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Transplant Flashcards

1
Q

Allograft

A

Unrelated

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2
Q

Syngraft

A

Monozygous twin

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3
Q

Xenograft

A

Different species

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4
Q

Autograft

A

Same person

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5
Q

Are syngrafts rejected

A

No

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6
Q

Allograft rejected

A

Yup

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7
Q

Xenograft

A

Hyperactive rejection

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8
Q

Xenograft

A

Foreign

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9
Q

Hyperactute rejection

A

Preformed antibodies to HLA class I antigens or antigens of the ABO blood group.

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10
Q

What causes acute or accelerated acute rejections

A

Cellular allorecognition of the graft

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11
Q

GVHD

A

Transfer of immunocompetent allogenic cells into an immune depressed individual leads to these rejecting the recipient

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12
Q

Good hla matching

A

Prolongs graft survival

Done for renal

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13
Q

Why is hla matching not done for liver, heart and lungs

A

Short periods for which the latter organs maintain their function when explanted

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14
Q

Presensitization

A

Presence of preformed antibodies to HLA class I or ABO antigens in the recipients blood, it tested for in renal but not others

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15
Q

When rejected organs are biopsies, what do they contain?

A

Inflammatory infiltrate with mononuclear white blood cells(lymphocytes and macrophages, CD4, 8, macrophages, B cells and NK cells)

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16
Q

When a virgin helper CD4 cell sees an alloantigen, presented by APC what two options can it become if there is costimulation

A

TH1 or TH2

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17
Q

If the surrounding medium is rich in IL12, a macrophage derived cytokine, what will the virgin THCD4 become with antigen presentation

A

TH1

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18
Q

What does TH1 do

A

Activate CD8 and macrophages through IL2 and IFNy

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19
Q

If the surrounding is rich in IL-4 the virgin CD4 T cell will become what

A

TH2

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20
Q

What does TH2 do

A

Secrete IL4 and IL10 and direct B cells and antibody production

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21
Q

What CD4 predominates in rejection

A

TH1

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22
Q

What does IFNy from TH1 do

A

Recruit and activate macrophages and enhance MHC expression on the graft, making it particularly susceptible to the cytotoxic action of CD8 cell

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23
Q

What does IL2 do

A

Fav our the activation of cytotoxic T cells

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24
Q

Alloantigen

A

Antigen recognized during rejection

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25
Q

What are the key allantigens

A

MHC-HLA molecules

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26
Q

Direct allorecognition

A

Recipients immune system can recognize an intact MHC

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27
Q

Indirect allorecognition

A

Peptide derived rom the foreign MHC could be presented on APC

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28
Q

Is direct or indirect allorecognition more common

A

Direct

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29
Q

Hyperacute rejection

A

Minutes

Preformed antibodies

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30
Q

Accelerated rejection

A

1-5 days

T cells

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31
Q

Acute rejection

A

From 2 week

T cells

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32
Q

Chronic rejection

A

Months to years

Antibodies, complement, adhesion molecules

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33
Q

Hyperacute rejection is mediated by ___ __ in the recipient that are directed against antigens of the donor organ

A

Preformed antibodies

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34
Q

Example of hyperacute rejection

A 
ABO blood group barrier 
Antibodies against HLA class I from previous transfusions, transplants or pregnancies
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35
Q

Where are ABO blood group antigens presented

A

Endothelial cells

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36
Q

How manage hyperacute rejection

A

Preventative

Accommodation

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37
Q

Accommodation

A

Temporary depletion of natural antibodies may result in long term graft survival, despite the return of antibodies in the presence of their specific target antigens

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38
Q

Acute rejection is mediated by ____ and becomes apparent _ days post op

A

T cells

7

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39
Q

In acute rejection, how do T cells see alloantigen

A

Mainly direct

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40
Q

What cells infiltrate in acute rejection

A

Lymphocyte and monocyte

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41
Q

Accelerated acute rejection

A

1-5 days

T cells that have been sensitized to alloantigen (pregnancy, transduction)

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42
Q

How treat acute rejection

A

Suppression

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43
Q

Chronic rejections appears _ or _ after successful transplantation

A

Moonthe years

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44
Q

Is cell infiltration a major feature of chronic rejection

A

No

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45
Q

in chronic rejection __ release IL1, 6 TNFa

A

Macrophages

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46
Q

How it is expected that chronic rejection occurs

A

Early damage to the vascular endothelium is predisposing
Endothelium further damaged by antibodies to alloantigen, deposition of immune complexes, activation of complement , exposure of collagen and activation of the clotting cascade
FAVORING ENDOTHELIAL CELL PROLIFERATION and narrowing of the vascular lumen

47
Q

GVH

A

Grafts have immunocompetent cells recognize alloantigen of the recipient

48
Q

GVH is common after transplantation of __ ___

A

Bone marrow

49
Q

What happens when GVH becomes symptomatic

A

It is GVHD

50
Q

GVHD divided into two entities

A 
Acute disease (1-2 months)
Chronic disease(develops 2-3 months)
51
Q

What does GVHD effect in humans

A

Skin, liver, intestinal tract, immune system

52
Q

How long does GVHD happen after bone transplant

A

Days weeks

53
Q

Characterization of GVH

A

Erythema on palms and soles and ears
Hyperbilirubinaemia
Diarrhea

54
Q

Characterization of severe GVHD

A

Jaundice, increased Alkaline phosphatase, which denotes cholestasis, and of transaminases, a ding of liver damage
Diarrhea abdominal pain

55
Q

What causes the symptoms of GVHD

A

Epithelial cell injury

56
Q

Chronic GVHD shares certain clinical characteristics with __ __

A

Systemic sclerosis

57
Q

Prophylaxis for acute GVHD

A

Combination of methotrexate and ciclosporin

58
Q

Treatment of established GVHD

A

Methylprednisolone, ciclosporin/tacrolimus

Anti-CD52 monoclonal antibody campath1

59
Q

Tissue typing

A

Kidneys bc robust-can bee 48 hours cold

60
Q

HLA types kidneys have a graft survival in 1st year os ___% while nonmatched have __%

61
Q

How test for presenstization

A

Incubating the serum of the recipient and the lymphocytes of the donor. Binding of antibodies in the recipient serum is analyzed by flow cytometry

62
Q

Presensitization is an absolute ___ in renal transplant

A

Contradiction

63
Q

Is presensitization evaluated in cardiac and liver transplantation

64
Q

Immunosuppressive drugs

A

Dampening down the immune system

65
Q

Azathioprine

A

Inhibits purine synthesis

66
Q

Corticosteroids

A

Block cytokine gene expression

67
Q

Ciclosporin A; tacrolimus

A

Block Ca2+ dependent T cell activation pathway

68
Q

Sirolimus

A

Blocks il2 triggered proliferation and CD28/CTLA4 mediated co stimulators signals

69
Q

Azathioprine

A

Purine antagonist and functions as an effective antiproliferative agent.

70
Q

Corticosteroids have multiple effects on the immune system

A

Decrease B cells and inhibit monocyte trafficking , T cell proliferation and cytokine gene expression

71
Q

Side effects of corticosteroids

A

Skin, bones, and other tissues continue to present problems in clinical

72
Q

Glucorticoid:prednisone

A

Given immediately before or at the time of transplantation

73
Q

Methylprednisone

A

Administered immediately upon diagnosis of beginning rejection and continued once daily for 3 days

74
Q

Do prednisone and azathioprine act non specifically on the immune system

75
Q

Ciclosporin a

A

Calcineurin inhibitor
Small fungal cyclic peptide
Reduce GVHD following bone marrow transplant

76
Q

Major effects of ciclosporin a

A

T cells-inhibit il2 secretion

Stimulate production of cell growth inhibitory cytokines, such as TGFb

77
Q

What does TGFb do

A

Inhibits both T cell proliferationa nd the generation of cytotoxic lymphocytes , a heightened production of tgfb may contribute to the immune suppressive activity of ciclosporin A

78
Q

Ciclosporin a side effect

A

Nephrotoxicity

79
Q

Tacrolimus

A

Macro life antibiotic isolated from a Japanese soil fungus, streptomyces T
Similar effects and side effects of ciclosporin

80
Q

Side effects tacrolimus

81
Q

Ciclosporin and tacrolimus are what

A

Calcineurin inhibitors

82
Q

Sirolimus

A

Rapamycin , macrocyclic lactose that inhibits biochemical pathways that are required for cell progression through the late G1 phase or entry into the S phase of the cell cycle and is labeled as an antiproliferatice

83
Q

Side effects sirolimus

A

Hypertriglyceridaemia

84
Q

Antibodies can be used to target specific immune cells thought to be involved in rejection

A

Target cells are abolished or lessened through antibody directed cell lysis or modulation of surface molecules

85
Q

Monoclonal antibody

A

Monospecificity and can be purified to homogeneity

86
Q

Since the 80s, ALG and ATG have been used by many transplant centers for the treatment of rejection episodes (antilymphocyte globulin and antimyocyte globulin)

A

These polyclonal antisera are composed of multiple antibodies specific for a variety of lymphocyte cell surface molecules

87
Q

Monoclonal anti CD3

A

OKT3 monoclonal antibody sees human cd3
Treat recipients of allograft in clinical transplantation
Intravenous administration of OKT3 clears T cell from circulation by opsonization

88
Q

Disadvantage of anticd3 molecule

A

Side effects and development of anti mouse antibodies in 75% of ppl

89
Q

Monoclonal anti-cd4 and anti-cd8

A

Okt4

In clinical trials

90
Q

Monoclonal antibodies specific for activation antigens

A

When T cells respond to antigen and become activated, they express IL2 receptor. Targeting this receptor may allow more selective immunosuppressive therapy. This antibody is used in islet transplantation

91
Q

Side effects of antibody therapy

A

Syndrome of fever and myalgia that is believed to be caused by systemic release of cytokines
Also develop lymphomas

92
Q

Lymphomas occur in _% of all recipients of transplanted organs

93
Q

Immunosuppressive regimen

A

Multiple immunosuppressive drugs acting at different levels of T cell activation
Standard:tacrolimus and corticosteroid

94
Q

__ antibodies are used in some centers before transplantation to prevent the activation of anti graft immune response

A

Antilymphocyte

95
Q

Antilymphocyte antibodies are effective but increase the incidence of what

A

Lymphoproliferatice disorders and possibly infections

96
Q

The administration of murine anti cd3 OKT3 is associated with what

A

Fever, chills, hypotension, pulmonary edema, encephalopathy, nephropathy…CAPILLRARY LEAK SYNDROME

97
Q

Complications of immunosuppressive regimen

A

Infections, malignancies, bacterial fungal viral

98
Q

Frequent agents of infection after transplant

A

CMV, herpes virus, fungal organisms, Aspergillus, Nocardia, cryptococcal, pneumocystis, toxoplasmosis

99
Q

What is the most frequent and pathologically important post transplant infection

100
Q

Does cmv infection last for life

101
Q

When does cmv deactivate

A

Impaired T cell immunity

102
Q

Primary cmv infection

A

If in organ that was transplanted

103
Q

In renal, cardiac, lung, liver and bone marrow transplant, CMV causes what

A

Fever, leukopenia, hepatitis, pneumonia is, oesophagitis, gastritis, colitis, 1month after surgery

104
Q

CMV retinitis can appear later

105
Q

How treat cmv infection

A

Ganciclovir, a guanosine derivative

106
Q

What are the most common cancers seen after organ transplant

A

Lymphoma, skin cancer, Kaposi Sarcoma

107
Q

The development of __ diseases is also dependent on immunosuppression, induced by drugs such as ciclosporin, tacrolimus, okt3

A

Lymphoproliferative

108
Q

In the setting of allotransplatation , lymphoproliferative diseases are aggressive with a high incidence of what

A

Central nervous system and extranodal involvement ; they are mainly classified as B cell derived large cell non Hodgkin lymphomas and can be polyclonal or monoclonal

109
Q

Outcome os lymphoproliferative disease

A

Poor unless immunosuppressive therapy can be stopped

110
Q

Origin of these lymphoproliferative diseases has been ascribed to the effect of the oncogenic ___ over B cells constantly stimulated by the allograft. Immusuppression would be a catalyst

111
Q

The use of immunosuppression controls rejection episodes

A

The introduction of ciclosporin a in the 1980s has dramatically improved the outcome of allotransplantation

112
Q

Immunosuppressive regimens typically include and use multiple drugs acting at different levels of what

A

T cell activation

113
Q

Episodes of rejection resistant to conventional immunosuppressive regimens are controlled by what

A

Use of high dose steroids, tacrolimus, and antilymphocyte antibodies

114
Q

Side effects of immunosuppression

A

Opportunistic microorganisms and malignancies

Immunology (14 decks)

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