MLT GlobeBlood Banking: ABO system – page 5
116 Blood Banking MCQs on ABO system with answers and explanations.
A patient with the Bombay (Oh) phenotype needs red cells. Which units are suitable?
Bombay plasma contains potent anti-H that is active at 37 °C and can cause severe hemolysis. Group O cells have the most H antigen, so only Oh cells are compatible; washing does not remove antigens.
A group A patient received several group O apheresis platelet units. Reverse typing now shows a weak reaction with A1 cells, and the DAT is weakly positive. The most likely cause is:
Group O platelet units contain plasma with anti-A, which can appear in reverse typing and coat the patient's A cells. The patient's forward type was A1-compatible, so anti-A1 production is unlikely.
Low-titer group O whole blood is used in trauma resuscitation mainly because:
Group O plasma does contain anti-A and anti-B, so units are selected for low titers to limit hemolysis when given to A, B or AB patients.
When red cell units arrive from a blood supplier, the transfusion service must confirm:
AABB requires confirmation of the ABO group of all red cell units and the D type of units labelled D-negative. Weak D testing and reverse typing are not required for this confirmation.
A technologist incubates reverse-typing tubes at 37 °C for 30 minutes before reading. The most likely effect is:
Anti-A and anti-B are mainly IgM and react best at room temperature or below. Warm incubation can weaken reactions and cause a false discrepancy.
In ABO forward typing, using a red cell suspension that is much too heavy most likely causes:
Too many red cells relative to antibody (antigen excess) can weaken agglutination and cause false negatives. Rouleaux come from abnormal plasma, not heavy cell suspensions.
A healthy, never-transfused donor has a mixed-field reaction with anti-A. The two cell populations type as A and O. Her plasma has anti-B but no anti-A, and her twin brother is group A. The most likely cause is:
Twin chimerism gives two separate red cell populations, and the person is tolerant to both, so no anti-A is made. A3 cells do not separate into cells typing as normal A and O.
Before an ABO-incompatible kidney transplant, what is usually done for the recipient?
ABO antigens are on vascular endothelium, so high recipient anti-A or anti-B causes hyperacute rejection. Titers are reduced by plasma exchange or immunoadsorption before transplant.
A 5-day-old group A neonate of a group O mother needs red cells. Maternal IgG anti-A is detected in the infant's plasma by IAT. Which red cells should be given?
Passive maternal anti-A would destroy group A cells, so group O cells are given until the antibody is no longer detected.
For a neonate younger than 4 months, repeat ABO/D typing during the same hospital admission is:
Infants under 4 months rarely make new antibodies, so one ABO/D type per admission is enough. Reverse typing is not done because antibodies are maternal.
A group A2 patient has anti-A1 that reacts at 37 °C and in the antiglobulin phase. Which red cells are the best choice?
Anti-A1 active at 37 °C may shorten survival of A1 cells, so group O or A2 cells are given. AB and B units carry antigens the plasma reacts with.
Some laboratories add group O reagent cells to reverse typing. A positive reaction with the O cells suggests:
Normal ABO antibodies do not react with O cells. Reaction points to a cold alloantibody, autoantibody or anti-H (e.g., Bombay).
Soluble ABH substances in the saliva of secretors are mainly:
In secretions ABH antigens are carried on glycoproteins (mucins). On red cells they are on both glycoproteins and glycolipids.
Forward typing shows group O, but the plasma contains only anti-B (A1 cells negative). To look for a weak A antigen, the best next step is:
Missing anti-A suggests a weak A subgroup. Longer incubation at room temperature or 4 °C, with anti-A,B, increases detection of weak A.
A group O patient receives group A apheresis platelets. Compared with group O platelets, a possible effect is:
Platelets carry A antigen, so the recipient's anti-A shortens their survival and can lower the increment. Anti-D formation depends on D, not ABO.
The H (FUT1) and secretor (FUT2) genes are located on which chromosome?
FUT1 and FUT2 are on chromosome 19. The ABO gene is on chromosome 9.
Forward and reverse ABO typing results do not agree. What is the first step?
Many discrepancies come from clerical or technical errors, so the tests are repeated first (with a new sample if a wrong-blood sample is suspected). The ABO group must not be reported until the discrepancy is resolved.
Naturally occurring anti-A and anti-B are thought to be stimulated by:
Gut bacteria and foods carry carbohydrates similar to A and B, which stimulate antibody against whichever antigen the person lacks, without any red cell exposure.
A group A patient with colon cancer suddenly types as AB with a weak anti-B reaction, while the plasma still contains anti-B. The most likely explanation is:
Bacterial deacetylase (in colon cancer, obstruction or gram-negative sepsis) turns N-acetylgalactosamine, the A sugar, into galactosamine, which resembles the B sugar and reacts with some anti-B reagents. The patient's own anti-B does not react with his cells.
A group A patient's plasma weakly agglutinates A1 reagent cells but not A2 cells. The red cells do not react with Dolichos biflorus lectin. The most likely cause is:
Dolichos biflorus lectin reacts with A1 but not A2 cells, so the patient is A2. About 1-8% of A2 and 22-35% of A2B people make anti-A1, which gives this reverse-typing discrepancy.