blood bank study guide questions 19-37 + discrepancy

what genes need to be present for A and B antigens to be expressed?

H-antigen is required for phenotypic expression, addition of immunodominant sugar to have ABO blood group present

precursor for red cell antigen and secretor status

Se located on chromosome 19, binds to precursor substance I found in secretions, fucosyl glycoprotein precursor for secretor status, H-antigen (L.fucose) for RBC precursor

universal donor for RBC

type O

universal recipient for RBC

type AB

universal donor for plasma

type AB

universal recipient for plasma

type O

if transfusing cells:

Make sure the recipient does not have preformed antibodies directed against donor RBC

if transfusing plasma:

Make sure the recipient’s red blood cells do not have antigens that donor plasma contains

type A blood can receive ___ RBC and ___ plasma

A and O; A and AB

type B blood can receive ___ RBC and ___ plasma

B and O; B and AB

type AB blood can receive ___ RBC and ___ plasma

A, B, AB and O; AB

type O can receive ___ RBC and ___ plasma

O; A, B, AB, and O

A1 cells are:

highly concentrated on branched and linear chains due to strong ability of the gene product to interact with H antigen, will agglutinate with D. biflorus

A2 cells have:

fewer antigen copies due to simpler linear forms of antigen, strong reaction with Ulex europaeus

false positives on ABO forward typing due to:

acquired B phenomenon, B(A) phenotype, poly-agglutination/rouleaux

false negatives on ABO forward typing due to:

patient conditions (leukemia/lymphoma) impacting antigen expression, A subgroup

Fisher race CDE =

weiner Rz

Fr cDE =

w R2

Fr CDe =

w R1

Fr cDe =

w R0

Fr CE =

w ry

Fr Ce =

w r’

Fr cE =

w r”

Fr ce =

w r

blood typed as weak D, we type that as

D positive or RhD +

Rh associated glycoprotein:

coded on chromosome 6, own unique glycoprotein antigens, absence has been noted to cause absences in RHCE & RHD proteins

RHD and RHCE genes are found on:

chromosome 1, two loci control phenotype

D antigen:

most immunogenic, 85% of D neg patients exposed to D pos RBCs will develop anti-D,  D-neg patients should receive D neg units to avoid seroconversion, Functions as cation transporter and is essential for membrane integrity

weak D (Du) is detected by:

indirect antiglobulin testing (IAT)

F antigen is formed when:

c and e are in the cis position

Ce antigen is formed when:

C and e are in the cis position

when C is inherited trans to D

the D allele expression is weaker

LW A =

A+

LW B =

B+

LW =

A-/B-

LW a LW a or LW a LW =

LW(a+ b-)

LW a LW b =

LW (a+ b+)

LW b LW b or LW b LW =

LW (a- b+)

LW LW =

LW (a- b-)

Rh control should always be:

negative

Rh system antibodies are:

unexpected antibodies, typically IgG that do not readily bind complement, best react at 37C and agglutination best at AHG phase, enhanced by LISS or albumin, can cause hemolytic reaction

missing or weak forward type discrepancy: Something decreasing antigen expression, Leukemia, lymphoma , A subgroup - A2 will not react well with A1 antisera

resolve: Incubate tubes at RT and repeat 

Incubate tubes at 4c and repeat 

Test with A1 lectin to rule out A1- should be neg

Use anti A,B reagent– reacts with most subgroups

Forward type discrepancy: extra reactions, Something enhancing ag expression or lattice formation, Acquired B phenomenon (Group A1 individual with lower gastrointestinal tract disease or gram negative septicemia who acquires reactivity with anti-B reagents, Usually due to gut bacteria deacetylating the immunodominant A antigen sugar and making it easier for Anti-B reagent to react with)

resolve: Determine patient’s diagnosis and transfusion history

Test patient serum against autologous red blood cells. Should be negative rxn

Use anti-B with different pH

Treat RBC’s with acetic anhydride to cause reacetylation to the molecules

forward type discrepancy: extra reaction, B(a) phenotype (Group B patient who acquires reactivity with Anti-A reagents in ABO red cell testing, The gene product of that B gene will sometimes add a small amount of the immunodominant sugar of A antigen to red cells and increased sensitivity of monoclonal reagents detects)

resolve: Determine patient diagnosis and transfusion history

Test RBC’s with additional monoclonal anti-A reagents or human polyclonal Anti-A

forward type discrepancy: extra reaction, poly-agglutination/ rouleaux (Elevated globulins due to multiple myeloma, waldenstroms or hodgkins lymphoma, Presence of plasma expanders like dextran and polyvinylpyrrolidone, Wharton’s Jelly in cord blood samples)

resolve: Washing the RBC’s several times with saline to remove proteins

Cord blood may require 6-8 washes

Saline replacement technique to remove rouleaux

• Centrifuge tube and note how much plasma is present, collect the plasma out of the tube

• Add saline to tube in volume equivalent to plasma removed

• Resuspend and then recentrifuged

In Wharton Jelly: remember that maternal antibodies could be implicated in causing discrepancy

Forward type discrepancy: mixed field reactions, 2 populations of cells are present in patient sample, Type O blood recently transfused into A, B, or AB patient, Recent history of bone marrow transplant

resolve: Medical and transfusion history

Reverse type discrepancy: missing/weak, Something limiting antibody production, Newborn: ABO antibodies non detectable until 3-6 months, Elderly: ABO ab production suppressed, Leukemia, lymphoma, agammaglobulinemia/immunodeficiency, Chemotherapy or immunosuppressive drugs, Recent massive transfusion: diluted abs

resolve: Review pt medical and transfusion history 

Reverse type discrepancy: extra reactions, A subgroups with Anti-A1 (Patients with A subgroup can produce an anti-A1)

resolve: Determine patient diagnosis and transfusion history

Test patient RBC’s with anti-A1 lectin to confirm ABO Subgroup

Test patients with A2 cells to confirm they will be negative reactions

• May require three A1 cells and three A2 cells

Reverse type discrepancy: extra reactions, Rouleaux can be present

resolve: saline replacement

Reverse type discrepancy: extra reactions, Cold reacting unexpected non-ABO abs (Reagent RBCs do not have JUST the ABO ags, An unexpected ab in the patient that reacts at room temp may bind to one of the non ABO ags causing false positive, Cold autoantibody that cause patients RBCs to be so heavily coated with ab that they spontaneously agglutinate)

resolve: Perform autocontrol to determine if autoantibody or alloantibody

• Autocontrol = patient RBC with Patient plasma

• If autocontrol is positive it is a cold autoantibody:

  • Incubate RBC’s at 37C for 10 minutes and wash patient RBC three times with saline

  • Can also treat patient RBC’s with 0.01M dithiothreitol (DTT) – disperses IgM agglutination

  • For reverse typing auto absorption may be needed if reverse typing is still discrepant

• If autocontrol is negative negative it is a cold alloantibody:

  • Run antibody ID screen/panel and look for cold reacting unexpected, non-ABO antibody

  • If non-ABO antibody found, use reagent A-cells or B-cells free of the complementary antigen