ABO GROUP PPT 2 Flashcards
(132 cards)
1
Q
_________ represent phenotypes that show weaker variable serologic reactivity
with the commonly used human polyclonal anti-A, anti-B, and anti-A,B
A
ABO Subgroups
2
Q
(A Subgroups)
in 1911, _______ described two different A antigens based on reactions between group
A RBCs and anti-A and anti-A1.
A
von Dungern
3
Q
(A Subgroups)
___ = Group A RBCs that react with both anti-A and anti-A1.
A
A1
4
Q
(A Subgroups)
___ = Group A RBCs that react with anti-A and not anti-A1.
A
A2
5
Q
(A Subgroups)
RBCs from A1 and A2 individuals react equally strong with current monoclonal _____ in
ABO forward typing tests
A
anti-A
6
Q
________ are generally common
A
A subgroups
7
Q
(A Subgroups)
The weaker serologic reactivity of ABO subgroups = attributed to the decreased number of
___ and ________ sites on their red cells.
A
A and B antigen
8
Q
(A Subgroups)
The cells of approximately 80% of all Group A (or AB) individuals are ______, the remaining 20% are ______ or ______
A
A1 (or A1B) ; A2 (or A2B) or weaker subgroups
9
Q
(A Subgroups)
The production of both types of antigens is a result of an inherited gene at the ______
A
ABO locus.
10
Q
(Difference between A1 and A2 = Quantitative Difference)
Inheritance of an A1 gene elicits production of high concentrations of the enzyme ___________, which converts almost all of the H precursor structure to A1 antigens on the RBCs.
A
a-3-N-acetylgalactosaminyltransferase
11
Q
(Difference between A1 and A2 = Quantitative Difference)
____ creates between 810,000 and 1,170,000 antigen sites of an adult _____
A
A1 ; A1 RBCs
12
Q
(Difference between A1 and A2 = Quantitative Difference)
_____ results in production of only 240,000 to 290,000 antigen sites on the adult ____
A
A2 gene ; A2 RBC.
13
Q
(Difference between A1 and A2 = Quantitative Difference)
The immunodominant sugar on both A1 and A2 RBCs is __________
A
N-acetyl-D-galactosamine.
14
Q
(Difference between A1 and A2 = Qualitative Difference)
1% to 8% of A2 individuals produce _____in their serum
A
anti-A1
15
Q
(Difference between A1 and A2 = Qualitative Difference)
25% of A2B individuals produce ____
A
anti-A1
16
Q
(Difference between A1 and A2 = Qualitative Difference)
Differentiation of A1 and A2 phenotypes is determined serologically using ______
- a reagent made from a seeds of the plant _______
- it agglutinate human cells with some degree of specificity.
A
anti-A1 lectin ; Dilochos biflorus
17
Q
(Difference between A1 and A2 = Qualitative Difference)
Anti-A1 lectin agglutinates ______ cells but does not agglutinate ______
A
A1 (A1B) ; A2
(A2B).
18
Q
(QUANTITATIVE AND QUALITATIVE DIFFERENCES OF SUBGROUPS A1 AND A2)
- ↓ number of antigen sites
- ↓ amount of transferase enzyme
- ↓ amount of branching
A
Quantitative Difference
19
Q
(QUANTITATIVE AND QUALITATIVE DIFFERENCES OF SUBGROUPS A1 AND A2)
- Differences in the precursor oligosaccharide chains
- Subtle differences in transferase enzymes
- Formation of anti-A1, in a percentage of some subgroups
A
Qualitative Differences
20
Q
Lectins Used in Blood Banking:
agglutinates A1 or A1B
A
Dolichos biflorus
21
Q
Lectins Used in Blood Banking:
agglutinates B cells
A
Bandeiraea simplicifolia
22
Q
Lectins Used in Blood Banking:
agglutinates O cells (H specificity) and other ABO blood groups depending on the amount of H antigen available.
A
Ulex europaeus
23
Q
(A SUBGROUPS)
The antigens present on the RBCs of A1 and A2 individuals can be depicted in two
ways:
1. A1 RBCs are illustrated as having both __ and __ antigens on the cell surface, in
contrast to A2 cells which only contain __.
2. Alternatively, A1 RBCs can also be conceptualized as having only ___ antigens sites and
A2 as only having __ antigen sites.
A
A and A1 ; A
A1 ; A
24
Q
(A SUBGROUPS)
_____ is found in greatest concentration on the RBCs of group O individuals
-may not be detectable in _____ individuals.
- in the presence of A2 gene, only some of the H antigen is converted to A antigens, and the remaining H antigen is detectable on the ____.
A
H antigen ; group A1 ; cell
25
(A SUBGROUPS)
____ subgroups of the A antigen will often have an inverse reciprocal relationship
between the amount of H antigen on the RBC and the amount of A antigens formed.
Weak
26
(A SUBGROUPS)
______ is a naturally occurring IgM cold agglutinin that reacts best below room
temperature.
This anti-H
27
(A SUBGROUPS)
this antibody is formed in response to a natural substance and reacts most strongly with cells of _____ individuals and weakly with the RBCs of ____ individuals.
group O ; A1B
28
(A SUBGROUPS)
REACTIVITY OF ANTI-H ANTISERA OR ANTI-H LECTIN WITH ABO BLOOD GROUPS : GREATEST TO LEAST AMOUNT OF H
O > A2 > B > A2B > A1 > A1B
29
(A SUBGROUPS)
it is an insignificant antibody in terms of transfusion purposes because it has no
reactivity at body temp.
ANTI-H
30
(A SUBGROUPS)
However, _______ may react at room temp. and present a problem in antibody screening procedures.
high-titered anti-H
31
(A SUBGROUPS)
________ agglutinate RBCs of group O and A2 and react very weakly or not at all
with groups A1 and A1B.
Anti-H lectin
32
(A SUBGROUPS)
More detailed, theory of ABO subgroups has been proposed by the identification of
four different forms of H antigens:
- 2 of which are unbranched straight chains (___, ____)
- 2 of which are complex branched chains (___, ___)
H1, H2 ; H3, H4
33
(A SUBGROUPS)
___ AND ___ correspond to the precursor structures on which the A enzyme can act to
convert H antigen to blood group A active glycolipids.
H1 and H4
34
(A SUBGROUPS)
Straight chain __ and __ glycolipids can be converted to A and A antigens,
respectively, by both A1 and A2 enzymes, with the A2 enzyme being less efficient.
H1 and H2
35
(WEAK A SUBGROUPS)
Subgroups weaker than A2 occur frequently and are most often recognized through an
_________
ABO discrepancy
36
(WEAK A SUBGROUPS)
These subgroups of A make up ___ of those encountered in the laboratory and therefore are mainly of academic interest.
1%
37
(WEAK A SUBGROUPS)
characteristics of weak A subgroups include the following:
1. decreased number A antigen sites per RBC
2. Varying degrees of agglutination by human anti-A,B
3. Increased variability in the detectability of H antigen, resulting in strong reactions
with anti-H
4. presence or absence of anti-A1 in the serum
38
(WEAK A SUBGROUPS)
_________, _________ and _______ can be utilized to subdivide A individual into A3,Ax, Aend, Am and Ael.
Secretory studies, adsorption-elution tests, and molecular testing
39
(WEAK A SUBGROUPS)
Weak A phenotypes can be serologically differentiated using the following techniques:
1. Forward grouping of A and H antigens with anti-A, anti-A,B, and anti-H
2. Reverse grouping of ABO isoagglutinins and the presence of anti-A1
3. Adsorption-elusion tests with anti-A
4. Saliva studies to detect the presence of A and H substances
40
(WEAK A SUBGROUPS)
Additional special procedures such as ________ for mutations or ________ studies for detecting the A enzyme can be performed for
differentiation of weak subgroups.
molecular testing ; serum glycosyltranferase
41
(WEAK A SUBGROUPS)
________ characteristically demonstrate a mixed-field pattern of agglutination with
anti-A and most anti-A,B reagents.
- The estimated number of A antigen sites is approximately ________ per RBC.
- ______ may be present in serum of A3 individuals, and A substance is detected in the saliva of ________.
A3 RBCs ; 35,000 ; Anti-A1 ; A3 secretors
42
(WEAK A SUBGROUPS)
________ characteristically are not agglutinated by anti-A reagent but do agglutinate with most examples of anti-A,B
- the estimated number of A antigen sites is approximately ______ per RBC.
Ax RBCs ; 4,000
43
(WEAK A SUBGROUPS)
________ characteristically demonstrate very weak mixed-field agglutination with
some anti-A and anti-A,B reagents.
- the estimated number of A antigen sites on the few agglutinable RBCs is approximately _____ per RBC, whereas no detectable A antigens are demonstrated on RBCs that do not agglutinate.
-no ________ is detectable in the serum or in the RBC membranes of Aend individuals.
Aend RBCs ; 3,500 ; A glycosyltransferase
44
(WEAK A SUBGROUPS)
______ are not agglutinated by anti-A or anti-A,B reagents.
Am RBCs
45
(WEAK A SUBGROUPS)
________ typically are unagglutinated by anti-A or anti-A,B reagents; adsorption and
elution can be used to demonstrate the presence of the A antigen
- the Ael phenotypes is inherited as a _____ at the ABO locus.
Ael RBCs ; rare gene
46
(Weak B Subgroups)
Subgroups of B are very ____ and much less frequent than A subgroups.
rare
47
(Weak B Subgroups)
Inheritance of B subgroups, similar to that majority of A subgroups, is considered to
be a result of ________ at the B locus.
alternate alleles
48
(Weak B Subgroups)
Criteria used for for differentiation of weak B phenotypes include the following
techniques:
1. Strenght and type of agglutination with anti-B, anti-A,B, and anti-H
2. Presence or absense of ABO isoagglutinins in the serum
3. Adsorption-elution studies with anti-B
4. Presence of B substance in saliva
5. Molecular testing
49
(Weak B Subgroups)
RBCs demontrating serologic activity that is weaker than normal are designed weak B
phenotypes or B subgroups and include ____, ____, ____, and ____ phenotypes.
B3, Bx, Bm and Bel
50
(Weak B Subgroups)
____ phenotype generally results from the inheritance 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
B3
51
(Weak B Subgroups)
______ typically demonstrate weak agglutination with anti-B and anti-A,B antisera.
- family studies suggest that Bx is a _____ at the ABO locus.
Bx RBCs ; rare allele
52
(Weak B Subgroups)
______ are characteristically unagglutinated by anti-B or anti-A,B antisera
- the ______ is reported to be more frequent in Japan.
Bm RBCs ; Bm subgroup
53
(Weak B Subgroups)
_____ are unagglutinated by anti-B or anti-A,B antisera.
- Bel is inherited as a unique mutation in _____ of the B gene at the ABO locus.
Bel RBCs ; exon 7
54
First reported by Bhende in 1952 in Bombay, India.
The Bombay Phenotypes (Oh)
55
(The Bombay Phenotypes (oh))
_____ cannot be expressed, and ______ cannot be formed.
ABO genes ; ABH antigens
56
(The Bombay Phenotypes (oh))
RBCs are devoid of normal ABH antigens and, therefore, fail to react with ______, ______ and ______
anti-A, anti-B, and anti-H
57
(The Bombay Phenotypes (oh))
In RBC testing using anti-A and anti-B, the Bombay would phenotype as an _________
- Do not react with _________, unlike those of the normal group O individual; which react strongly with anti-H lectin.
O blood group ; anti-H lectin (Ulex europaeus)
58
(The Bombay Phenotypes (oh))
Bombay serum contains ______, _____, ______, and _____
anti-A, anti-B, anti-A,B and anti-H
59
(The Bombay Phenotypes (oh))
Bombay anti-H can often be potent and reacts strongly at __________
37 degrees celsius.
60
(The Bombay Phenotypes (oh))
_________ is also absent in saliva.
ABH substance
61
(The Bombay Phenotypes (oh))
More than ____ Bombay phenotypes have been reported in various parts of the world.
130
62
(The Bombay Phenotypes (oh))
Only blood from another Bombay individual will be compatible and can be transfused to a Bombay recipient.
YES
63
(The Bombay Phenotypes (oh))
The Bombay phenotype is inherited as an ___________
autosomal recessive trait
64
(The Bombay Phenotypes (oh))
The underlying molecular defect is most often a mutation in the gene _________, producing a silenced gene incapable of coding for the enzyme, a-2-L-fucosyltransferase (H
transferase).
FUT1 (H gene)
65
(The Bombay Phenotypes (oh))
This enzyme (a-2-L-fucosyltransferase or H
transferase) normally catalyzes the transfer of _____ in an a-1,2 linkage to the terminal galactose of the precursor molecule on RBCs forming the H antigen.
This mutation underlying the Bombay phenotype is also associated with a silenced_______
L-fucose ; FUT2 gene (Se gene).
66
- 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
- Can only be transfused with blood from another Bombay (oH)
The Bombay Phenotype (Oh)
67
GENERAL CHARACTERISTICS OF BOMBAY Oh (Hnull) Phenotypes:
1. Absence of ___, ___, and ____; no agglutination with anti-A,
anti-B, or anti-H lectin
2. Presence of ____, ____, and ____ and a potent wide thermal
range of anti-H in the serum
3. ____, ____, ____ nonsecretor (no A, B, or H substances present in saliva)
4. Absence of ______ in serum and H antigen on red cells.
5. Presence of ___ or ___ enzymes in serum (depending on ABO
genotype)
6. A ______ mode of inheritance (identical phenotypes in children but not in parents)
7. RBCs of the Bombay phenotype (Oh) will not react with the ________
8. RBCs of the Bombay phenotype (Oh) are compatible only with the serum from another ________
1. H, A, and B, antigens
2. anti-A, anti-B, anti-A,B,
3. A, B, H
4. α-2-L-fucosyltransferase (H-enzyme)
5. A or B
6. recessive
7. anti-H lectin (Ulex europaeus)
8. Bombay individual
68
are those rare phenotypes in which the RBCs are completely devoid of H antigens or have small amount of H antigen present.
(The Para-Bombay Phenotypes)
69
(The Para-Bombay Phenotypes
these individuals express weak forms of ____ and _____
A and B antigens (Ah and Bh)
70
(The Para-Bombay Phenotypes)
_______ almost always present in the serum
- weak H-like antibody
- Reactive at low temperature.
Oh: anti-H
71
(ABH Antigens and Antibodies in Disease)
Associations between _____ and practically any disorder known to man can be found throughout medical literature.
ABH antigens
72
(ABH Antigens and Antibodies in Disease)
“_____” in A blood groups
“_____” in group B blood groups
“______” in group O
hangover ; criminality ; good teeth
73
(ABH Antigens and Antibodies in Disease)
Various disease states seem to alter RBC antigens, resulting in either progressively weaker reactions or additional acquired ____________, which can be seen during forward grouping
pseudoantigens
74
(ABH Antigens and Antibodies in Disease)
leukemia, chromosome 9 translocation, and any hemolytic disease that induces stress hematopoiesis have been shown to depress _______
antigen strength
75
(ABH Antigens and Antibodies in Disease)
________ reported to weaken or depress ABH red cell antigens, resulting in variable reactions during forward grouping similar to those found in leukemia.’
Hodgkin’s disease
76
(ABH Antigens and Antibodies in Disease)
The isoagglutinins also may be _____ or _____ in those leukemias demonstrating hypogammaglobulinemia, such as chronic lymphocytic leukemia.
weak or absent
77
(ABH Antigens and Antibodies in Disease)
Various lymphomas, such as the malignant variety, may yield ________, owing to moderate decreases in the gamma globulin fraction.
weak isoagglutinins
78
(ABH Antigens and Antibodies in Disease)
Acquired B phenomenon in group A individuals.
- Px with intestinal obstruction, colon or rectum carcinoma, or other disorders of the lower intestinal tract may have increased _______ of the intestinal wall which allows the bacterial polysaccharides from _________ into the patient's circulation and results in acquired B phenomenon in group A1 individuals.
- group A red cells absorb the B-like polysaccharide, which reacts with ____________
permeability ; Escherichia coli serotype O86 ; human-source anti-B
79
(ABH Antigens and Antibodies in Disease)
lack of detectable ABO antigens can occur in patients with ______ of the stomach or pancreas.
- The patient's rbc antigens have not been changed but the serum contains excessive amounts of ___________ may neutralize the antisera utilized in the forward grouping.
carcinoma ; blood group-specific soluble substances(BGSS)
80
(ABH Antigens and Antibodies in Disease)
All these disease states previously mentioned may result in discrepancies between the _____ and _____ groupings, indicating that the patient's red cell group is not what it seems.
forward and reverse
81
(ABH Antigens and Antibodies in Disease)
all __________ must be resolved before blood for transfusion is released for that patient.
-help confirm the patient's true ABO group: __________ or _______
ABO discrepancies ; secretor or molecular studies
82
(Common Sources of Technical Errors Resulting in ABO Discrepancies)
* Incorrect or inadequate identification of ______, _______, or _______
* Cell suspension either ______ or ______
* ________ or incorrect recording of results
* A mix-up in _____
* Missed observation of ______
* Failure to add ______
* Failure to add ______
* Failure to follow ___________
* Uncalibrated ______
* ___________ or ________
* Contaminated _________
* Warming during _________
1. blood specimens, test tubes, or slides
2. too heavy or too light
3. Clerical errors
4. samples
5. hemolysis
6. reagents
7. samples
8. manufacturer’s instructions
9. centrifuge
10. Overcentrifugation or undercentrifugation
11. reagents
12. centrifugation
83
Occurs when the red cell testing does not match the serum testing results.
(ABO Discrepancy)
84
(ABO Discrepancy)
reverse grouping = patient’s _____
forward grouping = patient’s ______
serum ; red cells
85
(ABO Discrepancy)
Usually technical in nature and can be simply resolved by correctly ______ the testing and carefully _____ reagents with meticulous _____ and ______ of results.
reporting ; checking ; reading and recording
86
(ABO Discrepancy)
most of the time, the problem is _________
technical
87
(ABO DISCREPANCY)
Other Technical Errors:
1. errors in labeling the blood sample at the patient's bedside or in the laboratory
2. contaminated reagents
3. Failure to add reagents or the addition of incorrect reagents or sample
YES
88
(ABO Discrepancy)
Resolution: using a _________ of RBCs if the initial test was performed using RBCs suspended in serum or plasma
saline suspension
89
(ABO Discrepancy)
new sample should be drawn and RBC and serum testing is repeated if due to an error in ________ or __________
specimen collection or identification.
90
(Types of Discrepancies)
most common type
GROUP I DISCREPANCY
91
- If a reaction in the reverse grouping is weak or missing
- it means that the patient has depressed antibody production or cannot produce the ABO antibodies.
GROUP I DISCREPANCY
92
Common populations with discrepancies in G1 discrepancy are:
1. __________ : the production of ABO antibodies is not detectable until 4-6 months of age.
2. _________ : the production of ABO antibodies is depressed.
3. __________ : chronic lymphocytic leukemia or lymphoma (malignant lymphoma) demonstrating hypogammaglobulinemia.
4. Patients using __________ that yield hypogammaglobulinemia
5. ___________ : patients develop hypogammaglobulinemia from therapy and start producing a different RBC population from that of the transplanted bone marrow.
6. Patients whose existing ABO antibodies may have been diluted by _________ or ______
7. _____ Subgroups
1. Newborns
2. Elderly Patients
3. Patients with a Leukemia
4. immunosuppressive drugs
5. Patients with bone marrow or stem cell transplantations
6. plasma transfusion or exchange transfusion
7. ABO Subgroups
93
(RESOLUTION OF GROUP 1 DISCREPANCY)
Obtaining the patient’s ______ may resolve this type of discrepancy.
history
94
(RESOLUTION OF GROUP 1 DISCREPANCY)
Hypogammaglobulinemia = best way to resolve this discrepancy is to enhance the ____ or _____ in the serum.
- Performed by _________ the patient serum with reagent A1 and B cells at room temp. for approximately _____ minutes or by adding ___ or ____ drops more plasma or serum to the test.
- if there is still no reaction after centrifugation, the serum-cell mixtures can be incubated at ___ degrees celsius for _____.
weak or missing reaction ;
- incubating ; 15-30 ; one or two
- 4 ; 15 mins
95
(RESOLUTION OF GROUP 1 DISCREPANCY)
an ________ and ______ control must always be tested concurrently with reverse typing when trying to solve the discrepancy since the lower temperature of testing will most likely enhance the reactivity of other commonly occurring cold agglutinins that react with all adult RBCs.
auto control and O cell
96
least common type of discrepancy
GROUP II DISCREPANCIES
97
unexpected reactions in the forward grouping due to weakly reacting or missing antigens.
(GROUP II DISCREPANCIES)
98
(GROUP II DISCREPANCIES)
Some of the causes of discrepancies in this group include:
1. ________ may be present
2. ________ may yield weakened A or B antigens and ____ disease has been reported in some cases to mimic the depression of antigens found in leukemia.
3. The _________ phenomenon will show weak reactions with anti-B antisera and is most often associated with diseases of the
digestive tract
1. Subgroups of A (or B)
2. Leukemias ; Hodgkin’s
3. “acquired B”
99
(RESOLUTION OF GROUP II DISCREPANCY)
The agglutination of weakly reactive antigens with the reagent antisera can be enhanced by ______ the test mixtures at _______. for up to ______, which will increase the
association of the antibody with the RBC antigen.
- if it is still negative, incubate the test mixture at ___ degrees celsius for ____ to ___ mins. include group O and autologous cells as controls. RBCs can also be penetrated with enzymes
and rested with reagent antisera.
incubating ; room temp ; 30 mins
- 4 ; 15 to 30
100
(RESOLUTION OF GROUP II DISCREPANCY)
__________ - arises when bacteria enzymes modify the immodominant blood group A sugar into D-galactosamine, which is similar to the group B sugar and cross-reacts with
anti-B antisera.
Acquired B antigen
101
(RESOLUTION OF GROUP II DISCREPANCY)
_________ is formed at the expense of the A1 antigen and disappears after recovery.
- the reaction of the appropriate antiserum with these acquired antigens demonstrates a _________, often yielding a mixed-field appearance.
Pseudo-B antigen ; weak reaction
102
(RESOLUTION OF GROUP II DISCREPANCY)
Testing the patient’s serum against autologous RBCs gives a __________ reaction because the anti-B in the serum does not agglutinate autologous RBCs with the acquired B Ag.
negative
103
Due to excess amounts of blood group-specific soluble (BGSS) substances present in the plasma.
- will neutralize the reagent anti-A or anti-B, leaving no unbound antibody to react with the patient cells which yields a false-negative or weak reaction in the forward grouping
RARE GROUP II DISCREPANCIES
104
(RARE GROUP II DISCREPANCIES)
Washing the patient cells free
of the BGSS substances with _______ should alleviate the problem, resulting in correlating forward and reverse groupings.
saline
105
(RARE GROUP II DISCREPANCIES: RESOLUTION)
antibodies to low-incidence antigens in reagent anti-A or anti-B can also cause ________ or ________ in RBC grouping.
weakly reactive or missing reactions
106
(RARE GROUP II DISCREPANCIES: RESOLUTION)
- Even though rarely, it has been reported that this additional antibody in the reagent antisera has reacted with the corresponding low-prevalence antigen present on the patient's RBCs. This produces an unexpected reaction of the patient’s cell with _______ or _____, or both, mimicking the presence of a __________.
- The best way to resolve this discrepancy is by _________, using antisera with a different _______
anti-A or anti-B ; weak antigen ;
- repeating the forward type ; lot number
107
______ is defined as the presence of two cell populations in a single individual
Chimerism
108
Chimerism was discovered in _____ (born to a group O mother and group B father) who had a mixture of both B and O cells instead of the expected group of either B or O.
twins
109
(chimerism)
Detecting a separate cell population may be easy or difficult, depending on what
percentage of cells of the minor population are present.
Reactions from chimerism are typically ________
mixed field.
110
_________, which occurs in twins, is rarely found, and the two cell populations will exist throughout the lives of the individuals.
True chimerism
111
In utero exchange of blood occurs because of vascular ______. As a result, two cell
populations emerge, both of which are recognized as self,
and the individuals do not make anti-A or anti-B.
- Therefore, expected isoagglutinins are not present in the _____ grouping, depending on the percentage of the population
of red cells that exist in each twin.
If the patient or donor has no history of a twin, then the chimera may be due to
_______ (two sperm fertilizing one egg) and indicates
______.
anastomosis ; reverse ; dispermy ; mosaicism
112
More commonly, artificial chimeras occur, which yield mixed cell populations as a result of:
* ________ (e.g., group O cells given to an A or
B patient)
* _______ bone marrows or peripheral blood stem
cells of a different ABO type
* Exchange _______
* _________ bleeding
1. Blood transfusions
2. Transplanted
3. transfusions
4. Fetal-maternal
113
discrepancies between forward and reverse groupings are caused by proteins or plasma abnormalities and result in rouleaux formation or pseudoagglutination
GROUP III DISCREPANCIES
114
Group III discrepancies is attributable to the following:
1. Elevated levels of globulin from certain disease states, such as _______, _________, other plasma cell ______, and certain moderately advanced
cases of _______
2. Elevated levels of _______
3. Plasma expanders, such as ________ and ________
4. ________ in cord blood samples
5. _______ formation
1. multiple myeloma, Waldenstrom’s macroglobulinemia ; dyscrasias, ; Hodgkin’s lymphomas
2. fibrinogen
3. dextran and polyvinylpyrrolidone
4. Wharton’s jelly
5. Rouleaux
115
(Resolution of Common Group III Discrepancies)
________ is a stacking of erythrocytes that adhere in a coin-like fashion, giving the appearance of agglutination. it can be observed on microcopic examination.
- cell grouping can usually be accomplished by ______ the patient’s RBCs several times with _____
Rouleaux ; washing ; saline
116
(Resolution of Common Group III Discrepancies)
* performing a ________ technique will free the cells in the case of rouleaux formation in the reverse type.
- in this procedure, ______ is removed and replaced by an equal volume of ______.
- in true agglutination, ________ will still remain after the addition of saline.
saline replacement ; serum ; saline ; RBC clumping
117
(Resolution of Common Group III Discrepancies)
cord blood - washing cord cell ____ to ______ times with saline should alleviate spontaneous rouleaux due to Wharton’s jelly (will cause the red cells to aggregate).
six to eight
118
(Resolution of Common Group III Discrepancies)
_________ is a viscous mucopolysaccharides material present on cord blood cells and thorough washing should result in an accurate ABO
grouping
Wharton’s jelly
119
(Resolution of Common Group III Discrepancies)
However, because testing is usually not performed
on cord serum (because the antibodies detected are usually
of __________), ________ may still not correlate with the RBC forward grouping.
maternal origin ; reverse grouping
120
Discrepancies Between forward and reverse groupings are due to miscellaneous problems.
GROUP IV DISCREPANCIES
121
GROUP IV DISCREPANCIES have the following causes:
1. Cold reactive autoantibodies in which RBCs are so heavily coated with antibody that they spontaneously agglutinate, independent of the specificity of the reagent antibody
2. Patient has circulating RBCs of more than one ABO group due to RBC transfusion or marrow/stem cell transplant
3. Unexpected ABO isoagglutinins
4. Unexpected non-ABO alloantibodies
- ______________ should be performed with the patient’s serum.
antibody identification panel
122
(Resolution of Common Group IV Discrepancies)
Potent cold autoantibodies can cause spontaneous agglutination of the patient’s cells.
These cells often yield ________
direct Coombs’ or antiglobulin test
positive
123
(Resolution of Common Group IV Discrepancies)
If the antibody in the serum reacts with all adult cells—for example, anti-I—the reagent A1 and B cells used in the reverse grouping also agglutinate.
- To resolve this discrepancy, the patient’s RBCs could be
incubated at_____ for a short period, then washed with saline
at 37°C ______ and _____
If this is not successful in
resolving the forward type, the patient’s RBCs can be treated
with _________ to disperse IgM-related agglutination.
37°C ; three times ; retyped.
- 0.01 M dithiothreitol (DTT)
124
(Resolution of Common Group IV Discrepancies)
As for the serum, the reagent RBCs and serum can be ______ to 37°C, then _____, _____, ______ at 37°C.
warmed ; mixed, tested, and read
125
(Resolution of Common Group IV Discrepancies)
The test can be converted to the _________ phase if necessary.
Weakly reactive anti-A or anti-B may not react at ______, which is outside their optimum thermal range.
If the reverse typing is still negative (and a positive result was expected), a _________ (patient cells with patient serum) could be performed to remove the cold autoantibody from the
serum.
The absorbed serum can then be used to repeat the _______ at room temperature.
antihuman globulin ; 37°C ; cold autoabsorption ; serum typing
126
antibodies other than anti-A and anti-B may react to form antigen-antibody complexes that may then adsorb onto patient’s RBCs
example: individual who has an antibody against acriflavine
RARE GROUP IV DISCREPANCIES
127
the yellow color in dye used in some commercial anti-B reagents is due to ________
the antisera A is blue color because of the presence of the dye ________-
acriflavine ; methyline blue
128
(RARE GROUP IV DISCREPANCIES)
___________ complex attaches to the pateint’s RBCs, causing agglutination in the forward type.
acriflavine-antiacriflavine
129
(RARE GROUP IV DISCREPANCIES: RESOLUTION)
washing the patient’s cells __________ with saline and then retyping them should resolve this discrepancy.
three times
130
(RARE GROUP IV DISCREPANCIES)
_________ refers to the inheritance of both AB genes from one parent carried on one chromosome and an O gene inherited from the other parent (Offspring inheriting three ABO genes instead of two)
Cis-AB
131
(RARE GROUP IV DISCREPANCIES)
Cis-AB phenotype was discovered in 1964, when a polish family was decribed in which the father was group O, and the mother was
group AB and gave birth to children who were all group AB.
Cis-AB phenotype
132
(RARE GROUP IV DISCREPANCIES)
A and B genes were inherited together and were both on the same, or ___, _________; thus the term cis-AB
- express a weakly reactive A antigen and a weak B antigen.
cis ; chromosome
