ABO Blood Group System Flashcards
Basic precursor substance
Paragloboside/Glycan
Described the theory for the inheritance of the ABO groups
Bernstein (1924)
Expression of ABO is through
Codominance expression
Inheritance pattern of group O phenotype
Autosomal recessive
Presence of two identical alleles
Homozygous genotype
Inheritance of different alleles
Heterozygous genotype
Sequence of DNA that is inherited
Genotype
Anything that is produced by the genotype
Phenotype
Glycosyltransferase coded by H gene
A-2-L-fucosyltransferase
Glycosyltransferase coded by A gene
A-3-N-acetylgalactosaminyltransferase
Glycosyltransferase coded by B gene
A-3-D-galactosyltransferase
Immunodominant sugar of H gene
L-fucose
Immunodominant sugar of A gene
N-acetyl-D-galactosamine
Immunodominant sugar of B gene
D-galactose
ABO antigens form as early as
37th day of fetal life
Full expression of ABO antigens occur at what age
2-4 years
Precursor chain of ABO antigens on RBCs
Type 2
Precursor chain of ABO antigens in secretions
Type 1
Linkage of ABO antigens on RBCs
Beta 1-4 linkage
Linkage of ABO antigens in secretions
Beta 1-3 linkage
ABH secretions can be found in
DUBSTAMP
Digestive juices
Urine
Bile
Saliva
Tears
Amniotic fluid
Milk
Pathogenic fluid
Excessive ABH substances in secretions can be observed in
PIC
Pseudomucious ovarian cyst
Intestinal obstruction
Carcinoma of stomach and pancreas
Determination secretor status is by
Hemagglutination Inhibition
Unbranched straight chains of H antigens
H1 and H2
Complex branched chains of H antigens
H3 and H4
Reactivity of anti-H antisera or anti-H lecti with ABO blood groups
O > A2 > B > A2B > A1 > A1B
Reacts with anti-A1, anti-A, and anti-AB
A1
Reacts with anti-A and anti-AB
A2
MF reaction with anti-A and anti-AB
A3
Reacts with anti-AB, no recation with anti-A
Ax
MF reaction with anti-A and anti-AB but with only few agglutinates (<10% of cells)
Aend
Weak/no reaction with anti-A and anti-AB
Am
No reaction with anti-A and anti-AB
Ael
No reaction with anti-A and anti-AB; observed in siblings; germline mutation of an A gene
Ay
Method used to confirm the presence of Am, Ael, and Ay antigens
Adsorption & Elution
Predominantly Aa and Ab and unconverted H3 and H4 antigen sites
A2 RBCs
Aa, Ab, Ac, and Ad determinants and no unconverted H3 and H4 antigen sites
A1 RBCs
Reacts with anti-B and anti-AB
B
MF reaction with anti-B and anti-AB; most frequent B subtype
B3
Weak reaction with anti-B and anti-AB
Bx
No/Weak reaction with anti-B and anti-AB
Bm
Converts Bm subgroup to B when incubated with
Uracil diphosphate
No reaction with anti-B and anti-AB: extremely rare phenotype
Bel
Method used to confirm the presence of Bm and Bel antigens
Adsorption & Elution
Phenotype that results in the inability to form the H antigen subsequently the A or B antigens
Bombay phenotype
Bombay phenotype was first reported by
Dr. Y. M. Bhende (1952) in Bombay (Mumbai), India
Causes silenced H gene
Mutation in FUT 1 gene
Causes silenced Se gene
Mutation in FUT2 gene
Antibodies in the serum of Bombay phenotype
Anti-A, Anti-B, Anti-AB, and Anti-H
Bombay phenotype blood group
Group O
Absent or only trace amount of ABH antigens on RBCs with normal expression in secretion or body fluids
Parabombay phenotype
Causes of Parabombay phenotype
1) Mutated FUT1 gene w/ or w/o an active FUT2 gene
2) Silenced FUT1 gene with an active FUT2 gene
Naturally occurring Abs directed against the A and/or B antigens absent from and individual’s RBCs
ABO Abs
ABO Abs are produced at_____but detected only at _____months of age
Birth, 4-6 months
ABO Abs are cold reacting
Predominantly IgM
ABO ABs react at what temp
Room temp or after IS phase
ABO Abs activate complement at what temp and can cause what
37 degC, cause in vitro/in vivo hemolysis
Plants or seed extracts that agglutinate human cells
Lectins
Anti-A1 lectin
Dolichos biflorus
Anti-B lectin
Bandeiraea simplicifolia/ Griffonia simplicifolia
Anti-H lectin
Ulex europaeus
Anti-N lectin
Vicia graminea
Anti-M lectin
Iberis amara
Anti-T, Th lectin
Arachis hypogaea
Anti-Tn lectin
Salvia sclarea
ABO Ags appear as early as ___ , peak at ___ , and decline at ___
37th day of fetal life, 2-4 years old, remain constant throughout life
ABO Abs appear as early as ___ , peak at ___ , and decline at ___
Birth (detected only at 3-6 months), 5-10 years old, after 10 years
Using antisera to detect Ags on px RBCs
Forward grouping
Typing sera must be:
1) monoclonal
2) IgG
3) highly specific
Typing sera preservative
Formalin/ sodium azide
Antisera QC that ensures the reactivity of antisera
Positive control
Antisera QC that ensures the specificity of the antisera
Negative control
Uses reagent RBCs to detect ABO Abs in px serum
Reverse grouping
Reagent for reverse grouping
4-5% human red cells (A1 and B cells)
Universal RBC donor
Type O
Universal plasma donor
Type AB
Universal RBC recipient
Type AB
Universal plasma recipient
Type O
Grading with one solid agglutinate
4+
Grading several large agglutinates, clear bg
3+
Grading with medium agglutinates, clear bg
2+
Grading with small agglutinates, turbid bg
1+
Grading with tiny agglutinates, turbid bg
W+
Grading with no agglutination or hemolysis
0
Conditions that cause weaker rxns
1) leukemia (MF)
2) chromosome 9 translocation
3) hemolytic dses
4) hogkin’s lymphoma
5) hypogammaglobulinemia/immunodeficiency
Conditions that cause pseudoantigens
1) acquired A phenomenon
2) acquired B phenomenon
Conditions that cause acquired A phenomenon: “PT”
1) P. mirabilis infxn
2) T cell inactivation
Conditions that cause acquired B phenomenon: “EPIC-C”
1) E.coli 086 infxn
2) P.vulgaris infxn
3) Intestinal obstruction
4) Carcinoma of colon & rectum
5) C.tetani infxn
How to differentiate acquired B fom true B
Acquired B cells will not react with pH <6 or > 8.5
Most common source of ABO discrepancy
Incorrect specimen/labelling/recording of results
Failure to add reagents/sample
False neg
Cell suspension too heavy
False pos
Cell suspension too light
False neg
Contaminated reagents/materials
False pos
Problem: reverse grouping
Causes: weakly reacting/missing Abs
Group l discrepancies
Causes of group l discrepancies: “NE-HAPA”
1) newborn
2) elderly
3) hypogammaglobulinemia
4) agammaglobulinemia
5) plasma transfusion/exchange therapy
6) ABO subgroups
Problem: forward grouping
Causes: weakly reacting Ags/missing Ags
Group ll discrepancies
Causes of group ll discrepancies: “AWP”
1) ABO subgroups
2) weakend expression of A and B Ags
3) pseudoantigens
A rare group ll discrepancy wherein the reagent anti-A or anti-B is neutralized, leaving no unbound Ab to react with px cells
Blood Group Specific Soluble (BGSS) substances
Problem: forward and reverse groupings
Causes: plasma/protein abnormalities
Group lll discrepancies
Causes of goup lll discrepancies: “EEP-W”
1) elevated globulin levels
2) eleavated fibrinogen
3) plasma expanders
4) wharton’s jelly in cord blood samples
Plasma expanders that may cause group lll discrepancies
1) dextran
2) polyvinylpyrrolidone
Problem: forward and reverse groupings
Causes: miscellaneous problems
Group IV discrepancies
Causes of group IV discrepancies: “CUUM-P”
1) cold reactive autoantibodies
2) unexpected ABO isoagglutinins
3) unexpected non-ABO alloantibodies
4) more than one ABO group RBCs (transfusion, BM or stem cell transplant)
5) polyagglutination
