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Blood Bank > Other Major Blood Group Systems > Flashcards

Other Major Blood Group Systems Flashcards

1
Q

Describe the unique characteristics of Lewis Antigens and where they are located? (3)

A
  • Not intrinsic to RBCs
  • Are on Type I glycosphingolipids
  • Passiely adsorbed on to RBC membrane from plasma
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2
Q

Who made the first Lewis Antibody and When was it reported?

A

Mourant, 1946

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3
Q

Lea and Leb do not result from _______ _______. Rather from the interaction of two ____________ encoded by independed genes _____ and ______.

A
  • alternative alleles
  • fucosyltransferases
  • Le and Se
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4
Q

Identify what type of chain Lewis antigens are?

A

Type I glycolipids

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5
Q

How are Lewis Antigens produced and where are they found?

A

By tissue cells and found primarily in in plasma and other body secretions.

NOT manufactured by RBCs

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6
Q

Idenify the chromosome the Se gene is located on?

A

Chromosome 19

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7
Q

What does the Se gene code for and what does it do?

A

It codes for a fucosyltransferase enzyme that adds L-fucose to Type I precursor chains.

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8
Q

What gene is similar to the Se gene and how is it similar, yet different?

A

H gene is similarly located on chromosome 19 and also codes for the same fucosyltransferase. HOWEVER the H gene adds L-fucose to the Type II precusor chain.

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9
Q

What are the Secretor phenotypes and what is the non-secretor phenotype?

A
  • SeSe
  • Sese
  • sese (amorph)
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10
Q

What percentage of the population are secretors?

A

80%

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11
Q

What percentage of the population are non-secretors?

A

20%

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12
Q

What genes encode the enzymes FUT1, FUT2, FUT3?

A
  • FUT1 = H gene
  • FUT2 = Se gene
  • FUT3 = Lewis gene
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13
Q

The Lewis gene is found on which chromosome?

A

19

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14
Q

What does the Le gene code for and what does it do?

A

Codes for alpha 1,4-L-fucosyltransferase (FUT3), which transfers L-fucose to the Type I precursor H chain forming Leb

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15
Q

If A and B genes are present along with Le what is the result?

A

Type I (1H) converted to A and B structures then Le fucosyltransferase will produce ALeb and BLeb

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16
Q

What is made is small amounts before the secretor enzyme adds terminal fucose?

A

Lea

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17
Q

Lewis Phenotypes: Describe Le (a+b-)

What genes are present?

What is present in secretions and why?

A
  • Le and H genes present
  • Lea produced
  • No Se gene present as no Leb made so are nonsecretors
  • Lea present in secretions beceause it is a type I chain
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18
Q

Lewis Phenotypes: Describe Le (a-b+)

What genes are present?

What is present in secretions and why?

A
  • Genes Le, H and Se
  • Se gene needed to make Leb
  • Leb is made preferentially over Lea
  • All are secretors (Se gene present) will have ABH Lea and Leb in secretions
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19
Q

Lewis Phenotypes: Describe Le (a-b-) Secretor and nonsecretors.

A
  • No Le gene
  • cannot make alpha 1,4 L-fucosyltransferase

​

  • Le (a-b-) Secretors do not make Lea/b but have ABH Antigens in secretions
  • Le (a-b-) nonsecretors lack Le and Se genes so NO ABH antigens present in secretions.
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20
Q

Which Lewis phenotype is 4 times more common in black than white?

A

Le(a-b-) Nonsecretors (lele)

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21
Q

Which Lewis Phenotype is insignificant an rare; with no secretions stated.

What results in this phenotype?

A
  • Le (a+b+)
  • Weak Se gene that produces a FUT2 that competes less effectivelt with Le fucosyltransferase (FUT3) resulting in the prescence of both Lewis Antigens.
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22
Q

What gene must be present for the formation of Leb?

A

Se gene

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23
Q

Are Lewis antigens well developed at birth?

A

No, but begin to appear shortly after because antigens are adsorbed on to RBC membrane

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24
Q

What Lewis phenotype is chord blood?

A

Le (a-b-)

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25
Q

When Le and sese genotypes are inerited, Lewis antigens are not detectabe on chord cells but infants secrete____ in their ______

A
  • Lea
  • Saliva
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26
Q

When are Lewis Antigens detectable in plasma after birth?

A

10 days

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27
Q

At what age will the true Lewis Phenotype show up?

How do the Lewis Phenotypes develop? (3)

A

6-7 years

  • Le and Se
    • Le (a-b-) –> Le(a+b-) –> Le(a-b+)
  • Le and sese
    • Le(a-b-) –> Le(a+b-) after 10 days
  • lele and sese
    • Le(a-b-) for life
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28
Q

T/F: Lewis antigens are readily shed from tansfused RBCs within a few days ofr transfusion?

A

True

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29
Q

What is the ISBT code for Lewis Antigens?

A

007

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30
Q

What is the ISBT # for Lea?

A

LE1

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31
Q

What is the ISBT # for Leb?

A

LE2

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32
Q

Identify the antibody and ISBT # of the Ab that reacts with Le(a+b-) and Le(a-b+) RBCs from adults and 90% of chord RBCs?

A
  • Anti-Leab (reacts with Leab)
  • LE3
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33
Q

What Ab reacts with Aleb and its ISBT #?

A
  • Anti-Aleb reacts with groupA1 Le(b+) and A1B Le(b+)
  • LE5
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34
Q

What Ab reacts with group O Le(b+) and A2 Le(b+)?

What is the ISBT #?

A
  • Anti-LebH
  • LE4
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35
Q

Identify the ISBT #s for Anti-ALeb and Anti-BLeb?

A
  • LE5
  • LE6
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36
Q

How does pregnancy affect Lewis antigens?

A
  • Decline dramatically
  • Transient Anti-Lea formed
  • Physiologic changes affect the Lewis glycolipid distribution between plasma and RBCs
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37
Q

What is the most commonly encoutered Antibody of the Lewis system?

A

Anti-Lea

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38
Q

Which microorganism is of biological significance in the Lewis system and why?

A
  • Helicobacter pylori - causes gastric and duodenal ulcers, mucosa-associated lymphiod tissue lymphoma, atrophic gastitis and ademocarcinoma.
  • Lewis antigens have receptors that interact with microorganism.
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39
Q

Lewis antigens ar3e associate with what other disease factors?

A
  • Peptic ulcers
  • Ischemic heart disease
  • cancer
  • kidney transplant rejection
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40
Q

Who discovered the S antigen that was linked to M and N?

A

Walsh and Montgomery

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41
Q

Identify the protein that M and N antigens are found on?

A

GYP A (Glycophorin A), the major sialic acid-rich glycoprotein (sialoglycoprotein - SGP)

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42
Q

M and N are antithetical and differ in amino acid sequence. What is the different amino acid residues in position 1 and 5 for M and N

A
  • M
    • 1 - Serine
    • 5 - glycine
  • N
    • 1 - Leucine
    • 5 - glutamic acid
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43
Q

What are the different M and N phenotypes?

A
  • M+N-
  • M+N+
  • M-N+
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44
Q

Which of the MNS system antigens are well developed at birth?

A

S and s

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45
Q

On what proteins are S and s antigens located?

A

GYP B (glycoprotein B)

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46
Q

Idenitfy the different amino acid residues between S and s antigens at position 29?

A

S - Methionine

s - Theronine

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47
Q

What are the S phenotypes of the MNS system?

A
  • S+s-
  • S+s+
  • S-s+
  • S-s-U-
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48
Q

Which MNS phenotype is seen almost exclusively in African Americans?

A

S-s-U-

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49
Q

What is the issue with the S-s-U- phenotype?

A
  • Most people have the U antigen, so anti-U will react with the cells of most people (100% white & 99% black).
  • Would need to consult the Rare Donor Registry
50
Q

What results in the En(a-) Phenotype?

A

homozygous for rare gene deletion of GYPA locus so no GYPA made. GYPB not affected.

Produce Anti-Ena

Difficult to transfuse; siblings may be a potential source

51
Q

What results in the Mk phenotype?

A

near complete deletion of the GYPA and GYPB genes, therfore MNS null phenotype

52
Q

Where are P (003) and Globoside (028) antigens found?

A
  • RBCs
  • Granulocytes
  • Lymphocytes
  • Monocytes
53
Q

Where is the GLOB gene located?

A

Chromosome 3

54
Q

What are the antigens of the P system?

A
  • P
  • P1
  • Pk
  • Luke (LKE)
55
Q

What does the GLOB gene code for and what does it do?

A

Codes for a transferase that converts Pk antigen into P1 antigen.

56
Q

What is the most common antigen in the P1PK (003) blood group system?

A

P1 antigen

57
Q

How well is the P1 antigen expressed at birth?

How long does it take for the P1 antigen to be expressed?

A

Poor

May take up to 7 years

58
Q

Which population has a stronger expression of the P1 antigen?

A

Black

59
Q

What might inhibit expression of the P1 antigen, causing some P1 people to type as P1 negative?

A

Rare dominant gene In(lu) type Lu(a-b-) RBCs

60
Q

Why may detection of anti-P1 with P1 antigens result in false positives?

A

Deteriorates rapidly on storage

61
Q

Where is the P1 and Pk gene located?

What do the genes code for and do?

A

Chromosome 22

  • Transferase which produces P1 (type 2H precursor chains)
  • Transferase converts Pk to P
62
Q

T/F: the Pk antigen is low frequency but is expressed on all RBCs?

A

True

63
Q

Why is Pk not readily detected?

A

P masks

64
Q
A
65
Q

What are the possible P phenotypes?

A
  • P1
  • P2
  • P
  • P1k
  • P2k
66
Q

This antibody is known as the Donath-Landsteiner antibody?

A

Anti-P

67
Q

Which antibody is a powerful biphasic hemolysin and what does this mean?

A

Anti-P

attaches to red cells in the cold and lyses them as they warm back up

68
Q

Identify the indviduals in which all three P/GlOB system antibodies are found in?

A

p (anti-P + P1 + Pk)

69
Q

What are the major diseases associated with the P/GLOB blood group system?

A
  • Hydatid cyst
  • Paroxysmal Cold Hemoglobinuria (PCH)
  • Tertiary Syphilis
  • E.coli associated hemolytic uremic syndrome
70
Q

How are P antigens affected by enzymes?

A

Resistant

71
Q

Describe the relationship between I and i antigens?

A

Reciprocal relationship; > I =

72
Q

Newborn red cells have linear stucture with repeating N-acetyllactosamine?

A

i

73
Q

The development of ____ depends on th addition of branching N-acetyllactosamine units.

A

I (big)

74
Q

Over what period does I(big) develop?

A

2 years

75
Q

Identify the rare phenotype in which adults produce alloanti-I?

A
  • retain I-i+
  • iadult
76
Q

When would alloanti-I (anti-I or iso) be an issue?

A

iadult

should be given i blood (rare)

77
Q

Anti-I is associated with which diseases/infections?

A

Cold agglutinin disease and Mycoplasma pneumonia infections

78
Q

Which antibody commonly interferes with in vitro testing?

A

Anti-I

  • compatibility, antibody studies, and ABO reverse grouping, if done at low temp
  • Anti-I can mask prescence of other antibodies
79
Q

a rare antibody, seen in patients with infectious mononucleosis, myeloid leukemia, alcoholic cirrhosis, and reticulosis?

A

Anti-i

80
Q

How do enzymes affect Ii antigens?

A

Enhanced - ficin and papain

Resistant - DTT, glycine-acid EDTA

81
Q

What are the two major alleles of the Kell system?

A

K and k

82
Q

What are the other alleles of the Kell system?

A
  • Kpa
  • Kpb
  • Jsa
  • Jsb
83
Q

What is the Kell amorph and its genoype?

What is the result of this phenotype

A

K0

Homozygous K0K0

Kell null and no Kell antigens produced

84
Q

What protein is covalently linked to the Kell glycoprotein and essential for Kell antigen expression?

A

Kx Blood group system

Kx protein

85
Q

What chromosome is the XK gene located?

A

X chromosome

86
Q

T/F - Kell antigens are well developed at birth?

A

True

87
Q

What reagents destroy Kell antigens?

A

Sulfahydryl reagens - DTT or 2-mercaptoethanol (2-ME)

88
Q

Identify the antigen that is a powerful immunogen, second only to the D antigen?

A

K antigens

89
Q

What is the frequency of occurence of the following antigens?

  • k
  • Kpa (higher in whites)
  • Kpb
  • Jsa (higher in blacks)
  • Jsb
A
  • a = low frequncy
  • b = high frequency
  • k = high frequency
90
Q

Define McLeod Syndrome?

What gene is missing?

A
  • Appear to be Kell null but weak expression of k, Kpb and Jsb
  • Lack XK gene
91
Q

How are red cells affected by McLeod syndrome?

A
  • Shortened survival
  • acanthocytosis
  • increased osmotic fragility
  • reticulocytosis
92
Q

How are K/Kx antigens affected by enzymes?

A
  • Destroyed - trypsin and chymotrypsin when used with thiol reducing agents.
  • No effect - ficin and papain
93
Q

What does the Fy gene produce?

A

Transmembrane carrier molecule for Duffy Glycoprotein.

94
Q

What does the Fy gene enable susceptibility to?

A

invasion by Plasmodium vivax, causative of malaria.

95
Q

What cells are resistant to malaria?

A

Fy(a-b-) and lack Fy6 receptor (West Africa, almost all African blacks have this resistance)

96
Q

What does the Fyx gene produce?

A

Does not produce a distinct antigen, but inherited weak form of Fyb that reacts with some forms of anti-Fyb

97
Q

How many Antigens are in the Duffy system? and what are they?

A
  • Fya
  • Fyb
  • Fy3
  • Fy4
  • Fy5
  • Fy6
98
Q

What Duffy genes are expressed co-dominatly?

A

Fya and Fyb

99
Q

Fya and Fyb are well developed at birth (T/F)?

A

True

100
Q

What are Duffy phenotype is found in 68% of American blacks and 100% of African Blacks?

A
  • Fy(a-b-)
101
Q

What are the different genetic origins of the Fy(a-b-) phenotype?

Why is identifying race important?

A

Black - also express Fy4 antigen

White - also express Fy3 antigen

Black patient receiving blood from white individuals can make anti-Fy3. this would react strongly with future transfusions of Fy3 positive blood.

102
Q

How do Proteolytic enzymes affect Duffy antigens?

What does not affect Duffy antigens

A
  • DESTROY
  • neuraminidase or purified trypsin
103
Q

What is the product of the Jk gene?

A

Urea transport molecule

104
Q

What is unquie about Jk(a-b-) RBCs?

A

Resistant to lysis in 2M urea

105
Q

What are the 3 Jk alleles?

A
  • Jka
  • Jkb
  • Jk3
106
Q

What are the two ways in which the Jk(a-b-) phenotype forms?

A
  • Genetic mutation - no Jka, Jkb, or Jk3 produced
  • In(Jk) gene - dominant supressor at the Jk locus
    • express decreased Jka, Jkb, and Jk3, but too weak to react.
107
Q

The Jk(a-b-) phenotype has been identified in which populations?

A

Polynesian

Chinese

108
Q

Anti-Jka and Anti-Jkb have a notorious blood bank because of these unique characteristics?

A

Difficult to detect; very weak reactions and antigen dosage effect.

109
Q

Kidd antibodies are norally made in response to?

A

Pregnancy or transfusion

110
Q

Which Antibody is produced by Jk(a-b-) individuals, reacts with all Jka and Jkb positive cells and is insperable from anti-Jka and anti-Jkb?

A

Anti-Jk3

111
Q

Why are Kidd antibodies a common cause of Delayed HTRs?

A

Titre of anti-Jka and anti-Jkb gradually declines in vivo.

112
Q

The Rare autoantibody-Jka has been documented in (4):

A
  • Warm autoimmune hemolytic anemia
  • Methly dopa (aldomet) drug-induced hemolytic anemia
  • Recent viral/bacterial infection
  • Paraben preserved medications
113
Q

How does Paraben affect the Jka antigen?

A

Paraben alters the Jka antigen causes the body to not recognize self and make an autoantibody.

114
Q

Which blood group is the first example of autosomal linkage in humans?

How many antigens?

A
  • Lutheran
  • 19
115
Q

The LU locus is linked to which locus?

A

SE Locus

116
Q

What does the LU gene produce?

What gives rise to the varios Lutheran Antigens?

A
  • Lutheran Glycoprotein
  • (antithetical) Amino acid changes gives rise to the various Lutheran Antigens
117
Q

What are the two most common Lu antigens and their frequency?

A

Lua - low

Lub - high

118
Q

What are the three methods that result in the Lu Null Phenotype Lu(a-b-)?

A
  • Dominant In(lu) supressor gene; supresses Lu antigens
  • Recessive LuLu gene; inherit 2 null genes
  • Recessive X-linked gene; supresses Lu antigens
119
Q

Of the Lutheran Null Phenotype methods, which results in the formation of Anti-Lua3 which reatcs with all Lua and Lub positive cells?

A

Recessive LuLu

120
Q

How do enzymes affect Lu antigens?

A

Routine BB enzymes like ficin, papain and bromelin have NO effect/ DO NOT destroy Lu antigens.

Blood Bank (8 decks)

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