Question | Answer |
Which antigens are associated with the P system? | P1 |
Which antigens are associated with the Globoside system | P, Pk |
What autoantibody is associated with Paroxysmal cold hemoglobinuria | Anti-P |
What lab test can confirm the presence of the Anti-P autoantibody | Donath Landstiener test |
What antibody is Mrs. Jay's Tumor (Anti-Tja) | Anti-PP1Pk |
What is the phenotype of a person presenting with the anti-PP1Pk antibody? | p null |
Give an example of a compound antigen | Anti-f |
Which Rh Antigen is the most immunogenic? | D |
Which I antigen is found in newborns? | i^infant |
What does the "I" stand for? | Individuality |
What is a compound antigen | Epitopes with more than one Rh genes on the same chromosome |
What is an antithetical antigen | A pair or more than a pair of antigens that are coded by different alleles of the same gene (high incidence/ low incidence) |
What is a high incidence (frequency) antigen? | An antigen that almost everyone has (almost 100%) |
Examples of high incidence antigens | k, Lub |
What is a low incidence (frequency) antigen? | An antigen that is very rare, almost no one has it (<1%) |
Examples of | |
What rbc morphology does one see in McLeod Syndrome? Why? | Ansio/Polkiocytosis because Kx protein isn't made = reduced K antigen |
Why does DTT neutralize Kell antigens | Breaks the disulfide bond |
Describe the significance of anti- "N" | Mimics the N on GPA (glycophorin A) and reacts at 37 degrees celsius |
What does HTLA | high titer, low avidity |
Kidd system is what kind of immunoglobulin? | IgG |
You need what to find Kidd | enzyme enhancement |
Why are HTLA antibodies usually clinically insignificant | Low avidity makes the antibodies weak and can be diluted out so they have not been implicated in causing transfusion reactions and therefore are not "clinically significant" |
KEL1 | K |
KEL2 | k (celano) |
KEL3 | Kpa (Penney) |
KEL4 | Kpb (Rautenberg) |
KEL5 | Ku (almost every RBC) |
KEL6 | Jsa (suttler) |
KEL7 | Jsb (matthews) |
History of the Kell system | Mrs. Kelleher; first to have hemolytic disease of the newborn |
Function of Kell gene on erythrocytes | Endothelian-d (converting enzyme) and vasocontrictor |
Function of duffy on erythrocytes | receptor for pro-inflammatory cytokines, transmembrane carrier |
If you have no Kx protein do you express Kell? | No |
DTT, 2-ME, and AET function | break disulfide bonds |
Cause of McLeod syndrome | no Kx protein |
Results of Mclead syndrome | ansio/polkiocytosis, decrease haptoglobin, increased reticulocytes, fragile, splenomegaly |
Enzymes papain and ficin destroy | Duffy, M, N |
Enzymes papain and ficin enhance | |
An antibody demonstrating dosage would mean that | Homozygous cells were stronger because you receive double the antigen, one allele from your mom and one from your dad |
What p-value must be observed in the rule of 3? | <=0.05 (gives a 95% confidence interval) |
A DAT performed on a clotted sample stored at 4 degrees celsius may demonstrate | in vitro complement attachment because a positive DAT demonstrates that the patients cells are coated with IgG antibodies and complement can be detected |
Elution | forcing off; acid elution's lower the ph and dissociates the antibody from the RBC membrane |
Adsorbtion procedures | remove autoantibody from serum to determine whether an underlying alloantibody exists |
The purpose of additional procedures when working up a warm autoantibody is to | identify potential underlying autoantibodies because warm autoantibodies agglutinate initially and mask underlying autoantibodies |