MIDTERM LEC: Other Major Blood Group System Flashcards
(198 cards)
1
Q
Both antigens are expressed
A
CODOMINANT
2
Q
Most blood group alleles are codominant and express a corresponding antigen
A
CODOMINANT
3
Q
“Silent alleles”
A
AMORPHIC
3
Q
alleles exist that make no antigen, but they are rare
A
AMORPHIC
4
Q
When paired chromosomes carry the same silent allele, it results to a null phenotype
A
AMORPHIC
5
Q
Cannot be expressed
A
AMORPHIC
6
Q
Only determines the phenotype only
A
SEROLOGIC TESTING
7
Q
actual gene of an individual; the genetic makeup
A
Genotype
8
Q
ISBT #007
A
LEWIS BLOOD GROUP SYSTEM
8
Q
MAJOR BLOOD GROUPS:
A
● LEWIS
● KELL
● KIDD
● DUFFY
● LUTHERAN
9
Q
Not intrinsic to Red Blood Cell
A
LEWIS BLOOD GROUP SYSTEM
10
Q
Not intrinsic to Red Blood Cell meaning?
A
Antigens are not produced by RBCs, it is being adsorb into the RBCs
11
Q
Manufactured by tissue cells and secreted into body fluids (adsorbed into RBCs)
A
LEWIS BLOOD GROUP SYSTEM
12
Q
LEWIS BLOOD GROUP SYSTEM
Le GENE Located at:
A
Chromosome 19p13.3
12
Q
LEWIS BLOOD GROUP SYSTEM
Se GENE Located at:
A
Chromosome 19q
12
Q
Production depends not only on the inheritance of Le genes but also on the inheritance of Se gene
A
LEWIS BLOOD GROUP SYSTEM
13
Q
LEWIS BLOOD GROUP SYSTEM
2 Major Antigens:
A
Lea and Leb
14
Q
Expression of these antigens would have an effect on the presence of the gene that will encode for the enzyme for a certain carbohydrate to attach
A
Lea and Leb
15
Q
Lewis antigen
A
Lea
16
Q
*
Se antigen
A
Leb
17
Q
LEWIS BLOOD GROUP SYSTEM
Antigens secreted and absorbed onto: [RLP]
A
○ RBC
○ Lymphocytes
○ Platelet membrane from plasma
18
Q
Somewhat related to the ABO blood group because of the sugars attached on the RBC membrane
A
LEWIS BLOOD GROUP SYSTEM
19
Q
Codes for fucosyltransferase-3 (FUT3) so that fucose molecules will attach to the N-acetyl-D-galactosamine (GalNac) = Lea
A
Le GENE
20
Q
Has genes that will produce the enzymes and therefore producing a
specific sugars
A
LEWIS BLOOD GROUP SYSTEM
21
Codes for the secretory enzyme, **fucosyltransferase-2 (FUT2)** so that 1 fucose molecule will attach to the **galactose** = Leb
Se GENE
22
80% of the individuals have this gene
Se GENE
23
Stronger in terms of expression compared to Le Gene
Se GENE
24
THE LEWIS PHENOTYPE:
Le (a+b-)
Le (a-b+)
Le (a-b-)
25
Both of the genes can be present
Le GENE
Se GENE
26
LE1 - 007.001
Le (a+b-)
27
Nonsecretor
Le (a+b-)
28
Secretor
Le (a-b+)
28
LE2 - 007.002
Le (a-b+)
29
Secretor or Nonsecretors
Le (a-b-)
30
Lea
■ Present in plasma:
glycolipids
30
Leb
■ Secretions
glycoprotein (20% carbohydrates and 15% amino acid)
31
_____ molecules are attached on type 1 chain
Fucose
32
Le2(a-b-) from plasma can be converted to Le(a+b-)/Le(a-b+)
T OR F
T
33
- Lewis antigen is present in saliva but absent in the plasma
○ All newborns started as **Le(a-b-)**
Newborns
34
Le(a-b-) → Le(a+b-) → Le(a+b+) → Le(a-b+)
Inherited Le and Se genes will develop overtime
35
○ Le(a-b-) → Le(a+b-)
○ persists throughout life
If the Inherited Le and Sese gene
36
If inherit lele gene:
○ Le(a-b-)
○ birth and for the rest of their life
37
CHANGES IN LEWIS PHENOTYPE:
● Phenotype changes
● Can vary all throughout life
● Not capable of causing:
38
CHANGES IN LEWIS PHENOTYPE
● Not capable of causing:
- Hemolytic Disease of the Fetus and Newborn (HDFN)
- Hemolytic Transfusion Reaction (HTR)
- Changes in Lewis phenotype can be seen in the following
39
Even if the mother has IgG antibodies that passes the placenta, there will be no reaction that will happen since fetuses start as Le(a-b-)
Hemolytic Disease of the Fetus and Newborn (HDFN)
40
■ RBCs change rapidly from donor to recipient
■ Example: Lewis antigen of the donor is different from the recipient. Even though the recipient receives the blood from the donor, there will be no reaction that will happen. The recipient’s RBCs will just adsorb whatever is present in the donor's Lewis blood type
Hemolytic Transfusion Reaction (HTR)
41
Changes in Lewis phenotype can be seen in the following: [PCAVG]
○ Pregnancy women: Le (a-b-)
○ Cancer
○ Alcoholic Cirrhosis
○ Viral and Parasitic Infection
○ Genetic Reasons
42
■ Pregnant women has higher plasma content
that will make the secretor status lower in numbers. (Similar to dilution effect)
■ Little secretor antigen will be adsorb by the pregnant women’s RBCs
Pregnancy women: Le (a-b-)
43
IgM, naturally occurring
LEWIS ANTIBODIES
44
Frequent in pregnant women (serum)
LEWIS ANTIBODIES
45
May occur together
LEWIS ANTIBODIES
46
# *
More reactive with O cells
LEWIS ANTIBODIES
46
Anti-Lea
do not make anti-Lea (anti-Lea structure is contained within Leb structure)
Le(a-b+)
46
LEWIS ANTIBODIES
Anti-Lea & Anti-Leb
46
Detected with saline-suspended cells at RT (agglutinates are often fragile and can be easily dispersed if the cell button is not gently resuspended after centrifugation)
Anti-Lea
46
Neutralized with plasma or saliva
Anti-Lea
46
Either IgG or IgM, but usually IgM
Anti-Lea
47
Anti-Lea
anti-Lea is commonly seen
Le(a-b-)
48
IgM
Anti-Leb
49
Most common
Anti-Leb
50
Produced by Le(a-b-)
Anti-Leb
51
Neutralized by plasma or saliva
Anti-Leb
52
# *
Has 2 categories
Anti-Leb
53
Anti-Leb
Has 2 categories:
* anti-Lebh
* anti-Lebl
54
reacts best when both the Leb and the H antigens are present on the RBC, such as group O and A2 cells. (H dependent)
anti-Lebh
55
recognizes any Leb antigen regardless of the ABO type (H independent)
anti-Lebl
56
Formed by Le(a-b-)
Anti-Lex
57
Agglutinates 90%
Anti-Lex
58
Can be neutralized by the Lewis substances present in the plasma
CLINICAL SIGNIFICANCE (Ab
59
Dissociates from the RBCs as readily as they bind to RBC
CLINICAL SIGNIFICANCE (Ab
60
# *
Generally IgM
CLINICAL SIGNIFICANCE (Ab
61
ISBT #002
MNS BLOOD GROUP SYSTEM
62
attached to glycoproteins, which is an important part of a cell membrane
M & N ANTIGEN
63
Found in glycophorin A
M & N ANTIGEN
64
Rich in sialic acid (sialoglycoprotein) coded by Glycophorin A (GPA)
M & N ANTIGEN
65
Well developed at birth
M & N ANTIGEN
66
M and N differ in amino acid residues at
positions 1 and 5
67
M =
Serine and Glycine
68
N =
Leucine and Glutamic Acid
69
Detected on renal endothelium, and epithelium
MNS BLOOD GROUP SYSTEM
70
Destroyed by enzyme treatment and ZZAP+ DTT + papain/ficin
MNS BLOOD GROUP SYSTEM
71
Both are codominant
MNS BLOOD GROUP SYSTEM
72
Found in glycophorin B
S & s ANTIGEN
73
Well developed at birth
S & s ANTIGEN
74
Destroyed by enzyme treatment (Ficin, Papain, Bromelin, Pronase & Chymotrypsin)
S & s ANTIGEN
75
S and s differ in amino acid at
position 29
76
S =
methionine
77
s =
threonine
78
MNS ANTIBODIES
- Anti-M
- Anti-N
- Anti-S & Anti-s
79
Naturally occurring
Anti-M
80
50-80% IgG
Anti-M
81
Do not bind complement
Anti-M
82
Do not react w/ enzyme treated RBCs
Anti-M
83
Common in children and patient with burns
Anti-M
84
pH dependent (pH 6.5)
Anti-M
85
Detected in plasma
Anti-M
86
Lectin: Iberis amara
Anti-M
87
Not a significant cause of HDFN
Anti-M
88
Cold reactive, IgM or IgG
Anti-N
89
Dosage effect
Anti-N
90
Not clinically significant
Anti-N
91
Does not bind complement
Anti-N
92
Seen in renal patients (Formaldehyde may alter the M and N antigens)
Anti-N
93
Anti-N
Lectins:
● Vicia graminea
● Bauhinia variegate
● Bauhinia purpura
94
Mostly IgG
Anti-S & Anti-s
95
Reactive at 37C
Anti-S & Anti-s
96
Dosage effect
Anti-S & Anti-s
97
Can bind complement
Anti-S & Anti-s
98
Implicated in severe HTR and HDN
Anti-S & Anti-s
99
ISBT #003
P BLOOD GROUP SYSTEM
100
Can be detected 12 weeks in fetal RBC
P1 ANTIGEN
101
**7 years old:** fully expressed
P1 ANTIGEN
102
Gestational age: **weaken**
P1 ANTIGEN
103
Strength can vary on **quantity and race**
P1 ANTIGEN
104
Deteriorates rapidly on storage → false negative (freshly prepared)
P1 ANTIGEN
105
naturally occurring, IgM
ANTI-P1 ANTIBODY
106
weak, cold reactive saline agglutinin
ANTI-P1 ANTIBODY
107
ANTI-P1 ANTIBODY
Enhance Reaction by: [FIP]
● Fresh RBC preparation
● Incubate cells at RT or lower
● Preheating cells with enzymes
108
ANTI-P1 ANTIBODY
neutralized by hydatid cyst fluid from: [EPT]
● Echinococcus granulosus infection
● Pigeon dropping
● Turtle dove egg white
109
SOURCES OF P1 ANTIGEN AND ANTIBODY:
Echinococcus granulosus
110
SOURCES OF P1 ANTIGEN: [PRED]
■ Plasma
■ RBCs
■ Egg white of turtle doves
■ Droppings of pigeons and turtle doves
111
SOURCES OF P₁ Antibody: [COAL]
■ Clonorchis sinensis
■ Opisthorchis viverrini
■ Ascaris suum
■ Lumbricoides terrestris
112
T in the Tja refers to tumor
Anti-PP1 Pk (Anti-Tja)
113
scovered in serum of patient "Mrs. Jay" with adenocarcinoma of stomach
Anti-PP1 Pk (Anti-Tja)
114
Produced by p individual
Anti-PP1 Pk (Anti-Tja)
114
IgM and IgG
Anti-PP1 Pk (Anti-Tja)
115
Associated with PCH (Paroxysmal Cold Hemoglobinuria)
Autoanti-P
115
associated with increased incidence of spontaneous abortions in early pregnancy
Anti-PP1 Pk (Anti-Tja)
116
IgG antibody
Autoanti-P
117
Cold reactive
Autoanti-P
118
Detects biphasic hemolysin
Donath-Landsteiner Test
119
**Biphasic hemolysin:** binds to RBCs at low temperature and activates complement to produce in-vitro hemolysis at warmer
temperatures
Donath-Landsteiner Test
120
Can be detected 12 weeks in fetal RBC
Donath-Landsteiner Test
120
binds to RBCs at low temperature and activates complement to produce in-vitro hemolysis at warmer temperatures
Biphasic hemolysin
121
P BLOOD GROUP SYSTEM
DISEASE ASSOCIATION:
○ Parasitic infection
○ Early abortion
○ PCH
○ Urinary Tract Infection
○ Septicemia and meningitis
○ P antigens
122
P antigens:
■ Pyelonephritogenic E. coli
■ Streptococcus suis
■ Shigella dysenteriae
123
ISBT #027
I BLOOD GROUP SYSTEM
124
1956 - Wiener and coworkers; I for “individuality.”
I ANTIGEN
125
I
undetectable
126
I = adults; i= infants
I ANTIGEN
127
i
slowly decreases (first 18 months)
128
adult RBCs are rich in I and have only trace amounts of i antigen
T OR F
T
129
I BLOOD GROUP SYSTEM
neutralized by
Human Milk
130
○ "I" activity is increased in individuals with Bombay phenotype and if ABH sugars are removed by enzymes
○ Adult "i"
I BLOOD GROUP SYSTEM
131
I BLOOD GROUP SYSTEM
Sources:
membrane of leukocytes and platelets
132
IgM
Anti-l
133
Strong agglutination: Adult
Anti-l
134
Weak agglutination: Cord RBCs
Anti-l
135
# *
Detectable at 4C
Anti-l
136
Can be found in serum
Anti-l
136
Strong Reaction: Cord RBCs, Adult "i"
Anti-i
137
IgM, detectable at 4C
Anti-i
138
Anti-i
Associated with: [IRAM]
■ Infectious Mononucleosis (Epstein barr Virus)
■ Reticuloses
■ Alcoholic cirrhosis
■ Myeloid leukemia
138
It Antigen and Antibody
1965:
Curtain and coworkers reported a cold agglutinin in Melanesians that did not demonstrate classical I or i specificity
138
It Antigen and Antibody
1966:
Booth and colleagues confirmed these observations
139
It (T for “transition”)
It Antigen and Antibody
140
It Antigen and Antibody
Reaction:
■ Strong: Cord RBC
■ Weak: Normal adult RBC
■ Most Weak: Adult "i"
141
○ IgM
○ Associated with organism or parasite
It Antigen and Antibody
142
ISBT #027
KELL BLOOD GROUP SYSTEM
142
Warm reactive, IgG, reactive in AHG phase, involved in HDN and HTR
○ I**gG1: cannot fix complemen**
KELL BLOOD GROUP SYSTEM
142
Originated from Mrs. Kellaher, from whom anti-K was first identified
○ Baby of Mrs. Kellaher has anemia
○ Mrs. Kellaher tested negative in her DAT test. They found out that it does not make agglutination
○ Antigen + Antibody = coats the RBC = extravascular
hemolysis
KELL BLOOD GROUP SYSTEM
143
Detection: 10 weeks at fetal RBC (k: 7 weeks)
KELL BLOOD GROUP SYSTEM
143
Most immunogenic second to D
KELL BLOOD GROUP SYSTEM
144
KEL gene at chromosome 7
KELL BLOOD GROUP SYSTEM
145
# *
Resistant proteolytic enzymes
KELL BLOOD GROUP SYSTEM
146
RBCs are acanthocytic
KELL BLOOD GROUP SYSTEM
147
X-linked, occurs when Kx antigen is not expressed
McLeod Phenotype
148
ISBT #008
DUFFY BLOOD GROUP SYSTEM
148
NADH-oxidase is deficient in WBCs
McLeod Phenotype
148
# *
Associated with Chronic Granulomatous Disease (CGD)
McLeod Phenotype
149
1950: named for Mr. Duffy, a multiply transfused hemophiliac
DUFFY BLOOD GROUP SYSTEM
149
RBC lack Kx and Km and other Kell antigens are depressed K-negative when transfused with Kpositive will create anti K as high as 10% chance
McLeod Phenotype
150
Has receptors IL-8 for inflammation
Duffy Antigen Receptor Cytokines (DARC) gene
150
Has receptors for **Plasmodium knowlesi & Plasmodium vivax**
Duffy Antigen Receptor Cytokines (DARC) gene
151
associated with African-American Population (1955 - Sanger & colleagues)
Fy(a-b-) phenotype
152
Confers resistance to Plasmodium vivax infections
Fy(a-b-) phenotype
153
do not store well in saline suspension
Fya and Fyb antigens
154
destroyed in enzyme treatment
Fya and Fyb antigens
155
usually warm reacting, reacts at AHG phase (IgG)
Anti-Fya and Anti-Fyb
156
antibody made by Duffy Null phenotype
Anti-Fy3
157
ISBT #009
KIDD BLOOD GROUP SYSTEM
158
1951: Allen and colleagues reported finding an antibody in the serum of Mrs. Kidd, whose infant had HDFN
KIDD BLOOD GROUP SYSTEM
159
Antibodies have notorious reputation in blood banking (associated with Delayed HTR)
KIDD BLOOD GROUP SYSTEM
160
ENHANCED in enzyme treatment
KIDD BLOOD GROUP SYSTEM
161
Antibodies disappear rapidly both in vivo and in vitro (major reason why they cause delayed HTR)
KIDD BLOOD GROUP SYSTEM
162
Demonstrate dosage effect, usually warm reactive and antibodies are labile on storage
KIDD BLOOD GROUP SYSTEM
163
RBCs resist lysis in 2M urea
Jk(a-b-)
164
Rh Null antibodies =
anti-Jk-3
164
abundant in Polynesians; also been found in Filipinos, Indonesians, Chinese, and Japanese
Jk null
165
Organism with Jkb-like specificity include:
○ Enterococcus faecium
○ Micrococcus
○ Proteus mirabilis
166
ISBT #005
LUTHERAN BLOOD GROUP SYSTEM
167
Antibody was first identified in a donor's name, Luteran
LUTHERAN BLOOD GROUP SYSTEM
168
Can produce a mixed field agglutination
LUTHERAN BLOOD GROUP SYSTEM
169
○ reacts well with saline
○ can produce mixed-field agglutination
○ thermal optimum is **12-23°C**
Anti-Luª
170
incomplete antibody, reacts better in AHG phase
Anti-Lub
171
Amorphic Gene= Lu(a-b-) while Inhibitor Gene =
InLu, dominant type
172
Amorphic Gene= Lu(a-b-) while Inhibitor Gene =
InLu, dominant type
173
Antibody demonstrates a characteristic loose mixed field agglutination pattern
LUTHERAN BLOOD GROUP SYSTEM
