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ABO Blood Groups

QuestionAnswer
Reagent plant lectin used to differentiate Bombay phenotype Ulex europaeus
Anti-H lectin; yields a negative result with Bombay cells Ulex europaeus
Primary function of ABO, H, and Se genes code for specific glycosyltransferase enzymes that attach terminal sugars to precursor molecules
precursor oligosaccharide chains found in body fluids and secretions Type 1
precursor oligosaccharide chains found on RBC cell membranes Type 2
If an antigen (Ag) is present on a patient's red blood cells, the corresponding antibody (Ab) will not be present in the patient's plasma under normal conditions. Landsteiner's Rule: Reciprocal Relationship
Autosomal codominant inheritance; offspring inherits one blood type allele from biological mother and one from biological father Mendelian genetics of Blood Group inheritance
β1-4 linkage Type 2 found in body fluids and secretions
β1-3 linkage Type 1 found on RBC membranes
Predominant immunoglobulin class of Anti-A,B in group O individuals IgG
IgG class of immunoglobulin capable of crossing the placenta and causing ABO Hemolytic Disease of Fetus and Newborn (HDFN)
Immunodominant sugar for the B-antigen D-galactose (Gal)
D-galactose (Gal), immunodominant sugar for the B-antigen is added by this enzyme D-galactosyltransferase
Immunodominant sugar for the H-antigen L-fucose (Fuc)
L-fucose (Fuc), immunodominant sugar for the H-antigen is added by this enzyme L-fucosyltransferase
N-Acetylgalactosamine (GalNAc), immunodominant sugar for the A-antigen is added by this enzyme N-acetylgalactosaminyltransferase
Immunodominant sugar for the A-antigen N-Acetylgalactosamine (GalNAc)
Reagent plant lectin used to differentiate A1 and A2 red blood cells Dolichos biflorous
Anti-A1 lectin; agglutinates A1 cells but not A2 cells Dolichos biflorous
H gene locus chromosome and its dominant/recessive alleles Chromosome 19: H allele is dominant (>99.99%), h allele is a rare amorph
Proportions of A1 and A2 phenotypes among Group A individuals A1 phenotype ~80%; A2 phenotype ~20%
Bombay phenotype Genotype h/h; lacks H antigen and ABO-antigen expression
Bombay phenotype has strong naturally occurring anti-H, anti-A and anti-B
Three separate genetic loci controlling ABH antigen expression H, Se (Secretor), and ABO
Order of blood groups by relative amount of H antigen (greatest to least) O > A2 > B > A2B > A1 > A1b
Safest RBC selection for transfusion in patients with resolved ABO discrepancies or weak subgroups Group O red blood cells
Primary clinical risk associated with weak B subgroups in the blood bank misidentifying the blood type in the forward typing (eg. mistaking group B for group O or A) leading to ABO incompatible transfusion
Predominant immunoglobulin class of naturally occurring ABO antibodies in Group A or B individuals IgM class
Forward typing in ABO testing detects RBC antigens using commercial antisera
Reverse typing in ABO testing detects plasma antibodies using known reagent red blood cells
cross-reacting Anti-A,B antibody a single IgG antibody found in Group O individuals that reacts with both A and B antigens, not a mixture of anti-A and anti-B
a single IgG antibody found in Group _ individuals that reacts with both A and B antigens, not a mixture of anti-A and anti-B Group O
True or False ABO antigens are detectable in utero. True
True or False ABO reciprocal antibodies are detectable at birth False
Prevalence of Anti-A1 antibody in A2 individuals ~ 8% of A2 individuals
Prevalence of Anti-A1 antibody in A2B individuals ~ 22% - 35% of A2B individuals
O allele produces an enzymatically inactive protein, leaving the H antigen unconverted Group O RBC expression
Serological pattern characteristic of B3 subgroup Mixed-field agglutination when tested with reagent Anti-B
Landsteiner's Rule If an antigen is present on a person's RBCs, the corresponding antibody will NOT be present in their plasma under normal conditions
Autosomal codominant inheritance (A and B are codominant, O is recessive) Mode of inheritance for ABO blood groups
Most frequent blood type(s) Group O and Group A
A silent allele that yields no detectable product or enzyme activity (eg: h allele, O allele) Amorph
Naturally occurring antibodies produced against antigens of the same species without foreign RBC sensitization Isoagglutinins
What is Landsteiner's rule, and why does it make forward and reverse typing an internal check for ABO blood group determination? Forward typing identifies RBC antigens, reverse typing identifies serum antibodies using reagent RBCs. Because the antibody pattern directly mirrors the antigen pattern, the two tests serve as a reciprocal check on each other.
Why do Group O red blood cells express the highest quantity of H antigen? O alleles that produce an enzymatically inactive protein; the H antigen produced by the H gene remains completely unconverted.
Why do Group A1B cells express the least H antigen Group A1B express active A1 and B transferases that convert almost all available H precursor structures leaving very few unconverted H antigen sites.
What genetic deficiency causes the Bombay phenotype (Oh), and why can Bombay individuals only receive blood from other Bombay donors? Without a functional H gene, individuals cannot produce the H antigen required as a foundation for A and B antigens. They naturally form potent Anti-H, Anti-A, and Anti-B antibodies.
Why are Group O mothers with IgG Anti-A,B antibodies at higher risk for causing ABO Hemolytic Disease of the Fetus and Newborn (HDFN) compared to Group A or B mothers? Naturally occurring Anti-A and Anti-B antibodies in Group A and B individuals are predominantly of the IgM class, which cannot cross the placenta. Group O individuals produce a cross-reacting Anti-A,B antibody that is predominantly IgG
Created by: MOrfCLS
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