• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/56

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

56 Cards in this Set

  • Front
  • Back
Name the neutrolizer of ABO Ab's
Saliva (secretor)
Name the neutrolizer of Lewis Ab's
Saliva (secretor for Leb)
Name 2 neutrolizers of P1 Ab's
1. Hydatid cyst fluid
2. Pigeon egg fluid

Note: Turtle dove egg fluid can apparently do it too.
Name the neutrolizer of Sda Ab's
Urine
Name the neutrolizer of Chido and Rodgers Ab's
Serum/Plasma
Name a neutralizer of anti-H Ab
Saliva

(Also neutralizes anti- Lewis a and anti-AB"O").
Name a neutralizer of anti-I Ab
Breast milk
Name the Ab's that most commonly show dosage
Kidd, Rh, Duffy, and MNSs

Mnem: Because of dosage, kidd rides duffy up mountains
The lectin Bandeiraea simplicifolia binds what Ag?
B Ag
What Ab class are most cold reacting Ab's?
IgM
The lectin Lotus tetragonolobus binds what Ag?
H Ag
The lectin Arachis hypogaea binds what Ag?
T Ag
What Ab class are most warm reacting (and clinically significant) Ab's?
IgG
What bld grp Ab system is the major exception to the general rule that most cold reacting Ab's are IgM and most warm reacting Ab's are IgG?
ABO (though often naturally occuring and IgM-except anti-A, anti-B, or anti-A,B in grp O folks which are in fact IgG Ab's-these are indeed clinically significant)
Name the enzyme enhanced blood groups
1. The ABO FAMILY (ABO, Lewis, I/i, P) Mnem: "ALIP"
2. Rh blood group
3. Kidd blood group
Name the enzyme decreased blood groups
1. MNSs (mainly MNS-s usu. not affected)
2. Duffy
Name the enzyme unaffected blood group(s)
Kell

Recall Kell Ag's are destroyed by thiol reagents (e.g. ZZAP, 2ME, DTT) but not by enzymes alone!
What is the approx.frequency of the Se gene?
About 80%
What is the approx. frequency of the H gene?
About 100%

So most folks are not Bombays.
Where are type 1 chains found and what is the composition of their R group?
They are found in secretions and in plasma. Their R grp is composed of glycoproteins.
What is the sugar added to type 1 chains in order to make H Ag and where is that sugar added?
Fucose is the sugar added. It is added to the terminal galactose of type 1 chains.
Where are type 2 chains found and what is the composition of their R group?
They are found on RBC's. Their R grp is composed of glycosphingolipids.
What is the sugar added to type 2 chains in order to make H Ag and where is that sugar added?
Fucose is the sugar added. It is added to the termial galatose of type 2 chains
What type of H Ag must be made before A and/or B Ag's can be made on rbc's?
Type II H Ag
What type of H Ag must be made before A and/or B Ag's can be made in secretions and/or plasma?
Type I H Ag
What sugar is added to the terminal galactose in order to make an A Ag?
N-acetylgalactosamine (Gal-NAc)
What sugar is added to the terminal galactose in order to make a B Ag?
Galactose
On what chromosome are the Se and/or H genes?
Chrm 19
On what chromosome are the ABO Ag genes?
Chrm 9
Besides their location (rbc's vs. secretions/plasma) what is the only big difference between type I and type 2 chains?
Their R grps. Type I chains have a glycoprotein as the R group. Type 2 chains have a glycosphingolipid as the R group.
What are lectins?
They are chemicals that cause agglutination of rbc's bearing a certain antigen for which they are specific.
For what Ag's is the lectin Dolichos biflorus specifc? Why is this important?
1. A1
2. Sda

Is important with regard to A1 b/c it helps differentiate A1 from A2 subgroups. Dolichos biflorus agglutinates A1 subgroup rbc's but not A2 subgroup rbc's.
For what Ag is the lectin Ulex europaeus specific?
H
For what Ag is the lectin Vicea graminea specific?
N
What is the pathogenesis behind an acquired B phenotype?
Bacteria deacetelyate the grp A sugar (GalNac) and the remaining (now exposed) terminal galactose cross reacts with reagent anti-B to give an AB fwd grping (with weak fwd reactions with reagent anti-B).
Name 4 "treatments" that can be used to deal with an acquired B phenotype.
1. Acidify the serum (acidified human anti-B does not react with acquired B Ag)
2. Acetic anhydride (re-acetylates)
3. Autoincubation
4. BS-1 lectin
What is the difference between a bombay and a para-bombay?
Bombays totally lack H, A, and B Ag's due to lack of H AND Se genes. Parabombays are similar but have Se gene to partially comensate for their lack of H. Thus their secretions/serum testing may show H and A or B Ag (unless they are grp O) but their rbc's may type like a Bombay(i.e. no H, A or B).
On what chain (type 1 vs. 2) only can Lewis Ag be made?
Type 1
Can you make Lewis b Ag if you are a non-secretor?
No. The reason is because H Ag is required to make Lewis b. And since Lewis Ag (regardless of Lewis A or Lewis B) is only made on type 1 chains, only those who make type 1H (i.e. secretors can make Lewis b Ag). Note that H Ag is not required to make Lewis A Ag. All you need is a type 1 chain (H Ag on it is not required).
If Lewis Ag's are only made on type I chains, then how is it that Lewis Ag's are rbc Ag's? Because recall, type I chains are found only in secretions and/or plasma, not on rbc surfaces.
They are absorbed onto the rbc surface (and Lewis B more so than A).
Is there an inverse relationship between the amount of H Ag present and the amount of Lewis Ag (e.g. Lewis B Ag) present on rbc's like there is with H Ag and ABO Ag?
No
With the exception of the ABO blood group, when Ab's are naturally occuring, are they clinically significant?
No
Name 2 "diseases" associated with the production of an auto-anti I.
1. Mycoplasma pna infection.
2. Cold agglutinin dz
Name a disease associated with the production of an auto-anti i.
Infectious mono.
Unlike most anti-P Ab's, the Donath-Landsteiner Ab (which is the anti-P Ab associated with PCH) is of what Ab class?
IgG.
Most of the Rh Ab's are immune mediated. But if one is naturally occuring, what is it MC to be?
Anti-E.
What is the other name for each of the following genes (i.e. FUT 1, 2, or 3)?
1. Se gene
2. H gene
3. Lewis gene
Se gene= FUT2
H gene=FUT1
Lewis gene=FUT3
What is the significance of LW Ag and anti-LW Ab?
The LW Ag is expressed more strongly on D+ cells than D- cells. If anti-LW Ab's are present, they may appear to be reacting with only D+ cells, thus simulating anti-D Ab's. Thus they can make it seem like an O+ person has an anti-D Ab.
What effect can Hodgkin lymphoma and/or leukemia have on A and B Ag's on rbcs'?
It can give decreased/weakened expression of them leading to mixed-field agglutination.
What effect can gastric CA have on A and B Ag's on rbc's?
It can give increased free serum A or B Ag's which may have the effect of binding your REAGENT anti-A and anti-B thereby rendering them unable to bind to A and B Ag's on rbc's thus giving the false impression that the patient has type O cells.
What 4 drugs are classically known to give a positive DAT/autocontrol?
1. PCN
2. Cephs
3. Procainamide
4. Aldomet
Name 2 relatively uncommon causes of a positive DAT/autocontrol that must be excluded (along with more common causes such as recent transfusion and drugs) before a primary autoimmunity is considered.
1. Post-bone marrow txplant
2. Pt taking anti-lymphocyte globulin (ALG)
The warm-reacting auto-Ab's in WAIHA are usu of what Ig class?
IgG
What is the only reliable CBC index in a pt with cold agglutinins?
The hgb.
What Ig class are most cold agglutinins?
IgM. Thus they can activate complement in vitro and rxns can thus be seen at the AHG phase using polyspecific antisera. If monospec. reagents are used, the cells are agglutinated by anti-C3d but not anti-IgG.
What are the Ab's in cold agglutin dz usu. against?
Anti-I is MC.
Anti-i.
Anti-H.