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Clinical Immunology > Transfusion & Transplantation > Flashcards

Transfusion & Transplantation Flashcards

1
Q

The demand for blood donation is

A

very high

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2
Q

3

A
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3
Q

how much whole blood is needed per year?

A

12.5 million units of whole blood per year, from 8 million volunteers

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4
Q

how many human blood groups?

A

There are 29 human blood groups carried by two types of structure on the surface of erythrocytes:

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5
Q

There are 29 human blood groups carried by two types of structure on the surface of erythrocytes:

A

1) Carbohydrates (AB0-glycolipids)
2) MEmbrane proteins (Rh)

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6
Q

The role of glycoprotein is to

A

give the erythrocyte an over all (-ve)
charge, aiding repulsion in capillaries

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7
Q

Carbohydrates can be joined direct to

A

phospholipids
or proteins

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8
Q

Glycolipids carry

A

A, B and H antigens

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9
Q

similiarites between innate and adaptive immune cells?

A

Both innate and adaptive immune cells recognise and become
activated towards foreign antigen i.e. ‘foreign cells’

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10
Q

differences between innate and adaptive immune cells?

A

Unlike innate immune cells, adaptive immune cells must communicate directly with ‘self cells’ to orchestrate their immune function

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11
Q

Adaptive immune cells (B and T cells) must recognise

A

‘self’ MHC for communication, but not become activated towards it (tolerance)

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12
Q

MHC are

A

co-dominant

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13
Q

MHC are co-dominant & we

A

inherit one allele (haplotype) from each parent

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14
Q

T and B cells are
educated to

A

tolerate self (+ve and -ve) selection for T cells and -ve selection for B cells)

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15
Q

Therefore, all of your adaptive immune cells are

A

self restricted via central tolerance

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16
Q

All nucleated cells in the body express

A

self MHC-I or MHC-II (antigen presenting cells)

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17
Q

erythrocytes have no

A

nucleus and no MHC

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18
Q

11

A
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19
Q

Blood group antigens cause

A

blood group incompatibility

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20
Q

Blood group antigens cause blood group incompatibility
Most important during transfusion, but also in

A

incompatible pregnancy

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21
Q

Antigens are epitopes expressed on

A

membrane proteins (e.g. Rh) of
glycosites on glycoprotein (e.g. Duffy, Kidd… Kell) or glycoliipid (glycosylation patterns eg: AB- and H

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22
Q

ABO and Rh will be

A

the
focus as these antigens are
the most immunogenic and
a screened for during
transfusion

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23
Q

13

A
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24
Q

same carbohydrate
core: O-group contains
only

A

the core

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25
Q

same carbohydrate
core: O-group contains
only the core (this core
includes the

A

H antigen

but for hisotrical reasons refferred to as O(unmodified core)

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26
Q

A and B antigens are

A

co dominant

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27
Q

ABO Incompatibility symptoms

A
  • Back pain
  • Haemoglobinuria (red urine)
  • Chills (fever)
  • Jaundice (due to haemolysis of transfused blood)
  • Feeling of impending do
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28
Q

Symptoms within

A

24h or can be delayed several days

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29
Q

Fucosyltransferase (FUT1 gene) adds

A

fucose subunits by (glyosidic bonds)

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30
Q

Fucose modifications
add

A

biochemical diversity, but have little impact on immunogenicity

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31
Q

Carbohydrate structures are widely

A

expressed throughout the body,
polymorphic due to genetic arms race

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32
Q

Blood group ‘O’ arises from

A

a frame-shift mutation, causes non functional transferase

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33
Q

Glycosylation occurs in

A

the golgi

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34
Q

A, B and H antigens are not just

A

confined to erythrocyte surface

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35
Q

A, B and H antigens are not just confined to erythrocyte surface and
may

A

be secreted in saliva, gastric and seminal fluid

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36
Q

Carbohydrate (CHO) secretion requires

A

the Se (secretor) gene
fucosyltransferase
Alpha-2
(FUT2), which is only expressed in ~70-80% of the
British population

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37
Q

FUT2 is active in

A

epithelial cells (FUT1 catalyses
the same reaction in erythrocytes)

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38
Q

FUT2 creates the

A

‘H antigen’ where further glycosylation’s can be added

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39
Q

H antigen is central to

A

CHO secrretion

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40
Q

FUT1 Active in

A

mesodermal / myeloid cell lineages (erythrocytes)

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41
Q

FUT1
Active in mesodermal / myeloid cell lineages (erythrocytes) and
catalyses the

A

transfer of fucose α1,2 glyosidic bonds to the terminal
galactose of a H-active substance (creates H antigen)

42
Q

FUT2
Active in

A

endodermal cells (mucosa)

43
Q

FUT2
Active in endodermal cells (mucosa) and catalyses

A

the identical
reaction as above: aka Se (secretion) factor

44
Q

FUT3
Lewis (or Le) active substance and is active in

A

endodermal cells an catalyses the transfer of fucose α1,3/4 to N-acetylglucosamine

45
Q

what are the two types of Rh proteins?

A

1) RhCcEe
2) RhCcEe

48
Q

In Caucasian Rh (-ve) the RhD
gene is

A

completely deleted, thus only RhCcEe is expressed

49
Q

In Black communities the RhDψ variant

A

exists, where the RhD gene is
mutated and is non-functional

50
Q

The human Rh genes are highly

A

polymorphic >40 variations

51
Q

The human Rh genes are highly polymorphic >40 variations
They represent the

A

second most immunogenic next to ABO

52
Q

Unlike H antigens, that are widely expressed Rh is

A

erythrocyte restricted

53
Q

Prophylactic anti-D is

A

administered in some pregnancies

54
Q

Mum is Rh (-ve), however, foetus
is

55
Q

Pregnancy fine, however foetal
and maternal bloods

A

mix during parturition

56
Q

Immunogenic, activates

A

RhD reactive T and B cells

57
Q

Second pregnancy, risk of

A

haemolytic disease of new born

58
Q

Anti-D immunoglobulin
neutralises

A

foetal RhD in materal blood (ADCC)

59
Q

Neonatal Fc receptor (FCRN) facilitates

A

maternal IgG trans-migration

60
Q

Anti-D (IgG) attacks

A

foetal blood

61
Q

Anti-D (IgG) attacks foetal blood, causing

A

haemolysis

62
Q

Anti-D (IgG) attacks foetal blood, causing haemolysis, resulting in

A

haem metabolites build up (bilirubin) and cause brain damage (kernicterus)

63
Q

Platelets (thrombocytes) arise from

A

a common myeloid progenitor

64
Q

Under thrombopoietin (TPO)
cytokine

65
Q

platelets start as

A

megakaryocyte

66
Q

platelets are important in

A

haemostasis

67
Q

why trasnfer platelets?

A

Thrombocytopaenia (shortage of platelets)

69
Q

Platelets are central to

A

haemostasis

70
Q

describe haemostasis?

A

collagen receptors detect tissue
damage → haemostatic plug formation (with other clotting factors)

71
Q

what is Plateletapheresis

A

whole blood separated into constituents, platelets retained

72
Q

what is Donor recipient compatibility

A

HLA class-I
antigens (see MHC lecture); platelets also
express AB0 antigens

73
Q

HPAs are

A

polymorphic

74
Q

HPAs are polymorphic, donor match important as

A

miss-match can cause post-transfusion purpura
(PTP)

75
Q

what is post-transfusion purpura
(PTP)

A

adverse reaction to blood transfusion
(caused by erythrocyte miss-match also)

76
Q

HPA-1a, HPA-1b and HPA-5a are

A

important antigens

77
Q

Recipient lacks

A

HPA-1a but donor expresses HPA-1a

78
Q

Recipient produces

A

anti-HPA1a antibodies, but become auto-reactive
(combining site redundancy) and destroy self platelets

79
Q

Recipient produces anti-HPA1a antibodies, but become auto-reactive(combining site redundancy) and destroy self platelets

Occurs …

A

1 - 2 weeks post-transfusion and can be fatal

80
Q

Degree of immune response (graft rejection)
Depends on…

A

… the class of graft

81
Q

what is autograft

A

Self-tissue transferred from one part
of the body to another (e.g. burns)

82
Q

what is an isograft?

A

Involves monozygotic twins

83
Q

what is an allograft?

A

Tissues / organs transferred between genetically different
individuals (good HLA match)

84
Q

what is Xenograft?

A

Tissues transferred between species

85
Q

36-40

86
Q

Histocompatibility is carried out in

87
Q

Histocompatibility is carried out in stages which are

A
  • Initial ABO typing (haemagglutination assay)
  • MHC matching 1) lymphocyte toxicity assay, identifies MCH-I and
    MCH-II via incubation with various HLA-type antibodies
    (or DNA hybridisation or PCR of HLA alleles)
    2) cross matching; recipient antibodies against donor HLA
88
Q

organ rejection occurs when

A

there are pre-existing organ
specific antibodies (rare) – patient has
had repeated blood transfusions
(H antigen mediated)

89
Q

organ rejection occurs very

A

rapidly (the more vasculature, they greater the effect)

90
Q

cell mediated organ rejecton?

A

T cells infiltrate can become activated, cause tissue damage (involves macrophages) and endotheliosis

91
Q

when does cell mediated organ rejection occur

A

7 – 10 days post-transplantation; set-1

92
Q

cell mediated also known as

A

histocompatibility mis match

93
Q

when does organ rejection occur?

A

Occurs months – years after the acute phase

94
Q

Chronic immune activity culminates in

A

damaged vessel wall (growth
and repair) leading to vessel occlusion → blood can no longer supply
organ → organ dies

95
Q

Histocompatibility mismatch means

A

that all grafts / organs will
eventually reject

96
Q

Graft / organ survival can be

A

improved through the use of immunosuppressive drugs

97
Q

Imuran is a an

A

azothioprine

98
Q

what does imuran do?

A

inhibits
mitosis, therefore T cell
proliferation

99
Q

cyclosporine targets?

A

calcineurin

100
Q

what is calcineurin?

A

a downstream phosphatase in the TCR signalling pathway

101
Q

Why are bone marrow transplants needed?

A
  • Blood cancers
  • Leukaemias
  • Lymphomas
  • Haemolytic disease
  • Sickle cell
  • Thalassemias
  • Aplastic anaemia

Clinical Immunology (8 decks)

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