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Metabolism 2 > Transplantation Immunology > Flashcards

Transplantation Immunology Flashcards

1
Q

What is rejection

A
  • rejection implies that there is something active that is attacking the graft, this is usually the immune system that attacks the graft and causes it to loose function
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2
Q

what are the three types of rejection that you can have

A
  • hyperacute
  • actue
  • chronic
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3
Q

describe the time periods that the three types of rejection can occur in

A

Hyperacute:minutes to hours

Acute:- one week to six months occasionally later

Chronic: months to years – can see the change in the biopsy after a small number of months

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4
Q

How does acute rejection happen

A
  • this is by activation of the adaptive immune system
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5
Q

name the two types of acute rejection

A
  • acute cellular rejection

- acute antibody mediated rejection

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6
Q

Describe how acute cellular rejection happens

A

this involves the activation of the helper T lymphocyte

- this causes the activation of cytotoxic T lymphocyte and macrophage

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7
Q

what can be caused by acute cellular rejection

A

endarteritis

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8
Q

describe how acute antibody mediated rejection occurs

A
  • the Helper T lymphocyte becomes activated

- this causes the B lymphocyte to become activated and produce antibodies

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9
Q

what is the primary target for the antibodies in acute anitbody mediated rejection

A

endothelium of the arteries and capillaries

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10
Q

List the antibodies that can be activated in antibody mediated rejection

A

ABO antigens
MHC antigens (class I, II)
MHC class I-related chain A (MICA)
others (including anti-AT1 receptor)

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11
Q

What are the histological features of antibody mediated rejeciton

A

Neutrophils (or mononuclear cells) in peritubular capillaries

Thrombosis

Severe arteritis/fibrinoid necrosis of vessels

This results in
Haemorrhage and Infarction

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12
Q

describe the classical pathway of complement activation

A
  • antibody - antigen complex activates C1
  • the activate C1 causes activation of C2 and C4
  • this produces C3
    and this also produces C4d which is clinically important as it shows up and can show that antibodies have been activated
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13
Q

what correlates with antibody activation

A

C4d

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14
Q

what is the criteria for acute antibody mediated rejection

A

1, Evidence of acute renal injury on histology
2, Evidence of antibody activity C4d staining in peritubular capillaries
3. Circulating anti-donor specific antibodies

Suspicious if 2 out of 3 are present

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15
Q

what is it important to define the mechanism of acute rejection between acute cellular rejection and acute antibody mediated rejection

A

because. ..
- projection is different
- treatment is different

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16
Q

what is more common acute cellular rejection or antibody mediated rejection

A

acute cellular rejection

17
Q

Why is it harder to treat acute antibody mediated rejection

A

= harder to treat as you can remove the antibodies but you cannot remove the b cells which will carry on producing antibodies

18
Q

what is hyperacute rejection

A
  • this happens within minutes and house

- these people have been previously primed and sensitiesed to the antibodies

19
Q

describe the 3 mechanisms of hyperacute rejection

A

previous transplant
previous transfusion
previous pregnancy

20
Q

what causes hyperactue rejection

A

1 hour – neutrophils in peritubular capillaries and glomeruli

21
Q

why does chronic acute rejection happen

A

It was damaged before transplantation

Surgical complications

Recurrence of original disease

Rejection

22
Q

what factors lead to chronic rejection

A
  • pre-transplant damage and surgicial complciations

- immune mediated damage

23
Q

how do you prevent hyperacute rejection

A
  • test ABO compatibility
24
Q

how do you screen for hyperactue

A

Direct cross-match

  • complement flow cytometry
  • complement cytoxicity

Most preformed antibodies are specific for HLA

25
Q

describe how complement flow cytometry works

A

Add serum form the potential recipietnt and add a second layer antibody that will shine in the dark when a laster is pointed at it
If there is a antibody that is specific to the layer – then the flueroqueine will shine
If the antibody is not present then there will be now fluroeine near the cell and it will be negative

26
Q

describe how complement cytoxcitiy works

A

add complement and the complement destroys the cell – it will be activated adjacent to the cell if there is a serum that is antigen that is linked to the antibody of the cell
Continually screening patients

27
Q

why do we get an immune response

A

This is why get an immune response because if the difference between the donor and recipient is not a peptide but part of HLA the T cell will assume the difference is the same as a viral infection and will attack the graft

28
Q

how do you prevent rejection in acute rejection

A

HLA matching

Minimising ischaemia

  • Ischaemia upregulates adhesion molecules
  • Increases adhesion of leucocytes during re-perfusion
  • Increases non-specific damage
  • Also increases acute rejection

= ISCHAEMIA-REPERFUSION INJURY
- therefore you should perfuse it with fusions that reduce the risk of ischaemia reperfusion injury

29
Q

how do you prevent chronic rejection

A

Choosing best organ

Minimising surgical damage

Minimising acute rejection

Minimising drug-toxicity

30
Q

why do we get rejection

A

allorecognition direct
- CD8 nad CD4 cells

allorecgonition indirect
- CD8 and CD4 cells from an APC reaction

31
Q

How does a T cell become activated

A
  • T cell recongises the antigne as well as a non specific antigen whcih sends signals to the nucleus
  • this causes cytokine activation
  • IL2 is produced
  • this causes other T lymphocytes to become proliferated
32
Q

What sites do immunosupressive agents work at

A

1, calcineurin inhibits – inhibits signalling to the nucleus to release cytokines
2, Corticoisteroids- inhibit cytokine release
3 , antiproliferative drugs(azathioprine, MMF) – stop the nucleus dividing

Metabolism 2 (40 decks)

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