MLT GlobeBlood Banking: Antibody screen & identification – page 5
90 Blood Banking MCQs on Antibody screen & identification with answers and explanations.
Rabbit erythrocyte stroma (RESt) is used for cold autoadsorption. An important limitation is that it may also remove:
RESt removes anti-I and anti-IH but can also adsorb anti-B, and some anti-D and anti-E. Adsorbed plasma should therefore not be used for ABO reverse typing.
A group A1 patient's cold antibody reacts strongly with group O cells, weakly with A2 cells and hardly with A1 cells or his own cells. The most likely antibody is:
Anti-IH reacts with cells having the most H and I antigen; group O and A2 cells have much more H than A1 cells. Anti-A1 would react with A1 cells, not O cells.
An antibody gives weak reactions with all panel cells at AHG, is neutralized by pooled normal plasma, and the patient is well. The likely specificity is:
Chido and Rodgers antigens are on complement C4 adsorbed to red cells, so C4 in plasma neutralizes the antibody. These high-titer, low-avidity antibodies are generally not clinically significant.
A myeloma patient on daratumumab (anti-CD38) has all panel cells reactive at IAT. How is this interference usually removed?
DTT removes CD38 from reagent cells, so the drug no longer reacts. DTT also destroys Kell antigens, so K-negative units are usually given unless the patient is K-positive.
Warm autoantibodies in autoimmune hemolytic anemia most often show apparent specificity within which system?
Many warm autoantibodies react more strongly with cells carrying certain Rh antigens, such as e. The practical value is limited, but antigen-negative blood may be chosen in some cases.
For allogeneic adsorption in a recently transfused patient with a warm autoantibody, adsorbing cells such as R1R1, R2R2 and rr are chosen so that:
Each adsorbed aliquot then keeps any alloantibody whose antigen is absent from that cell, so alloantibodies are not removed with the autoantibody.
A child on ceftriaxone develops sudden intravascular hemolysis. The DAT is strongly positive with anti-C3 and weak with anti-IgG. The most likely mechanism is:
Ceftriaxone causes drug-dependent antibodies that activate complement, giving C3 on cells and severe intravascular hemolysis. The penicillin type gives IgG coating and slower extravascular hemolysis.
Plasma reacts with all cells of one manufacturer's LISS-suspended panel, but not when the same cells are washed and resuspended in saline. The most likely cause is:
Reactivity that disappears once the reagent diluent is washed away points to an antibody against a diluent component. A red cell antibody would still react after washing.
Plasma contains anti-Fya and a second antibody that is hard to identify. A useful way to separate them is to:
Adsorbing with cells carrying only one antigen removes that antibody and leaves the other for identification.
Red cells treated with EDTA–glycine–acid (EGA) to remove IgG cannot be reliably typed for which antigens?
EGA removes IgG but destroys Kell system antigens, so Kell typing needs another method, e.g., chloroquine.