MLT GlobeBlood Banking: ABO system – page 6
116 Blood Banking MCQs on ABO system with answers and explanations.
ABH antigens on the red cell membrane are built mainly on which type of precursor oligosaccharide chain?
Red cell ABH antigens are made mainly on type 2 chains by FUT1. Type 1 chains are used in secretions and plasma (FUT2), which is why Lewis and soluble ABH relate to type 1.
A donor's red cells do not react with monoclonal anti-A, react 1+ with anti-A,B, and the plasma contains anti-B but no anti-A. The most likely phenotype is:
Ax cells typically react weakly or not at all with anti-A but agglutinate with anti-A,B from group O people. A2 cells react strongly with anti-A, and Bombay plasma would contain anti-H.
Forward type: group A. Reverse: A1 cells 1+, B cells 4+, A2 cells 1+. The antibody screen is positive at immediate spin. What is the most likely cause of the discrepancy?
Reactions with both A1 and A2 cells plus a positive room-temperature screen point to a cold alloantibody (e.g., anti-M) on the reagent cells. Anti-A1 would not react with A2 cells. Use antigen-negative A1 cells after identification.
Which plant lectin is used as a reagent to detect the B antigen?
Griffonia (Bandeiraea) simplicifolia lectin reacts with B antigen. Dolichos biflorus detects A1, Ulex europaeus detects H, and Arachis hypogaea detects T antigen.
Red cells type as group O and react only weakly with anti-H lectin. The plasma contains weak anti-H plus anti-A and anti-B, and saliva contains H substance. The best description is:
Para-Bombay people lack or have weak red-cell H (FUT1 inactive) but are secretors (FUT2 active), so H is present in saliva. Classical Bombay people have no H in saliva or on cells.
A healthy donor's cells react 2+ with anti-A and 2+ with anti-B, and the plasma has weak anti-B. The donor's mother is group O and the father is group AB with the same weak pattern. This is most likely:
In cis-AB, one ABO allele codes a transferase that makes both A and B antigen, usually weakly. Weak B expression often allows a weak anti-B in the plasma.
A group B donor's red cells react weakly with one monoclonal anti-A clone but not with other anti-A reagents. The plasma has strong anti-A, and secretor saliva contains B and H only. The best explanation is:
In B(A), a highly active B transferase adds small amounts of GalNAc, detected by some sensitive monoclonal anti-A clones. Cis-AB would give weak A and B with usually weak anti-B, not strong anti-A with normal B.
A group A patient received a group O hematopoietic stem cell transplant (minor ABO mismatch). Which red cells should be transfused after the transplant?
Donor-derived lymphocytes make anti-A that can hemolyse group A cells (passenger lymphocyte syndrome). Group O red cells are compatible with both recipient and donor.
Red cells do not agglutinate with anti-A or anti-A,B, but anti-A can be adsorbed onto and eluted from them. The plasma lacks anti-A, and secretor saliva contains A and H. The subgroup is:
Am cells are not agglutinated but adsorb and elute anti-A, the plasma lacks anti-A, and secretors have normal A in saliva. Ael differs because its saliva contains H only.
Red cells are not agglutinated by anti-A; A is shown only by adsorption–elution. The plasma often has an anti-A1-like antibody, and secretor saliva contains H only. The subgroup is:
Ael is shown only by adsorption–elution, has no A in saliva and often has anti-A in plasma. Am has A substance in the saliva of secretors.
The anti-A,B present in group O plasma is best described as:
Anti-A,B is a cross-reacting antibody: after adsorption with A cells, the eluate still reacts with B cells. This is why anti-A,B detects some weak A subgroups better than anti-A.
Type 1 and type 2 precursor chains of the ABH antigens differ in:
Type 1 chains have Gal β1→3 GlcNAc (mainly in secretions and plasma); type 2 chains have Gal β1→4 GlcNAc (mainly on red cells). Fucose is added later by the H or Se enzymes.
The most common O allele produces no active glycosyltransferase because of:
The common O allele has a single guanine deletion near the start of the gene (exon 6), causing a frameshift and a truncated inactive protein. FUT1 mutations cause the Bombay phenotype, not group O.
A patient with severe pneumococcal infection has red cells agglutinated by almost all adult ABO-compatible plasmas but not by cord plasma. The cells react with peanut (Arachis hypogaea) lectin. This is:
Bacterial neuraminidase exposes the T antigen; almost all adults have anti-T but newborns do not. Arachis lectin reacts with T; Tn is persistent and reacts with Salvia lectins.
A group O patient with a myelodysplastic neoplasm has persistent polyagglutination, weak mixed-field reactions with some anti-A reagents, and reactivity with Salvia sclarea lectin. Most likely:
Tn is a persistent somatic change in hematopoietic cells that exposes GalNAc, which can react like a weak A. T activation is transient and linked to infection.
A group O patient receives a group A stem cell transplant. Months later, reticulocytes remain very low and anti-A persists. The most likely complication is:
In a major ABO mismatch, persisting recipient anti-A destroys donor-derived A red cell precursors, delaying red cell engraftment. Passenger lymphocyte hemolysis occurs in minor mismatch.