[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
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
3
Q
ABO
ABO
A
001
4
Q
MNS
MNS
A
002
5
Q
P1PK
P1PK
A
003
6
Q
Rh
RH
A
004
7
Q
Lutheran
LU
A
005
8
Q
Kell
KEL
A
006
9
Q
Lewis
LE
A
007
10
Q
Duffy
FY
A
008
11
Q
Kidd
JK
A
009
12
Q
Diego
DI
A
010
13
Q
Yt
YT
A
011
14
Q
Xg
XG
A
012
15
Q
Scianna
SC
A
013
16
Q
Dombrock
DO
A
014
17
Q
Colton
CO
A
015
18
Q
Landsteiner-Wiener
LW
A
016
19
Q
Chido/Rodgers
CH/RG
A
017
20
Q
H
H
A
018
21
Q
Kx
XK
A
019
22
Q
Gerbich
GE
A
020
23
Q
Cromer
CROM
A
021
24
Q
Knops
KN
A
022
25
Indian
IN
023
26
Ok
OK
024
27
Raph
RAPH
025
28
John Milton Hagen
JMH
026
29
I
I
027
30
Globoside
GLOB
028
31
Gill
GIL
029
32
Rh-associated glycoprotein
RHAG
030
33
Note: many of these functional relationships have been predicted based on [?] and remain under investigation.
molecular cloning studies
34
Glycosyltransferases
ABO, P1PK, Lewis, and H blood group systems
35
Structural relationship to Red Cell
MNS, Diego, and Gerbich blood group systems
36
Transport Proteins
Rh, Kidd, Diego, Colton, and Kx blood group systems
37
Complement Pathway Molecules
Chido/Rodgers, Cromer, and Knops blood group systems
38
Adhesion Molecules
Lutheran, Xg, Lansteiner-Wiener, and Indian blood group systems
39
Microbial Receptors
MNS, Duffy, P, Lewis, and Cromer blood group systems
40
Biologic Receptors
Duffy, Knops, and Indian blood group system
41
It was named after one of the first individuals to make the antibody, reported by Mourant in 1946.
Lewis Blood Group System
42
The Lewis (Le, FUT3) gene is located on
chromosome 19 (at 19p13.3).
43
The Secretor (Se, FUT2) gene is located on
chromosome 19 (at 19q13.3)
44
There are two alleles at the Lewis locus, [?], and there are two alleles at the secretor locus, [?]
Le and the amorph le
Se and the amorph se
45
Le gene must be present for a precursor substance to be converted to [?], but the Se gene must also be present for conversion to [?].
Lea
Leb
46
Are not expressed on cord RBCs and are often diminished on the mother’s RBCs during pregnancy.
Lewis Antigens: Lea and Leb
47
They are found on lymphocytes and platelets and on other tissues such as the pancreas, stomach, intestine, skeletal muscle, renal cortex, and adrenal glands.
Lewis Antigens: Lea and Leb
48
are resistant to treatment with the enzymes ficin and papain, DTT and glycine acid EDTA.
Lewis Antigens: Lea and Leb
49
are not intrinsic to RBCs but are on Type 1 glycosphingolipids that are passively adsorbed onto the RBC membrane from the plasma.
Lewis Antigens: Lea and Leb
50
Are IgM and have no clinical significance.
Lewis Antibodies: Anti-Lea and Anti-Leb
51
Have not been implicated in HDFN because the antibodies do not cross the placenta, and the antigens are not well developed at birth.
Lewis Antibodies: Anti-Lea and Anti-Leb
52
It can bind complement.
Lewis Antibodies: Anti-Lea and Anti-Leb
53
The most commonly encountered of the Lewis
Lewis Antibodies: Anti-Lea and Anti-Leb
54
is the receptor for Helicobacter pylori, a gram-negative bacterium associated with gastritis, PUD, gastric carcinoma, and the Norwalk virus.
The Leb antigen
55
Whites: 22
Blacks: 23
Le (a+b-)
56
Whites: 72
Blacks: 55
Le (a-b+)
57
Whites: 6
Blacks: 22
Le (a-b-)
58
Whites: Rare
Blacks: Rare
Le (a+b+)
59
Le (a-b+) red cell phenotype arises from the inheritance of
Le, Se, and H gene.
60
Lewis glycolipids are not detectable in plasma until about
10 days after birth.
61
Cord blood and RBCs from newborn infant’s phenotype as
Le (a-b-).
62
In children who inherit the both the Le and Se gene:
Le(a-b-) at birth
Le (a+b-) after 10 days
Le (a+b+) and finally Le (a-b+), the TRUE Lewis phenotype, after about 6 years.
63
In contrast, children who inherit Le and sese genes phenotype as:
Le (a-b-) at birth
Le (a+b-) after 10 days
Le (a+b-) phenotype persist throughout life.
64
Individuals with lele genes phenotype as [?] at birth and for the rest of their lives.
Le (a-b-)
65
Lewis antigens found in the secretions are
glycoproteins
66
Lewis antigens found in the plasma are
glycolipids
67
adsorb only glycolipids, not glycoproteins, onto membrane
Red cells
68
A person can be a nonsecretor (sese) and still secrete [?] into the body fluid.
Lea
69
Le sese H
Lea
Le (a+b-)
70
Le Se H
Lea Leb H
Le (a-b+)
71
lele sese H
None
Le (a-b-)
72
lele Se H
H
Le (a-b-)
73
Le sese hh
Lea
Le (a+b-)
74
Le Se hh
Lea
Le (a+b-)
75
lele sese hh
None
Le (a-b-)
76
lele Se hh
None
Le (a-b-)
77
are not alleles
Lea and Leb
78
Individuals who have a phenotype of [?] are not secretors with the exception of the Bombay phenotype.
Le (a+b-)
79
A Bombay phenotype (hh) cannot express the
Leb antigen
80
Adult red cells with a phenotype of [?] are very rare.
Le (a+b+)
81
Traditionally, the P blood group comprised the
P, P1 and Pk abtigens and later, Luke (LKE).
82
are assigned to the P1Pk blood group system (003, P1PK)
P1 and Pk
83
is assigned to the globoside blood group system (028, symbol GLOB)
P
84
are assigned to the Globoside Collection (029, GLOB)
LKE and PX2
85
P1PK gene is located at
chromosome 22q11.2
86
P gene is located at
chromosome 3q26.1
87
: Biosynthetic Pathways of the P blood group antigens
Biochemistry
88
There are two distinct pathways for the synthesis of the P blood group antigens.
Biosynthetic Pathways of the P blood group antigens
89
The common precursor is [?] (or Gb2, also known as ceramide dihexose or CDH).
lactosylceramide
90
The pathway on the figure’s left results in the formation of
paragloboside and P1
91
is also the type 2 precursor for ABH.
Paragloboside
92
The pathway shown on the figure’s right side leads to the production of the globoside series:
Pk, P, and Luke (LKE).
93
The P blood group was introduced in
1927 by Landsteiner and Levine in 1927
94
Matson and coworkers:
Pk
95
may be found on RBCs, lymphocytes, granulocytes, and monocytes
P1, P, or Pk
96
can be found on platelets, epithelial cells, and fibroblasts.
P
97
have also been found in plasma as glycosphingolipids and as glycoproteins in hydatid cyst fluid
P and Pk
98
The antigens have not been identified in secretions.
P Antigen
99
Poorly expressed at birth and may take up to 7 years to be fully expressed.
The P1 Antigen
100
It deteriorates rapidly on storage.
The P1 Antigen
101
Blacks have stronger expression of P1 than whites
The P1 Antigen
102
P Antibodies 2 Categories:
Clinically insignificant
Potently hemolytic
103
: Parasitic Infections
*Anti-P1
104
: Early abortions
*Anti-PP1Pk or anti-P
105
: PCH
*Autoanti-P
106
tors for P-fimbriated uropathogenic E.coli (causes UTI).
*The P system v: recep
107
: receptor for shiga toxins, which cause shigella dysentery and E.coli-associated HUS.
*The Pk antigen
108
is the receptor of human parvovirus B19 Pk provides some protection against HIV infection of peripheral blood mononuclear cells.
*P
109
Common, naturally occurring IgM antibody in the sera of P- individuals.
Anti-P1
110
Anti-P1 in 2 P1 individuals infected with Echinococcus granulosus tapeworms led to the identification of P1 and Pk substance in hydatid cyst fluid.
Anti-P1
111
Typically weak, cold reactive saline agglutinin optimally reactive at 4oC and not seen in routine testing.
Anti-P1
112
Associated with parasitic infections.
Anti-P1
113
Strong antibodies to P1 have also been found in patients with fascioliasis and in bird handlers.
Anti-P1
114
Originally called anti-Tja.
Anti-PP1Pk
115
It was first described in the serum of Mrs. Jay, a p individual with adenocarcinoma of the stomach.
Anti-PP1Pk
116
It has the potential to cause severe HTRs and HDFN
Anti-PP1Pk
117
It is also associated with an increased incidence of spontaneous abortions in early pregnancy.
Anti-PP1Pk
118
Rarely seen but it is very significant in transfusion.
Alloanti-P
119
IgG class anti-P may occur and has been associated with habitual early abortion.
Alloanti-P
120
Associated with the cold reactive IgG autoantibody in patients with PCH.
Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)
121
The IgG autoantibody in PCH is described as a biphasic hemolysin.
Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)
122
Antibody binds to RBCs in the cold
Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)
123
Via complement activation, the coated RBCs lyse as they are warmed to 37 degrees Celsius.
Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)
124
It typically does not react in routine test systems but is demonstrable only by the DonathLandsteiner Test.
Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)
125
Described by Tippett and colleagues in 1965 in the serum of a patient with Hodgkin’s Lymphoma.
Luke (LKE) Antigen
126
Luke (LKE) Antigen Three phenotypes:
80% tested Luke+
14% Lule (w)
2% Luke-
127
*All individuals with the p and Pk phenotype are
Luke-
128
Rare
p Phenotype
129
Slightly more common in Japan, North Sweden, and in an amish group in Ohio.
p Phenotype
130
Antigens Present: P1, P, Pk
Possible Antibodies: None
P1
131
Antigens Present: P,Pk
Possible Antibodies: Anti-P1
P2
132
Antigens Present: None
Possible Antibodies: Anti-PP1Pk
P
133
Antigens Present: P1,Pk
Possible Antibodies: Anti-P
P1k
134
Antigens Present: Pk
Possible Antibodies: Anti-P, anti-P1
P2k
135
Whites: 79%
Blacks: 94%
P1
136
Whites: 21%
Blacks: 6%
P2
137
Whites: Rare
Blacks: Rare
P
138
Whites: Very rare
Blacks: Very rare
P1k
P2k
139
: I for Individuality
Wiener and coworkers
140
: reported finding anti-i
Marsh and Jenkins
141
I and i antigens are found on the
membranes of leukocytes and platelets in addition to RBCs
142
I and i have also been found in the [?] of adults and newborns and in [?]
plasma and serum
saliva, human milk, amniotic fluid, urine, and ovarian cyst fluid
143
is associated with much greater i activity on RBCs than control cord RBCs.
Chronic dyserythropoietic anemia type II or HEMPAS
144
In Asians, the adult i phenotype has been associated with
congenital cataracts
145
Both [?] are high-prevalence antigens
I and I Antigens
146
Infant RBCs are rich in
i
147
is almost undetectable
I
148
During the [?], the quantity of i slowly decreases as I increases until adult proportions are reached.
first 18 months of life
149
Adult RBCs are rich in
I
150
Anti-I: Strong
Anti-i: Weak
Anti-IT: Weak
Adult I
151
Anti-I: Weak
Anti-i: Strong
Anti-IT: Strong
Cord
152
Anti-I: Weak
Anti-i: Strong
Anti-IT: Weakest
Adult i
153
It is a common autoantibody that can be found in virtually all sera.
Anti-I
154
Testing at 4oC and/or against enzyme treated RBCs may be required to detect the reactivity.
Anti-I
155
It is not associated with HDFN because the antibody is IgM, and the I antigen is poorly expressed on infant RBCs.
Anti-I
156
Found in the serum of many normal healthy individuals and is benign- it is not associated with in vivo RBC destruction.
Autoanti-I
157
Weak, naturally occurring, saline reactive IgM agglutinin.
Autoanti-I
158
The production of autoanti-I may be stimulated by microorganisms carrying I-like antigen on their surface.
Autoanti-I
159
Associated with Mycoplasma pneumoniae infections
Autoanti-I
160
Associated with Cold agglutinin syndrome
Pathogenic autoanti-I
161
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.
Pathogenic autoanti-I
162
Typically reacts with adult and cord RBCs equally well at room temperature and at 4oC.
Pathogenic anti-I
163
Exists as an IgM and IgG antibody in the serum of most individuals with the adult I phenotype.
Alloanti-I
164
: never been described
Allanti-i
165
Potent examples are associated with Infectious mononucleosis (Epstein Barr virus infections) and some lymphoproliferative disorders.
Autoanti-i
166
have also been described and have been associated with HDFN.
IgG Anti-i
167
The agglutinin recognizes a transition state of I into I and designated the specificity IT (T for “Transition”).
IT Antigen and Antibody
168
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.
IT Antigen and Antibody
