MLT GlobeBlood Banking: Antibody screen & identification – page 3
90 Blood Banking MCQs on Antibody screen & identification with answers and explanations.
Why is an EDTA sample preferred for the direct antiglobulin test?
EDTA chelates calcium and magnesium needed for complement activation, so any C3 found reflects in vivo binding. Clotted samples stored cold can pick up complement in vitro.
After a negative antiglobulin test, IgG-coated check cells are added and do not agglutinate. The most likely cause is:
Check cells should react with free anti-IgG. No reaction means the AHG was neutralized by leftover plasma globulin, was not added, or was inactive, so the test is invalid and must be repeated.
Which error can cause a FALSE-POSITIVE antiglobulin test result?
Excess centrifugation packs cells tightly so they are hard to resuspend and look agglutinated. Delay after washing lets IgG elute and causes false negatives; a heavy suspension also weakens reactions.
In a solid-phase red cell adherence antibody screen, a positive reaction looks like:
When antibody is present, indicator cells bind across the coated well and form a carpet. With no antibody, indicator cells roll down and form a small button.
A 70-year-old with painful blue fingers in cold weather has a DAT positive with anti-C3d and negative with anti-IgG. This pattern best fits:
Cold IgM autoantibodies bind in the cold, fix complement, then detach on warming, leaving only C3d. Warm AIHA usually shows IgG with or without C3.
The prewarm technique in antibody testing is used to:
Cells and plasma are warmed to 37 °C separately before mixing, so cold antibodies cannot bind and carry into the AHG phase. It may weaken some clinically significant antibodies, so it is used with care.
All panel cells react 2+ at AHG, the autocontrol and DAT are negative, and the patient was never transfused but had pregnancies. The most likely cause is:
Uniform reactivity with a negative autocontrol points to an alloantibody against an antigen present on almost all cells. Next steps include testing cells lacking high-prevalence antigens and seeking rare donors or siblings.
A panel shows reactions of different strengths at different phases, and no single specificity fits. The best explanation is:
Varied strengths and phases suggest multiple antibodies, each with its own pattern. Selected cells, enzyme-treated cells and antigen typing help separate them.
A patient transfused 5 days ago needs a red cell phenotype. What is the best approach?
Donor cells give mixed-field results. The patient's own reticulocytes, which are less dense, can be separated by microhematocrit centrifugation, or DNA-based typing can be used.
Plasma is treated with dithiothreitol (DTT), and an antibody's reactivity disappears. This shows the antibody is mainly:
DTT breaks the disulfide bonds joining IgM subunits, destroying its agglutinating ability, while IgG stays reactive. This helps judge whether an antibody could cross the placenta.
A patient given intravenous immunoglobulin (IVIG) now has weak anti-A and anti-D in the plasma, with no history of exposure. The most likely source is:
IVIG is pooled from many donors and can contain ABO and other antibodies. Passive antibodies are usually weak and disappear within weeks.
For investigating ABO hemolytic disease of the newborn, which elution method works well?
Heat elution is effective for ABO antibodies, which have relatively low affinity. Chloroquine removes IgG to allow typing and is not an elution method.
A patient with warm AIHA has life-threatening anemia, and all crossmatches are incompatible. After alloantibodies are excluded by adsorption, what should be done?
Transfusion should not be withheld when life is at risk. Once alloantibodies are excluded, compatible-type units are given slowly with close monitoring, even if the crossmatch is incompatible.
Pooled screening cells (red cells from two donors mixed) are acceptable for:
Pooling dilutes each antigen and can miss weak antibodies, so pooled cells are allowed only for donor screening. Patient testing uses unpooled cells.
Chloroquine diphosphate treatment of DAT-positive red cells is used to:
Chloroquine dissociates IgG from red cells with little antigen damage, allowing typing with IAT reagents. It does not remove complement.
The antibody screen is negative, but the AHG crossmatch is incompatible with one of four units. The DAT on that unit is negative. The most likely cause is:
Screening cells rarely carry low-prevalence antigens, so such antibodies are found only by crossmatch. A high-prevalence antibody or autoantibody would react with the screen and most units.
An antibody to a high-prevalence antigen is identified, and no compatible blood is available locally. The best source of compatible donors is:
Siblings are the most likely to share a rare antigen-negative phenotype, and rare donor programs keep frozen rare units. Washing does not remove antigens.
Which elution method is commonly used to remove warm IgG autoantibodies from red cells?
Acid elution recovers IgG warm antibodies well. Heat and freeze–thaw methods are mainly used for ABO antibodies.
A patient on long-term methyldopa has a positive IgG DAT. The eluate reacts with all panel cells without any drug added. This indicates:
Methyldopa induces true autoantibodies that react without the drug, serologically identical to warm AIHA. Drug-dependent antibodies need drug present.
Whether a cold autoantibody causes hemolysis is best predicted by its:
An antibody that reacts at 30 °C or above can bind in peripheral circulation and cause hemolysis. A high 4 °C titer alone may be harmless.