Immunology 2: Transplantation Flashcards

1
Q

When do you transplant organs? 2 categories? how many a year?

A

When they organs have failed
either life saving-liver heart, small bowel
Life enhancing-kidneys (less dyalisis)
Pancreas-in selecte case better than insulin injection
QOL-cornea, reconstructive surgery

5000 a year-kidneys, pancrease, heart, liver, intestine-but manage 50000

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2
Q

Why do organs fail?

A

tons-and each organs have specific diseases and reasons-
liver-infection, drugs, alcohol
Kidneys-diabetic and other

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3
Q

What is an allograft? Autograft? Iso? Xeno? what is the main used one

A

allo-same species
auto-same person-if could grow organs
iso-same genetic make up
xeno-different specie-heart vavles from cow/pig, skin

mainly use allografts-solid organs, cells (BM, pancreas), temporary-blood, cornea, framwork (bone), composite-face, hand. Uterus

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4
Q

What are the 2 sources of organ?

A

Decreased donor-2 types-after brain death (DBD) and after circulatoiry death (CBD) (usually seen as less efficient)
Living donor-bone marrow, kidney, liver –better match if related

be sure to establish neurological death

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5
Q

What are things that must be true for an organ to be donated in deceased donor?

A

be sure of death-neurological
exclude-viral inferction, malignancy, drug abuse, disease
once done-organ removed and rapidely cooled (done by NHS blood and transplant

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6
Q

What is the difference between transplant selection and allocation?

A

selection-done by local team-decide if you have what it takes
allocation-how they are given once they become available
-> need to be fair and efficient-waiting for long, hard to match, best match?, surival efficiency
patient seprated in tiers-peads or adult, sensitised or not

main elements: Waiting time, HLA mathc, donor recipient age difference
gap has been going better-but stil 6000 people waiting

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7
Q

How have organ transplant acitivity been increased?

A

Deceased donation-more marginal cases taken
living- transplant across tissue compatibility, exchnage programs

future-xeno? Stem cell?

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8
Q

What are the 2 main reason for immune system rejects of organs?

A

HLA and ABO groups

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9
Q

What is the ABO groups and why does it matter in transplantation? whats the solution?

A

carbohydrate chains on RBC but also on endothelial cels
naturally occuring against anti A/B (opposite of what you have-AB-has none, O has both

group-A-has A chain, B-B chain, AB-both, O-none

endothelial chains are the one that are bad in transplant-inflammation of vessels

modern solution-remove the AB’s with plasma exchange-works veyr well

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10
Q

what are HLA molecules?

A

Human leukocyte antigens, or MHC
vary a lot between people
important in defence infection and neoplasia (presenting antigen to adaptive immune system)
Remember MHC and stuff

transplanted cells have their own HLA (1 or 2)-and they are seen as foreign AG by APC-uptaken and shown to Tcells like bacterial Ag on their own HLA

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11
Q

What are the different forms of HLA types?

A

Class I-A,B,C -1 a chain, 1 b microglobulin
Class II-Dr, DQ, DP-1a and 1b (symetrical)

each are very polymorphic

A, B , DR are usually the ones seen in transplant issues

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12
Q

How are mistatches calculated and notes?

A

well have 2 alleles in each HLA molecule-
compares A-can have 2 mismatches-noted as 0/1/2
Compare B-same
DR-again
potentially 6 mismathc there
MM: 1,2,0 (if 1 miss on A, 2 on B and 0 DR)

Other HLA are becoming more important as discoveries happen

siblings match better but not alawys perfect

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13
Q

What are the types of organ rejection?

A

Can be classified either by what the reaction is (T cell, antibody, mixed) or when it happens (hyperacute, acute, chronic)

More common are acute and chronic because careful on transplant

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14
Q

what are the features of T cell rejection?

A

Ag from donor shedded and taken by host APC-activate T cells-> home to the foreign Ag (teher, roll, arrest, diapesis)–then attack everything
interitial infiltraion, rupture or tubular BM, tubulitis
also recruit CD8 T cells, macrophages, etc-with cytokines-amplify

on biopsy-dark cells (immune) in the interstitium-usually T cells-tubulitis

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15
Q

what are the features of AB mediated rejection?

A

AB against ABO or HLA (rarely to other things)
either pre transplant (like Anti ABO), or post transplantation-de novo
pre-transplant are worse-faster bigger response

AB bind donor HLA antigen-activate complement, increase immune cell adhesion/recruitment to area-increase inflammation => necrosis and innlam
see immune cells in tubules-but mainly INTRAVASCULAR-unlike t cell medaited-can also see complement activation

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16
Q

How do you monitor rejection in organs? prevent it?

A

each organ special-kidneys-check GFR, liver-check LE
heart-not visible-need to take biosies

always treated on immunosupressants-pre transplant start-then from tranplant-base line immunosupressantm then if needed—and monitor whuch type (T cell/Bcell) and how bad the reaction is–change drug or dose to adapt
mainly target the APC-activated pathways-azothiaprine, anti CD3,-often downstream
or just anti T cells-depelte them

For B-cell-remove B cell (reitximab), or remove AB-reduce production. Or reduce complement activation

17
Q

What are, other than rejection, problems transplant patients get?

A

increase risk of conventional and commensals (even fungal) infection because of immunosupressant–can cause graft loss

also post transplant malignancy-skin cancer, epstein barr, other -slight increase because of immunosupressants again
r

risk of surgery