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blood bank > ABO/Rh > Flashcards

ABO/Rh Flashcards

1
Q

most important antigen group for transfusion and transplant

A

ABO Blood group

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2
Q

exception when there won’t be rejection

A

incompatible bone marrow with high immunosuppressive drugs

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3
Q

forward grouping

A

detect ABO antigen on patient RBCs

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4
Q

reverse grouping

A

detect ABO antibodies in patient serum

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5
Q

if back typing weak

A

add additional patient serum and incubate longer at RT

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6
Q

abo antibodies are

A

naturally occuring

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7
Q

anti-A and anti-B class

A

IgM

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8
Q

ABO antibodies detectable

A

3-6 months are birth

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9
Q

Anti-A,B occur naturally in

A

group O

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10
Q

anti-A, B

A

predominantly IgG

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11
Q

abo locus

A

chromsome 9

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12
Q

fucosyltransferase

A

produces H antigen to type 2 precursor chains

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13
Q

FUT2 produces

A

soluble H antigen will end up in secretions and body fluids and fixes fucose to type 1 precursor

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14
Q

type 1

A

B 1-3

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15
Q

type 2

A

b 1-4

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16
Q

A

A

N-acetylgalactosaminyl transferase

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17
Q

B

A

galactosaminyl transferase

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18
Q

AB

A

N-acetylgalactosaminyl transferase and galactoasminyl transferase

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19
Q

most amount of H

A

A2

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20
Q

ABH expression complete at

A

2-4 age

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21
Q

ABH antigens in

A

body fluids and secretions (secretor trait)

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22
Q

FUT2 modifies type 1 precursor chains to form

A

soluble H antigen

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23
Q

non secretor

A

Le a

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24
Q

secretor

A

Le b

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25
Q

agglutinate with A1

A

dolichos biflorus

26
Q

agglutinates cells with H antigen

A

ulex europaeus

27
Q

bandeiraea simplicifolia

A

agglutinated cells with B antigen

28
Q

produce less antigen

A

A2

29
Q

subgroups of A

A

very weak front typing with anti-A or unexpected A cells in back typing

30
Q

if suspect an A2 use

A

A1 lectin and will show no reactivity

31
Q

B3 is most common subgroup of B

A

shows mixed field agglutination

32
Q

hh genotype caused by

A

lack of H, lack fucosyltransferase = no ABO genes

33
Q

bombay can only receive

A

bombay

34
Q

parabombay

A

-H expression is near 0

dysfunctional FUT1 with functional FUT2

35
Q

dysfunctional FUT1 with functional FUT2

A

very small A, B, H; makes anti-H unless AHG phase

36
Q

dysfunctional FUT but no FUT2

A

very small amounts of ABH on RBCs, none in secretions

37
Q

silenced FUT1 active FUT2

A

make soluble ABH antigens ; make anti- IH

38
Q

2nd most important blood group following ABO

A

Rh system

39
Q

Rh reside of

A

proteins

40
Q

Rh antigens are

A

not naturally occuring; require foreign RBC’s

41
Q

Rh null

A

no Rh antigens (-1,-2,-3,-4,-5)

42
Q

f antigen

A

present on cells for homozygous for ce

43
Q

G antigen

A

present on all C positive and many D positive cells

44
Q

Cw antithetical to

A

near universal antigen MAR

45
Q

partial D/ mosaic D

A

-missing or incomplete epitopes for D antigen
-these people can make anti-D against missing portions of antigen so = Rh -

46
Q

weak d

A

express d weakling but it still there so Rh +

47
Q

positional effect C: D

A

D antigen is complete just reduced, so receive D + units

48
Q

Rh antibodies class

A

IgG

49
Q

Rh donors

A

weak d testing done on every unit, but be done all the way through

50
Q

Rh patients

A

if typed initially as weak d, DO NOT have to follow all the way through

51
Q

delayed hemolytic transfusion reactions

A

caused by giving a patient a unit of blood that is positive for an antigen and they have an anamnestic response to that antigen (extravascular lyse)

52
Q

HDFN

A

severve from Rh antibody
Rh antigens well developed on fetal cells and cross placenta

53
Q

rhogam given to what type mother

A

negative

54
Q

Rh deficiency syndrome

A

lack all Rh proteins on RBCs

55
Q

regulator type

A

RhAG required to traffic RhD and RhCE to cell surface

RhAG mutated- none produced

56
Q

amorphic type

A

mutation in RhCE and deletion of RhD in lack of Rh proteins

57
Q

symptoms of Rh def

A

hemolytic anemia, decrease serum haptoglobin, slight elevation in bili

58
Q

Rh null patients can develop

A

anti-Rh29 “total Rh” reacts will all Rh antigens

59
Q

Rh Mod

A

partial suppression of Rh genes caused by mutations in RhAG protein

60
Q
A

blood bank (8 decks)

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