The ABO and Rh Blood Group Systems Flashcards
(110 cards)
1
Q
Who discovered the ABO Blood Group Systems?
A
Karl Landsteiner
2
Q
At what age do antibodies appear?
A
3- 6 months
3
Q
At what age do naturally occurring antibodies peak?
A
10 years old
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.
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.
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.
7
Q
What is the result of ABO incompatible blood transfusion?
A
Acute intravascular hemolysis, renal failure and can be fatal.
8
Q
ABO typing reagents are manufactured from ?
A
Monoclonal antibodies
9
Q
What color are the anti-A and anti-B reagents?
A
Anti-A = Blue Anti-B = Yellow
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.
11
Q
Forward typing identifies?
A
Antigen
12
Q
Reverse typing identifies?
A
Antibodies
13
Q
What are the major antigens of the ABO system?
A
A, B, and H (O)
14
Q
What ABO Phenotype is most common to Hispanic and African Americans?
A
O - AA 50% and Hispanic 56%
15
Q
The A Blood group is most common to?
A
Caucasians
16
Q
The B Blood group is most common to?
A
A. Americans 20% and Asians 25%
17
Q
The AB blood group is lease common to?
A
Hispanics
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)
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
20
Q
What statement best describes naturally occurring antibodies?
A
Produced without any exposure to RBCs.
21
Q
The ABO genes are located on which chromosome?
A
Chromosome 9
22
Q
Which genes are co-dominant and both expressed?
A
A and B
23
Q
What is an Amorph?
A
No detectable antigen is produced with the O gene
24
Q
What blood group is amorphous?
A
O
25
T/F: ABO Antigens result from the interactions of the genes at 3 separate loci (ABO, Hh, and Se)
True
26
What do the ABO genes code for and what does it do?
A specific Glycosyltransferase enzyme that adds a sugar to the basic precursor substance.
27
Identify the precursor chains that RBC antigens are constructed on? What is this precursor material called?
oligosaccharide chains of a type 2 precursor substance called a paragloboside / glycan. These chains are attached through the RBC membrane onto ceramide proteins.
28
Identify the difference between type 1 and type 2 chains?
Type 2 chains are found in body fluids
29
Where is the H-gene located? What are its alleles?
Chromosome 19, H and H
30
Identify the enzyme produced by the H-gene and what it does?
alpha-2-L-fucosyltransferase which transfers fucose to the end of the type II precursor chain.
31
The amount of H antigen on red cells is based on agglutination and is represented as?
O\>A2\>B\>A2B\>A1\>A1B
32
Identify the blood group with the least H antigen?
A1B
33
Identify the enzyme coded for by the A gene?
What sugar is transferred by this enzyme?
* N-acetylgalactoseaminyltrasferase
* N-acetyl-D-Galactoseamine
34
Identify the enzyme coded for by the B gene?
What sugar is transferred?
D-galasyltransferase
D-galactose
35
What Lectin do O blood group react strongly with?
Ulex europaeus
36
What percentage of the US population are secretors?
80%
37
What enzyme does the Se gene code for?
alpha-2-L fucosyltransferase which modifies type I chains
38
What is the most common A subgroup?
A1
39
Why does the A1 subgroup have the least H antigen?
It has a higher concentration of the transferase enzyme that converts the H chains into A antigens.
40
What subgroup has the strongest reation with Anti-A1 at cold temperatures but is alsoi clinically significant at 37oC
A1
41
Identify the second most common A subgroup which represents how many group A and AB people?
A2; 19.9% (20%)
42
1-8% of A2 people with for which naturally occuring antibody?
Anti-A1
43
What percentage of group A2B will for naturally occuring Anti-A1?
22-35%
44
This subgroup represents approximately 1:1000 of group A and AB people?
A3
45
Which subgroups have mixed field aggutination?
* A3
* Aend
46
Which Lectin is specific to A1?
Dolichus biflorus
47
How are A1 and A2 phenotypes determined?
Dolichus biflorus
48
What reagent is known as Anti-A1 Lectin?
Dolichus biflorus
49
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?
* All of the above
* Homozygous recessive
50
Which antibodies does the Bombay phenotype have?
* Anti-A
* Anti-B
* Anti-A,B
* Anti-H
51
T/F anti-H in the bombay phenotype is potent and often reacts strongly at 37oC?
True
52
What blood group does not react with the lectin Ulex europas?
* A1B
* A2B
* Oh
* B
Oh (Bombay) and A2B
53
What statement best describes an ABO discrepancy?
The forward and reverse typing do not agree
54
Most ABO descrepancies are the result of what?
Technical error
55
If after a technical review the discrepancy persists, what step should be taken next?
Aqcuire essential info regarding patient info such as age, history, medication, Ig levels.
56
What blood type may be agminstered while a dsicepancy has not yet been resolved?
O-compatible
57
What are the four Non-technical ABO discrepancies?
1. Group I Antibodies
2. Group II Antigens
3. Group III Protein
4. Group IV Miscellaneous
58
Describe what a Group I discrepancy is?
discrepancy between forward and reverse due to weakly reacting or missing antibodies.
59
Identify the patients Group I discrepancies are common amoung? (6)
* Elderly
* Newborns
* Immunodeficient
* Hypergammaglobulinemia
* Leukemia or lymphomas
* immunosuppresive drug thereapy
60
Describe chimerism?
the prescence of two cell populations
61
What are some causes of chimerism? (4)
* Transfusion
* Bone marrow transplant
* Exchange transfusions
* Fetal-maternal bleeding
62
How are group I discrepancies resolved?
* Incubate 15-30 mins at room temp.
* Spin and read
* If necessary incubate at 4oC
63
Describe group II discrepancies?
Unexpected reactions in forward grouping due to weak reacting or missing antigens?
64
What are causes of group II descrepancies?
* A and B subgroups
* Leukemia\*
* Hodgkin's Lymphoma
* **Acquired B Phenomenom**
65
How are group II discrepancies resolved?
* Incubate 15-30 mins at room temp.
* Spin and read
* If necessary incubate at 4oC
66
What control must always be tested with concurrently with reverse typing to resolve discrepancies?
* Auto-control
* O cell control
67
Describe group III descrepancies?
descrepancies in forward and reverse grouping due to caused by protien or plasma abnormalities
68
Identify causes of group III descrepancies?
* Multiple Myeloma
* Hodgkin's Lymphoma\*
* Plasma expanders (i.e. Detran and Polyvinylpyrrolidone (PVP))
* **Chord blood cells contaminated by Wharton's Jelly**
69
How are group III descrepancies resolved?
Wash patients cell several times with saline
70
What are group IV descrepancies?
descrepancies between forward and reverse groupings from miscellaneous causes.
71
Identify causes of group IV desrepancies?
* Polyaggtination (T-antigen)
* Cold reactive antibodies (allo and auto)
* Warm autoantibodies
* unexpected ABO isoagglutins
* antibodies against the anti sera
72
How are group IV descrepancies resolved? (5)
* Test patient cells with lectin if Tactivation susupected
* warm blood to 37oC
* Autoantobody absorbed out
* Elutions
* check patient history
73
Who identified the Rh system?
Landsteiner and Weiner in 1940
74
How many antigens make up the Rh system?
5
* D
* C
* c
* E
* e
**\*d is abscent**
75
What is the most complex human blood group system?
Rh
76
how many specificities make up the Rh system?
\>50
77
What percentage are categorized as D positive?
85%
78
Which theory proposed that the Rh locus contained 3 ditinct genes?
Fisher-race
79
What is the basis of the Weiner theory?
One gene for Rh, which produced 3 factors
80
What are the Fisher-Race Haplotypes?
1. DCe
2. DcE
3. Dce
4. DCE
5. dCe
6. dcE
7. dce
8. dCE
9.
81
What Rh Fisher-Race haplotype is most common to caucasians?
DCe (R1)
82
Identify the Fisher-Race haplotype most common to Asians?
DCe (R1) (70%)
83
What Rh Fisher-Race haplotype is most common to A.Americans?
Dce (R0)
84
What Rh Fisher-Race haplotype is the least common across all ethnicities?
dCE (ry)
85
Identiy the Rosenfield nomenclature?
* D = 1
* C = 2
* E = 3
* c = 4
* e = 5
86
For red cells that type D+ C+ E = c+ e+ what is the Rosenfield designation?
Rh: 1, 2, -3, 4, 5
87
Which nomenclarture systen has no genetic basis?
Rosenfield
88
How are Rh alleles inherited?
Codominant
89
On what chromosome is the Rh loci?
Chromosome 1
90
What genes are on the Rh loci? What do they determine the prescence of?
* RHD - prescence or abscence of D
* RHCE - production of C or c and E or e
91
What gene does a D-negative individual inherit?
One RHCE gene from each parent
92
Which gene is called a **Coexpressor**?
RHAG
93
What chromosome is the RHAG (Rh-associated glycoprotein located)?
Chromosome 6
94
The lack of RHAG gene is responsible for which Rh type?
Rhnull
95
The RhD and RhCE protiens are made up of how many amino acids and traverse RBC membranes how many times?
* 417
* 12
96
What are the 3 Rh negative mutations arising from?
* White - RHD deletion
* Black - Unusual RHD (pseudogene)
* Asian - Altered RHD gene making them type negative
97
What are the 4 genetic mechanisms of weak D?
* Genetic weak
* Position effect
* Partial D
* Del (Rhnull)
98
Describe Genetic Weak D?
What ethnicity is this common to?
Inheritance of genes that code for weak expression of D antigen. D antigen is normal but few in number.
Black
99
Decribe Position effect?
C is Trans to RHD
RHD is in the trans position on the chromosome carrying C.
Antigen is normal, expression is weakened
100
Describe Partial D?
* 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
Rh antibodies react strongly at which phases of testing?
* 37oC incubatio w LISS
* AHG
102
T/F: Rh antibodies bind complement?
False, it is very rare
103
Which Rh antibodies show dosage?
Anti-E
Anti-D rarely shows dosage
104
What antigen is the most immunogenic outside the ABO blood group system?
D antigen
105
Most Rh antibodies are which immunoglobulin? When are they produced?
IgG (IgG1, IgG2, IgG3, IgG4)
After exposure to foreign RBCs
106
Which Rh IgG subclasses are the most clinically significant?
IgG1 and IgG3
107
HDFN caused by Rh antibodies is often severe, how is this prevented?
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
What is Amorph Rhnull?
* Mutations in RHCE and Deletion on RHD
* RHAG is normal
109
Describe Rhnull syndrome?
not express and Rh antigens or severely reduced Rh antigen expression
110
Describe Rhmod?
Partial supression of Rh gene expression caused by mutations in RHAG
