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Immunohematology Lec > [13] CHAPTER VI LESSON 1 > Flashcards

[13] CHAPTER VI LESSON 1 Flashcards

1
Q

DISCOVERY/CHARACTERISTICS OF OTHER MAJOR BLOOD GROUP SYSTEM

A

a. Kell Blood Group
b. Duffy Blood Group
c. Kidd Blood Group
d. Lewis Blood Group
e. MNSs Blood Group
f. Lutheran Blood Group
g. P Blood Group
h. I Blood Group

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2
Q

DISCOVERY/CHARACTERISTICS OF OTHER MAJOR BLOOD GROUP SYSTEM

A

a. Diego Blood Group
b. Cartwright Blood Group
c. Chido Blood Group
d. Xg Blood Group
e. Scianna Blood Group
f. Gerbich Blood Group
g. Milton Blood Group
h. Knops Blood Group
i. Bg Blood Group
j. Indian Blood Group
k. Others

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3
Q

ABO
ABO

A

001

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4
Q

MNS
MNS

A

002

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5
Q

P1PK
P1PK

A

003

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6
Q

Rh
RH

A

004

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7
Q

Lutheran
LU

A

005

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8
Q

Kell
KEL

A

006

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9
Q

Lewis
LE

A

007

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10
Q

Duffy
FY

A

008

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11
Q

Kidd
JK

A

009

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12
Q

Diego
DI

A

010

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13
Q

Yt
YT

A

011

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14
Q

Xg
XG

A

012

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15
Q

Scianna
SC

A

013

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16
Q

Dombrock
DO

A

014

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17
Q

Colton
CO

A

015

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18
Q

Landsteiner-Wiener
LW

A

016

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19
Q

Chido/Rodgers
CH/RG

A

017

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20
Q

H
H

A

018

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21
Q

Kx
XK

A

019

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22
Q

Gerbich
GE

A

020

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23
Q

Cromer
CROM

A

021

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24
Q

Knops
KN

A

022

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25
Q

Indian
IN

A

023

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26
Q

Ok
OK

A

024

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27
Q

Raph
RAPH

A

025

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28
Q

John Milton Hagen
JMH

A

026

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29
Q

I
I

A

027

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30
Q

Globoside
GLOB

A

028

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31
Q

Gill
GIL

A

029

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32
Q

Rh-associated glycoprotein
RHAG

A

030

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33
Q

Note: many of these functional relationships have been predicted based on [?] and remain under investigation.

A

molecular cloning studies

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34
Q

Glycosyltransferases

A

ABO, P1PK, Lewis, and H blood group systems

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35
Q

Structural relationship to Red Cell

A

MNS, Diego, and Gerbich blood group systems

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36
Q

Transport Proteins

A

Rh, Kidd, Diego, Colton, and Kx blood group systems

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37
Q

Complement Pathway Molecules

A

Chido/Rodgers, Cromer, and Knops blood group systems

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38
Q

Adhesion Molecules

A

Lutheran, Xg, Lansteiner-Wiener, and Indian blood group systems

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39
Q

Microbial Receptors

A

MNS, Duffy, P, Lewis, and Cromer blood group systems

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40
Q

Biologic Receptors

A

Duffy, Knops, and Indian blood group system

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41
Q

It was named after one of the first individuals to make the antibody, reported by Mourant in 1946.

A

Lewis Blood Group System

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42
Q

The Lewis (Le, FUT3) gene is located on

A

chromosome 19 (at 19p13.3).

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43
Q

The Secretor (Se, FUT2) gene is located on

A

chromosome 19 (at 19q13.3)

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44
Q

There are two alleles at the Lewis locus, [?], and there are two alleles at the secretor locus, [?]

A

Le and the amorph le

Se and the amorph se

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45
Q

Le gene must be present for a precursor substance to be converted to [?], but the Se gene must also be present for conversion to [?].

A

Lea

Leb

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46
Q

Are not expressed on cord RBCs and are often diminished on the mother’s RBCs during pregnancy.

A

Lewis Antigens: Lea and Leb

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47
Q

They are found on lymphocytes and platelets and on other tissues such as the pancreas, stomach, intestine, skeletal muscle, renal cortex, and adrenal glands.

A

Lewis Antigens: Lea and Leb

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48
Q

are resistant to treatment with the enzymes ficin and papain, DTT and glycine acid EDTA.

A

Lewis Antigens: Lea and Leb

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49
Q

are not intrinsic to RBCs but are on Type 1 glycosphingolipids that are passively adsorbed onto the RBC membrane from the plasma.

A

Lewis Antigens: Lea and Leb

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50
Q

Are IgM and have no clinical significance.

A

Lewis Antibodies: Anti-Lea and Anti-Leb

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51
Q

Have not been implicated in HDFN because the antibodies do not cross the placenta, and the antigens are not well developed at birth.

A

Lewis Antibodies: Anti-Lea and Anti-Leb

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52
Q

It can bind complement.

A

Lewis Antibodies: Anti-Lea and Anti-Leb

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53
Q

The most commonly encountered of the Lewis

A

Lewis Antibodies: Anti-Lea and Anti-Leb

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54
Q

is the receptor for Helicobacter pylori, a gram-negative bacterium associated with gastritis, PUD, gastric carcinoma, and the Norwalk virus.

A

The Leb antigen

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55
Q

Whites: 22
Blacks: 23

A

Le (a+b-)

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56
Q

Whites: 72
Blacks: 55

A

Le (a-b+)

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57
Q

Whites: 6
Blacks: 22

A

Le (a-b-)

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58
Q

Whites: Rare
Blacks: Rare

A

Le (a+b+)

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59
Q

Le (a-b+) red cell phenotype arises from the inheritance of

A

Le, Se, and H gene.

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60
Q

Lewis glycolipids are not detectable in plasma until about

A

10 days after birth.

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61
Q

Cord blood and RBCs from newborn infant’s phenotype as

A

Le (a-b-).

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62
Q

In children who inherit the both the Le and Se gene:
Le(a-b-) at birth
Le (a+b-) after 10 days

A

Le (a+b+) and finally Le (a-b+), the TRUE Lewis phenotype, after about 6 years.

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63
Q

In contrast, children who inherit Le and sese genes phenotype as:
Le (a-b-) at birth
Le (a+b-) after 10 days

A

Le (a+b-) phenotype persist throughout life.

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64
Q

Individuals with lele genes phenotype as [?] at birth and for the rest of their lives.

A

Le (a-b-)

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65
Q

Lewis antigens found in the secretions are

A

glycoproteins

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66
Q

Lewis antigens found in the plasma are

A

glycolipids

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67
Q

adsorb only glycolipids, not glycoproteins, onto membrane

A

Red cells

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68
Q

A person can be a nonsecretor (sese) and still secrete [?] into the body fluid.

A

Lea

69
Q

Le sese H

Lea

A

Le (a+b-)

70
Q

Le Se H

Lea Leb H

A

Le (a-b+)

71
Q

lele sese H

None

A

Le (a-b-)

72
Q

lele Se H

H

A

Le (a-b-)

73
Q

Le sese hh
Lea

A

Le (a+b-)

74
Q

Le Se hh
Lea

A

Le (a+b-)

75
Q

lele sese hh
None

A

Le (a-b-)

76
Q

lele Se hh
None

A

Le (a-b-)

77
Q

are not alleles

A

Lea and Leb

78
Q

Individuals who have a phenotype of [?] are not secretors with the exception of the Bombay phenotype.

A

Le (a+b-)

79
Q

A Bombay phenotype (hh) cannot express the

A

Leb antigen

80
Q

Adult red cells with a phenotype of [?] are very rare.

A

Le (a+b+)

81
Q

Traditionally, the P blood group comprised the

A

P, P1 and Pk abtigens and later, Luke (LKE).

82
Q

are assigned to the P1Pk blood group system (003, P1PK)

A

P1 and Pk

83
Q

is assigned to the globoside blood group system (028, symbol GLOB)

A

P

84
Q

are assigned to the Globoside Collection (029, GLOB)

A

LKE and PX2

85
Q

P1PK gene is located at

A

chromosome 22q11.2

86
Q

P gene is located at

A

chromosome 3q26.1

87
Q

: Biosynthetic Pathways of the P blood group antigens

A

Biochemistry

88
Q

There are two distinct pathways for the synthesis of the P blood group antigens.

A

Biosynthetic Pathways of the P blood group antigens

89
Q

The common precursor is [?] (or Gb2, also known as ceramide dihexose or CDH).

A

lactosylceramide

90
Q

The pathway on the figure’s left results in the formation of

A

paragloboside and P1

91
Q

is also the type 2 precursor for ABH.

A

Paragloboside

92
Q

The pathway shown on the figure’s right side leads to the production of the globoside series:

A

Pk, P, and Luke (LKE).

93
Q

The P blood group was introduced in

A

1927 by Landsteiner and Levine in 1927

94
Q

Matson and coworkers:

A

Pk

95
Q

may be found on RBCs, lymphocytes, granulocytes, and monocytes

A

P1, P, or Pk

96
Q

can be found on platelets, epithelial cells, and fibroblasts.

A

P

97
Q

have also been found in plasma as glycosphingolipids and as glycoproteins in hydatid cyst fluid

A

P and Pk

98
Q

The antigens have not been identified in secretions.

A

P Antigen

99
Q

Poorly expressed at birth and may take up to 7 years to be fully expressed.

A

The P1 Antigen

100
Q

It deteriorates rapidly on storage.

A

The P1 Antigen

101
Q

Blacks have stronger expression of P1 than whites

A

The P1 Antigen

102
Q

P Antibodies 2 Categories:

A

Clinically insignificant
Potently hemolytic

103
Q

: Parasitic Infections

A

*Anti-P1

104
Q

: Early abortions

A

*Anti-PP1Pk or anti-P

105
Q

: PCH

A

*Autoanti-P

106
Q

tors for P-fimbriated uropathogenic E.coli (causes UTI).

A

*The P system v: recep

107
Q

: receptor for shiga toxins, which cause shigella dysentery and E.coli-associated HUS.

A

*The Pk antigen

108
Q

is the receptor of human parvovirus B19 Pk provides some protection against HIV infection of peripheral blood mononuclear cells.

A

*P

109
Q

Common, naturally occurring IgM antibody in the sera of P- individuals.

A

Anti-P1

110
Q

Anti-P1 in 2 P1 individuals infected with Echinococcus granulosus tapeworms led to the identification of P1 and Pk substance in hydatid cyst fluid.

A

Anti-P1

111
Q

Typically weak, cold reactive saline agglutinin optimally reactive at 4oC and not seen in routine testing.

A

Anti-P1

112
Q

Associated with parasitic infections.

A

Anti-P1

113
Q

Strong antibodies to P1 have also been found in patients with fascioliasis and in bird handlers.

A

Anti-P1

114
Q

Originally called anti-Tja.

A

Anti-PP1Pk

115
Q

It was first described in the serum of Mrs. Jay, a p individual with adenocarcinoma of the stomach.

A

Anti-PP1Pk

116
Q

It has the potential to cause severe HTRs and HDFN

A

Anti-PP1Pk

117
Q

It is also associated with an increased incidence of spontaneous abortions in early pregnancy.

A

Anti-PP1Pk

118
Q

Rarely seen but it is very significant in transfusion.

A

Alloanti-P

119
Q

IgG class anti-P may occur and has been associated with habitual early abortion.

A

Alloanti-P

120
Q

Associated with the cold reactive IgG autoantibody in patients with PCH.

A

Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)

121
Q

The IgG autoantibody in PCH is described as a biphasic hemolysin.

A

Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)

122
Q

Antibody binds to RBCs in the cold

A

Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)

123
Q

Via complement activation, the coated RBCs lyse as they are warmed to 37 degrees Celsius.

A

Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)

124
Q

It typically does not react in routine test systems but is demonstrable only by the DonathLandsteiner Test.

A

Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)

125
Q

Described by Tippett and colleagues in 1965 in the serum of a patient with Hodgkin’s Lymphoma.

A

Luke (LKE) Antigen

126
Q

Luke (LKE) Antigen Three phenotypes:

A

80% tested Luke+
14% Lule (w)
2% Luke-

127
Q

*All individuals with the p and Pk phenotype are

A

Luke-

128
Q

Rare

A

p Phenotype

129
Q

Slightly more common in Japan, North Sweden, and in an amish group in Ohio.

A

p Phenotype

130
Q

Antigens Present: P1, P, Pk
Possible Antibodies: None

A

P1

131
Q

Antigens Present: P,Pk
Possible Antibodies: Anti-P1

A

P2

132
Q

Antigens Present: None
Possible Antibodies: Anti-PP1Pk

A

P

133
Q

Antigens Present: P1,Pk
Possible Antibodies: Anti-P

A

P1k

134
Q

Antigens Present: Pk
Possible Antibodies: Anti-P, anti-P1

A

P2k

135
Q

Whites: 79%
Blacks: 94%

A

P1

136
Q

Whites: 21%
Blacks: 6%

A

P2

137
Q

Whites: Rare
Blacks: Rare

A

P

138
Q

Whites: Very rare
Blacks: Very rare

A

P1k

P2k

139
Q

: I for Individuality

A

Wiener and coworkers

140
Q

: reported finding anti-i

A

Marsh and Jenkins

141
Q

I and i antigens are found on the

A

membranes of leukocytes and platelets in addition to RBCs

142
Q

I and i have also been found in the [?] of adults and newborns and in [?]

A

plasma and serum

saliva, human milk, amniotic fluid, urine, and ovarian cyst fluid

143
Q

is associated with much greater i activity on RBCs than control cord RBCs.

A

Chronic dyserythropoietic anemia type II or HEMPAS

144
Q

In Asians, the adult i phenotype has been associated with

A

congenital cataracts

145
Q

Both [?] are high-prevalence antigens

A

I and I Antigens

146
Q

Infant RBCs are rich in

A

i

147
Q

is almost undetectable

A

I

148
Q

During the [?], the quantity of i slowly decreases as I increases until adult proportions are reached.

A

first 18 months of life

149
Q

Adult RBCs are rich in

A

I

150
Q

Anti-I: Strong
Anti-i: Weak
Anti-IT: Weak

A

Adult I

151
Q

Anti-I: Weak
Anti-i: Strong
Anti-IT: Strong

A

Cord

152
Q

Anti-I: Weak
Anti-i: Strong
Anti-IT: Weakest

A

Adult i

153
Q

It is a common autoantibody that can be found in virtually all sera.

A

Anti-I

154
Q

Testing at 4oC and/or against enzyme treated RBCs may be required to detect the reactivity.

A

Anti-I

155
Q

It is not associated with HDFN because the antibody is IgM, and the I antigen is poorly expressed on infant RBCs.

A

Anti-I

156
Q

Found in the serum of many normal healthy individuals and is benign- it is not associated with in vivo RBC destruction.

A

Autoanti-I

157
Q

Weak, naturally occurring, saline reactive IgM agglutinin.

A

Autoanti-I

158
Q

The production of autoanti-I may be stimulated by microorganisms carrying I-like antigen on their surface.

A

Autoanti-I

159
Q

Associated with Mycoplasma pneumoniae infections

A

Autoanti-I

160
Q

Associated with Cold agglutinin syndrome

A

Pathogenic autoanti-I

161
Q

When peripheral circulation cools in response to low ambient temperatures, these antibodies attach in vivo and cause autoagglutination and peripheral vascular occlusion (acrocyanosis) or hemolytic anemia.

A

Pathogenic autoanti-I

162
Q

Typically reacts with adult and cord RBCs equally well at room temperature and at 4oC.

A

Pathogenic anti-I

163
Q

Exists as an IgM and IgG antibody in the serum of most individuals with the adult I phenotype.

A

Alloanti-I

164
Q

: never been described

A

Allanti-i

165
Q

Potent examples are associated with Infectious mononucleosis (Epstein Barr virus infections) and some lymphoproliferative disorders.

A

Autoanti-i

166
Q

have also been described and have been associated with HDFN.

A

IgG Anti-i

167
Q

The agglutinin recognizes a transition state of I into I and designated the specificity IT (T for “Transition”).

A

IT Antigen and Antibody

168
Q

Examples of IgM and IgG anti-I reacting preferentially at 37oC have also been found in patients with WAIHA, with a special association with Hodgkin’s disease.

A

IT Antigen and Antibody

Immunohematology Lec (35 decks)

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