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Pharmacology > Immunosuppresants > Flashcards

Immunosuppresants Flashcards

1
Q

What is being used more in renal transplants? What is being used less?

A

More: thymoglobulin
Less: ATGAM and muromonab

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2
Q

Immunosuppressive regimen given at time of transplant

A

induction

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3
Q

Describe induction

A

relatively intense; can’t be tolerated long term, may include donor specific transfusion or irradiation

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4
Q

Describe maintenance

A

lower potency than induction and rescue, tolerable in chronic use

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5
Q

Describe rescue

A

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

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6
Q

maintenance therapy usually consists of triple drug therapy using agents that work at different levels of the inflammatory cascade. What are the 3 drugs usually used?

A

Calcineurin inhibitor, anti-proliferative, steroid

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7
Q

What 2 antibodies bind parts of the T cell receptor to prevent activation?

A

Anti-CD3 Ab, CTLA-4 Ig

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8
Q

What 2 drugs inhibit T cells at the level of calcineurin?

A

tacrolimus, cyclosporine

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9
Q

What is calcineurin

A

a phosphatase in the T cell that controls nuclear access of NFAT. It allows upregulation of IL-2 (for proliferation)

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10
Q

What Ab target TCR? And what is the result?

A

Anti-CD3 Ab: binds CD3 component of TCR. No activation

CTLA-4 Ig: binds CD28. anergy, apoptosis

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11
Q

What happens when drugs bind calcineurin?

A

IL-2 is not upregulated

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12
Q

What do glucocorticoids do?

A

inhibit transcription of pro-inflammatory genes and diminish the ability of the T-cell to produce and release IL-2

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13
Q

What would Anti-CD25 mAB do?

A

bind to CD25, which is the IL-2 receptor. This inhibits the ability of adjacent T cells to be activated, diminishing clonal expansion

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14
Q

What is mTOR?

A

mTOR is activated after IL-2 activates the T cell. this causes initiation of cell cycle

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15
Q

What happens when mTOR is inhibited?

A

proliferative signal at IL-2 receptor has no consquences

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16
Q

What drugs inhibit mTOR?

A

serolimus, everolimus

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17
Q

What happens when Anti-CD52 mAb binds the CD52 target?

A

identifies cell for lysis via Ab cytotoxicity and complement mediated cytotoxicity

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18
Q

“xi” in a drug means that it is ____.

A

chimeric antibody

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19
Q

Muronomab class? is it lymphocyte depleting? antigenic target?

A

monoclonal, yes, CD3

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20
Q

Basiliximab class? lymphocyte depleting? antigenic target?

A

monoclonal, no, IL-2 receptor (CD25)

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21
Q

Daclizumab class? lymphocyte depleting? target?

A

monoclonal, no, IL-2 receptor (CD25)

22
Q

Rabbit ATG class? depleting lymphocytes? target?

A

polyclonal, yes, multiple

23
Q

Alemtuzumab class? depleting lymphocytes? target?

A

monoclonal, yes, CD52

24
Q

Belatacept class? depleting lymphocytes? target?

A

monoclonal, yes, CD80 (B7)

25
Q

What black box warning is found only with muromonab?

A

angiodema, hypovolemia, pulmonary edema, siezures

26
Q

In what patients is belatacept contraindicated? Why?

A

recipients who are EBV negative. reduce likelihood of PML and PTLD which can ve deadly

27
Q

What is PTLD?

A

B cell proliferation due to therapeutic immunosuppression after transplantation. These pt may develop mono like lesions or poly- clonal/morphic B cell hyperplasia that can give rise to lymphoma.

28
Q

How is calcineurin activated?

A

increased cytoplasmic calcium activates calcineurin via calmodulin

29
Q

What are the calcineurin inhibitors?

A

cyclosporine A and tacrolimus

30
Q

What is the cyclosporine A target? tacrolimus target?

A

cyclophilin; FKBP12

31
Q

What is the major problem with CNI?

A

dose/duration dependent nephrotoxicity

32
Q

What are problems with CNI?

A

renal toxicity, CV, neuro, gingival hyperplasia, hypertrichosis, 2ndary malignancies

33
Q

What do CBPs do?

A

They have intrinsic HAT activity. Acetylation of core histones and consequent increased expression of multiple inflammatory proteins,

34
Q

What do glucocorticoid receptors do?

A

bind corticosteroids, inhibit HAT by recruiting HDAC2, suppression of activated inflammatory genes

35
Q

What are the effects of corticosteroids on the immune system?

A

inhibition of T lymphocyte activity, neutrophilia, eosinopenia, monocytopenia

36
Q

What adverse effects are mediated by the cell-surface steroid receptors?

A

neurologic issues (insomnia, depression, anxiety)

37
Q

What are some general adverse effects to chronic use of corticosteroids?

A

protein metabolism dysfunction, reactivation of TB due to increased susceptibility to infection, hyerporticism, hypercholesterolemia, neurologic effects, skin atrophy and impaired wound healing

38
Q

Sirolimus binds ______ and inhibits _____.

A

FKBP12; 2nd phase of activation

39
Q

Sirolimus is synergistic with _____

A

cyclosporine

40
Q

What is the effect of sirolimus on B cells?

A

prevents differentiation into Ab producing cells, decreased IgG, A, M

41
Q

How does the drug target of sirolimus lead to adverse effects?

A

it is also expressed in non-immune cells

42
Q

adverse effects of sirolimus

A

life-threatening hepatotoxicity, renal function, opportunisitic infections and secondary malignancies, DVT

43
Q

What does mycophenolate mofetil do?

A

inhibits ionsine monophosphate dehydrogenase–> interupt DNA synthesis

44
Q

What cell types are most affected by mycophenolate mofetil?

A

B and T lymphocytes (inhibits T cell proliferation)

45
Q

What are advantages to using mycophenolate mofetil ?

A

blocks 2ndary antibody responses mediated by memory B cells. selective to lymphocyte proliferation, no chromosomal breaks

46
Q

most common side effect of mycophenolate mofetil involves the ____

A

GI tract. Myelosuppression occurs infrequently

47
Q

What is azathioprine?

A

cell cycle disruptor

48
Q

Metabolism of azathioprine leads to what products?

A

6MP (anti-cancer), 6- tioguanin triphosphate which blocks stimulation of T cell–> apoptosis in IL2 stimulated memory T cells

49
Q

Azathioprine is class ____

A

D

50
Q

What is cyclophosphamide?

A

anticancer drug that requires metabolic activation to its pharmacologically active form. It is an alkylating agent that produces cross links

51
Q

What is the dose limiting toxicity of cyclophosphamide?

A

hematologic

52
Q

Does cyclophosphamide affect B or T cells more?

A

B cells….lymphopenic: humoral immunity

Pharmacology (4 decks)

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