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MLSCI 270 > ABO Group > Flashcards

ABO Group Flashcards

1
Q

When were the ABO blood groups discovered?

A

1900; located on chromosome #9

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2
Q

ABO and H genes are ….

A

glycosyltransferases (enzymes)

  • add carbohydrates to type-2 paragloboside chain = Precursor Substance
  • made of four sugars attached to ceramide (lipid backbone) which is embedded in the RBC membrane
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3
Q

L-fucosyl transferase

A
  • gene = H

- antigen= H

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4
Q

N-acetyl D galactosaminyl

A

A

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5
Q

D- galactosyl

A

B

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6
Q

T or F. Almost 100% of the population will inherit two H genes

A

T!
as long as one H is inherited, then L-fucosyl transferase will be produced giving rise to an L-fucose being added to the PS

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7
Q

the __ antigen allows for other transferases to add sugars and form A and B antigens

A

H

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8
Q

antigen structure

A

glycosphingolipids or glycoproteins

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9
Q

lectins

A
  • proteins (found in nature) that bind specific carbs

- act as artificial Abs that bind certain antigens

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10
Q

Ulex europaeus

A
  • Anti-H

- seeds have lectin that binds H

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11
Q

Secretors

A
  • 80% of population (SeSe, Sese)

- make soluble proteins found in plasma, sweat, tears, etc.

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12
Q

ABO group with most amount of H

A

O

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13
Q

who produces Anti-H

A

produced by people who did not inherit at least one H allele

  • Bombay blood group
  • IgM & naturally occurring
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14
Q

determination of ABO

A
  • forward = testing for ABO involves determination of the antigen on the patient’s cells
  • reverse = presence of ABO antibodies in their plasma
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15
Q

Anti-A,B

A

can be used to check on the forward grouping (newborn)

or help pick up weak subgroups of A or B causing ABO discrepancies

seldom used routinely

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16
Q

What do Bombay people type as?

A

O

- must be transfused ith Bombay blood due to anti-H

17
Q

How do we test for Bombay?

A
  • test patient’s red cells with anti-H lectin (Ulex europaeus) => will be 0 because Bombay don’t have H at all
  • test for anti-H (which Bombaypeople should have) with O cells which is rich in H => positive!
18
Q

Subgroups of A

A
  • A1 = 80%
    A1A1, A1A2, A1O
  • A2 = 20%
    A2A2, A2O

** no difference in Ags; just clustering that is different **

  • A3 = rare; weak in the forward group; 1+ MFA; reverse group is normal
19
Q

this subgroup of A is a more efficient transferase and puts more terminal sugars on the H antigen

A
  • A1 = one million antigens per RBC
  • A2 = 250 000 antigens per RBC
  • A3 = 30 000 A antigens per RBC
20
Q

Anti-A1

A
  • made in response to something else in the environment (naturally occurring)
  • cross-reacts with A1
  • cold, clinically insignificant IgM (not same properties as anti-A, -B)
  • anti-A1 is unexpected; only made by 2-5% of people; <10% of A2B
21
Q

Dolichus biflorus

A

anti-A1 lectin

- monoclonal anti-A1

22
Q

Who makes anti-A1

A

A2 people and A2B people

23
Q

T or F. A1 people can make anti-A2, anti-A2B

A

F!

24
Q

Other subgroups of A

A

Ael, Aend, Ax

- small amounts of A or no A antigens on the cell; but have Ag in secretions

25
Q

Subgroups of B

A

exist but rare

- B3, Bx, Bm

26
Q

This may be useful in resolving a discrepancy

A

auto-control
- 2 drops of patient plasma with 1 drop of patient cells
OR
- anti-A,B may be useful in resolving a discrepancy

27
Q

missing/weak antibodies

A
  • newborns; <4 mos - <6 mos

- older person (70-90s)

28
Q

hypo/agammaglobulinemia

A
  • decreased Ab production
29
Q

how to resolve missing/weak antibodies

A

either coax it to react stronger or inhibit Abs

  • 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 at4C (react best in cold)

if not resolved = ABO questionable

30
Q

extra antibodies

A
  • irregular IgM alloantibodies (Lewis, P1, M, N)
  • cold autoagglutinins (anti-I, -IH, -H, -IA, -IB)
  • anti-A1
  • Rouleaux
31
Q

extra Abs = irregular IgM alloantibodies

A
  • Lewis, P1, M, N
  • naturally occurring IgM that some patients have; insignificant; read 4C (usually <15C)
  • resolve by prewarming; aliquot of plasma, warm 10 mins, drop of B cells and warm for 10 mins; use pipette that has been warmed; mix
  • if all else fails, then identify Ab (anti-M for ex), use own M negative B reverse grouping cell
32
Q

extra Abs = cold agglutinins

A
  • clinically insignificant for the most part
  • autoAb
  • naturally occurring
  • behave like regular IgM => react in cold, not warm
  • resolve by prewarming

** can vary in titre; ex: responding to infection = can increase that month, etc. **

33
Q

extra Abs = anti-A1

A
  • only made A2 or A2B ppl
  • usually 1-2+ strength
  • IgM; clinically insignificant; reacts in the cold
  • investigate by using the lectin => if pos = A1; if neg = A2; ID the Ab => confirm
  • resolve by driving rxn to the left
  • use A2
  • pre-warm (quicker + easier so start with this first)
34
Q

extra Abs = Rouleaux

A
  • increased protein in the plasma (multiple myeloma, acute phase reactants)
  • rxn will only be 1+
  • resolve by doing saline replace = remove plasma, replace with 2 drops of saline, mix, spin read, reaction should be 0
35
Q

other causes of discrepancies not resolved serologically

A
  • recent transfusion with non-identical ABO red cells
  • hematopoietic stem cell transplants (BM)
  • chimerism
  • passive ABO antibody from blood products

MLSCI 270 (15 decks)

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