OTHER BLOOD GROUPS Flashcards

(64 cards)

1
Q

are manufactured by tissue cells and secreted into the body fluids then adsorbed onto the red cell membrane

A

LEWIS SYSTEM

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2
Q

Lewis substances (in secretions) -

A

Glycoproteins

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3
Q

Lewis antigens (cell bound Ags) -

A

Glycosphingolipids

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4
Q

Lewis true phenotype

A

Le(a-b+)

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5
Q

Lewis newborn phenotype

A

Le(a-b-)

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6
Q

Lewis phenotype 10 days after birth

A

Le(a+b-)

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7
Q
  • located on the (p arm) short arm of chromosome 19
  • produces a specific L-fucosyltransferase to type I
    precursor substances.
A

Le genes

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8
Q

usually naturally occurring IgM; react best at RT or lower ; considered clinically insignificant

A

Lewis abs

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9
Q

most commonly encountered antibodies of the
Lewis system

A

Anti-Lea

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10
Q

Leb (Leb​ ​) has receptors for

A

Helicobacter pylori

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11
Q

Lex (Lex​ ​) antigen is marker for

A

Reed-Sternberg cells of Hodgkin’s disease

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12
Q

● The two loci system; includes 46 antigens
● The designation is 002 in the ISBT nomenclature. ● Genes are located in chromosome 4
● Genes are inherited as haplotypes
○ Half of genes from mother, half from father

A

MNSs U BLOOD GROUP

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13
Q

inherited as close linkage.
is associated with glycophorin A

A

M and N

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14
Q

associated with glycophorin B.

A

Ss

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15
Q

important markers in paternity testing
● Are found on red cells, not in body fluids and secretions

A

MNS antigens

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16
Q

the first amino acid is serine while the 5th is glycine.

A

M antigen

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17
Q

the first amino acid is leucine while the 5th amino acid is glutamic acid.

A

N antigen

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18
Q

S, the 29th amino acid is methionine.
For s, the 29th amino acid is threonine.

A

Ss

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19
Q

○ Are not clinically significant antibodies
○ Have limited biological activity
○ Mostly IgM, naturally occurring cold reactive saline agglutinins that do not bind, complement or react with enzyme-treated cells (DESTROYED by ENZYMES!)

A

Anti M and N

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20
Q

seen in renal patients who are dialyzed with equipment sterilized with formaldehyde

A

Anti N

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21
Q

reaction is enhanced by acidification

A

Anti M

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22
Q

Clinically significant
Mostly are IgG, reactive at 37C and the antiglobulin phase

A

Anti S and s

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23
Q

P1, P, or Pk may be found on

A

RBCs, lymphocytes, granulocytes, and monocytes.

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24
Q

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

A

P

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25
found in plasma as glycosphingolipids and as glycoproteins in hydatid cyst fluid.
P and Pk
26
antigens are poorly developed at birth
P1 ags
27
antigens are analogous to A1 and A2 in ABO.
P1 and P2 antigens
28
a precursor of P antigen.
Pk
29
the most common phenotype.
P1
30
a null phenotype because of absence of antigens. It is associated with the Parvovirus B19 in which it serves as receptor
P
31
antigen is associated with shiga toxin, ​E.coli, ​and Hemolytic Uremic Syndrome (HUS)
Pk
32
○ Naturally occurring IgM Abs in the sera of P​2 individuals; a weak cold reactive saline agglutinin ○ Can be ​neutralized with soluble ​P1 substance in hydatid cyst fluid​ (​Echinococcus granulosus ​infection)
Anti-P1
33
○ Naturally occurring alloantibody in the sera of all Pk individuals ○ Allo-anti-P ​is clinically significant. It is associated with rare spontaneous abortion.
Anti-P
34
IgG biphasic hemolysins associated with ​PAROXYSMAL COLD HEMOGLOBINURIA
AUTOANTI-P (Donath Landsteiner antibody)
35
○ Predominantly IgM; binds complement ○ Associated with spontaneous abortions in early pregnancy may demonstrate in vitro hemolysis
Anti-PP1Pk (Anti-Tja)
36
● At birth, infant red cells are rich in
i antigen
37
Weak naturally occurring saline reactive IgM autoagglutinin detectable only at 4C
Benign Anti-I
38
○ Potent cold autoagglutinin that demonstrates high titer reactivity and reacts over a wide thermal range (0-30​C) ○ Pxs with ​Mycoplasma pneumoniae ​infections may develop strong cold agglutinins with ​autoanti-I specificity
Pathologic Anti-Inflammatory
39
○ An IgM agglutinin and reacts optimally at 4C ○ Associated with ​infectious mononucleosis
Anti-i
40
○ T ​stands for transition ○ Found in Melanesians and Yanomama Indians in Venezuela ○ Associated with ​Hodgkin’s Disease
Anti-I ^T
41
- Found only on red cells, are well-developed at birth and are not destroyed by enzymes - rated ​second ​to ​D antigen in immunogenicity - Destroyed or inactivated ​by ​sulfhydryl reagents like ​AEY, DTT, ZZAP ​(artificial Kell null)
Kell antigens
42
- Lacks Kell antigens - Have no membrane abnormality
KO or K NULL phenotype
43
Lacks the Kx antigen (which might be a precursor for Kell antigens)
McLeod phenotype
44
Common among ​males suffering from ​Chronic Granulomatous Disease (CGD)
Mcleod Phenotype
45
the most common antibody seen in blood bank ○ Located at chromosome 7 ○ IgG “immune” antibodies reactive in AHG phase ○ Can cause both HDN and HTR
Anti-K
46
○ Two most important antigens associated with transfusion medicine in the Duffy blood group system ○ Well-developed at birth ○ Easily destroyed by common proteolytic enzymes
Fya​ ​ and Fyb​
47
Important anthropological marker for African blacks
Fy (a-b-)
48
Were shown to resist infection cause by Plasmodium vivax and Plasmodium knowlesi
Fya​ ​ and Fyb​
49
○ Usually IgG antibodies and react best at the AHG phase ○ Both are implicated in delayed HTR (DHTR) and HDN - shows dosage effect
Anti-Fya​ ​ and Anti-Fyb​
50
Anti-Fya​ ​ and Anti-Fyb​, which is more common
Anti-Fya
51
○ Well-developed at birth, contributing to the potential for HDN ○ SHow in vitro hemolysis - Reactivity enhanced by ​enzyme treatment
Jka and Jkb
52
Resists lysis in 2M urea and occurs mainly in Mongoloids
Jk (a-b-)
53
○ Show dosage ○ Both are IgG immune antibodies (primarily IgG3) and antiglobulin reactive ○ Bind complement ○ Common cause of delayed HTRs
Anti-Jka​ ​ and Anti-Jkb​
54
located on chromosome 19, closely linked with the​ secretor locus
Lutheran
55
○ Naturally occurring saline agglutinins​ (IgM in nature) ​that react best at RT ○ Characteristically show loose and mixed-fixed reactivity in vitro
Anti-Lua
56
○ Most are IgG (often IgG4) immune antibodies; reactive at AHG phase at 37o​ ​C and the AHG phase
Anti-Lub
57
Antibodies that causes HDN/EF (erythroblastosis fetalis)
Anti-C/Anti-AB (ABO) Anti-f (Rh) Anti-U (MNSs U) Anti-D Anti-Fya​ Anti-K Anti-Ss Anti-Jk
58
IgM ‘naturally occurring’ IgG ‘immune’ antibodies antibodies (generally) but can become IgG
Le P I Lu P1
59
IgG ‘immune’ antibodies
K Fy Jk Ss Xga​
60
Blood groups associated with secretor genes
Lewis Lutheran ABH
61
Enhanced by proteolytic enzymes
Kidd Rh I P1 Lewis
62
Inactivated/Destroyed by proteolytic enzymes
Duffy MNS
63
Antigens that are well-developed at birth
MNSs U Kidd Kell Duffy
64
Antigens that are poorly-developed at birth
Lewis P I Lutheran