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Pharmacology > Immunosupressents > Flashcards

Immunosupressents Flashcards

1
Q

What are the poly clonal IgG against human T-lymphocytes?

A

Anthihymocyte globulin

Atgam; thymoglobulin

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2
Q

What are the co-stimulatory molecutles?

A

muromonab-CD3

Belatacept

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3
Q

What are the CD-25 inhibitors?

A

Daclizumab

Basiliximab

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4
Q

What are the CD52 inhibitors?

A

Alemtuzumab

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5
Q

What are the calcineurin inhibitors?

A

Cyclosporine
Tacrolimus
Pimecrolimus

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6
Q

What are the nuclear transcription inhibitors?

A

Methylprednisolone

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7
Q

What are teh mTOR inhibitors?

A

Sirolimus

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8
Q

What are teh cell cycle disruptors?

A

Mycophenolate mofetil
Azathioprine
MEthotr4exate
Cyclophosphamide

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9
Q

What is the point of cancer chemotherapy outside of anti-cancer?

A

controlling proliferation of T cell populations

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10
Q

release of what cytokine leads to T cell proliferation and clonal expansion?

A

IL-2

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11
Q

What is induction?

A

at time of transplantation; relatively intense; prolonged use of prohibitively toxic; may include donor specific transfusion or irradication as drug alternative

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12
Q

What is maintenance?

A

lower potency; tolerable in choric use; not with out side effects
ususally have tripple durg therapy
may recive only 1-2 drugs
can have long term toxicity

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13
Q

what are the three drugs uszed in maintenacne?

A

Calcineurin inhibitor
anti-proliferative
steroid

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14
Q

What is rescue?

A

intense, effective

chrinically intolerable; applied in response to rejeciton episode

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15
Q

What are the 9 ways to block T cell activation?

A

1) block CD3 tcell receptor
2) surface receptor target; CD28-CD80/86
3) inhibiting calcineurin– cant activate NFAT (nuclear factor of activated transcription)
4) block transcriptional regulation of pro-inflammatory genes
5) block CD25 with monoclonal antibodies
6) inhibiting mTOR
7) inhibit cell ceycle (2 ways)
- a) CD 52 recetpor– ADCC tagging
- b)target the Tcel lvia polyclonal IgG against human T-lymphocytes

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16
Q

what are the ways that monocolonal antibodies can act on a t-Cell?

A

antagonism
signalling
CDC
ADCC

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17
Q

What are the types of monoclonal antibodies?

A

murine
chimeric
humanized
human

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18
Q

What drugs act via antagonism?

A

Infliximab (ligand)
omalizumab (ligand)
natalizumab (receptor)
davlizumab (receptor)

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19
Q

What drug acts via signalling?

A

TGN1412 (acts as a CD28 superagonist)

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20
Q

What drug acts via CDC and ADCC?

A

Alemtuzumab

rituzximab

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21
Q

What are these patients recieving these drugs at risk for>

A

opportunistic infections and secondary maligancies, lymphoma and skin cancer

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22
Q

What are calcineurin inhibitors?

A

act by blocking calcineuring from activating NFAT, and not allowing it to enter the nucleus
which is the first phase of T-cell activation
functionally associated with ion channel regulation, receptor signalling, cell secretions etc
-each bind to specific proteins that aid in calcineurin fucntioning.
cyclosporine A - cyclophilin
tracrolimus to FK binding protein 12

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23
Q

Which of the calcineurins inhibitors is most potent?

A

tacrolimus compared to cyclosporine

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24
Q

what toxicity is related to calcinurine inhibitors?

A 
Renal Toxicity
doe/dependent nephrotoxicity
HTN (cardiovascular)
Neurotoxicity (Tacrolimus)
gingival hyperplasia (cyclosporine)
Secondary malignacies (lymphomas and skin cancer)
25
Q

What is the mechanism of action for Cortiosteroids?

A

bind to the GR (glucocorticoid receptors) and the receptor-lingand complexes translocate to the nucleus and bind to coactivators to inhibit HAT in two ways.

26
Q

What are the two ways of inhibiting HAT?

A

1) recruiting HDAC2 - reverses the histone acetylation (suppresion of inflammatory genes)
2) directl inhibition

27
Q

What do the corticosteroids produce?

A

Neutrophila (^porduction; Vapoptosis)
Esoinopenia (^apoptosis)
monocytopenia (^apoptosis)

28
Q

What are the adverse effects of corticosteroids?

A

-one of hte most potent classes of anti-inflammatory and immunosuppressive drugs
-protein metabolism dysfuntion (myopathy, impaired wound healing etc)
-increased susceptibility to infection
-hypercorticism (cushing’s sundrome)
-menstrual irregularity
-hyperglycemia
-hypercholesterolemia
etherosclerosis
fat embolism, thrombosis, thromboembolism, phlebittis
neurologic effects - insomnia, depression, anxiety
skin atrophy-

29
Q

What is the mechanism of mTOR inhibitors?

A

bidns to FKBP12 (like tacrolimus) but inhibits activation of mammalian target of rapamycin (mTOR)

  • inhibits second phase of activation: signal transduction adn clonal proliferation of T-cells
  • prevents B-cell differentiation into antibody-producting cells, decreasing the levels of IgM, IgG, and IgA
30
Q

What are mTOR inhibitors synergistic with?

A

cyclosporine (in vivo and in vitro)

31
Q

What is a mTOR inhibitor and what are its adverse effects?

A

Sirolimus
-dose-related hyperlipidemia
thrombophlebitis, thromboembolism (pulomary DVT)
anemia, leukopenia, thrombocytopenia, hypokalemia, fecer and diarrhea
HYP
hepatotoxicity (fatal!!!!!)
opportunistic infections and secondary malignancies

32
Q

What are the cell cycle disruptors?

A

micophenolate mofetil
azathioprine
cyclophosphamide
methotrexate

33
Q

What is the mechanism of micophenolate mofetil?

A

a cell-cycle disruptor
blocks IMD and interupts DNA synthesase
affects primarity T adn B lymphocytes (cant synthesize GMP via salvage pahtway)

34
Q

What are the side effects of micophenolate mofetil?

A

constipation, diarrhea, dyspepsia and nausea/vomiting
myelosuppression (neutropenia)- infrequently
infections and tumors

35
Q

What are the advantages of mycophenolate mofetil?

A
  • blocks the secondary antibody responses mediated by memory B cells
  • selective effect on lymphocyte proliferation, unlike azathioprine or methotrexate
  • no chromosomal breaks
36
Q

What is the mechanism of azathioprine?

A

extensive metabolic conversion: 6-mercaptopurine (anti-cancer drug), 6 thioguanine
-a purine antagoinst; 6thio-IMP converted to 6-thi-GMP and is incorporated into DNA and stops cell cycle

37
Q

What is the mechanism of 6 thoguanine triphosphate?

A

blocks co. stimulation of T cells to promote apoptosis in IL-2 stimulated memory T cells.

  • inhibits RAC1
  • blocks CD28 co. stimulation
38
Q

What category is azathioprine in?

A

D

39
Q

What are the adverse effects of azathioprine?

A

-decreased warfarin leves (V INR values)
TPMT inhibiotn by 5-aminosalicylates (^ azathioprine toxicity)
-mild GI upset
^ risk of skin cancer, esp with UV exposure

40
Q

What enzyme test should be done on patients who are going to take azathioprine and what should be canged due to the results?

A

TPMT enzyme levels check; with deficent levels, azathiprine dose should be reduced

41
Q

What is the cyclophosphamide mechanism?

A

must be metabolically actiated
is an alkylating agent and produces DNA cross-linds (intrastrand adn interstrand)
-effects B cells more thand T cells

42
Q

What are the adcerse effects of cyclophosphamide?

A

dose limiting toxicity of— Hematologic
hemorrhagi cysits due to acrolein (metabolic by product)
-CV adn pulmonary issues
-long term use– fertility issues

43
Q

What is the mechanism of methotrexate?

A
  • a diyhydrofolate reductase inhibitor
  • polyglutamated in cytoplasm to increase retention
  • cause accumulation of AICAR
44
Q

What is the purpose of AICAR accumulation?

A

inhibits ADA and AMP deaminase– adenosine accumulation

45
Q

What are the effects of adenosine accumulation?

A

anti-inflammatory via AR on cells like macrophages to V IL-12, TNF-alpha, MIP-1a, and nitric oxide,
also ^ IL-10 and VEGF (both anti-inflamnatory)
-also leads to decreased Th1 and Th2 developemnt due to IL-12 release by DCs

46
Q

What does methotrexate inhibit?

A

s-phase specific inhition

-tissues with high rate of cellular division (most snesitive)

47
Q

What are the toxic effects of MEthotrexate? and is premedication requried?

A
  • darrhea, N/V - premedication may be necessary (5HT3 antagonist and corticosteroid)
  • Hematologic Toxicity
  • Elevated hepatic enxmes
  • Hepatotoxisity
  • infections and neurologic syndrome
  • a teratogen
48
Q 
Corticosteroids
Drugs:
Mechanism
Route of admistration 
Route of Excreation 
Useage (maintaince or indcution)
establish organ rejection..?
A

1) predinsone; methylprednisolone
2) antiinflammatory; inhibition of IL-2 production
3) IV/PO
4) Hepatic
5) Maintenance immunotherapy
6) Established rejection pulsed high-dose

49
Q 
Calcineurin inhibitors
Drugs:
Mechanism
Route of admistration 
Route of Excreation 
Useage (maintaince or indcution)
establish organ rejection..?
A

1) Cyclosporine; Tacrolimus
2) IL-2 bloackade; ihibitionof T-lymphocyte activation adn proliferation
3) IV/PO variable
4) Hepatic (CYP)
5) Maintenance immunotherapy
6) Ineffective

50
Q 
IL-2 Recetptor antagonist
Drugs:
Mechanism
Route of admistration 
Route of Excreation 
Useage (maintaince or indcution)
establish organ rejection..?
A

1) Basiliximab; Daclizumab
2) bloackade IL-2 receptor
3) IV
4) -
5) Induction agents for > 70% of de novo transplantation
6) Ineffective

51
Q 
Anti-lymphocyte antibodies
Drugs:
Mechanism
Route of admistration 
Route of Excreation 
Useage (maintaince or indcution)
establish organ rejection..?
A

1) Muromonab; Thymoglobulin
2) Anti-CD3 antibody; Anti-thymocyte Globuline– Deplete CD3 and Cells
3) IV
4) -
5) Induction agents for > 70% of de novo transplantation
6) Established rejection

52
Q 
Cell cycle and mTOR inhibitors
Drugs:
Mechanism
Route of admistration 
Route of Excreation 
Useage (maintaince or indcution)
establish organ rejection..?
A

1) Azathioprine; mycopheonolate; sirolimus
2) purine antagonist; purine biosynthesis inhibiotr; inhibition of IL-2 driven cell-cycle progression
3) IV/ PO; sirolimus- PO only
4) A & M Renal; S Hepatic (CYP)
5) maintenacne immunotherapy
6) ineffective

53
Q

what drugs are contranindicated in breastfeeding?

A 
cyclosporine
tacrolimu
azathioprine
methotrexate
cyclophosphamide
54
Q

What categorey is MTX? and what are the other cell cycle disruptors?

A

cat X; cat D

55
Q

What are the three monoclonal antibodies that casue cyokine relase upon infusion?

A

alemtuzumab, muromonabe-CD3, and TGN1412

56
Q

What does alemtuzumab recognize?

A

CD52 on T cells, efficient complement- dependent lysis of lymphocytes

57
Q

What does Muromonabe target?

A

CD3 on Tcell receptor comples

58
Q

What does TGN1412 targert?

A

CD28

59
Q

What is TGN1412

A

a superagopnist, that co-stimulates activation of naive T cells

Pharmacology (3 decks)

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