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Immunosuppressants Flashcards

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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?

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A

mAb, depletes T cells, binds CD52

21
Q

What does Belatacept do?

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A

mAb, depletes T cells, binds oto CD28

22
Q

What are so regular issues of cell surface drugs?

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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?

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A

angioedmea, hypovolemia, pulmonary edema

24
Q

What is special about Belatacept?

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A

don’t give in EBV negative patients

25
What are the two CNI drugs? | take IV/PO
1. cyclosporine + cyclophilin | 2. tacrolimus + FKBP12
26
Side effects of CNI drugs?
1. renal toxicity - increased CK, BUN 2. sometimes difficult to differentiate kidney rejection from drug toxicity 3. CV, neurotoxicity, ginival hyperplasia, hypertrichosis, HTN
27
How do corticosteriods work? | IV/PO
Bind to Gr and translocate to nucleus and bind to CBP, recruit HDAC2 to deacetylate histones to decrease gene expression of inflammatory genes
28
Adverse effects of steriods?
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
What is a mTOR inhibitor?
sirolimus
30
how does sirolimus work? | PO only
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
side effects of sirolimus?
hepatotoxicit, renal toxicity, HTN, anemia, etc
32
What are cell cycle disruptors?
1. micophenolate mofetil 2. Azathioprine 3. Cyclophosphamide 4. Methotrexate
33
How does micophenolate mofetil work? | IV/PO
inhibits IMP DH and prevents DNA synthesis and affects S phase
34
What cells are primarily affected by MM?
T and B cells - can't make GMP through salvage pathway | - blocks secondary Ab responses, inhibits T cell proliferation, no chromosomal breaks
35
What is the most common side effect of MM?
GI tract
36
How does azathioprine work? | IV/PO
metabolic products = 6MP and 6 thioGTP | -6thioGTP blocks co-stimulation of Tcells and promotes apoptosis in IL2 stimulated memory T cells
37
Category D?
regards to potential for birth defects | Azathioprine
38
Side effects of azathioprine?
- . skin cancer - avoid UV | - monitor CBC and liver E's, take pregnancy test before taking drug, dose reduction is impaired TPMT
39
How do cyclophosphamides work?
pro-drug that needs to be activated - alklyating agent that cross links DNA - lymphogenic drug that affects B cells more than T cells
40
Adverse effects of cyclophosphamides?
CV and pulmonary issues, pulmonary fibrosis and interstitial pneumonaie
41
Methotrexate basics?
DHF reductase inhibitor, effluxed by ABC transporters, and polymorphisms in genes affect efficacy and toxicity, S phase inhibition
42
How does methotrexate work?
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
What does adenosine do?
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
Adverse effects of Methotrexate?
hematologic effects, high liver enzymes, heptatoxicity, neurologic syndrome, TERATOGEN, acute reactions
45
What are maintenace drugs?
steriods, CNI, Azathioprine, mycophenolate, and sirolimus
46
What are induction drugs?
Basiliximab, daclizumbas, muromonab, ATG (all cell surface targets)
47
Drugs and pregnancy and lactation?
Cat D and X - never give Cat C and B - give w/ cation -don't give most of the cells during breastfeeding
48
What 2 drugs causes cytokine release?
1. alemtuzumab 2. muromonab 3. TGN1412

Pharmacology (5 decks)

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