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PHRM 865 > Exam 6: Transplant > Flashcards

Exam 6: Transplant Flashcards

1
Q

What is allograft rejection

A

immune response causing inflammation and direct tissue destruction

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2
Q

what is ACR

A

infiltration of the allograft by lymphocytes and other inflammatory cells

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3
Q

what is AMR

A
  1. circulating donor-specific antibodies

2. immunological evidence of an antibody-mediated process

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4
Q

hyperacute rejection

A

within minutes to hours after transplant

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5
Q

what mediates hyperacute rejection

A

preformed circulating antibodies

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6
Q

acute rejection

A

within days to months after transplant

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7
Q

what mediates acute rejection

A

host t-lymphocytes

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8
Q

chronic rejection

A

over months to years after transplans

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9
Q

what mediates chronic rejection

A

both cell-mediated and humoral processes

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10
Q

A blood type antigens

A

A antigens

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11
Q

A blood type antibodies

A

antibodies against B

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12
Q

B blood type antigens

A

B antigens

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13
Q

B blood type antibodies

A

antibodies against A

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14
Q

AB blood type antigens

A

A and B antigens

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15
Q

AB blood type antibodies

A

No antibodies AKA universal recipient

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16
Q

O blood type antigens

A

No antigens AKA universal donor

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17
Q

O blood type antibodies

A

Antibodies against A and B

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18
Q

ABO mismatch

A

Absolute CI for all deceased donor transplants

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19
Q

How does the immune system determine self vs non-self

A

HLA

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20
Q

HLA matching and outcomes

A

HLA matching= better outcomes

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21
Q

HLA antibodies

A

Do not occur naturally and are formed in response to non-self HLA exposure

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22
Q

Why is DSA testing used

A

To estimate risk of rejection and indicate failure of immunosuppression

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23
Q

Goals of immunosuppressive therapy

A
  1. Balance therapy in terms of graft and patient survival
  2. combination therapy
  3. individualized therapy
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24
Q

induction immunosuppressive agents

A
  1. thymoglobulin
  2. atgam
  3. campath
  4. simulect
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25
which induction immunosuppressive agents are polyclonal antibodies
1. thymoglobulin | 2. atgam
26
which induction immunosuppressive agents are monoclonal antibodies
campath
27
which induction immunosuppressive agents are IL-2 receptor antagonists
simulect
28
antithymocyte globulin mechanism
reduces the number of cirulating t-lymphocytes and ultimately affects cell-mediated and humoral immunity- leading to lymphocyte depletion
29
antithymocyte globulin duration
duration depends on indication and patient tolerance
30
antithymocyte globulin AE
leukopenia, thrombocytopenia fever, chills tachycardia pruritis
31
antithymocyte globulin monitoring parameters
WBC, ALC, platelts
32
campath mechanism
- CD52 cell surface glycoprotein located on T and B lymphocytes, NK cells, and less densely on monocytes and macrophages - antibody dependent cellular cytotoxicity - profound depletion of T cells and to a lesser degree B cells and monocytes
33
campath (alemtuzumab) AE
profound neutropenia, which is why it is off-labeled use
34
simulect (basiliximab) mechanism
competitively inhibits IL-2 mediated activation of lymphocytes
35
simulect AE
minimal
36
DOC for lymphocyte depleting therapy, especially for patients with high immunologic risk
thymoglobulin, alemtuzumab
37
DOC for non-lymphocyte depleting therapy: history of malignancy, high infection risk, immunocompromised, advanced aged
basiliximab
38
Calcineurin inhibitors
cyclosporin | tacrolimus
39
anitmetabolites
azathioprine | mycophenolate
40
m-TOR inhibitor
sirolimus | everolimus
41
corticosteroid
methylprednisolone | prednisone
42
selective t-cell costimulation blocker
belatacept
43
calcineurin inhibitor MOA
inducing immunosuppression by inhibiting signal-1 of t-cell activation
44
tacrolimus formulations
1. prograf 2. astagraf 3. envarsus
45
prograf conversion
1 mg PO= 0.5 mg SL= 0.2mg IV
46
envarsus conversion
1mg prograf= 0.8 mg envarsus
47
Tacrolimus target trough
5-15 ng/ml
48
cyclosporine formulations | are they interchangeable?
non-modified modified NOT Interchangeable
49
which cyclosporine formulation has improved bioavailability
modified
50
cyclosporine target torugh
100-400 ng/ml
51
which drugs raise calcinuerin inhibitor levels
``` verapamil diltiazem azoles erythromycin clarithromycin ritonavir grapefruit ```
52
which drugs can decrease calcineurin inhibitor levels
rifampin/rifabutin phenytoin/phenobarbital carbamazepine st. johns wort
53
cyclosporine AE
hypercholesterolemia hypertriglyceridemia hypertension nephrotoxicity
54
tacrolimus AE
``` neurotoxicity diabetes+hyperglycemia nephrotoxicity alopecia Gi ```
55
How does CNI PK change in liver dysfunction
half life increased
56
how CNI PK change in renal dysfunction
no change
57
Azathioprine MOA
incorporated into nucleic acids to inhibit RNA and DNA synthesis to inhibit immune cell proliferation
58
Azathioprine drug interactions
Allopurinol! Due to affecting xanthine oxidase Must reduce AZA to one-quarter of the original dose but likely best to avoid all together
59
Mycophenolic acid MOA
inhibits the de novo pathway of purine synthesis, which limits progression of activated T and B cells
60
mycophenolic acid AE
GI hematologic and lymphatic Pregnancy category D
61
Mycophenolic acid types
mofetil (IR) | sodium (EC DR)
62
mycophenolic acid interchange
therapeutically equivalent and interchangable mofetil 250mg = sodium 180mg
63
mTOR inhibitors MOA
inhibits signal-3 of t-cell activation and ultimately t-cell proliferation
64
what drugs are mTOR inhibitors
sirolimus | everolimus
65
sirolimus target trough
4-12 ng/ml
66
everolimus target trough
goal 12 hour trough is 3-8
67
corticosteroid equivalent dosing
20mg H= 5 mg P= 4 mg M= 0.75mg D
68
Belatacept use
kidney transplant
69
belatacept MOA
Blocks the CD28 mediated costimulation of T lymphocytes by binding to CD80 and CD86 on antigen-presenting cells to be a selective t-cell costimulation blocker

PHRM 865 (59 decks)

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