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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
same carbohydrate core: O-group contains only the core (this core includes the
H antigen but for hisotrical reasons refferred to as O(unmodified core)
26
A and B antigens are
co dominant
27
ABO Incompatibility symptoms
- Back pain - Haemoglobinuria (red urine) - Chills (fever) - Jaundice (due to haemolysis of transfused blood) - Feeling of impending do
28
Symptoms within
24h or can be delayed several days
29
Fucosyltransferase (FUT1 gene) adds
fucose subunits by (glyosidic bonds)
30
Fucose modifications add
biochemical diversity, but have little impact on immunogenicity
31
Carbohydrate structures are widely
expressed throughout the body, polymorphic due to genetic arms race
32
Blood group ‘O’ arises from
a frame-shift mutation, causes non functional transferase
33
Glycosylation occurs in
the golgi
34
A, B and H antigens are not just
confined to erythrocyte surface
35
A, B and H antigens are not just confined to erythrocyte surface and may
be secreted in saliva, gastric and seminal fluid
36
Carbohydrate (CHO) secretion requires
the Se (secretor) gene fucosyltransferase Alpha-2 (FUT2), which is only expressed in ~70-80% of the British population
37
FUT2 is active in
epithelial cells (FUT1 catalyses the same reaction in erythrocytes)
38
FUT2 creates the
‘H antigen’ where further glycosylation's can be added
39
H antigen is central to
CHO secrretion
40
FUT1 Active in
mesodermal / myeloid cell lineages (erythrocytes)
41
FUT1 Active in mesodermal / myeloid cell lineages (erythrocytes) and catalyses the
transfer of fucose α1,2 glyosidic bonds to the terminal galactose of a H-active substance (creates H antigen)
42
FUT2 Active in
endodermal cells (mucosa)
43
FUT2 Active in endodermal cells (mucosa) and catalyses
the identical reaction as above: aka Se (secretion) factor
44
FUT3 Lewis (or Le) active substance and is active in
endodermal cells an catalyses the transfer of fucose α1,3/4 to N-acetylglucosamine
45
what are the two types of Rh proteins?
1) RhCcEe 2) RhCcEe
46
23
47
24
48
In Caucasian Rh (-ve) the RhD gene is
completely deleted, thus only RhCcEe is expressed
49
In Black communities the RhDψ variant
exists, where the RhD gene is mutated and is non-functional
50
The human Rh genes are highly
polymorphic >40 variations
51
The human Rh genes are highly polymorphic >40 variations They represent the
second most immunogenic next to ABO
52
Unlike H antigens, that are widely expressed Rh is
erythrocyte restricted
53
Prophylactic anti-D is
administered in some pregnancies
54
Mum is Rh (-ve), however, foetus is
Rh (+ve)
55
Pregnancy fine, however foetal and maternal bloods
mix during parturition
56
Immunogenic, activates
RhD reactive T and B cells
57
Second pregnancy, risk of
haemolytic disease of new born
58
Anti-D immunoglobulin neutralises
foetal RhD in materal blood (ADCC)
59
Neonatal Fc receptor (FCRN) facilitates
maternal IgG trans-migration
60
Anti-D (IgG) attacks
foetal blood
61
Anti-D (IgG) attacks foetal blood, causing
haemolysis
62
Anti-D (IgG) attacks foetal blood, causing haemolysis, resulting in
haem metabolites build up (bilirubin) and cause brain damage (kernicterus)
63
Platelets (thrombocytes) arise from
a common myeloid progenitor
64
Under thrombopoietin (TPO) cytokine
control
65
platelets start as
megakaryocyte
66
platelets are important in
haemostasis
67
why trasnfer platelets?
Thrombocytopaenia (shortage of platelets)
68
30
69
Platelets are central to
haemostasis
70
describe haemostasis?
collagen receptors detect tissue damage → haemostatic plug formation (with other clotting factors)
71
what is Plateletapheresis
whole blood separated into constituents, platelets retained
72
what is Donor recipient compatibility
HLA class-I antigens (see MHC lecture); platelets also express AB0 antigens
73
HPAs are
polymorphic
74
HPAs are polymorphic, donor match important as
miss-match can cause post-transfusion purpura (PTP)
75
what is post-transfusion purpura (PTP)
adverse reaction to blood transfusion (caused by erythrocyte miss-match also)
76
HPA-1a, HPA-1b and HPA-5a are
important antigens
77
Recipient lacks
HPA-1a but donor expresses HPA-1a
78
Recipient produces
anti-HPA1a antibodies, but become auto-reactive (combining site redundancy) and destroy self platelets
79
Recipient produces anti-HPA1a antibodies, but become auto-reactive(combining site redundancy) and destroy self platelets Occurs ...
1 - 2 weeks post-transfusion and can be fatal
80
Degree of immune response (graft rejection) Depends on...
... the class of graft
81
what is autograft
Self-tissue transferred from one part of the body to another (e.g. burns)
82
what is an isograft?
Involves monozygotic twins
83
what is an allograft?
Tissues / organs transferred between genetically different individuals (good HLA match)
84
what is Xenograft?
Tissues transferred between species
85
36-40
86
Histocompatibility is carried out in
stages
87
Histocompatibility is carried out in stages which are
- 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
organ rejection occurs when
there are pre-existing organ specific antibodies (rare) – patient has had repeated blood transfusions (H antigen mediated)
89
organ rejection occurs very
rapidly (the more vasculature, they greater the effect)
90
cell mediated organ rejecton?
T cells infiltrate can become activated, cause tissue damage (involves macrophages) and endotheliosis
91
when does cell mediated organ rejection occur
7 – 10 days post-transplantation; set-1
92
cell mediated also known as
histocompatibility mis match
93
when does organ rejection occur?
Occurs months – years after the acute phase
94
Chronic immune activity culminates in
damaged vessel wall (growth and repair) leading to vessel occlusion → blood can no longer supply organ → organ dies
95
Histocompatibility mismatch means
that all grafts / organs will eventually reject
96
Graft / organ survival can be
improved through the use of immunosuppressive drugs
97
Imuran is a an
azothioprine
98
what does imuran do?
inhibits mitosis, therefore T cell proliferation
99
cyclosporine targets?
calcineurin
100
what is calcineurin?
a downstream phosphatase in the TCR signalling pathway
101
Why are bone marrow transplants needed?
- Blood cancers - Leukaemias - Lymphomas - Haemolytic disease - Sickle cell - Thalassemias - Aplastic anaemia
102

Clinical Immunology (9 decks)

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