Bb lec Flashcards

(147 cards)

1
Q

Found and soluble in plasma and saliva

A

Lewis

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2
Q

“Plasma
antigen”

A

Lewis

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3
Q

Expression of the Lewis antigens are influenced by

A

Hh and Sese antigens

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4
Q

is weak during pregnancy - Mothers
who are Le(a-b+), may be Le(a-b-)

A

Lewis

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5
Q

When was Lewis first discovered?

A

1946

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6
Q

Agglutinated RBCs from about 25% of English people

A

Lewis

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7
Q

When was Anti-Leb discovered?

A

1948

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8
Q

Le genes (Le/FUT3) are located at

A

short arm of chromosome 19p13.3

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9
Q

Le gene is linked to

A

Se and H genes

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10
Q

The gene does not actually code for the production of Lewis antigens but rather produce specific

A

L-fucosyltransferase to type 1 precursor substance

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11
Q

The system depends on 3 genes to produce the Lewis antigen

A

H, Se, Le genes

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12
Q

There are two alleles at the Lewis locus:

A

Le and le genes

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13
Q

There are two alleles at the secretor locus:

A

Se and se genes

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14
Q

Development of Lewis antigen structure begins in

A

first week after birth and may continue for six years

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15
Q

Also found on lymphocytes and platelets

A

Lewis antigens

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16
Q

-Lea substance is secreted regardless of secretor status

-Le gene adds “L-fucose” to the N- acetylglucosamine of the type 1 precursor substance to form the Lea antigen

A

Le(a+b-)

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17
Q

Le gene adds “L-fucose” to the N- acetylglucosamine, and H gene adds “L-fucose” to galactose of the precursor substance forming the Leb antigen

A

Le(a-b+)

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18
Q

Lewis antigens are resistant to treatment by enzymes

A

(Ficin and Papain), Dithiothreitol, and Glycine-acid EDTA

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19
Q

IgM, Naturally occuring

A

Lewis antibodies

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20
Q

Reacts at immediate spin

A

Lewis antibodies

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21
Q

Binds complement, and triggers in-vitro hemolysis

A

Lewis antibodies

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22
Q

(History) The antibody Anti-K was first identified in the serum of Mrs. Kelleher. It reacted with the RBCs of her newborn infant, her older daughter, and her husband. Discovery by Robin Coombs

A

1946

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23
Q

Kpa antigen and the null phenotype (Ko) were first described in

A

1957

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24
Q

Jsa were first described, named after the first producer

A

John Sutter

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25
The low-incidence antigen of Kell
K24
26
The Kel gene is found on chromosome
7q33/34
27
The different Kell antigens are due to
single base mutations that results to amino acid substitutions
28
Member of Neprilysin family
Kell
29
The Kell antigens are located on a
type II glycoprotein with 731 amino acids
30
The glycoprotein is linked with XK protein by a disulfide bond at
Cys72
31
The glycoprotein is linked with XK glycoprotein by a disulfide bond at
Cys347
32
Found only on RBCs
Kell antigens
33
Appears on fetal red cells earlier than Rh proteins
Kell antigens
34
Kell glycoprotein has been characterized as a _________which is central to zinc binding and catalytic activity
Zinc endopeptidase
35
Very immunogenic (second only to D)
K antigen
36
Detected to as early as 7 weeks
k
37
Gene encoding for the antigen is associated with suppression of other Kell antigens
Kpa
38
Can be detected on fetal RBCs as early as 10 weeks gestation and is fully developed at birth
K
39
Found in 20% of blacks
Jsa
40
A patient’s red cells lacks the entire Kell glycoprotein, therefore, no Kell antigens
Kell null phenotype
41
Who identified Kell null phenotype
Bruce Chown, Marion Lewis, and Kiroko Kaita in 1957
42
The most encountered antibody next to ABO and Rh
Anti-K
43
Associated with severe HTRs and severe HDFN
Anti-K
44
Patients should receive antigen-negative blood
Anti-K
45
Are not commonly detected because individuals who lack these high-incidence antigens are scarce
Anti-Kpa, Anti-Kpb, Anti-Kpc, Anti-Jsa, Anti-Jsb
46
This antigens are only found in asians
Kpc
47
Found in erythroid tissues, brain, lymphoid organs, heart, skeletal muscle
Kx
48
The XK gene that encodes for the Xk protein is independent to KEL gene and found in the
short arm of chromosome Xp21.1
49
Kx antigens present on all RBCs except those of the
Mcleod phenotype
50
Who described Mcleod phenotype
Allen and his coworkers
51
Rare and are common in males via inheritance of X- linked through a carrier mother
Mcleod phenotype
52
The McLeod phenotype RBC lacks ___ and ___, with decreased expression of other Kell antigens
Kx and Km
53
a neuroacanthocytosis syndrome
Mcleod syndrom
54
Acanthocytosis, Reticulocytosis, Bilirubinemia, Low haptoglobin, and Splenomegaly
Mcleod syndrome
55
From a multiply transfused hemophiliac who in 1950 was found out to produce antibodies against an antigen named “Fya”
Duffy
56
They reported that majority of the African americans tested were Fy (a- b-). The gene responsible for such result was “Fy” - the gene is rare in whites
Sanger and colleagues in 1955
57
The Duffy genes is located at what chromosome
Chromosome 1
58
There are three alleles at the Fy locus
Fya, Fyb, Fy
59
a major allele in blacks
Fy
60
Can be detected at 6 weeks gestation and are fully developed at birth
Duffy antigens
61
Found in other body tissues (brain, Colon, Endothelium, Lungs, Spleen, Thyroid, Thymus, Kidneys)
Duffy antigens
62
Duffy Antigens reside on
Glycoprotein of 336 amino acids
63
a member of the superfamily of chemokine receptors
Duffy glycoproteins
64
Enhanced in a low ionic strength medium
Duffy antibodies
65
The antithetical partner of Jka was found in
1953
66
present on RBCs positive for Jka or Jkb
Jk3
67
significant cause of Hemolytic transfusion reactions
Kidd antibodies
68
lacks the 3 antigens, common in Filipinos, Chinese, Japanese and Indonesians
Jk(a-b-)
69
Kidd resist lysis in
2M Urea
70
Both are well developed at birth
Jka and Jkb
71
___ can be detected on fetal RBCs at 11 weeks gestation while ___ can be detected at 7 weeksgestation
Jka; Jkb
72
The antigens are not found on other blood cells
Kidd antigens
73
Weak and demonstrates dosage (reacts strongly with RBCs with double dose antigen)
Kidd antibodies
74
Kidd antibody reactivity can be enhanced by using
LISS or PEG
75
Reactivity is enhanced by enzyme pretreatment of the RBCs
Anti-Jk3
76
Found in combination with other antibodies
Anti-Jka and Anti-Jkb
77
associated with both immediate and delayed HTRs and mild HDFN
Anti-Jk3
78
Who discovered “Ii” blood group
Weiner and his coworkers in 1956
79
The antigen for that agglutinin is “I” for
Individuality
80
A branched carbohydrate
I
81
Linear carbohydrate
i
82
I and i are both formed due to
activity of glycosyl transferase
83
Expressed in a reciprocal relationship
I and i
84
Infant RBCs are rich in
i
85
During the first 18 months of life, the quantity of “i”
Decreases
86
adults that retains their “i” antigen
Adult-i
87
are precursor for the synthesis of ABO and Lewis antigens
I and i
88
“i”antigen activity is defined by atleast two repeating ___________ in linear form
N-acetyllactosamine units
89
found on chromosome 6p24
IGnt gene (GCNT2)
90
Encodes the ___________ that adds N- Acetylglucosamine (G1cNAc) to form the branches
N-acetylglucosaminyltransferase
91
Increased “i” antigen expression is seen in
Acute Leukemia Hypoplastic anemia Megaloblastic anemia Sideroblastic anemia Thalassemia Sickle cell disease Paroxysmal hemoglobinuria Chronic hemolytic anemia
92
Membranes of leukocytes and platelets
Ii antigens
93
Also found in serum, saliva, human milk, amniotic fluid, urine, and ovarian cyst fluid
Ii antigens
94
Common autoantibody found in virtually all sera
Anti-I
95
Tested at 4C and with enzyme treated RBCs
Anti-I
96
Reacts with adult and cord RBCs at room temperature and at 4C
Pathogenic autoanti-I
97
Exist as IgG or IgM in the serum of most Adult-i individuals
Alloanti-I
98
Production can be stimulated by microorganisms carrying I-like antigen
Anti-I
99
Detected by polyspecific AHG reagent
Anti-I
100
a rare antibody that gives strong reactions with cord RBCs and adult-i RBCs
Autoanti-i
101
Is a strong IgM agglutinin with higher titers and a broad thermal range of activity (may reach 30-32C)
Pathogenic autoanti-I
102
not associated with in- vivo RBC destruction
A benign antibody
103
Some are associated with Infectious mononucleosis and lymphoproliferative disorders
Anti-i
104
IgG types are rare but are associated with HDFN
Anti-i
105
P1 and Pk are assigned to
P1PK blood group system (003)
106
P is assigned to
Globoside blood group system (028)
107
LKE and PX2 are assigned to
Globoside collection (209)
108
Via injection of human RBCs to rabbits to produced new antibodies
P blood group
109
In 1951, Levine and colleagues described Anti-Tja which is now known as _____
anti-PP1Pk
110
P+ became “__” and P became __”, the rare P null became “__”
P1; P2; p
111
described the antigen Pk
Matson and coworker in 1959
112
P1 describes RBCs that react with
Anti-P1 and Anti-P
113
P2 describes RBCs that do not react with
Anti-P1 but reacts with Anti-P
114
“p” phenotypes do not react with
Anti-P1, Anti- P, or Anti-Pk
115
Common in Japan, North Sweden, and in Ohio
p, P1k, and P2k
116
P1k phenotypes reacts with
Anti-P1 and Anti-Pk but not with Anti-P
117
P2k phenotypes reacts with
Anti-Pk but do not react with Anti-P1 or Anti-P
118
located on chromosome 22q13.2 encodes the 4-a-galactosyltransferase
P1PK gene (A4GALT)
119
located on chromosome 3q25 encodes the 3-B-N- acetylgalactosaminyltransferase
Globoside gene (B3GALNT1)
120
P antigens is synthesized by
glycosyltransferases
121
can be found on platelets, epithelial cells, and fibroblasts
P
122
have been found in plasma as glycosphingolipids and glycoproteins in hydatid cyst fluid
P and Pk
123
Antigen strength varies: From inheritance to Race
P1 antigen
124
Poorly expressed at birth (may even take 7years for full expression)
P1 antigen
125
Deteriorates rapidly on storage
P1 antigen
126
infected with Echinococcus granulosus worms led to the discovery of P1 and Pk substance in hydatid cyst fluid
anti-P1
127
have also been found in patients with Fascioliasis (bovine liver fluke disease)
Strong antibodies to P1
128
The common precursor of P antigens
“Lactosylceramide” (Gb2, Ceramide dihexose, or CDH)
129
Pk synthesis is carried out by
4-α- galactosyltransferase (Gb3, Pk synthase)
130
P synthesis formation is carried out
3-β-N- acetylgalactosaminyltransferase (Gb4 synthase)
131
described an antibody in the serum of a Hodgkin’s lymphoma patient in 1965
Tippett and colleagues
132
Group under P Blood group since the antibody reacted in all RBCs except 2% of P1 and P2 phenotypes
Luke Antigens (LKE)
133
All p and Pk phenotypes are
Luke(-)
134
Common, naturally occurring IgM antibody in the serum of P1(-) individuals
Anti-P1
135
Formerly “Anti-Tja”
Anti-PP1Pk
136
A component of anti-PP1Pk in “p” individuals
Alloanti-P
137
IgMs that reacts at room temperature
Anti-LKE
138
Poorly developed on fetal RBCs
Anti-P1
139
May cause in-vivo RBC destruction, immediate or delayed HTRs
Anti-P1
140
Reaction varies especially if old RBCs are used.
Anti-P1
141
Reacts over a wide thermal range and bind complement
Anti-PP1Pk
142
The antibodies had cytotoxic properties that may have helped prevent metastatic growth post surgery
Anti-PP1Pk
143
Can be separated by adsorption
Anti-PP1Pk
144
Produced by “p” individuals early in life without RBC sensitization and reacts with all RBCs except those of the “p” phenotype
Anti-PP1Pk
145
Produced by “p” individuals early in life without RBC sensitization and reacts with all RBCs except those of the “p” phenotype
Anti-PP1Pk
146
Naturally occurring in the sera of Pk individuals
Alloanti-P
147
Bga antigen = ____ Bgb antigen = ____ Bgc antigen = ____
HLA-B7 HLA-B17 HLA-A28