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
Reading...
Front

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

image

Play button

image

Play button

image

Progress

1/58

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?
Codominant.
Poor immunogens.
Well developed.
How many alleles do we know about for duffy antigens?
What are they?
Four:
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?
Yes.
Yes.
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.
(1,2,3,4,6,7)
Of all the kell antigens, which is most frequent?
K
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
Kpb
Jsa
K
Ko
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?
k/Jsb/Kpb
What situates kell antigens on the RBC?
what cells lack it?
what phenotypes is it diminished in?
-a 93-kD protein.
-Ko, null cells.
-McLeod
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.
Yes.
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 :)

Xga/Xg
(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?
-HTR/HDN?
-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?
Glycoproteins
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.
-RARE cause HDN/HTR
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.
-YES
-It may
-How does Anti-S react to enzymes?
-Does it cause HTR/HDN?
Variably.
Yes.
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.
-Yes.
-How does Anti-U react to enzymes?
-Does it cause HTR/HDN?
-What type of blood crossmatch?
-Enzymes HAVE NO EFFECT!
-Yes.
-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?
Codominant.
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.
Coomb's.
Yes.
Weak reactions.
-How can you enhance Kidd group reactions?
-Do the antibodies show dosage?
-By using enzyme-treated RBCs.
-Yes.
What spcfc type of IgG are the Kidd antibodies?
how does it alter their rxtns?
IgG-3
-Makes them "notorious" for delayed HTR.