak or missing reaction in the serum by incubating the patient serum with reagent A1 and B cells at room temperature for approximately 15 to 30 minutes.

**If there is still no reaction after centrifugation, the serum-cell mixtures can be incubated at 4°C for 15 to 30 minutes. An auto control and O cell control must always be tested concurrently with the reverse typing.

67
Q

Mixed-field may also appear as

A

“halo” or “puff of smoke”

68
Q

presence of two cell populations in a single individual

A

Chimerism

69
Q

occurs only in twins and is rarely found.

A

True chimerism

70
Q

If the patient or donor has no history of a twin, then the chimera may be due to

A

Dispermy and Mosaicism

71
Q

occurs when the donor’s red RBCs are incompatible with the recipient’s plasma

A

major ABO incompatibility

72
Q

occurs when the donor’s plasma is incompatible with the recipient’s RBCs

A

minor ABO incompatibility

73
Q

occurs when both a major and minor incompatibility are present

A

Bidirectional incompatibility

74
Q

associated with unexpected reactions in the forward grouping due to weakly reacting or miss- ing antigens.

A

Group II Discrepancies

75
Q

causes of discrepancies in this group 2:

A

-Subgroups of A or B may be present
- Leukemia
- “acquired B” phenomenon

76
Q

Resolution of Common Group II Discrepancies

A

enhanced by incubating the test mix- ture at room temperature for up to 30 minutes to increase the association of the antibody with the RBC antigen.

**If the reaction is still negative, incubate the text mixture at 4°C for 15 to 30 minutes.

77
Q

arises when bacterial enzymes modify the immunodominant blood group A sugar (N-acetyl- D-galactosamine) into D-galactosamine, which is sufficiently similar to the group B sugar (D-galactose) to cross-react with anti-B antisera.

A

Acquired B Antigen

78
Q

formed at the ex- pense of the A1 antigen and disappears following the patient’s recovery.

A

Pseudo B antigen

79
Q

discrepancies between forward and reverse groupings are caused by protein or plasma abnormalities and result in rouleaux formation or pseudoagglutination

A

Group III Discrepancies

80
Q

Causes of Group 3 Discrepancies

A

• Elevatedlevelsofglobulinfromcertaindiseasestates,such as multiple myeloma, Waldenström’s macroglobulinemia, other plasma cell dyscrasias, and certain moderately advanced cases of Hodgkin’s lymphomas

• Elevated levels of fibrinogen
• Plasma expanders, such as dextranandpolyvinylpyrrolidone
• Wharton’s jelly in cord blood samples

81
Q

a stacking of erythrocytes that adhere in a coin- like fashion, giving the appearance of agglutination

A

Rouleax

82
Q

Resolution of Common Group III Discrepancies

A

accomplished by washing the patient’s RBCs several times with saline.

** observed on microscopic examination

83
Q

If Cord blood samples contaminated with a substance called Wharton’s jelly. What is the resolution?

A

washing cord cells six to eight times with saline

**it should alleviate spontaneous rouleaux due to Wharton’s jelly and result in an accurate ABO grouping.

84
Q

These discrepancies between forward and reverse groupings are due to miscellaneous problems.

A

Group IV Discrepancies

85
Q

Causes of group IV discrepancies:

A

• Cold reactive autoantibodies
• Circulating RBCs of more than one ABO group due to RBC transfusion of marrow/stem cell transplant
• Unexpected ABO Isoagglutinins
• Unexpected non-ABO Alloantibodies

86
Q

Resolution of Common Group IV Discrepancies

A

patient’s RBCs could be incubated at 37°C for a short period, then washed with saline at 37°C three times and retyped.

**If this is not successful in resolving the forward type, the patient’s RBCs can be treated with 0.01 M dithiothreitol (DTT) to disperse IgM-related agglutination.

*** As for the serum, the reagent RBCs and serum can be warmed to 37°C for 10 to 15 minutes, mixed, tested, and read at 37°C. The test can be converted to the antihuman globulin phase if necessary.

87
Q

PARA-BOMBAY PHENOTYPE

A

rare phenotypes in which the RBCs are completely devoid of H antigens or have small amounts of H antigens present
*** ● A​h a​nd B​h,​ AB​h

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