MLT GlobeBlood Banking: Other blood group systems – page 3
74 Blood Banking MCQs on Other blood group systems with answers and explanations.
A patient needs red cells. Which antibody requires antigen-negative, AHG-crossmatch-compatible units?
Anti-Fya is IgG and clinically significant, so Fy(a−) units are given. Cold-reactive Lewis, P1 and M antibodies that do not react at 37 °C/AHG usually need only crossmatch-compatible blood.
Which antigen commonly shows dosage, giving stronger reactions with homozygous cells?
Duffy, Kidd, MNS and most Rh antigens (not D) show dosage because homozygous cells carry more antigen. K, Lea and P1 do not typically show dosage.
The Xga antigen is unusual because its gene is located on the:
Xga is encoded on the short arm of the X chromosome, so it is more common in females (about 89%) than males (about 66%). Anti-Xga is rarely clinically significant.
The Diego antigen Di(a) is found mainly in which populations?
Di(a) is carried on band 3 and is common in Indigenous peoples of the Americas and in East Asians but very rare in Europeans and Africans. Anti-Dia can cause HDFN.
A patient with the Ko (Kell-null) phenotype has an antibody reacting with all panel cells. The antibody is most likely:
Ko cells lack all Kell antigens, and immunized people make anti-Ku (anti-KEL5), which reacts with all cells except Ko. Kx is present on Ko cells.
The Jk(a−b−) phenotype is most often found in people of:
The Kidd-null phenotype is rare overall but most frequent in Polynesians. These cells resist lysis in 2 M urea.
The Le(a−b−) phenotype is most common in people of:
About a fifth of people of African descent are Le(a−b−), compared with about 6% of Europeans.
The Pk antigen (Gb3, CD77) is the cellular receptor for:
Gb3 (Pk) binds Shiga and Shiga-like toxins. Parvovirus B19 uses globoside, the P antigen.
Colton antigens are carried on which red cell protein?
The Colton antigens are on the water channel aquaporin-1. The Kidd glycoprotein is a urea transporter.
Cromer blood group antigens are carried on:
Cromer antigens are on DAF (CD55), a GPI-linked protein, so they are weak on PNH type III cells. CR1 carries Knops antigens.
Antibodies in the Knops system (carried on CR1, CD35) are generally:
Knops antibodies give weak, variable (HTLA-type) antiglobulin reactions because CR1 levels vary between people, and they do not cause hemolysis.
Which red cell protein carries the Yt (Cartwright) antigens?
Yt antigens are on acetylcholinesterase, a GPI-linked enzyme on red cells.
An antibody gives small, shiny, refractile mixed-field agglutinates at AHG and is neutralized by guinea pig urine. The specificity is:
Anti-Sda gives refractile mixed-field agglutinates and is neutralized by guinea pig urine. Anti-Ch is neutralized by pooled plasma.
Bg (Bennett-Goodspeed) antigens on red cells are:
Bga, Bgb and Bgc correspond to HLA-B7, B17 and A28. Their antibodies are usually weak and rarely clinically significant.
Unusually strong anti-P1 is associated with infection by:
Hydatid cyst fluid contains P1-like substance that boosts anti-P1. Mycoplasma is linked to anti-I and EBV to anti-i.
Anti-Lea rarely destroys transfused red cells mainly because:
Lewis antigens are adsorbed from plasma; soluble Lewis substance in transfused plasma neutralizes the antibody, and donor cells shed Lewis antigens in the recipient.
Which blood group system, like ABO, has carbohydrate antigens?
Lewis antigens are carbohydrates made by fucosyltransferases and adsorbed onto red cells from plasma. Kell, Kidd and Duffy antigens are carried on proteins.
In blood group serology, 'dosage' means that an antibody:
Homozygous cells (for example Jk(a+b−)) carry a double dose of antigen and react more strongly than heterozygous cells. This is typical of Kidd, Duffy, MNS and some Rh antibodies.
An antibody reacts only at the AHG phase with Fy(a+) panel cells and stops reacting when the cells are treated with ficin. The most likely specificity is:
Fya is destroyed by ficin, so anti-Fya reactivity disappears. Kidd, Rh and Lewis antibodies are enhanced by enzyme treatment, not abolished.
Most Fy(a−b−) people of African descent do not make anti-Fyb after transfusion. Why?
In these people a GATA-1 promoter mutation silences FY*B only in red cell precursors, so Fyb is still made in other tissues and they are tolerant to it. They may, however, make anti-Fya.