Antigen/Antibodies other an ABO Flashcards

1
Q

Antibodies that react at the RT phase

A

P, I, H, Lewis
M, N,
Lutheran(a)

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2
Q

Antibodies that react at AHG phase

A

S, s, U, Kell
Duff, Kidd
Lutheran (b), Xga
Rh, rarely lewis

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3
Q

5 phenotypes of P system

A

P1, P2, p, P1k, P2k

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4
Q

Detectable antigens for P1

A

P1P

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5
Q

Detectable antigens for P2

A

PP

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6
Q

Detectable antigens for p

A

None

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7
Q

Detectable antigens for P1k

A

P1Pk

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8
Q

Detectable antigens for P2k

A

PkPk

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9
Q

Antibody that can be inhibited by hydatid cyst fluid

A

Anti-P1

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10
Q

Antibody/antibody class associated with paroxysmal cold hemoglobinuria

A

Auto anti-P
IgG biphasic
ID by Donath-Landsteiner test

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11
Q

What antigen in the P system deteriorates rapidly during storage?

A

P1 antigen

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12
Q

What is the Donath-Lansteiner test used for?

A

Anti-P autoantibody

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13
Q
  • No gene for I or i but the presence or absence of many glycosyl transferases results in different sequences added to the original structure
  • I and i antigens are the subterminal portions of the molecules that are eventually converted to H, A, or B
A

Transition of i to I antigen

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14
Q

Antibody characteristics of Ii system

A

IgM - only significant if it is masking the presence of another antibody. Not RBC stimulated, usually autoantibody

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15
Q

Transient antibody associated with infectious mononucleosis

A

Anti-i

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16
Q

Anti-I thermal activity

A

usually weak IgM

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17
Q

Potent anti-I thermal activity

A

Can occur with an IgM molecule that has a wide thermal range - reacting at 30 C or warmer.

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18
Q

Anti-i

A

Usually IgM and react best at 4 C

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19
Q

Antibody associated with Mycoplasma infections

A

Anti-I (cold agglutinin disease)

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20
Q

Anti-I cord blood activity

A

Does NOT agglutinate with cord cells

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21
Q

Anti-i cord blood activity

A

Agglutinates with cord blood

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22
Q

How can you differentiate pathogenic anti-I and non pathogenic anti-I?

A

Pathogenic anti-I will react equally with adult or cord cells (ii)

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23
Q

Which blood group is most likely to make anti-H?

A

A1B combination because they have the least amount of H on the surface

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24
Q

Acquisition of Le (a)

A

Substance is produced if the individual has inherited the Le gene. This substance will absorb onto the surface of the RBC & become an RBC surface antigen & is a glycolipid Le (a+b-)

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25
Q

Acquisition of Le (b)

A

Substance is interaction of the Le gene, the H gene, & the Se gene. If all three are present, the Le (b) soluble antigen is produced in addition to Le (a) when both are in secretions.

  • More successful at absorbing onto the surface of RBC
  • Le (a-b+)
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26
Q

Is Le (a+b-) a secretor?

A

No

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27
Q

Is Le (a-b+) a secretor?

A

Yes

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28
Q

Is Le (a-b-) a secretor?

A

Unkown

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29
Q

Do enzymes affect the Lewis antigen?

A

Yes, by enhancing the activity

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30
Q

Where are the Lewis antigens produced?

A

Tissue

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31
Q

Significance of anti-Le(a), anti-Le(b)

A

Considered insignificant because of their neutralization by Lewis substances, poor attachment to RBC, IgM class

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32
Q

Do the Lewis antigens show dosage and are the reactions changed with enzymes?

A

No dosage, reactions are enhanced by enzymes

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33
Q

Who is most likely to make anti-Le(a) or Le(b)?

A

Pregnant women sometimes change to Le(a-b-) no matter what Lewis genes they have inherited.

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34
Q

Chromosome MNSsU is on

A

4

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35
Q

Does MNSsU show dosage?

A

Yes

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36
Q

Enzyme reaction of MNSsU system

A

All decrease with enzymes

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37
Q

When MNSsU system is developed

A

At birth

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38
Q

Precursor to MN

A

Glycophorin A

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39
Q

Precursor to SsU

A

Glycophorin B

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40
Q

Anti-M antibody Class

A

Naturally occurring IgM or rarely immune IgG

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41
Q

Anti-M complement fixation

A

Does not fix complement

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42
Q

Anti-M temp of reactivity

A

Not reaction above or at 30 C - not clinically significant

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43
Q

Anti-M cause of HDN/HTR

A

Should be concerned about HDN

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44
Q

Is anti-M RBC stimulated?

A

No

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45
Q

Anti-N antibody class

A

IgM or occasional IgG

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46
Q

Does anti-N fix complement?

A

Does not fix complement

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47
Q

Anti-N temp of reactivity

A

Only significant if reacting at or above 30 degrees

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48
Q

Does anti-N have the ability to cause HDN/HTR?

A

No

49
Q

Is anti-N RBC stimulated?

A

No

50
Q

En(a-) pheotype

A

Individuals make anti-En(a)

Appears to be antibody to various portions of glycophorin A

51
Q

M(k) phenotype

A

Silent gene, no M, N, S or s

52
Q

Anti-S antibody class

A

IgG, occasionally IgM

53
Q

Does anti-S fix complement?

A

Poorly

54
Q

Anti-S temp of reactivity

A

usually 37 degrees and AHG phase

55
Q

Does anti-S have the ability to cause HDN/HTR?

A

Yes

56
Q

Is anti-S RBC stimulated?

A

yes

57
Q

Anti-s antibody class

A

IgG

58
Q

Can anti-s fix complement?

A

poorly

59
Q

Anti-s temp of reactivity

A

Usually 37 degrees and at AHG phase

60
Q

Does anti-s have the ability to cause HDN/HTR?

A

Yes

61
Q

Is anti-s RBC stimulated?

A

yes

62
Q

What is the prevalence of the U antigen if S and s antigen is negative?

A

U is part of the S structure, so if no S or s, then no U

63
Q

Kell system dosage

A

Occasional

64
Q

When is the Kell system developed?

A

It is well developed at birth

65
Q

How do enzymes affect the Kell system?

A

No change, but will decrease with AET & ZZAP

66
Q

McLeod phenotype & syndrome

A

Rare, lacks K(x) & K(m), x-linked

Patients have a variety of muscle and nerve disorders

67
Q

Anti-K antibody class

A

IgG

68
Q

Can anti-K fix complement?

A

Yes, sometimes

69
Q

Anti-K temp of reactivity

A

AHG phase

70
Q

Does anti-K have the ability to cause HDN/HTR?

A

yes

71
Q

Is anti-K RBC stimulated?

A

Yes

72
Q

Rare antibodies of the Kell system

A

Kp(a), Js(a), k, Kp(b), Js(b)

73
Q

How antigenic are the Kell antigens?

A

Very antigenic

74
Q

Why don’t we see anything other than anti-K very much in the Kell system?

A

Antigens are either very high frequency or very low frequency so exposure to an antigen that is foreign would be rare

75
Q

Does the Duffy system have dosage?

A

Yes

76
Q

When is the Duffy system developed?

A

At birth

77
Q

How does enzymes affect the Duffy system?

A

It decreases the reactivity

78
Q

Which antigen has a relationship to the Rh blood group?

A

Fy(6)

79
Q

Duffy system antibody clas

A

IgG

80
Q

Can duffy system antibodies fix complement?

A

Can bind compliment but not usually to lysis

81
Q

Duffy system antibody temp of reactivity

A

AHG phase

82
Q

Does the Duffy system antibodies have the ability to cause HDN/HTR?

A

yes

83
Q

Are the Duffy system antibodies RBC stimulated?

A

yes

84
Q

What is the antigen inheritance and significance of Fy(a-b-) in the black population?

A

68% of blacks will inherit. This allows them to resist Plasmodium vivax.

85
Q

Describe Fy(x) antigen and antibody

A

Antigen: weak form of Fy(b)
Antibody: none

86
Q

Describe Fy3 antigen and antibody

A

Antigen: probably part of the Fya and/or Fyb structure
Antibody: Seen most often in blacks that are Fy(a-b-)

87
Q

Describe Fy5 antigen and antibody

A

Antigen: not entire understood but different than Fy3. There is interaction between Rh and Duffy glycoprotein
Antibody: Reacts with Fy(a-b-)Fy3- cells

88
Q

Kidd System antibody class

A

IgG

89
Q

Can the Kidd system fix complement?

A

It binds compliment well

90
Q

Kidd system temp of reactivity

A

AHG phase

91
Q

Does the Kidd system have the ability to cause HDN/HTR?

A

Yes

92
Q

Is the Kidd system RBC stimulated?

A

Yes

93
Q

Why are the kidd antibodies particularly problematic?

A

Anti-Jk(a) and anti-Jk(b) quantity fade quickly from circulation and if stimulated, may make an anamnestic response with delayed intravascular & extravascular hemolysis

94
Q

Do Kidd antigens have dosage?

A

Yes

95
Q

When are Kidd antigens developed?

A

By birth

96
Q

What affect does enzymes have on Kidd antigens?

A

Increased activity

97
Q

Does Lutheran antigens have dosage?

A

Yes

98
Q

When are Lutherans antigens developed?

A

Poor at birth

99
Q

How are Lutheran antigens affected by enzymes?

A

No effect

100
Q

Anti-Lu(a) antibody class

A

IgM, and rare IgG

101
Q

Does Anti-Lu(a) fix complement?

A

Will bind compliment but not to lysis

102
Q

Anti-Lu(a) temp of reactivity

A

RT

103
Q

Does Anti-Lu(a) have the ability to cause HDN/HTR?

A

Not usually but can be mild

104
Q

Is Anti-Lu(a) RBC stimulated

A

No

105
Q

Anti-Lu(b) antibody class

A

IgM/IgG

106
Q

Does Anti-Lu(b) fix complement?

A

Occasionally

107
Q

Anti-Lu(b) temp of reactivity

A

37/AGH phase

108
Q

Does Anti-Lu(b) have the ability to cause HDN/HTR?

A

Yes but very mild

109
Q

Is Anti-Lu(b) RBC stimulated?

A

Yes

110
Q

2 non-RBC stimulated antibodies that may occur in Rh group

A

Anti-Cw

Anti-E

111
Q

Xg(a) chromosome location

A

X chromosome

112
Q

Xg(a) antigen genetics

A

Only blood group that is produced from a gene on the X chromosome

113
Q

Anti-Xg(a) antibody charactersitics

A
IgG - AHG phase reactivity
Can bind complement but not to hemolysis
Not implicated in HDN/HTR
Destroyed by enzymes
Rare
114
Q

What is the Bg antigen

A

Residual MHC I on RBC surface

115
Q

Define High Titer Low Avidity Antibodies (HTLA)

A

High titer (>64) reactivity but low avidity for agglutination when binding to its antigen (weak reactions)

116
Q

Characteristics of HTLA antibodies

A
IgG
AHG phase
Usual titer > 64
Poor agglutination response with corresponding antigen
Clinically insignificant
React poorly with LISS
117
Q

Antigens that are defined as HTLA

A

Chido, Rodgers, Knops, McCoy, York, Cost

118
Q

What is unique about Chido and Rodgers antibodies?

A

Can be neutralized or inhibited by plasma containing C4d