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MET 2 > Transplantation immunology > Flashcards

Transplantation immunology Flashcards

1
Q

3 classifications of rejection

A

Hyperacute

Acute Chronic

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2
Q

When does hyperacute rejection occur

A

Minutes or hours of transplantation

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3
Q

When does acute rejection occur

A

1 week to 6 months later

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4
Q

When does chronic rejection occur

A

Months to years

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5
Q

What mechanism happens in acute rejection

A

Acute cellular rejection

Acute antibody rejection

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6
Q

How does kidney appear in cell mediated rejection

A

Interstitital tuberlitis
Endothelialitis
Lumen compromised by presence of lymphocytes

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7
Q

What happens in acute cellular rejection

A

Helper T cell stimulates cytotoxic T cell to produce immune response

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8
Q

What is antibody mediated rejection

A

Help T cell produces B lymphocyte which produces antibodies

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9
Q

What is the primary target of antibodies in antibody mediated rejection

A

Endothelium of arteries adn capillaries

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10
Q

How does blood vessel appear histologically after antidboy mediated rejection

A

Inflammation

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11
Q

How is cell vs antibody mediated rejection differentiated

A

Antibody activates complement cascade

C4d forms covalent bonds with thio-ester groups on endothelial cell surfaces and these can be detected

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12
Q

What happens when you have complement mediated activation

A

C1 activated, then C2 and C4

C4d is lost

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13
Q

Criteria for acute AMR

A

1) Evidence of acute renal injury on histology
2) Evidence of antibody activity
3) Circulating anti-donor specific antibodies

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14
Q

Is antibody or cell mediated rejection more common

A

Cell

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15
Q

Is antibody or cell rejection more dangerous

A

Antibody

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16
Q

In what kind of person does a hyperacute rejection occur

A

A person who has been ‘immunologically primed’- they have had a previous transplant, transfusion or pregnancy

17
Q

What kind of response is involved in hyperacute rejection

A

Antibody mediated

18
Q

How does hyperactive rejection lead to endothelial damage

A

Preformed antibodies bind to the vessel lumen, activating the endothelium into pro-coagulant state
Leads to thrombosis and damage

19
Q

Reasons why a graft can fail (4)

A
  • It was damaged before transplantation
  • Surgical complication
  • Recurrence of original disease
  • Rejection
20
Q

Define rejection

A

Recognition and destruction by recipient immune system

21
Q

How do grafts appear after chronic rejection

A

Lost majority of structure
Not as many tubules
Replaced in large measure by collagen- fibrotic process

22
Q

Who can the following blood groups receive donated organs from

a) A
b) B
c) 0
d) AB

A

a) A or O
b) B or O
c) O
d) A, B or O

23
Q

How do you prevent hyperacute rejection

A

Screen for the presence of preformed antibodies.

24
Q

What are most preformed antibodies specific for?

A

HLA

25
Q

How do you prevent acute rejection

A

HLA matching

Minimising ischaemia

26
Q

What is the HLA molecule responsible for

A

Sampling all the proteins around the presenting the antigen on an antigen presenting cell for the T cell receptor

27
Q

What is the advantage of an individual having several different MHC molecules

A

Increases the number of peptides that can be bound

28
Q

What is the difference between MHC class 1 and class 2

A 
MHC class 1 found on every cell
MHC class 2 only found on antigen presenting cells
29
Q

Why does ischaemia need to be minimised to prevent rejection

A
  • Ischaemia upregulates adhesion molecules
  • Increases adhesions of leucocytes during rreperfursion
  • Increases non specific damage
30
Q

How to prevent chronic rejection (4)

A

Choose best organ
Minimise surgical damage
Minimise acute rejection
Minimise drug toxicity

31
Q

Why is the immune response to graft less aggresive over time

A

Loss of bone marrow derived cells of donor

Development of active regulation

32
Q

What factors affect the ‘load’ (how much stress the kidney undergoes)

A 
Hypertension
Hyperlipidaemia
CNI toxicity
Senescence
Alloimmune injury
Hyperfiltration
CMV
33
Q

What can cause inflammation of the transplant (3)

A

Ischaemia reperfusion
CNI toxicity
Alloimmune injury

34
Q

Where can imunosuppresants target

A
  • Take out T cell receptor
  • Calcineurin inhibitors which inhibit transduction of signal
  • Steroids inhibit gene activation
  • Anti IL-2
  • Anti metabolites present cells from dividing

MET 2 (32 decks)

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