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SBB Review > Carbohydrate Antigens > Flashcards

Carbohydrate Antigens Flashcards

1
Q

Enzyme that converts i to I

A

B-1,6-acetylglucosaminyltransferase

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2
Q

Gene

I

A

IGnT or GCNT2

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3
Q

Number of antigen sites

I

A

32,000-500,000

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4
Q

Number of antigen sites

i

A

20,000-70,000

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5
Q

Location in RBC membrane:

I/i

A

Glycoproteins, glycolipids, Band 3

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6
Q

Present in which body fluids:

I/i

A 
Saliva
Milk
Amniotic fluid
Urine
Ovarian cyst
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7
Q

Present on which other blood cells:

I/i

A

Lymphocytes
Monocytes
Platelets
Granulocytes

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8
Q

Expression on adult cells:

I/i

A

I: strong

i: weak

Complete conversion around age 2

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9
Q

Expression on cord cells:

I/i

A

I: weak

i: strong

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10
Q

i adult phenotype without cataracts

A

Autosomal recessive

Mutation in exon 3 of GCNT2

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11
Q

Auto anti-I

Ig class

A

IgM

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12
Q

Auto anti-I

Temp of reactivity

A

RT to 4C- benign

30-37: pathogenic

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13
Q

Auto anti-I

Bind complement

A

Rarely

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14
Q

Auto anti-I

Hemolysis in vitro

A

No

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15
Q

Auto anti-I

Reactivity with enzyme treated RBCs

A

Increased

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16
Q

Auto anti-I

HTR/HDFN

A

No

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17
Q

Alloanti-I

Ig class

A

IgM

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18
Q

Alloanti-I

Bind complement

A

Rarely

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19
Q

Alloanti-I

Hemolysis in vitro

A

No

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20
Q

Alloanti-I

Temp of reactivity

A

RT - 4 C

Rarely 37

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21
Q

Alloanti-I

Reactivity with enzyme treated RBCs

A

Increased

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22
Q

Alloanti-I

HDFN

A

No

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23
Q

Alloanti-I

HTR

A

None to rare

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24
Q

Auto anti-i

Ig class

A

IgM

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25
Q

Auto anti-i

Temp of reactivity

A

RT-4C: benign

30-37: pathologic

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26
Q

Auto anti-i

Bind complement

A

Rarely

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27
Q

Auto anti-i

Hemolysis in vitro

A

No

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28
Q

Auto anti-i

Reactivity with enzyme treated RBCs

A

Increased

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29
Q

Auto anti-i

HTR/HDFN

A

No

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30
Q

Chain type of ABH In secretions

Also adsorbed onto RBCs

A

Type 1 chain

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31
Q

Chain type of most ABH on RBCs

A

Type 2 chain

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32
Q

H gene (FUT1) encodes

A

a-2-L-fucosyltransferase

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33
Q

H antigen expression

A

O>A2>B>A2B>A1>A1B>Bombay

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34
Q

ABO antibodies

Detection age

A

3-6 months

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35
Q

ABO antibodies

Adult levels reached

A

5-10 years

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36
Q

ABO antibodies

Titers

A

Vary from 4- >2048

Anti-A titers higher than anti-B

Titers higher in group O individuals than A or B

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37
Q

ABO antibodies

Ig class

A

Mostly IgM

Group Os have a mix of IgG and IgM

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38
Q

ABO antibodies

Temp of reactivity

A

4C

IgG will also react at 37

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39
Q

ABO antibodies

In vitro hemolysis

A

Yes (intravascular)

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40
Q

ABO antibodies

HTR

A

Yes

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41
Q

ABO antibodies

HDFN

A

Yes, usually mild

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42
Q

Lectin

Bandeiraea simplicifolia

A

Anti-B

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43
Q

Lectin

Dolichos biflorus

A

Anti-A1

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44
Q

Lectin

Ulex europaeus

A

Anti-H

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45
Q

Lectin

Phaseolus limensis

A

Anti-A

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46
Q

Lectin

Helix pomatia

A

Anti-A

Snails

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47
Q

Lectin

Anguilla japonica

A

Anti-H

Eel

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48
Q

Terminal epitope

A antigen

A

N-acetylgalactosamine

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49
Q

Terminal epitope

B antigen

A

Galactose

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50
Q

Terminal epitope

H antigen

A

Fucose

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51
Q

ABO antigen age of detection

A

5-6 week gestation

Adult levels 2-4 years (precursor chains branch with age allowing for more antigen expression)

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52
Q

ABO gene location

A

Chromosome 9q34

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53
Q

A1

A

80% of A donors

Approx 5x the A than A2

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54
Q

A2

A

Most common subtype @ 20%

Inefficient conversion of H
Less A antigen more H

55
Q

Acquired B

A

Deacetylation of the A antigen yields a B like galactosamine

Typically shows weak agglutination with anti-B reagents w/ negative auto control

56
Q

Acquired B disease associations

A

Infection by gastrointestinal bacteria

57
Q

Acquired B resolution

A

Type patient cells with different monoclonal reagent or acidified (pH 6) anti-B

58
Q

Anti-A1 frequency in A2 individuals

A

1-8% A2

22-35% A2B

59
Q

Anti-A1

Ig class

A

Usually IgM

60
Q

Anti-A1

Temp of reactivity

A

Usually RT or below- clinically insignificant

Rarely 37- clinically significant

61
Q

Lewis antigen present on which cells/tissues

A

Platelets
Endothelial cells
Kidney tissue
Genitourinary and gastrointestinal epithelium

62
Q

Lewis antigen on RBCs

A

NOT synthesized by RBCs
Passively adsorbed onto the cell membrane

May be eluted with increase plasma volume or increased circulating lipoprotein

Levels decrease on stored RBCs

63
Q

Lewis and secretor gene

A

Leb +

64
Q

Lewis gene but no secretor gene

A

Lea+

65
Q

Le(a+b+)

A

Transiently seen in infants while secretor activity increases

Seen in Asian populations where weak secretor gene is common (18% Japanese)

66
Q

Lewis expression in newborns

A

Le(a-b-)

Valid phenotype not present til age 5-6

67
Q

Lewis phenotype prevalence:

European

A

Le(a+b-): 22%
Le(a-b+): 72%
Le(a-b-): 6%
Le(a+b+): rare

68
Q

Lewis phenotype prevalence:

African

A

Le(a+b-): 23%
Le(a-b+): 55%
Le(a-b-): 22%
Le(a+b+): rare

69
Q

Lewis antibodies

Ig class

A

Generally IgM

70
Q

Lewis antibodies

In Le(a-b+) individuals

A

Do not make anti-Lea as trace amount of Lea is synthesized

71
Q

Anti-Leb

A

May show abo specificity

Most common anti-Leb H

72
Q

Lewis antibodies

HDN

A

Unlikely

Antigens readily shed from cells after transfusion
Antigen negative RBCs generally not indicated for most patients

73
Q

Lewis antibodies

HDFN

A

No

Predominantly IgM and antigen poorly expressed on neonate RBCs

74
Q

GCNT2 (I) chromosome location

A

6p24

75
Q

Difference between i adult w/cataracts and w/o cataracts

A

W/o cataracts mutation is in Exon 1c which is specific for I synthesis in RBCs (so none on red cells but present on other tissue)

W/ cataracts is gene deletion or mutation in exon 2 or 3 meaning I synthesis is lost in all tissues

76
Q

Anti-i disease association

A

Infectious mononucleosis

77
Q

P1 and P2 phenotypes both express

A

Pk and P

78
Q

Rare recessive phenotypes in P1PK/GLOB

A

P1k, P2k, p

Associated with natural production of antibodies

79
Q

P, Pk, P1 synthesis

A

Stepwise addition of sugars to lactosylceramide

Pk synthesized first- precursor of all globo-series glycosphingolipids

80
Q

Pk requires what gene

A

A4GALT

81
Q

Pk is a substrate for what enzyme

A

B1-3-N-acetylgalactosaminyltransferase
(B3GALNT1)

forms P antigen

82
Q

P1

A

A4GALT adds galactose to paragloboside

83
Q

p phenotype

A

Mutation in A4GALT

Loss of all globo family and P1

84
Q

ABO discrepancies

Missing/Weak antigen

A

subgroup of A/B

suppressed antigen

85
Q

ABO discrepancies

extra/unexpected antigen

A

acquired B
B(A)
antibody coating cells

86
Q

ABO discrepancies

missing/weak antibody

A

age

Hypo or agammaglobuliemia
Disease (Lymphomas, Waldenstrom’s marcroglobuliemia, CLL, Immusuppressive, and Immudeficiency)

87
Q

ABO discrepancy

extra/unexpected antibody

A 
rouleaux
anti-A1
autoantibody
cold alloantibody
passively acquired antibody
88
Q

A3

A

weakly positive with anti-A

mf

89
Q

Aend

A

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

90
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

91
Q

Am

A

negative with anti-A
adsorbs/elutes anti-A or -A,B

secretes A & H

92
Q

Ay

A

negative with anti-A
adsorbs/elutes anti-A or -A,B

secretes weak A and H

93
Q

Ael

A

negative with anti-A
adsorbs/elutes anti-A or -A,B

secretes only H

94
Q

B(A)

A

super B gene produces a–3-N-acetylgalactosaminyltransferase

extra “A like” antigen

95
Q

Lewis gene/chromosome

A

FUT3

chromosome 19

96
Q

P phenotypes frequency

Caucasion

A 
P1: 79%
P2: 21%
p: rare
P1k: very rare
P2k: very rare
97
Q

P phenotypes frequency

African American

A 
P1: 94%
P2: 6%
p: rare
P1k: very rare
P2k: very rare
98
Q

p (null phenotype)

A

lack P1, P, and Pk

99
Q

High prevalence in P1PK/GLOB

A

Pk, P, PX2, LKE

100
Q

P Asian frequencies:

A 
P1: 20%
P2: 80%
p: rare
P1k: rare
P2k: rare
101
Q

B3GALNT1 mutation

A

Pk phenotype

Loss of P, LKE, and PX2

102
Q

Anti-P1

A

Naturally occurring IgM present in 25-33% of P2 individuals

103
Q

Anti-P1

HDFN/HTR

A

Rarely crossed placenta- no HDFN

Rare reactivity at 37 or invitro hemolysis

104
Q

P1 levels during storage

A

Decrease

105
Q

P1 expression

A

Varies in strength among individuals

Anti-P1 may not react with all P1 + cells

106
Q

Anti-P1 with enzyme treated cells

A

Reactivity enhanced

107
Q

Anti-P1 inhibited by:

A

Hydatid cyst fluid

P1 substance from pigeon eggs

108
Q

Anti-PP1Pk (anti-Tja)

A

Separable mixture of the antibodies found in p people

109
Q

Alloanti-P (in P1k, P2k, and p) characteristics

A

Naturally occurring
Predominantly IgM or a mix of IgM and IgG

Associated with hemolytic transfusion reaction and occasional HDFN

ASSOCIATED WITH RECURRENT SPONTANEOUS ABORTIONS (placenta rich in P and Pk antigen)

110
Q

Auto anti-P association

A

Paroxysmal cold hemoglobinuria

Donath landsteiner test

111
Q

FORS1 characteristics

A

Addition of N-acetylgalactosamine to the P antigen

Resembles the A antigen and may be picked up by certain anti-A reagents (originally thought to be an A subgroup)

Gene: GBGT1

Most people have naturally occurring anti-FORS1

112
Q

How is Pk antigen formed?

A

A4GALT enzyme adds galactose to Lactosylceramide

113
Q

How is P antigen formed?

A

P antigen is formed from Pk

B3GALNT-1 adds GalNAc to Pk > P antigen

114
Q

How is NOR antigen formed?

A

Formed from P antigen

A4GALT enzyme adds galactose to P antigen

115
Q

How is LKE antigen formed?

A

Formed from P antigen

A4GALT enzyme adds galactose and sialic acid is added to form LKE

116
Q

Characteristics of P1 antigen

A

Weaker on cord cells until 10 years of age
Antigen varies in strength and is weaker on older cells
Enzymes enhance reactivity
Not destroyed by Papain, Ficin, EGA, DTT, Chloroquine

117
Q

What disease is Pk antigen associated with?

A

Receptor for shiga toxin

Receptor for Streptoccocus suis

118
Q

What disease is P antigen associated with

A

Receptor for parvovirus

119
Q

Disease associated with anti-I

A

Mycoplasma pnuemoniae

120
Q

Characteristics of pathological auto anti-I in CHD

A

Reacts at 32C and activates complement at 30-37C
Titer is > 500 at 4C and >128 at room temp
Will hemolyze enzyme treated cells at low pH
Antibody is typically monoclonal or idiopathic

121
Q

Characteristics of benign auto-I?

A

Reacts at <25C and activates Complement at <25C
Titer is < 64 at 4C and <16 at room temp
Antibody is polyclonal

122
Q

Diseases and Ii concentration

A

Increased I and i is found in chronic hemolytic disorders and is a sign of stresses erythropoiesis

  • Thalassemia major
  • Hypoplastic anemia
  • CLL
  • Acute leukemia
  • Bombay phenotype
123
Q

What chromosome is Le gene located on?

A

Chromosome 19

124
Q

Leb is a receptor for…

A

H. pylori - bacteria responsible for causing gastritis

Norovirus

125
Q

What is Le(a-b-) associated with?

A

Increased susceptibility to E. Coli, candida, Cardiovascular disease, and possibly graft failure in renal transplant patients

126
Q

What chromosome is H gene located on

A

Chromosome 19

127
Q

What disease is also produces Oh phenotype

A

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

128
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

129
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

130
Q

ABO frequency

European

A

O: 45%
A: 40%
B: 11%
AB: 4%

131
Q

ABO frequency

African American

A

O: 49%
A: 27%
B: 20%
AB: 4%

132
Q

H disease associations

A

Helicobacter pylori

Norovirus

133
Q

Anti-Le^ab

A

Inseparable anti-lea and -Leb

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