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Immunosuppresive agents Flashcards

1
Q

Calcineurin inhibitors (2)

A

Cyclosporin

Tacrolimus

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2
Q

Nuclear transcription inhibitors (1)

A

prednisone

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3
Q

mTOR inhibitors (1)

A

sirolimus (Rapamune)

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4
Q

Cell Cycle disruptors (4)

A

mycophenolate mofetil (CellCept)
azathioprine (imuran)
Methotrexate (trexall)
Cyclophosphamide (cytoxan)

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5
Q

Overall goal of immunosuppresive therapy

A

reduce T cell population

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6
Q

Critical cytokine released by an activated T cell, for proliferation/clonal expansion

A

IL-2

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7
Q

CD28 on T cell binds to?

A

B7 on APC

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8
Q

3 types of immunosuppressive therapies

A
  1. induction
  2. maintenance
  3. Rescue
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9
Q

Hallmarks of induction therapy

A
  1. at the time of the transplant
  2. relatively intense
  3. prolonged use prihibitively toxic
  4. may include donor specific transfusion or irradiation as drug alternatives
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10
Q

hallmarks of maintenance therapy

A

tolerable in chronic use, but not without side effects

*tends to employ drugs of milder potency that are more tolerable throughout the course of treatment

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11
Q

hallmarks of rescue therapy

A

intense and effective
chronically intolerable
*applied in response to rejection episode

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12
Q

classic maintenance therapy 3-drug combo

A
  1. calcineurin inhibitor (cylosporin)
  2. anti-proliferative (mycophenolate mofetil)
  3. steroids (prednisone)
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13
Q

list the order of graft immunogenicity

A

lungs > heart > kidney > liver > dick

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14
Q

Bind FKB12 protein

A

Tacrolimus

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15
Q

Polyclonal IgG drugs against human T-Lymphocytes

A

Thymoglobulin

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16
Q

Nuclear Transcription inhibitors

A

Prednisone

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17
Q

Binds to FKBP12 (2)

A

Tacrolimus

Sirolimus

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18
Q

Where do most of these immunosuppressive drugs work?

A

T cells: Targets include:

  • cell surface inhibitors
  • calcineurin inhibitors
  • transcription inhibitors
  • mTOR inhibitors
  • cell-cycle inhibitors
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19
Q

Most common drug used in renal transplantation currently

A

thymoglobulin (poly clonal IgG against T cells)

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20
Q

transplantation between two non-identical organisms

A

allograft

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21
Q

second signal required for activation of T cell

A

CD28 must bind to B7 of APC to release autocrine growth factor IL2
IL-2 activated adjacent t cells to udndergo proliferation and differentiation

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22
Q

drugs that target T cell surface would be attempting to inhibit what

A
  1. proliferation of T cells in response to IL2

2. targeting the t cell for death by other immuno components

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23
Q

normal treatment path for induction therapy

A

there is none–> tx is different in each specific case
more similarites between donor/recipient will probably require less potent drugs
more dissimilar–>more potent drugs at higher concentrations

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24
Q

Calcineurin inhibitors MOA

A

a phosphatase that controls NFAT–>This prevents T cell from upregulate IL-2–>inhibits t cell proliferation and differentiation signal

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25
Monoclonal Ab's MOA
block secreted IL from an activated T cell from binding to the CD25 receptor on adjacent T cells *diminishes t cell proliferation
26
glucocorticoids MOA
act in the cell nucleus to INHIBIT REGULATION of transcription of many proinflammatory cytokines...one of which is IL-2 this downregulate t cell proliferation
27
Normally, activation by IL-2 leads to what
activation of mTOR and initiation of cell-cycling | *inhibition of mTOR causes the IL-signal to be irrelevant
28
Where is CD52 expressed
surface of mature lymphocytes
29
Binding of CD52 by mAb's leads to what processes
1. ADCC (NK cell and is FC dependent) FCgammaR3 | 2. compliment mediated cytotoxicity
30
Thymoglobulin MOA
polyclonal IgG against human T lymphocytes--> leads to t lymphocyte depletion via Compliemnt dependent opsonization and lysis
31
mAb's that bind to a ligand (2)
infliximab | omalizumab
32
mAb's that bind to a receptor (2)
natalizumab | daclizumab
33
TGN1412 is what
mAb that is a CD28 superagonist | *binding to CD28 receptor can activate the Tcell without TCR ligation to antigen
34
What does FcRn do
controls transpot or IgG across cell barriers | *fucking Miller keeps calling this the FcRb receptor
35
Does drugs acting on IL-2 receptor or release lead to cell depletion
NO
36
target of muromonab
CD3 (transduction unit for a t cell)
37
target of basiliximab
Cd-25 the IL2 receptor
38
target of daclizumab
IL 2 receptor (cd25)
39
drugs that target B7
belacept
40
drug that targets CD52
alemtuzumab (leads to ADCC and CDC)
41
problems associated with imunosuppressive
I. increased risk for opportunistc infections | 2. secondary malignancies
42
toxicity associated with CNI's
1. renal toxicity (calcification, vasoconstricton etc) 2. mild-moderate HTN from renal vasoconstrcition and increased sympathetic tone 3. secondary malignancies
43
does CNI's affect T cell, Bcells or both
Both INHIBITS IFg and IL-2 production in t cells Il-4 production in B cells
44
Hirsutism or hypertrichosis is associated with
cyclosporine
45
CNI with neurotoxicity
Tac (headache, insomnia, parasthesias and dizziness)
46
Gingival hyperplasia is associated with
cyclosporine
47
two ways in which corticosteroids+GR inhibit gene transcription of inflammatory proteins
1. directly | 2. indirectly by recruitment of HDAC--> leads to diminished transcription bc the DNA is too tightly wound up
48
Blood content reactions (other than inhibition of T cell activity) due to prolonged corticosteroid therapy
1. neutrophilia: increased production and decreased apoptosis 2. eosinopenia: increased apoptosis 3. monocytopenia: decreased production and differentiation
49
Sirolimus MOA
binds to FKB12-->inhibits mTOR-->leading to cell-cycle arrest
50
"first phase of T cell activation"
production of autocrine growth factors like IL-2 that lead to proliferation and differentiation
51
"second phase of T cell activation"
signal transduction and clonal proliferation of T cells (G1 arrest)
52
synergistic drug that you can give with cyclosporin
sirolimus (does not affect CN activity)
53
Sirolimus affect on B cells
prevents differntition into antibody producing cells -->decreased host levels of IgM, IgG and IGa
54
Pt's taking sirolimus must be monitored for
hyperlipidemia. HTN, fever, diarrhea,
55
Blood content reaction to sirolimus
anemia, leukopenia, thrompocytopenia, hypokalemia, azotemia (high nitrogen),increased serum creatinine, defreased GFR
56
pt.s taking sirolimus are at increased risk for?
thromboembolism and DVT's, secondary malignancies, infections
57
organ affected by sirolimus
liver-->hepatotoxicity including fatal necrosis of the liver | kidney as well
58
risk of secondary malignancies is associated with which drug classes
Sirolimus (mTOR inhibitor) CNI's (cyclosporin) mAb's MMF azothiprine (skin cancer with increased UV) *all due to weakend self-monitoring respnses by immunosuppression
59
MMF MOA
inhibits inosine monophosphate dehydrogenase-->interrupts DNA synthesis
60
Cell cycle disruptors affect which cell lines the most?
B and T cells *cannot synthesize GTP sufficiently through the salvage pathway-->therby if DNA becomes a rate limiting reagent T cell proliferation is inhibited
61
drug wtih selective effect on lymphocyte proliferation
MMF
62
drugs without selctive effect on lymphocyte proliferation
methotrexate | asathioprine
63
Adverse effects of MMF
secondary malignancies Gi upset neutropenia (myelosuppression)
64
Azathioprine is converted to
6 mercaptopurine (an anticancer drug in its own right)
65
Metabolism for azothiprine
azo->6mc--> 6 thioguanine triphosphate-->
66
6 thioguanine triphosphate does what
1.Inhibits RAC1 blocks CD28 co stimulation promotes apoptosis especially CD45RO (IL2 stimulated)memory T cells 2. leads to cell cycle arrest by incorporating a decoy DNA precursor (6 thio GTP) in to chain
67
cannot give azothioprine in concert with which drugs
1. allopurinol (increases azothioprine toxicity) | 2. warfarin (decreased INR)
68
cyclophosphamide
requires activation of its pro-drug form
69
greatest effect of cyclophosphamide
suppression of humoral immunity
70
ADE's of cyclophosphamide
``` cardiovascular risks: CHF, toxicity, PE skin cancer azoospermia fibrosis of bladder fibrosis of lungs ```
71
uptake of MTX follows
folate pathway
72
efflux of MTX is via
ABC transporter
73
MTXPG leads to accumulation of
AICAR
74
AICAR inhibits ADA and AMp deaminase and leads to
build up of adenosine (which is anti-inflammatory)
75
where would you find adenosine receptors
APC's
76
Adenosine-AR binding does what in APC's
via cAMP and increased cytosolic calcium - ->dimnished production of ILa anf TNF-a, MIP1a, and NO - ->increase production of IL10 and VEGF
77
S phase specific cell-cycle disruptor
methotrexate dirreah, NV pulmonary fibrosis
78
blood reactions cause by MTX
anemia | leuko, thrompo, neutro, pancytopenias
79
MTX is a teratogen
yes
80
drug with no pGp or cyp34 involvment
MMF
81
substrate + inhibitor for pGp and CYP3a4
cyclosporine
82
substrate for cyp3a4/ no involvement with pGp
tacrolimus
83
substrate for CYP3a4 and substrate + inhibitor for PGP
sirolimus
84
drug used for established rejection pulsed high dosage
muromonab CD3 and Thymoglobulin (anti-t lumphocyte ab's)
85
used for cardiac transplant via impregnanted stents
sirolimus

CMOD (19 decks)

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