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SBB > A, B, and H > Flashcards

A, B, and H Flashcards

1
Q

What is a blood group system?

A

Series of allelic genes and their modifiers
may be 2 or many alleles
Produce chemical related but serologically distinct antigens
Antibody is how the antigen is recognized and antigen is defined by antibody

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2
Q

Red cell antigens are?

A

chemical structures embedded or protruding from the RBC membrane
May be a soluble substance
genotype determines the presence or absence of antigens

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3
Q

Where are ABO antigens found in blood?

A

RBC’s, Plt’s, lymphocytes, and circulating proteins

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4
Q

Where are ABO antigens found in the body

A

Kidney, heart, lungs, liver, pancrease, gastric mucosa, and endothelium

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5
Q

Where are ABO antigens found in secretors?

A

glands, goblet cells, tears, urine, saliva, digestive juices, milk, sweat, bile, pericardial fluid, and peritoneal fluid

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6
Q

What chromosome in h gene located on?

What enzyme does H code for?

A

19

FUT1

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7
Q

What does FUT1 do?

A

Fucosyl transferase
adds L-fucose to terminal sugar on type 2 chain
a1-2 linkage
Gluc>Gal>GlcNAN>(1-4)Gal >(1-2) Fuc

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8
Q

What chromosome are ABO genes on?

A

Chromosome 9

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9
Q

What does A gene code for?

A

N-acetylgalactosamyl transferase

add GalNAc to Gal of H chain in a1-3 linkage

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10
Q

What does B gene code for?

A

D-galactose transferase

adds D-galactose to Gal of H chain in a1-3 chain

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11
Q

What causes O phenotype?

A

O gene codes for non-functional transferase

O01 and O02 caused by a deletion and framshift leading to truncated protein

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12
Q

AA critical in determining A and B genes?

A

Gly235Ser, Leu266Met, Gly268Ala

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13
Q

What type of chains are ABO antigens carried on?

A

A and B antigens are a terminal sugar attached to oliosaccharide chain carried on glycoproteins 90% and glycosphingolipids 10%

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14
Q

ABH antigens on glycoproteins are on what kind of chain

A

ABH antigens are mainly on N-GLycans containing polyactosaminyl units on Band 3 (DI), the glucose transport protein, RhAG, and CHIP-1 (CO)

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15
Q

What gestational age is ABO antigen detected?

A

5-6 weeks

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16
Q

What age are ABO antigens full formed?

A

By 2-4 years of age

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17
Q

What race has a stronger B antigens

A

Blacks, also have 20% Group B

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18
Q

Most to least H antigen

A

O > A2 > A2B > B > A1 > A1B

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19
Q

What is classic Bombay?

A

hh, sese, = Lea on RBC if Le gene present
Types as Group O, ABS pan-reactive and AC negative
Patient is negative with anti-H and AB is non-reactive with Oh cells

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20
Q

Allo Anti-H

A

Anti-H in bombay is very potent
Predominatly IgM that reacts at 4-37C
Often stronger at IS then AHG phase

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21
Q

What disease is also produces Oh phenotype?

A

LAD - Leukocyte adhesion deficiency also produces Oh cells due to deficiency in GDP-fucose transporter

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22
Q

What is gene epitasis?

A

where gene masks expresssion of another gene
Epistatic reactions occur because to transferase are required
Ex) H is required for A and B production

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23
Q

What is Para-Bombay?

A

hh, Se gene present
A, B, H in secretions and can adsorb onto RBC’s
Serum may still have weak anti-H or -IH and may be clinically significant
Anti-A1 may present because less A antigen present
May need adsorption/elution to detect antigens

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24
Q

What is auto-H?

A 
cold agglutin
may be seen with anti-I
More common in group A or AB people = less H
IgM antibody that reacts at RT or lower
Not clinically significant
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25
Q

What is CIS AB?

A

non-mendelian inheritance
1 gene produces mutant enzyme that makes both A and B transferase
Cis AB/O, Cis, AB/A, Cis, CisAB/B

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26
Q

What blood group is gastric cancer more common?

A

Group A

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27
Q

What blood group is gastric and duodenal ulcers more common in?

A

Group O

28
Q

Group O and coag factors

A

Group O has 25% less VIII and vWf?

May tend to bleed more

29
Q

Characteristics of ABO antibodies

A

IgM, reactive at RT
binds complement
Group O has anti-A,B - recognizes a shared determinant

30
Q

What age are ABO antibodies formed?

A

Antibodies can be seen at 3 months
1 year everyone should have antibodies
by 5-10 years antibodies will be at adult levels

31
Q

What does Se gene do?

A

Se gene, FUT2, add a fucose to type 1 chains
fucose is added to terminal galactose in -2 linkage
H substance in secretions

32
Q

Type 1 chains

A

Terminal galactose attached in 1-3 linkage
present in secretions/ adsorbed onto membrane
attached to protein
first sugar is GalNAc

33
Q

Type 2 chains

A

terminal galactose attached to GlcNAc in 1-4 linkage
present on RBC’s
attached to lipid (ceramide or glycospingolipid)
First sugar is glucose

34
Q

Anti-A1 lectin - Diluted

A

Dolichos biflorus Diluted
reacts with only A1 cells
also aglutinates strong Sda pos cells and Tn polyagglutinable regardless of ABO type

35
Q

Anti-A lectin - Undiltuted

A

Dolichos biflorus undiluted

reacts with any group A

36
Q

Anti-B lectin

A

Griffonia simplicifolia (aged)
may also be found as GS II + GalNAc
Used to detect acquired B -

37
Q

Anti-A + B lectin

A

Griffonia simplicifolia (fresh)
has weak anti-A activity
detects A and B activity

38
Q

Anti-H

A

Ulex europeaus

39
Q

What causes ABO subgroups?

A

AA substitution, resulting from a mutation, deletion, or gene recombination, within exon 6 and 7
less efficient transferase = weaker serological reactions

40
Q

A2 subgroup

A

20% of group A are A2

A2 is same transferase as A1 but less efficient

41
Q

A1 vs A2 phenotype

A

A1 converts nearly all H substances to A >1,000,000
A2 converts only 1/4 of H substance 200,000
A1 is on branched chains (H3 and H4)
A2 is on unbranched chains (H1 and H2)

42
Q

Why do A subgroups make Anti-A1?

A

Anti-A1 is really antibody against branched chains
Anti-A(cd)
AsubB have less A(cd) so more likely to make Anti-A1
A2 = 1-8%
A2B = 20-30%

43
Q

A3

A

mixed field agglutination

Anti-A1 may be present

44
Q

Ax

A

not agglutinated by Anti-A but sometimes weak with Anti-A,B human sera
most monoclonal reagents detect
similar to Am except A substance not in secretions
Ax has substance that is only detected using Ax cells
Anti-A can be adsorbed and eluted off

45
Q

Aend

A

MF agglutination but very weak
only 10% of cells agglutination
No A substance in secretions
Anti-A1 usually present

46
Q

Am

A

Weak or negative with Anti-A or Anti-A,b
Adsorption/elution required
Usually do not produce Anti-A1
Looks like Ax but Am has A substance in secretions

47
Q

Ael

A

usually so weak antigens not detected
may have weak reaction with anti-A,B
Usually has Anti-A1 present which make person look like a group O
no A substance in secretions
need adsorption/elution to detect A antigen

48
Q

Advantages of monoclonal reagents

A

Detection of Ax phenotype
fewer false positive due to anti-T, anti-Tk, anti-Tm
most will not detect acquired B (except MH04)

49
Q

Causes of Missing reactions in forward type

A 
Neutralization of Anti-A/B with high A/B substance
Massive transfusion of Group O
BMT
Large fetomaternal bleed
True chimerism
Disease (AML, Leukemia, Hodgkin's)
50
Q

Describe neutralization of Anti-A or Anti-B

A

Occurs with plasma suspended cells in patients with carcinoma of stomach or pancreas. Patients have an increased A or B substance that binds to Anti-A or -B reagent making antibody unable to bind to patient RBC ag

51
Q

What is adsorption/elution?

A

Incubate cells w/ Anti-A from human sera if possible for 30-60 min
Lui freeze thaw to elute antibody bound to cells
test Eluate with A1, A2, O cells.
If A antigen present, A cells will react because Anti-A will be present in Eluate

52
Q

What is B(A)?

A

Autosomal dominate phenotype (BB)
Weak expression of A antigen is due to an elevated D-galactosyl transferase that transfers a small amt of GalNAc = A
Agglutination is weak and easily dispersed
Only MH04 detects it
rare (1 in 1000 group B)
2+ with Anti-A 4+ with anti-B and strong 4+ with A Cells

53
Q

What is A(B)?

A

Associated with elevated H antigen and plasma H-transferase
increased H precursor allows for synthesis of B antigen by A antigen
Be described with monoclonal B reagent

54
Q

Causes of extra reactions in forward type

A 
Acquired B
Polyagglutination
BMT
Antibody coated cells
Rouleaux
55
Q

What is Acquired B?

A

Strong reaction with Anti-A but weak reaction with Anti-B
Seen with infected bowel
Bacterial enzymes remove an acetyl group from GalNAc > resembles galactose = B antigen
Not seen with monoclonal reagents
lower pH to 6.0 of human anti-B
GS I +GalNAc lectin (aged) will reacts with true B antigen

56
Q

What is polyagglutination?

A

A cell problem where crypt antigens (T, Tn) that are normally masked are exposed by disease such as sepsis or bowel infection
Crypt antigens react with Anti-T and Anti-Tn that are present in normal human sera. = Avoid plasma TRN
Persons wtih polyagglutination lack Anti-T, Tn

57
Q

What is Tn polyagglutination?

A

Only seen in Group O or B
Sialic acid residues on glycophorin A and B give RBC net negative charge
Mutation on X chromosome leads to decreased synthesis of Sialic residues exposing crypt antigens that resembles A antigen.
Reacts strongly with A1 lectin but should not react with monoclonal Anti-A. Seen using human polyclonal antisera.
Enzyme treat cells to remove M and N antigen

58
Q

What is cis A/B

A

Appear as A2. A antigen is more than A2 but less than A1. B antigen is weakly expressed with Anti-B present
Secretors have normal A, Large amt H, and weak B
High levels of H antigen cells
Mutated enzyme is capable of producing A and B

59
Q

Resolve antibody coated cells interfering with ABO

A

IgM antibodies can be washed away with warm saline or DTT treatment
IgG antibodies treat with EGA = EDTA glycine-acid

60
Q

What causes rouleaux?

A

Abnormal proteins in the plasma seen in MM, cryoglobulinemia, macroglobulinemia

61
Q

Causes of weak reactions in back typing

A

Decreased antibodies due to age
Hypo or agammaglobuliemia
Disease (Lymphomas, Waldenstrom’s marcroglobuliemia, CLL, Immusuppressive, and Immudeficiency)

62
Q

Causes of extra reactions in back typing

A

Rouleaux
Cold antibodies (Anti-A1, IgM, or cold auto)
Antibodies to media in reagent red cells
Passively acquired allo antibodies (IVIG, PLT’s, Many Group O RBC’s)

63
Q

Cold autoadsorption procedure

A

Treat patient RBC’s with ficin or ZZAP to remove antibody.
Mix 1 mL of patient’s ficin cells with 1 mL of serum at 4C for 30 min
Centrifuge and transfer adsorbed serum to a clean test tube to repeat testing with fresh ficin treated cells

64
Q

B3 phenotype

A

MF reactivity with B substance in secretions

65
Q

Bm

A

Weak B with B substance in secretions

66
Q

Bx

A

Weak or negative reaction with anti-B

May have very weak Anit-B present in serum

67
Q

Bel

A

Weak or negative reaction with Anti-B
requires adsorption/elution to detect
May have weak anti-B present in serum

SBB (37 decks)

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