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Pharmacology > Immunosuppressants > Flashcards

Immunosuppressants Flashcards

1
Q

Why did allograft transplants become widespread in 1983?

A

cyclosporine - it replaced steriods and azathioprine

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2
Q

What has been a new therapy?

A

ATG

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3
Q

Induction?

A

drugs given at time of transplantation, relatively intense, prolonged use

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4
Q

Maintenance?

A

lower potency, tolerable in chronic use

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5
Q

Rescue?

A

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

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6
Q

What does maintenace therapy usually involved?

A

3 drugs: CNI, anti-proliferative, and steriods

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7
Q

What does an anti-CD3 ab do?

A

prevents T cell activation

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8
Q

What does an antiCD28 ab do?

A

blocks co-stimualtory signal so no activation of T cells so apoptosis

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9
Q

Anti-CD25 ab?

A

prevents adjacent T cell from becoming activated by IL2 so diminished T cell clonal expansion

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10
Q

mTOR inhibition?

A

normally activated by IL2 so w/ inhibition prevents cell cycle

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11
Q

anti CD52 ab?

A

binding of mAb identifies cell for lysis

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12
Q

Calneurin normal roles?

A

APC interacts w/ TCR and increase ctoplasmic Ca –> calmodulin –> calneurin activated. controls nuclear access of NFAT via dephosphorylation to activate IL2 genes

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13
Q

CNI effect?

A

prevention of upregulation of IL2

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14
Q

CDRs w/ Fab reiong can do what?

A

antagonism or signalling

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15
Q

F2 region of mAb can do what?

A

complement fixation or bind Fc receptors for ADCC

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16
Q

What are cell surface drugs?

A

Muronomab, Basiliximab, Daclizumab, Rabbit ATG, Alamtuzumab, Belatacept

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17
Q

What does Muronomab do?

A

mAb, depletes T cells, binds CD3, IV

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18
Q

What does Basiliximab and Daclizumab do?

A

mAb, bind CD25 (IL2 receptor), take via IV

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19
Q

What does Rabbit ATG do?

A

depletes T cell and has many Ags, IV

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20
Q

What does Alamtuzumas do?

A

mAb, depletes T cells, binds CD52

21
Q

What does Belatacept do?

A

mAb, depletes T cells, binds oto CD28

22
Q

What are so regular issues of cell surface drugs?

A

risk of opporunitistic infections so give them prophylactic drugs to prevent infection. Secondary malignicies and cytokine release syndrome

23
Q

What are side effects of Muronomab?

A

angioedmea, hypovolemia, pulmonary edema

24
Q

What is special about Belatacept?

A

don’t give in EBV negative patients

25
Q

What are the two CNI drugs?

take IV/PO

A
  1. cyclosporine + cyclophilin

2. tacrolimus + FKBP12

26
Q

Side effects of CNI drugs?

A
  1. renal toxicity - increased CK, BUN
  2. sometimes difficult to differentiate kidney rejection from drug toxicity
  3. CV, neurotoxicity, ginival hyperplasia, hypertrichosis, HTN
27
Q

How do corticosteriods work?

IV/PO

A

Bind to Gr and translocate to nucleus and bind to CBP, recruit HDAC2 to deacetylate histones to decrease gene expression of inflammatory genes

28
Q

Adverse effects of steriods?

A

chronic use associated w/ a lot of problems
- protein metabolism dysfunction, hypercorticism, hyperglycemia, increased DM, neurologic effects due to cell surface receptor, skin strophy, impairs wound healing

29
Q

What is a mTOR inhibitor?

A

sirolimus

30
Q

how does sirolimus work?

PO only

A

binds FKBP12 and inhibits signal transduction and clonal proliferation of T cells (second phase activation).

  • no effect on calcineurin activity, synergistic w/ cyclosporine
  • drug targets also expressed in nonimmune cells - side effects
  • prevents clonal expansion and B cell differentiation into Ab producing cells
31
Q

side effects of sirolimus?

A

hepatotoxicit, renal toxicity, HTN, anemia, etc

32
Q

What are cell cycle disruptors?

A
  1. micophenolate mofetil
  2. Azathioprine
  3. Cyclophosphamide
  4. Methotrexate
33
Q

How does micophenolate mofetil work?

IV/PO

A

inhibits IMP DH and prevents DNA synthesis and affects S phase

34
Q

What cells are primarily affected by MM?

A

T and B cells - can’t make GMP through salvage pathway

- blocks secondary Ab responses, inhibits T cell proliferation, no chromosomal breaks

35
Q

What is the most common side effect of MM?

A

GI tract

36
Q

How does azathioprine work?

IV/PO

A

metabolic products = 6MP and 6 thioGTP

-6thioGTP blocks co-stimulation of Tcells and promotes apoptosis in IL2 stimulated memory T cells

37
Q

Category D?

A

regards to potential for birth defects

Azathioprine

38
Q

Side effects of azathioprine?

A
  • . skin cancer - avoid UV

- monitor CBC and liver E’s, take pregnancy test before taking drug, dose reduction is impaired TPMT

39
Q

How do cyclophosphamides work?

A

pro-drug that needs to be activated

  • alklyating agent that cross links DNA
  • lymphogenic drug that affects B cells more than T cells
40
Q

Adverse effects of cyclophosphamides?

A

CV and pulmonary issues, pulmonary fibrosis and interstitial pneumonaie

41
Q

Methotrexate basics?

A

DHF reductase inhibitor, effluxed by ABC transporters, and polymorphisms in genes affect efficacy and toxicity, S phase inhibition

42
Q

How does methotrexate work?

A

converted to MTXPG via GGH. MTXPG impedes folate and inhibits de nove pyrimidine synthesis so AICAR builds up. AICAR inhibts ADA and AMP deaminase – adenosine accumulates

43
Q

What does adenosine do?

A

Binds to receptors on monocytes and macrophages and decreases IL12, TNF alpha, MIP1a, and NO and increases secretion of anti-inflammatory IL10 and VEGF

44
Q

Adverse effects of Methotrexate?

A

hematologic effects, high liver enzymes, heptatoxicity, neurologic syndrome, TERATOGEN, acute reactions

45
Q

What are maintenace drugs?

A

steriods, CNI, Azathioprine, mycophenolate, and sirolimus

46
Q

What are induction drugs?

A

Basiliximab, daclizumbas, muromonab, ATG (all cell surface targets)

47
Q

Drugs and pregnancy and lactation?

A

Cat D and X - never give
Cat C and B - give w/ cation
-don’t give most of the cells during breastfeeding

48
Q

What 2 drugs causes cytokine release?

A
  1. alemtuzumab
  2. muromonab
  3. TGN1412

Pharmacology (5 decks)

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