Transplantation Flashcards

1
Q

autologous transplant

A

the transplant tissue is from the same individual e.g. skin graft

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2
Q

syngeneic transplant

A

between twins

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3
Q

allogenic transplant

A

between genetically non-identical members of the same species

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4
Q

xenogenic transplant

A

between different species

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5
Q

cadaveric transplant

A

organs from dead donor

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6
Q

what is rejection

A

when the immune system attacks the transplant

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7
Q

what can reduce the risk of rejection

A

donor and recipient must be AOB compatible close as possible HLA match recipient must not have anti-donor HLA antibodies immunosuppression

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8
Q

what is hyperacute rejection

A

immune system rejects organ/translant within hours

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9
Q

pathophysiology of hyperacute rejection

A

antibodies bind to ABO blood group or HLA class I antigens on the graft type II hypersensitivity reaction is triggered IgG and IgM bind and recruit macrophages and complement system causing cell damage

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10
Q

acute rejection

A

delayed type IV hypersensitivity reaction days-weeksusually due to HLA incompatibility

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11
Q

pathophysiology of acute rejection

A

dendritic cells from donor stimulate an allogenic response in lymph node node releases T cells which target donor organ

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12
Q

afferent phase of acute rejection

A

donor MHC molecules on dendritic cells recognised by patients CD4+ T cells

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13
Q

efferent phase of acute rejection

A

T cell recruit macrophages< NK cells, B cellsgraft is targeted

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14
Q

what is chronic rejection

A

takes place over months/years often mediated by T cells can be caused by pre-existing autoimmune disease

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15
Q

role of immunosuppresants in transplants

A

prevent rejection at the time of the transplant if the drugs are stopped rejection will occur

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16
Q

role of corticosteroids in transplants

A

low dose prevent early stages of rejection target antigen presenting cells at a high dose they can treat rejection

17
Q

how does ciclosporin work

A

immunosuppressant interacts with proteins in T cell signalling cascade

18
Q

examples of monoclonal antibodies

A

basiliximab daclizumab

19
Q

role of monoclonal antibodies in transplants

A

used in acute graft rejection

20
Q

rapamycin mechanism of action

A

inhibits signals from IL-2 receptor

21
Q

role of rapamycin in transplants

A

prevents acute graft rejection

22
Q

side effects of rapamycin

A

raises lipid and cholesterol levels anaemia hypertension rash thrombocytopenia

23
Q

what are anti-proliferatives

A

drugs that inhibit DNA production

24
Q

anti-proliferatives examples

A

azathioprine mycophenolate mofetil methotrexate

25
stem cell sources for transplant
bone marrow peripheral bloodcord blood
26
when is stem cell transplantation used
last resort for haematological malignancies primary immunodeficiency severe combined immunodeficiency
27
autologus stem cell therapy
marrow is removed frozen and reinfused after chemotherapy has been given
28
allogenic stem cell therapy
higher risk risk of graft vs host disease
29
what is conditioning for SCT
high dose chemo/radiotherapy to destroy stem cells before new ones are given
30
what is graft vs host disease
multi-system complication of allogenic bone marrow transplantationT cells respond to allogenic recipient antigens
31
what is the billingham criteria
criteria used to diagnose graft vs host disease
32
three requirements to meet the billingham criteria
transplanted tissue has immunologically functioning cells recipient and donor are immunologically differenr recipient is immunocompromised
33
when does acute graft vs host disease happen
within 100 days
34
features of acute graft vs host disease
affects skin, liver, GImaculopapular rashjaundicewatery/bloody diarrhoea nausea vomiting fever
35
features of chronic graft vs host disease
any organ system can be involved scleroderma vitiligo corneal ulcers scleriti dysphagia oral ulcers oral lichenous changes obtructive or restrictive lung disease
36
what drugs would you use in graft vs host disease
immunosuppressants
37
how can hyperacute rejection be triggered in xenotransplantation
humans make antibodies against sugar side chains that they are exposed to in the gut the antibodies can target the organ and activate the complement system