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Immunoheme Exam 2
| 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 |
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