Study your flashcards anywhere!

Download the official Cram app for free >

  • 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

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

58 Cards in this Set

  • Front
  • Back
-What type of inheritance are the Lu antigens?
-Are they immunogenic?
-How developed at birth?
-Co-dominant; expression varies
-No; not very immunogenic.
-Poorly developed at birth.
What type of antibodies are Anti-Lua?
-Nat'ly occurring IgA, M, or G.
What temp is optimal for Lua?
Does it bind complement?
Enzyme response?
-Usually roomtemp; rare warm.
-Occasionally binds complement.
-Enzymes make reactivity variab.
How frequent is LuA as a Ag?
Does it cause HDR/HTN?
Low frequency.
No, does not cause HTR; may cause mild HDN if IgG.
What's the diffnc betwenn LuA and LuB?
LuB is significant, warm-rctv, IgG.
What type of antibodies are Anti-LuB?
Immune or Naturally occurring IgA, M, or G.
What temp is optimal for LuB?
Does it bind complement?
Enzyme response?
37, Warm.
Occasionally binds complement.
-Enzymes make reactivity variab.
Does Anti-LuB cause HDN/HTR?
MAy cause either.
What are the duffy antigens?
Fya and Fyb
-What type of inheritance are the duffy antigens?
-How immunogenic are they?
-How developed at birth?
Poor immunogens.
Well developed.
How many alleles do we know about for duffy antigens?
What are they?
Fya, Fyb, Fy, and Fyx.
What is Fy?
What population is it seen in, and why?
the third allele that codes for the absence of Fya or Fyb.
Seen in blacks, a natural defense against malaria.
What is Fyx?
Variant gene that encodes weakened Fyb antigen.
What temp optimal for Anti-Fya?
Does it bind complement?
Enzyme response?
Warm, IgG.
Yes; activates complement.
Won't react - enzyme destroys these antigens.
Does Fya show dosage?
Does it cause HDN/HTR?
How does Fyb compare to Fya?
Pretty similar, but very rare and often found with Anti-K and Anti-c
In whom would you find Fya3, 4, or 5?
Blacks with phenotype Fya-b-
How many and what antigens are in the Kell Blood Group system?
Six: K, k, Kpa, Kpb, Jsa, Jsb.
Of all the kell antigens, which is most frequent?
How are Kell antigens inherited?
How developed at birth?
-Inherited as spcfc haplotypes, gene complex. Codominant.
-Well developd at birth.
What are the haplotypes inherited, what's more common?
K/k, Jsa/Jsb, Kpa/Kpb.

k/Jsb/Kpb is much more common than K/Jsa/Kpa.
What are the frequencies of:
Kpa = rare, in blacks
Kpb = common in both
Jsa = common in blacks, rare in whites.
K = neg in 90% of population.
Ko = very rare, kell null
What is the most common Kell haplotype?
What situates kell antigens on the RBC?
what cells lack it?
what phenotypes is it diminished in?
-a 93-kD protein.
-Ko, null cells.
What is Kx?
Not part of the Kell glycoprotein; stabilizes RBC membrane/cytoskeleton.
Who is missing Kx, and what is the result?
McLeod phenotypes; results in membrane defects, problems.
What are the 2 diseases associated with Kell null cells?
-McLeod Phenotypes
-Chronic Granulomatous Disease
What causes Chronic Granulomat. disease?
The lack of Kx antigen on WBCs. Result: defective WBC function.
Quick: you see a chronic bacterial infection; what do you think?
Check for absence of Kx antgen, may be chr. granulamatous dises.
What type of Ab are Kell?
Are they immunogenic?
-Natural OR Immune occuring, usually IgG (IgM is rare).
-YES! these antigens rate second only to D in immunogenicity!
Should we care about Kell antibodies?
YES! they are 2/3 of the non-Rh antibodies we'll see in labs.
What temp do Kell abs react at?
Do they show dosage?
Do they cause HDN/HTR?
Warm - AHG.
Yes, occasionally.
How often would you see Anti-k, and why?
VERY rarely, because only .2% is K/K, able to make the antibody.
How do you normally detect anti-Kpa or anti-Jsa?
With incompatible donor screens, because these rare antigens not typically on screen cells.
What on earth is the Xg blood group system?
What are the alleles?
The sex linked system :)

(Xg is amorphic)
Who is the Xga gene more frequently found in?
Females -> 89%

Males -> 66%
If an Xga pos male mated with an Xg female, what would result?
All neg males (Xg)
All pos females (Xga)
Anti-Xga characteristics:
-Type? How stimulated?
-Optimal reaction at?
-Complement? enzymes?
-IgG, immune stimulated.
-Reacts at warm better than IAT.
-May bind complement. Enzymes depress it.
-Maybe HTR, NOT HDN.
What holds the MNSs antigens onto RBCs?
GPA for M/N
GPB for S/s
Do enzymes alter MN antigens?
Which enzymes?
How are MN antigens inherited?
Do they show dosage?
Yes; destroys them.
Ficin trypsin and papain.
Codominant; show dosage
How developed at birth are M/N?
Are they only on RBCs or other?
-Well; 9 wks post-birth.
-Also on renal tissue.
What phenotype denotes M/N neg cells?
En(a-) --> represents the 2 En genes encoding GPA negative.
-How do Ss antigens respond to enzymes?
-How often does U occur?
-Variably inhibited by FICIN and papain.
-U is high incident.
what is unique about U- and U variant cells?
Lack the 'N' antigen, GPB; so are S-s-U-.
This is seen only in blacks.
What type of Ab is Anti-M?
What optimal temp does it react?
Does it activate complement?
Does it show dosage?
-Usually IgM, maybe IgG.
-Optimal at R.T. if IgM.
-Does NOT activate complement.
-Shows dosage.
What enhances some Anti-M's?
What destroys them?
Does Anti-M cause HDN/HTR?
-Enhance w/ acid environment.
-Destroy with enzymes.
What type of Ab is Anti-N?
What optimal temp does it react?
Does it activate complement?
Does it show dosage?
-Naturally occuring, IgM.
-Optimal is R.T.
-Does not activate complement.
-Shows dosage.
What destroys Anti-N?
Does Anti-N cause HDN/HTR?
Is it clinically significant?
-Enzymes destroy
-Rare cause of HDN/HTR.
-Only if reacts at 37.
What type of Ab is Anti-S?
What optimal temp does it react?
Does it activate complement?
Does it show dosage?
-Immune, IgG!!
-Coomb's phase.
-It may
-How does Anti-S react to enzymes?
-Does it cause HTR/HDN?
How does anti-s compare to Anti-S?
-Also immune IgG, but rarer.
What type of Ab is Anti-U?
What optimal temp does it react?
Does it activate complement?
-A rare immune IgG.
-Coomb's phase.
-How does Anti-U react to enzymes?
-Does it cause HTR/HDN?
-What type of blood crossmatch?
-S-s-U- from blacks.
What antigens are in the Kidd blood group system?
How developed are they at birth?
-Jka and Jkb.
-Well developed.
What type of inheritence is in the Kidd group?
What type of Ab are anti-Jka/b?
What optimal temp does it react?
Does it activate complement?
How immunogenic are the rxns?
Immune, IgG.
Weak reactions.
-How can you enhance Kidd group reactions?
-Do the antibodies show dosage?
-By using enzyme-treated RBCs.
What spcfc type of IgG are the Kidd antibodies?
how does it alter their rxtns?
-Makes them "notorious" for delayed HTR.