ABO BLOOD GROUP SYSTEM Flashcards
1
Q
● most important system in transfusion and transplantation therapy
A
ABO BLOOD GROUP SYSTEM
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
3
Q
discovered ABO blood group system in 1901
A
Karl Landsteiner
4
Q
the first one to perform the forward and reverse blood
typing.
A
Karl Landsteiner
5
Q
genetic makeup of an individual
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Genotype
6
Q
physically manifested/physical characteristics of an
individual
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Phenotype
7
Q
two subgroups of A
A
A1 (80%) and A2 (20%)
8
Q
WHAT IS YOUR GENOTYPE if you are O
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O
9
Q
Genotype: if B
A
BB / BO
10
Q
T or F: A1 is more dominant than A2
A
True
11
Q
T or F: A and B genes are codominantly expressed
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True
12
Q
T or F: A and B genes are more dominant than O gene
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True. When you combine O with A and B, O will not be
expressed. Only A and B genes will be expressed phenotypically
13
Q
ABO genes are located on what chromosome?
A
Chromosome 9
14
Q
used to show the codominant manner of
inheritance of the ABO blood group system
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Punnett square
15
Q
Are inherited in a codominant manner following simple Mendelian genetics laws
A
ABO GENES
16
Q
A, B, and H Antigens are expressed on
A
Surface of RBC
17
Q
H gene
Glycosyltransferase:
Immunodominant sugar:
A
Glycosyltransferase: L- fucosyltransferase
Immunodominant sugar: L-fucose
18
Q
A gene
Glycosyltransferase:
Immunodominant sugar:
A
Glycosyltransferase: N-acetylgalactosaminyl-transferase
Immunodominant sugar: N-acetyl-D-galactosamine
19
Q
B gene
Glycosyltransferase:
Immunodominant sugar:
A
Glycosyltransferase: D-galactosyltransferase
Immunodominant sugar: D-galactose
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
21
Q
These antigens are not fully expressed until about
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2-4 years of age
22
Q
Compositions of the paragloboside:
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○ Glucose
○ Galactose
○ N-acetylgalactosamine sugar
○ Terminal galactose
Sugars in type O individuals
23
Q
Antigens under ABO are found on the
A
RBC membrane
24
Q
ABO antibodies are predominantly and react at what temperature?
A
Igm, react at room temperature/ambient/cold
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using known sources of commercial antisera (anti-A, anti-B) to detect antigens on an individual’s RBCs.
Forward grouping
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defined as detecting ABO antibodies in the patient’s serum by using known reagent RBCs, namely A1 and B cells.
Reverse grouping
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can be performed using the slide method or the tube
method.
Forward grouping
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also known as serum typing or back typing.
Reverse grouping
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Anti-A (blue): dye
Anti-B (yellow): dye
Anti-A (blue): TRYPAN BLUE
Anti-B (yellow): ACRIFLAVINE
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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.
Both true
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Regulates the formation of H antigen and subsequently, of A and B antigens in secretory cells
Sese system (secretor)
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Are regulatory genes that will control the formation
of H antigens in the secretions in the erythrocytes.
Zz and Se genes
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TorF:
You can’t used saliva as a back-up specimen for blood typing in case there are ABO discrepancies.
False
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In red cells, epithelium tissues, BM, other cells
Glycolipids
Glucose Type 2
1 → 4 linkage
FUT1 (Zz gene)
ABH Antigens
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In all body secretions Glycoproteins
N-acetylgalactosamine Type 1
1 → 3 linkage FUT2 (Se gene)
ABH SOLUBLE SUBSTANCES
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Anti-H is derived from
Ulex europaeus (lectin)
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Anti-A1 lectin is derived from
Dolichos biflorus
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has more antigenic sites for H antigen thus giving (+) reaction with anti-H lectin; no A1 antigen
A2 cells
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H antigen sites occupied by both A and A1
A1 cell
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B lectin is derived from
Bandeiraea simplicifolia
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Reactivity of anti-H antisera or anti-H lectin with ABO blood
groups from least to greatest amount of H antigen
A1B>A1>A2B>B>A2>O
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are most often recognized through an ABO discrepancy (unex- pected reactions in the forward and reverse grouping).
Weak A SUBGROUPS
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Weak A phenotypes can be serologically differentiated using the following techniques:
• 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
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Weak A subgroups can be distinguished as
A3, Ax, Aend, Am, Ay, and Ael
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characteristically demonstrate a mixed-field pattern of agglutination with anti-A and most anti-A,B reagents
A3 RBC
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characteristically are not agglutinated by anti-A reagent but do agglutinate with most examples of anti-A,B
Ax RBC
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characteristically demonstrate very weak mixed-field agglutination with some anti-A and anti-A,B reagents.
Aend RBC
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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.
Am RBC
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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.
Ay RBC
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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.
Ael RBC
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usually recognized by variations in reaction strength using anti-B and anti-A,B.
Weak B subgroups
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Serologic techniques can be used to characterize B sub- groups in the following categories:
B3, Bx, Bm, and Bel
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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.
B3 phenotype
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demonstrate weak agglutination with anti-B and anti-A,B antisera
Bx RBCs
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characteristically unagglutinated by anti-B or anti-A,B antisera. The Bm RBCs easily adsorb and elute anti-B.
Bm RBCs
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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.
Bel RBC
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Bombay phenotype was first reported
Bhende in 1952 in Bombay, India
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• 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
The Bombay Phenotype (Oh)
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Bombay phenotype (Oh) do not react with what lectin
Anti-H lectin
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Bombay serum contains
anti-A, anti-B, anti-A,B, and anti-H
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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.
ABO Discrepancies
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Technical errors can also cause ABO discrepancies. Examples include:
blood sample and test tube labeling errors, failure to add reagents, or the addition of incorrect reagents or sample.
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Resolution if there is an ABO Discrepancies
- 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.
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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.
Group 1 Discrepancies
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Common populations with discrepancies in this group are:
• 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
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Resolution of Common Group I Discrepancies
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.
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Mixed-field may also appear as
“halo” or “puff of smoke”
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presence of two cell populations in a single individual
Chimerism
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occurs only in twins and is rarely found.
True chimerism
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If the patient or donor has no history of a twin, then the chimera may be due to
Dispermy and Mosaicism
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occurs when the donor’s red RBCs are incompatible with the recipient’s plasma
major ABO incompatibility
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occurs when the donor’s plasma is incompatible with the recipient’s RBCs
minor ABO incompatibility
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occurs when both a major and minor incompatibility are present
Bidirectional incompatibility
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associated with unexpected reactions in the forward grouping due to weakly reacting or miss- ing antigens.
Group II Discrepancies
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causes of discrepancies in this group 2:
-Subgroups of A or B may be present
- Leukemia
- “acquired B” phenomenon
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Resolution of Common Group II Discrepancies
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
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.
Acquired B Antigen
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formed at the ex- pense of the A1 antigen and disappears following the patient’s recovery.
Pseudo B antigen
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discrepancies between forward and reverse groupings are caused by protein or plasma abnormalities and result in rouleaux formation or pseudoagglutination
Group III Discrepancies
80
Causes of Group 3 Discrepancies
• 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
a stacking of erythrocytes that adhere in a coin- like fashion, giving the appearance of agglutination
Rouleax
82
Resolution of Common Group III Discrepancies
accomplished by washing the patient’s RBCs several times with saline.
** observed on microscopic examination
83
If Cord blood samples contaminated with a substance called Wharton’s jelly. What is the resolution?
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.
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These discrepancies between forward and reverse groupings are due to miscellaneous problems.
Group IV Discrepancies
85
Causes of group IV discrepancies:
• 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
Resolution of Common Group IV Discrepancies
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.
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PARA-BOMBAY PHENOTYPE
rare phenotypes in which the RBCs are completely devoid of H antigens or have small amounts of H antigens present
*** ● Ah and Bh, ABh
