Term
| How common are blood transfusions? |
|
Definition
| extremely common (1 in 4 people) |
|
|
Term
| T/F Tranfusing blood is considered a mini-transplant. |
|
Definition
|
|
Term
| How many different antigens can contribute to a blood transfusion reaction? |
|
Definition
|
|
Term
| T/F Erythroblastosis Fetalis can cause heart failure. |
|
Definition
| True, anemia means the heart has to work faster to supply the rest of the tissues with blood |
|
|
Term
|
Definition
| edema in multiple compartments of a fetus. can be caused by heart failure due to erythroblastosis fetalis |
|
|
Term
|
Definition
| when you mix the recipient's serum with the red cells to be transfused to test for an immune response |
|
|
Term
| How many nurses have to check the cross-match and the unit of blood to be transfused prior to initiation? |
|
Definition
|
|
Term
| How long is a patient watched for when they get a transfusion? |
|
Definition
|
|
Term
| What are the symptoms of a transfusion reaction? What are the possible negative outcomes of a transfusion reaction |
|
Definition
mild: hives (allergic reaction), low grade fever
severe: fever, chills, shock (drop in bp)
renal failure and death |
|
|
Term
| How long does it take for each unit of blood to be transfused? |
|
Definition
|
|
Term
| Minor transfusion reactions can be treated with _________. |
|
Definition
|
|
Term
|
Definition
| hematogenous stem cell transplant |
|
|
Term
| What does xenographic mean? |
|
Definition
|
|
Term
| What does allogenic mean? |
|
Definition
|
|
Term
| What are the most common and most likely to take SOT? |
|
Definition
|
|
Term
| What are the top 4 most common transplanted organs? |
|
Definition
| corneas, kidney, liver, then heart (then lung and pancreas) |
|
|
Term
| Which antigens are normally expressed on vascular endothelial cells? |
|
Definition
|
|
Term
| What cauess hyperacute reaction? |
|
Definition
| existing antibodies against ABO and HLA class I vascular antigens cause complement fixation and clotting cascade. Organ dies due to lack of blood supply |
|
|
Term
| How do you prevent a hyperacute reaction? |
|
Definition
| cross matching: serum from recipient mixed with WBCs from donor |
|
|
Term
| Which class of HLA is more important in hyperacute reaction? why? |
|
Definition
Class I
anti HLA class I reacts with both B and T cells
anti HLA class II reacts only with B cells |
|
|
Term
| How do we get anti-HLA antibodies? |
|
Definition
| pregnancy, blood transfusions, previous organ transplant, IVDU, sexual activity |
|
|
Term
| T/F Unless the organ is from an identical twin, you will pretty much always have HLA mismatches in SOT. |
|
Definition
|
|
Term
| What causes acute SOT rejection? |
|
Definition
| donor dendritic cells are activated by inflammation and go to recipient spleen to activate effector T cells that then migrate to graft and destroy it. Mediated via CD8 CTLs |
|
|
Term
| How do you prevent acute SOT rejection? |
|
Definition
| mixed lymphocyte reaction--> donor cell is irradiated and used as antigens recipient peripheral blood cells respond to them. You then measure proliferation of recipient T cells and the ability of recipient T cells to kill |
|
|
Term
| Which HLAs are the most important to match? |
|
Definition
|
|
Term
| How long after transplantation does chronic rejection take place? |
|
Definition
|
|
Term
| What causes chronic rejection of a SOT? |
|
Definition
| antibodies to HLA class I binds to antigens on endothelium. This causes thickening of blood vessels and ischemia. Fc binding to monocytes and macrophages causes infiltration of smooth muscle with macrophages, granulocytes, alloreactive T cells and antibodies. |
|
|
Term
| What causes antibodies to be made in chronic SOT rejection? |
|
Definition
| indirect pathway of allorecognition: donor DC dies and is phagocytosed by recipient DC. HLA molcules are presented to CD4 cell which in turn can get a B cell to make antibodies against HLA |
|
|
Term
| What are the four categories of immune ruppressive drugs used with SOT? |
|
Definition
| 1) corticosteroids 2) cytotoxic drugs 3) microbial products 4) deplete T cells |
|
|
Term
| How does the steroid prednisone get into cells? |
|
Definition
| diffuses across cell membrane then binds to steroid receptor complex releasing Hsp90. This complex then can cross the nuclear membrane |
|
|
Term
| What are the various effects of steroids on immune system functions? |
|
Definition
| decreases inflammation, decreases NOS and thereby NO, decreases prostaglandins and leukotrienes, decreases emigration of leukocytes from vessels, and induces apoptosis in lymphocytes and eosinophils via induction of endonucleases |
|
|
Term
| What is the dose of steroids? |
|
Definition
|
|
Term
| What are side effects of steroids? |
|
Definition
| thin skin, brittle bones, water retention, diabetes, infection |
|
|
Term
|
Definition
| azathioprine: a cytotoxic drug that inhibits synthesis of adenine and guanine which inhibits DNA replication |
|
|
Term
|
Definition
| (mycophenolic acid) a cytotoxic drug that inhibits guanine synthesis |
|
|
Term
|
Definition
| cyclophosphamine: a cytotoxic drug that crosslinks and alkylates DNA |
|
|
Term
|
Definition
| methotrexate: a cytotoxic drug that inhibits dihydrofolate reductase and there by inhibits thymidine synthesis |
|
|
Term
| How does the TCR binding to antigen activate NFAT? |
|
Definition
| signals from TCR raise intracellular Ca which binds to calcineurin a phosphatase that activates NFAT |
|
|
Term
| How does cyclosporin A (CspA) work? |
|
Definition
| Csp A binds to cyclophilins which then binds to calcineurin to prevent NFAT activation |
|
|
Term
| How does tacrolimus work? |
|
Definition
| binds to FKBP which then binds to calcineurin to prevent NFAT activation |
|
|
Term
| What aresome examples of microbial products used in SOT patients? |
|
Definition
|
|
Term
| What are negative side effects of microbial products? |
|
Definition
| significant renal toxicities |
|
|
Term
|
Definition
| made in animals, first does work but then an immune response is created against this agent less effective with subsequent doses |
|
|
Term
| What drug is able to inhibit all T cell functions? |
|
Definition
|
|
Term
|
Definition
| monoclonal antibody against IL-2 receptor- targets only activated T cells |
|
|
Term
| What type of matchign has to be done with a liver transplant? |
|
Definition
| doesn't need HLA matching only ABO |
|
|
Term
| The basis of the main allogeneic reaction in BMT is mediated by: |
|
Definition
| cells from the infused bone marrow attacking the recipient's cells |
|
|
Term
| What are the main categories of diseases treated by BMT? |
|
Definition
| inborn errors of metabolism/genetic diseases and malignant diseases, |
|
|
Term
| Which cells do you isolate when purifying donor's bone marrow from peripheral blood? |
|
Definition
|
|
Term
| What are the negative side effects of "conditioning" a patient to receive a bone marrow transplant? |
|
Definition
| fever, abdominal pain, increased bilirubin |
|
|
Term
| How long does it take for a bone marrow transplant to engraft? What do you do until then? |
|
Definition
| 2-3 weeks (support with RBCs, platelets, antibiotics) |
|
|
Term
|
Definition
| an alloreaction, i.e. when the mature T cells in graft attack the recipient's HLA allotypes that are mismatched |
|
|
Term
|
Definition
| 10-28 days after transplantation |
|
|
Term
|
Definition
| steroids, cyclosporine, methotrexateeither prophylactically or therapeutically |
|
|
Term
| Name the three tissues affected in GVHD. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| T/F HLA matching is more critical for BMT than for SOT. |
|
Definition
|
|
Term
| T/F Absolutely identical HLA prevents GVHD. |
|
Definition
| False, there are still different antigens being presented despite identical HLA |
|
|
Term
| What are the pros/cons of removing T cells from BMT? |
|
Definition
| leads to less engraftment and increased cancer relapse but you reduce GVHD |
|
|
Term
| T/F It is better to have autologous BMT to prevent cancer relapse. |
|
Definition
|
|
