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Transfusion 231 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What are Co-Dominant Alleles

A

The product of each allele is expressed

Equal expression of 2 different inherited alleles

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2
Q

What are Dominant Alleles

A

Expressed even in a Heterozygous
state

when one gene product is expressed over another

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3
Q

What are Recessive Alleles

A

Expressed in a Homozygous state

recessive alleles are only expressed in a homozygous state
only expressed when inherited by both parents

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4
Q

What is the dosage effect

A
  • AB reaction strength depends on the quantity of target antigen present on a target RBC

Kidd blood group system; alleles are codominant, meaning that the product of each allele is expressed
Jka and Jkb

-the more binding sites that are present the stronger the reaction
-stronger agglutination grading when RBC AG are expressed in homozygous form

-identified with ABs associated with Duffy, Kidd, Rh MNs group

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5
Q

What does phenotyping describe

A

which antigens are present on the red cell and determined through
serological testing. Positive indicates that antigens are present. A negative indicates that the antigens are not present.

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6
Q

What are the duffy AG

A

Fya and Fyb

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7
Q

How can Enzymes affect reactions with Ag

A

-enhance, suppress, and inhibit entirely the antigen reactivity with the antibody.
-Ficin, Trypsin, Papain, and Bromelin are examples of the proteolytic enzymes used.
* Removes the net negative charge on red cell membranes and denaturing the antigenic determinants.
* Reduces the Zeta potential and enhances the agglutination of some other antigens.
-Duffy and MNS are destroyed by the enzyme-treated cells, but Kidd Rh and Lewis blood group systems are enhanced by enzyme-treated cells. Kell has no effect.

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8
Q

Where can ABO AG be found

A

-RBC, endothelial cells, platelets,
lymphocytes, epithelial cells, and tissue cells. If the secretor gene is inherited, ABO antigens can be found in body fluids such as saliva.

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9
Q

The ABO-H-Link

A

-Before A/B sugar is added to precursor , L-Fucose needs to be added
-H gene codes for enzyme FUT 1 to add the
L-Fucose (sugar) to the precursor substance.
-this forms the H ag which is needed for the expression of A and B AG since gene produces of ABO alleles need H AG to be the acceptor molecule from A & B transferases

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10
Q

H Gene

A

-codes for L-fucosyltransferase, which adds the L-fucose to the precursor substance to
produce the H antigen.
-H Locus has 2 significant alleles: H and h
- little h allele is considered an amorph with a rare frequency, does not code for enzyme and is the silent h
-hh is rare

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11
Q

What is the bombay phenotype

A
  • hh genotype
    -no fucose added to precursor
    -no A or B sugar can be added
    -group like its a group O and serum contains Anti-A, Anti-B and Anti-A,B, and even Anti-H.
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12
Q

Why is Anti H important

A

-antibody is capable of high thermal activity and complement activation, which results in hemolysis.

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13
Q

how to detect Bombay in the lab

A

-bombay phenotype is Oh
-pt have Anti H so they react with all cells except rbc from other bombays so if they need a transfusion it has to be from another bombay
-reaction strength depends on number of H ag on the cells
-pf types as group O and the AB screen would positive across the whole panel
-

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14
Q

slide 19

A
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15
Q

What is the lewis system

A

-Ag are not produced on the RBC membrane
-not intrinsic
-produced and secreted on Type 1 precursor chains and then absorbed onto RBC membrane
-Ag development depends on 3 independent inherited genes -H, Secretor gene, and the Lewis gene.
-Le gene -dominant and le -amorph with no enzyme being produced

-Antigens present on RBC are Lea or Leb

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16
Q

Le, H, and Se Genes

Le, H, and Se Gene = Lewis and Secretor

A

Le, H, and Se Gene = Lewis and Secretor

-when these genes are inherited varying amounts of precursor chains
converted depending on the ABO type (H antigens are increased in O individuals).
-H, A, B, Lea, and Leb substances can be found in secretions
-Most of the Lea is converted to Leb by the Se gene
-Red cell absorbs only Leb in significant amounts so there is none or a trace of Lea AG on RBC

17
Q

Le, H, and se Genes

Le, H, and sese Gene = Lewis and Non-Secretor

A

Le, H, and sese Gene = Lewis and Non-Secretor

1) Only Lea produced
2) NO further addition of sugars
3) Red cell Membrane only absorbs Lea
4) Plasma contains only Lea soluble antigens
5) sese gene, NO H, A, B in soluble form

18
Q

Lewis Genes

A

-only the LE gene
* NO Lea or Leb gene
* They are not alleles Lea or Leb

They are the AG found on the rbc

Only one antigen is absorbed onto the red cell membrane

19
Q

Lewis Ag

A

-not fully developed at birth
-NB are usually Le(a-b-) and maybe typed as Le(a+b+) until the transition to Le(a-b+)
-phenotyping is unreliable until 6 years of age, because phenotyping is able to change because AG can be reabsorbed so it wouldnt be an prominent on the RBC membrane

20
Q

Lewis Antibodies

A

-IgM AB with no significance
-wide temperature range
-not well developed at birth but can bind complement and cause hemolysis
-does not cause a transfusion reaction
-enhances effect on enzymes
* Possible for Le(a-b-) individuals to make Anti-Lea and Anti-Leb
* Anti-Leb is rare in Le(a+b-) individuals
* Le(a-b+) would NOT produce Anti-Lea

21
Q

Major OBG Systems

A

Kell - Warm AB
Duffy - Warm AB
Kidd - Warm AB
MNSs
P - carb -Cold AB
Li - carb
Lewis - carb - cold AB

blood group system grouped according to similar antigens inherited by alleles at a single
gene locus or linked loci.

Antigens can be multi-pass proteins like (Rh), single-pass proteins with carbohydrates components or carbohydrate branches (ABO).

22
Q

Ficin or
Papain

A

an antibody no longer reacts with the panel of red cells, after the red cells have been pretreated these enzymes

23
Q

MNSs System

A
  • on chromosome 4. due to proximity, they are inherited as a haplotype
    -* M and N antigens are co-dominant alleles
  • S and s antigens are co-dominant alleles

-inherited like the Rh system and well developed at birth
- high phenotype frequency
-single pass glycoproteins
-integrated into the RBC membrane
-GYPA and GYPB genes encode for the MNS system

-* Glycophorin A (GPA) codes for M and N antigens
* Glycophorin B (GPB) codes for S and s antigen
* U antigen is always present when S or s is inherited.

24
Q

Anti M
Antibody M

A

IgM
-cold reacting, depending on pH
-doesnt need RBC stimulation like ABO grouping
- can be IgG
-if it reacts at 37 with AHG and doesn’t disappear it is important
-rarely causes HDFN
-does show dosage so it reacts stronger with HOMO cells
-destroyed by enzyme-treated cells

25
Q

Anti N
Antibody N

A

-IgM immunoglobulin
-clinically insignificant
-shows dosage
-destroyed by enzyme treated panel cells

26
Q

Anti-S and Anti-s

Antibody S or s

A

-red cell immune (produced after exposure) and can cause transfusion reactions and HDFN
-clinically significant because they are IgG immunoglobulins and react at the IAT phase
-destroyed by enzymes
- show dosage

27
Q

Anti U

Antibody U

A

-red cell immune can cause transfusion reactions and HDFN
-IgG
-IAT reactions
-resistant to enzyme destruction
- only seen in S-s- and U- patients
-reacts with S+s+

28
Q

Kell AB

A

-antiK can cross the placenta
-give K negative to women of child baring age
-k is high frequency AG as alot of people have k on their AG
- low frequency AG but anti k is high frequency
-red cell immune and dont bind complement
-transfusion and HDFN reactions
-IgG
-optimal at IAT and 37
-activity depressed with LISS
* K, Kpa and Jsa are low-frequency antigens
* K, Kpb and Jsb are high frequency antigens
-folding in cell membrane - integrated
-sensitive to sulfhydryl reagents such as DTT, 2ME and AET because it disrupts the disulphide bonds between the amino acids.
-e five sets of alleles in total
-immunogenic 2nd to D antigen
* Kell null phenotype can produce Anti-Ku

29
Q

The McLeod Phenotype

A

-XK gene is not inherited, the Kx antigen is
not expressed on red cells.
-absence of this antigen reduces expression of Kell blood group system antigens.
-Acanthocytes with spur-like projections are present in these individuals.

30
Q

Duffy System AB

A

-well developed at birth and detected on fetal cells
-can cause delayed or quick transfusion reactions
-codominant alleles
-red cell immune and dont bind complement
-Anti Fya can bind complement and cause reactions
-IgG
-Anti-Fya is much more common than Anti-Fyb
-reaction at IAT and 37
-Reactions are destroyed by enzyme treated cells.
-show dosage
-just like Kell they are not on granulocytes, lymps, monos or platelets
-glycoprotein found on lipid bilayer of rbc membrane
-The Duffy antigens are Fya and Fyb, and they are codominant. A silent FY allele has no Fya or Fyb antigens present on the red cells.
* Susceptible to proteolytic degradation by enzymes, like papain and ficin
* Receptor for proinflammatory chemokines (activation of white cells)

31
Q

Duffy System and Malaria

A

-SS pt can be Fya and Fyb negative.
-SS pt have a mutation that affects Fyb antigent expression on RBC and ss pt wont produce Anti Fyb therefore they can be given Fyb pos blood even if they are Fya and Fyb neg
–Fy(a-b-) phenotype has a resistance to malaria
Fy allele provides a genetic selective advantage in geographic areas where P.vivax is endemic.
-CBS has to do genetic testing to see if a FyFy pt will produce Anti Fyb
-* GATA1 mutation impacts the Fyb antigen expression

32
Q

Fy(a-b-) produce?

A

AntiFya, Anti-Fy3, and Anti-Fy5

both fy3/5 are resistant to ficin or papain treatment and are expressed on cord blood

33
Q

The Kidd AB

A

-developed in the fetus , red cell immune
-grouped in clusters because they are so close when the AB attach they can activate complement causing INTRAVASC- HDFN
-IgG
-IAT at 37
-enhances its effect on enzymes
-Jk(a-b-) red cells are more resistant to lysis in the presence of 2 M urea
* JK glycoprotein facilitates rapid urea transport across the red cell membrane.
-show dosage
* Co-dominant alleles JKA and JKB= high-frequency antigens
* JK allele is a silent allele
-allo antibodies hard to detect linked to extravascular hemolysis in delayed hemolytic transfusion reactions.
-anti Jka and anti Jkb disappear quickly from circulation are low in titre

34
Q

Ii System AB

A
  • on all adult cells
  • I antigen -branched chains
  • i antigen - in infants (cord blood from placenta) and linear chain
    -i can convert into I in 2 years
    -both found on RC membrane and body secretions
    -nti I and Anti i can be autoantibodies

-gM and cold reacting
-Anti i is transient found with infectious mono
-Auto Anti I can cause CAD associated with mycoplasma pneumonia
-Anti I binds complement and Anti C3d can be used to detect the reaction
-prewarming helps to prevent reactions
-have a compound AB Anti HI

35
Q

P antigens

A

-poorly developed at birth and have genes that code for enzyme for AG development
- found in different amount on different RBC
-have a strong expression but diminish in storage
-found on tissues and RBC
-similar AG are found in nature like bird poop, pigeons, eggs, hydatid cyst fluid

P1 is most common phenotype and expresses P, P1 and PK AG had no antibodies
P1K associated with spontaneous abortions

36
Q

P Antibodies

Anti-P1

A

common in P2 ppl
-no RBC stimulation
- IgM, cold reacting, and enhanced with enzymes.
-Commercially purchased P1 substance used to neutralize the antibody.

37
Q

P Antibodies

Auto Anti-P

A

-seen in P1 or P2 individuals and causes clinically significant Paroxysmal Cold Hemoglobinuria (PCH).
-IgG antibody -Donath Landsteiner antibody. It is a biphasic hemolysin that binds to P red cells at low temps in extremities. Since complement is attached it can affect hemolysis
-can appear in kids after viral infections

Transfusion 231 (10 decks)

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