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BLOODBANK > OTHER BLOOD GROUPS > Flashcards

OTHER BLOOD GROUPS Flashcards

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
Q

found in plasma as glycosphingolipids and as glycoproteins in hydatid cyst fluid.

A

P and Pk

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26
Q

antigens are poorly developed at birth

27
Q

antigens are analogous to A1 and A2 in ABO.

A

P1 and P2 antigens

28
Q

a precursor of P antigen.

29
Q

the most common phenotype.

30
Q

a null phenotype because of absence of antigens. It is
associated with the Parvovirus B19 in which it serves as receptor

31
Q

antigen is associated with shiga toxin, ​E.coli, ​and Hemolytic
Uremic Syndrome (HUS)

32
Q

○ 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)

33
Q

○ Naturally occurring alloantibody in the sera of all Pk individuals
○ Allo-anti-P ​is clinically significant. It is associated with rare spontaneous abortion.

34
Q

IgG biphasic hemolysins associated with ​PAROXYSMAL COLD HEMOGLOBINURIA

A

AUTOANTI-P (Donath Landsteiner antibody)

35
Q

○ Predominantly IgM; binds complement
○ Associated with spontaneous abortions in early pregnancy may demonstrate in vitro hemolysis

A

Anti-PP1Pk (Anti-Tja)

36
Q

● At birth, infant red cells are rich in

37
Q

Weak naturally occurring saline reactive IgM autoagglutinin detectable only at 4C

A

Benign Anti-I

38
Q

○ 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

A

Pathologic Anti-Inflammatory

39
Q

○ An IgM agglutinin and reacts optimally at 4C
○ Associated with ​infectious mononucleosis

40
Q

○ T ​stands for transition
○ Found in Melanesians and Yanomama Indians in Venezuela
○ Associated with ​Hodgkin’s Disease

41
Q
  • 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)
A

Kell antigens

42
Q
  • Lacks Kell antigens
  • Have no membrane abnormality
A

KO or K NULL phenotype

43
Q

Lacks the Kx antigen (which might be a precursor for Kell antigens)

A

McLeod phenotype

44
Q

Common among ​males suffering from ​Chronic Granulomatous Disease (CGD)

A

Mcleod Phenotype

45
Q

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

46
Q

○ Two most important antigens associated with transfusion medicine in the Duffy blood group system
○ Well-developed at birth
○ Easily destroyed by common proteolytic enzymes

A

Fya​ ​ and Fyb​

47
Q

Important anthropological marker for African blacks

48
Q

Were shown to resist infection cause by Plasmodium vivax and Plasmodium knowlesi

A

Fya​ ​ and Fyb​

49
Q

○ Usually IgG antibodies and react best at the AHG phase
○ Both are implicated in delayed HTR (DHTR) and HDN
- shows dosage effect

A

Anti-Fya​ ​ and Anti-Fyb​

50
Q

Anti-Fya​ ​ and Anti-Fyb​, which is more common

51
Q

○ Well-developed at birth, contributing to the potential for HDN
○ SHow in vitro hemolysis
- Reactivity enhanced by ​enzyme treatment

A

Jka and Jkb

52
Q

Resists lysis in 2M urea and occurs mainly in Mongoloids

53
Q

○ Show dosage
○ Both are IgG immune antibodies (primarily IgG3) and antiglobulin reactive
○ Bind complement
○ Common cause of delayed HTRs

A

Anti-Jka​ ​ and Anti-Jkb​

54
Q

located on chromosome 19, closely linked with the​ secretor locus

55
Q

○ Naturally occurring saline agglutinins​ (IgM in nature) ​that react best at RT
○ Characteristically show loose and mixed-fixed reactivity in vitro

56
Q

○ Most are IgG (often IgG4) immune antibodies; reactive at AHG phase at 37o​ ​C and the AHG phase

57
Q

Antibodies that causes HDN/EF (erythroblastosis fetalis)

A

Anti-C/Anti-AB (ABO)
Anti-f (Rh)
Anti-U (MNSs U)
Anti-D
Anti-Fya​
Anti-K
Anti-Ss
Anti-Jk

58
Q

IgM ‘naturally occurring’ IgG ‘immune’ antibodies antibodies (generally) but can become IgG

A

Le
P
I
Lu
P1

59
Q

IgG ‘immune’ antibodies

A

K
Fy
Jk
Ss
Xga​

60
Q

Blood groups associated with secretor genes

A

Lewis Lutheran ABH

61
Q

Enhanced by proteolytic enzymes

A

Kidd
Rh
I
P1
Lewis

62
Q

Inactivated/Destroyed by proteolytic enzymes

63
Q

Antigens that are well-developed at birth

A

MNSs U
Kidd
Kell
Duffy

64
Q

Antigens that are poorly-developed at birth

A

Lewis
P
I
Lutheran

BLOODBANK (7 decks)

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