MLT GlobeBlood Banking: ABO system – page 3
116 Blood Banking MCQs on ABO system with answers and explanations.
The most common cause of acute ABO-incompatible hemolytic transfusion reactions is:
Most ABO-incompatible transfusions result from misidentification during sample collection or bedside administration, not from technical testing errors.
About what proportion of people in most populations are ABH secretors?
Around 80% of people have at least one functional Se (FUT2) gene and secrete ABH substances.
In a column (gel) ABO test, a mixed-field reaction appears as:
Agglutinated cells stay at the top while unagglutinated cells pass to the bottom, showing two populations. A single top band is 4+; a bottom button alone is negative.
Group O red cells can be given to group A, B and AB patients because:
Group O cells have no A or B antigens, and people (except Bombay) do not make anti-H. They do carry much H antigen.
Who discovered the ABO blood group system?
Karl Landsteiner described the ABO groups in 1900–1901 and later received the Nobel Prize. Coombs developed the antiglobulin test.
Landsteiner's rule states that:
Landsteiner's rule: healthy people have anti-A and/or anti-B against the ABO antigens they lack. For example, a group A person has anti-B.
Naturally occurring anti-A and anti-B usually become detectable at about what age?
Infants begin making their own ABO antibodies at about 3–6 months. This is why reverse grouping is not done on newborns.
How are the A and B alleles expressed when a person inherits both?
A and B are codominant, so both antigens are made and the person is group AB. The O allele is recessive (amorphic).
Red cells react with both anti-A and anti-B, and the plasma reacts with neither A1 nor B reagent cells. The ABO group is:
Both antigens on the cells and no anti-A or anti-B in plasma is the pattern of group AB, and forward and reverse results agree.
The Bombay (Oh) phenotype was first described in:
The Bombay phenotype was first found in 1952 in Bombay (now Mumbai), India. These people lack H antigen and make strong anti-H.
In tube agglutination grading, a single solid clump with a clear background is graded as:
4+ is one solid agglutinate with a clear background. Weaker grades show smaller clumps with a cloudy red background.
Reverse (serum) grouping is important in ABO typing mainly because it:
Forward and reverse grouping must agree. The reverse group confirms the forward result and helps to reveal errors and discrepancies.
The H antigen, precursor of the A and B blood group antigens, is formed by adding which sugar to a terminal galactose?
Fucosyltransferase (FUT1) adds L-fucose to make H substance; A and B transferases then add N-acetylgalactosamine or galactose. Fructose is not part of blood group antigens.
The immunodominant sugar that defines the blood group A antigen is:
A transferase adds N-acetylgalactosamine to H substance; B transferase adds galactose. Fucose forms the H antigen itself, present on all common groups.
A child is blood group A. Which pair of parental ABO groups could NOT have produced this child?
The child needs an A allele from one parent. An O (OO) parent and a B (BO or BB) parent carry no A allele, so a group A child is impossible.
The immunodominant part of the A, B and H antigens is:
ABH specificity is set by terminal sugars (N-acetylgalactosamine for A, galactose for B, fucose for H) on glycoproteins and glycolipids.
Red cells of subgroup A2 typically give which pattern?
A2 cells carry fewer A antigen sites and lack the A1 epitope, so Dolichos biflorus lectin does not agglutinate them.
Which ABO group has the MOST H antigen on its red cells?
H is the precursor that A and B transferases convert. Group O cells have no transferase, so H is left unchanged. The order is O > A2 > B > A2B > A1 > A1B.
Red cells of a patient do not react with anti-A, anti-B or anti-H lectin (Ulex europaeus), and the plasma agglutinates all group O cells. The most likely phenotype is:
Bombay (Oh) people lack the H gene, so they cannot make H, A or B antigens. They make strong anti-H as well as anti-A and anti-B, and can only receive blood from another Bombay donor.
Why does an ABO-incompatible transfusion typically cause acute intravascular hemolysis?
Naturally occurring anti-A and anti-B are mostly IgM. IgM fixes complement efficiently through to the membrane attack complex, lysing red cells in the circulation and causing haemoglobinaemia, haemoglobinuria and possibly DIC.