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DMD 5244 (Immunity) > Transplantation immunology (complete) > Flashcards

Transplantation immunology (complete) Flashcards

1
Q

When is transplant indicated (needed)

A

1, good evidence of irreversable organ damage

  1. alternative treatments not applicable or helpful
  2. when the organ is in the end-stage of organ failure
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2
Q

What is the main complication of transplantation

A

the grafted tissue/organ is recognized as foreign and attacked by the bodies immune system
(host vs. graft response)

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3
Q

what is host vs. graft response, and what does it lead to

A

the host’s immune system attacks the graft because it sees it as foreign. this leads to transplant/graft rejection

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4
Q

what causes host vs. graft response

A
  1. differences in major HLA
  2. high frequency of host T-cells recognizing the graft HLA
  3. indirect recognition
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5
Q

what is graft vs. host reaction

A

when donor lymphocytes attack the host

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6
Q

when do you see graft vs. host reaction

A

bone marrow transplants

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7
Q

what is the treatment/prevention of graft vs. host reaction

A

removal of all t-cells from the graft

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8
Q

what are the different types of grafts

A

autograft - from one part of the body to another
isograft - from one geneticallly identical person to another
allograft - from another unidentical person
xenograft - from a different species

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9
Q

Are all grafts rejected at the same rate? if not, what are the different rates?

A

no
hyperacute rejection
acute rejection
chronic rejection

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10
Q

what is hyper acute rejection

A

rejection occuring within minutes or hours, that is usually Ab mediated

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11
Q

what is acute rejection

A

rejection occuring in days or weeks, usually initiated by alloreactive T-cells

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12
Q

what is chronic rejection

A

happens over months or years

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13
Q

what are the methodes that are used to test for transplant compatibility

A
  1. ABO compatibility
  2. HLA matching (tissue typing)
  3. Tissue cross matching
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14
Q

what else can be used along with best compatability to prevent graft rejection

A

immunosupressive drugs (blocking T-cells, or both B and T-cells)

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15
Q

how critical is ABO blood type compatibility for transplants, and why

A

essential, because it isn’t only found on the blood, but on other tissues

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16
Q

how critical is RhD blood type compatibility for transplants and why

A

it is unimportant, because it is only on RBCs

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17
Q

what is tissue typing

A

testing to see how closely HLA’s between the donor and recipient match up (the closer the better)

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18
Q

what is tissue cross matching

A

determining whether a patient has Abs that will react specifically with donor WBCs

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19
Q

how is tissue cross matching done

A

the recipients serum is mixed with donor leukocytes. if there is a reaction (positive result) then the transplantation is contra-indicated

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20
Q

what are the possible consequences of using an immunosuppresive drug to prevent transplant rejection

A

they are at an increased risk for infections (especially opportunistic ones) and cancer

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21
Q

what are some examples of opportunistic infections

A 
candida
Epstein-Barr virus (EBV)
cytomegalovirus (CMV)
Listeria
Mycobacterial
22
Q

what are the 4 types of immunosuppressors that affect T-cell function

A

Calcineurin inhibitors
T-cell activation and proliferation inhibitors
Anti-T-cell immunoglobins
IL-2 receptor antagonists

23
Q

how do calcineurin inhibitors affect T-cell function

A

it inhibits calcineurin enzymes and activation of NFAT

BLOCKS TRANSCRIPTION and PRODUCTION OF IL-2

24
Q

what is the function of IL-2

A

it stimulates T-cells to grow and proliferate

25
Q

what drugs are calcineurin inhibitors, and thus block transcription and production of IL-2

A

cyclosporine(sandimmune)

Tacrolimus/FK-506 (Prograf)

26
Q

What is MTOR

A

mammalian target of rapamycin inhibitor

27
Q

what does MTOR do to T-cell activation

A

it inhibits MTOR, it inhibits IL-2 driven proliferation of T-cells

28
Q

what are examples of MTOR

A

sirolimus (rapamune)(rapamycin)

29
Q

how do anti-Tcell immunoglobins block T-celll function

A

the antibodies bind to T-cells

30
Q

what are examples of anti T-cell immunoglobins drugs

A
  1. antithymyocyte Globin (Atgam)

2. murononab, a-CD3 (OKT3)

31
Q

what does Atgam (antithymyocyte Globin) do

A

binds to Tcells, Bcells, platelets, and other leukocytes

NON-SPECIFIC

32
Q

what does murononab, a-CD3 (OKT3) do

A

binds to CD3, and depletes all T-cells via complement and opsonization/phagocytosis

33
Q

which immunosuppresive drug is used to treat acute rejection

A

murononab, a-CD3 (OKT3)

34
Q

what do IL-2 receptor antagonists do

A

bind the IL-2 receptor of activated T-cells so that IL-2 can’t. this stops T-cells from proliferating

35
Q

what are two examples of IL-2 receptor antagonists

A

DAclizumab (zenapax)

Basilixumab (simulect)

36
Q

What are the drugs that affect B and T cell development

A

antimetabolites and corticosteroids

37
Q

how do antimetabolites affect B and T cells

A

they inhibit purine synthesis in lymphocytes which blocks proliferation

38
Q

what are two antimetabolites that block proliferation of B and T cells

A 
azathioprine (Imuran)
mycophenolate mofetil (cellcept)
39
Q

how do corticosteroids affect T and B cell function

A

they inhibit PLA2 which leads to decreased synthesis of prostaglandins and leukotrienes
low prostaglandins lead to decreased inflammation and T-cell function
low leukotrienes leads to decreased inflammation, chemotaxis and degranulation of PMNs, and CTL proliferation

40
Q

what are two examples of corticosteroiids

A

prednisone (orasone, deltasone)

methypredinisone (methylpred, solumedrol)

41
Q

what happens to the immune system as a whole on corticosteroids

A

the whole system is supressed

42
Q

what is oral chronic GVHD (cGVHD)

A

pathology of the oral cavity due to graft vs. host disease

43
Q

what are the oral manifestations of oral chronic GVHD

A

lichenoid changes
mucosal atrophy and ulcerations
taste disturbances
salivary gland hypofunction

44
Q

what are candidal superinfections

A

yeast like infections

45
Q

what is the treatment for patients with extensive cGVHD

A

immunosupressive drugs

46
Q

what is the problem with frequent use of inmmunosupressive drugs

A

more likely to get infections
more likely to have malignancy
sometimes death

47
Q

what are the first drugs used for cGVHD

A

cyclosporine and corticosteroids (prednisone)

48
Q

when in cGVHD would you use tacrolimus instead of cyclosporine

A

if the disease is manifest in the liver

49
Q

what does thalidomide do

A

anti-inflammatory (decrease TNF-a)

50
Q

what does methotrexate do

A

anti-metabolite

51
Q

what would be the benefit of using topical/local immunosupressants for those with cGVHD

A

it doesn’t supress the entire immune system, just the local immune system

52
Q

what are the topical drugs for cGVHD

A
  1. topical corticosteroids
  2. topical cyclosporine
  3. local phototherapy
  4. topical azathioprine
  5. topical tacrolimus

DMD 5244 (Immunity) (16 decks)

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