TM ABO Group Flashcards
ABO and H genes code for..
glycosyltransferases (enzymes)
= adds carbohydrates to type-2 paragloboside chain (Precursor Substance)
What is the ABO type ?
Anti-A = 4+
Anti-B = 4+
A1 cells = 0
B cells = 0
AB
What is the ABO type ?
Anti-A = 0
Anti-B = 0
A1 cells = 4+
B cells = 3+
O
L-fucosyl transferase
- encoded by gene H
- adds L-fucose = H antigens
N-acetyl-D-galactosaminyl
- encoded by gene A
- adds N-acetyl-D-galactosamine
D- galactosyl
- encoded by gene B
- adds D-galactose
T or F: Almost 100% of the population will inherit two H genes
TRUE;
only one H needs to be inherited for L-fucosyl transferase to be produced = adds L-fucose to the PS
the __ antigen allows for other transferases to add sugars and form A and B antigens
H antigen
What kind of molecules are ABO antigens ?
glycoproteins
What are lectins ?
- proteins (found in nature) that bind specific carbs
- act as artificial Abs that bind certain antigens
Ulex europaeus
Anti-H
- seeds have lectin that binds H
Genotype for ABH secretors ?
- SeSe
- Sese
NOTE: only need one “Se” allele
Describe secretors of ABH antigens
- 80% of population (SeSe, Sese)
- make soluble antigens found in plasma, sweat, tears, etc.
ABO group with most amount of H
Type O
NOTE: H antigens have been added to PS
who produces Anti-H ?
- people who did not inherit at least one H allele (only have PS on RBC membrances)
- Bombay blood group
- IgM & naturally occurring
anti-H
- IgM
- naturally occurring*
*NOTE: IN BOMBAY, not in others
IgM
naturally occurring
IgG: naturally occurring or RBC-stimulated ?
RBC-stimulated
What do the forward vs reverse group in ABO testing determine ?
Forward = tests antigens on the patient’s cells
Reverse = tests for ABO antibodies in patient plasma
What do Bombay people type as ?
Type O
- must be transfused with Bombay blood due to anti-H in plasma
How do we test for Bombay ?
- test patient RBCs with anti-H lectin (Ulex europaeus) = will be 0 because Bombay don’t have H antigens at all
- test for anti-H (which Bombay people should have) with O cells (which is rich in H) = positive !
anti-A1
- naturally occurring
- cross-reacts with A1 cells
- cold, clinically insignificant IgM (not same properties as anti-A, -B)
- unexpected; only made by 2-5% of people; <10% of A2B
Dolichus biflorus
anti-A1 lectin
Who can make anti-A1 ?
- ONLY A2 people and A2B people
- NOT A1
What is an auto-control ?
- 2 drops of patient plasma with 1 drop of patient cells = SHOULD NOT CLOT
- can be useful in resolving a discrepancy
Cause: missing/weak antibodies (RG <2+)
- newborns <6 months
- seniors >70 years
- hypo/agammaglobulinemia
How to resolve missing/weak antibodies (RG <2+)
- add more plasma (4 drops instead of 2) to cells to promote shift to right (4:1 ratio of plasma cells)
- incubate RT for 30 mins
- incubate at 4℃ (ABO reacts best in cold)
Cause: extra antibodies
- irregular IgM alloantibodies (Lewis, P1, M, N)
- cold autoagglutinins (anti-I, -IH, -H, -IA, -IB)
- anti-A1
- rouleaux
What are the extra irregular IgM alloantibodies ? How do you resolve them ?
- Lewis, P1, M, N
- naturally occurring IgM that some patients have; insignificant; read 4℃
- resolve by PRE-WARMING: use aliquot of plasma, drop of B cells, and pipette that have been warmed for 10 minutes = mix
- if all else fails, then identify Ab (ie. anti-M)
What are cold agglutinins ? How do you resolve them ?
ie. anti-I
- clinically insignificant (mostly)
- autoAb
- IgM; naturally occurring
- resolve by PRE-WARMING
How is anti-A1 resolved ?
- made by Type A2 or A2B individuals
- IgM; clinically insignificant; reacts in the cold
- autocontrol = 1+
Resolve by:
1. PRE-WARM plasma, cells and pipette for testing
2. investigate using lectin (Dolichus biflorus): true anti-A1 will be pos with A1 cells and neg with A2 cells
3. use A2 cells in reverse group testing
What is rouleaux ? How is it resolved ?
- increased protein in the plasma (multiple myeloma, acute phase reactants)
- RG rxns will all be 1+, including auto-control
- resolve by doing SALINE REPLACEMENT = remove plasma, replace with 2 drops of saline, mix, spin read = rxn should now be 0
Differentiate A1 vs A2 cells
- A1 will have a more efficient transferase (N-acetyl D galactosaminyl) = more A antigens on cells
- A1 cells have more branched carbohydrates
If both parents are Type AB, why might the child not have any A or B antigens ?
The child is bombay (hh) = will Type as O
In TM, what rxn strength is considered abnormal and requires follow-up ?
less than 2+
Which antibodies are expected ?
- anti A, -B, -AB
- anti-H in bombay
