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Pharmacology for Amjad > EXAM #4: IMMUNOSUPPRESSANTS > Flashcards

EXAM #4: IMMUNOSUPPRESSANTS Flashcards

1
Q

What types of grafts will NOT provoke an immune response?

A

1) Autografts (self)

2) Isografts (identical twins)

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2
Q

What is an allograft?

A

Transplant between two non genetically identical individuals

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3
Q

What are the two hallmark Calicneurin inhibitors used as immunosuppressants?

A

Cyclosporine

Tarcolimus

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4
Q

What are the anti-proliferative/ anti-metabolic immunosuppressants?

A

Azathioprine
Mycophenolate mofetil
Sirolimus

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5
Q

What are the “biological” immunosuppressants?

A

Antithymocyte globulin
Muromonab-CD3
Anti-TNF-a

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6
Q

What are the two adverse effects associated with immunsuppressants as a drug class?

A

1) Infection

2) Malignancy

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7
Q

What are the “genomic” effects of glucocorticoids i.e. MOA related to the genome?

A

1) Bind cytosolic receptor
2) Translocate to nucleus
3) Alter gene expression to decrease pro-inflammatory cytokines

Can also alter transcription factors to decrease production of proinflammatory cytokines

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8
Q

What are the “non-genomic” effects of glucocorticoids?

A

1) Alter signaling pathways

2) Insertion into cell membrane to alter ion transport

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9
Q

What are the effects of glucocorticoid administration?

A

1) Decreased peripheral lymphocytes
2) Decreased pro-inflammatory cytokines
3) Inhibition IL-2
4) Reduced neutrophil chemotaxis

*Little effect on humoral immunity

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10
Q

What are the pro-inflammatory cytokines?

A

IL-1
IL-6
TNF-a
IFN-gamma

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11
Q

What is the function of IL-2?

A

T-cell proliferation

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12
Q

What are the indications for glucocorticoid administration?

A

1) Prevent transplant rejection
2) GVHD
3) Autoimmune disease
4) Prevention of initial “cytokine storm” with biological immunosuppressants

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13
Q

What adverse effects are seen with glucocorticoids?

A

1) Growth retardation
2) Poor wound healing
3) HTN
4) AVN
5) Cataracts
6) Hyperglycemia
7) Adrenal crisis upon discontinuation

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14
Q

What is low dose glucocorticoid therapy?

A

Less than 7.5 mg prednisone/ predisoe equivalent per day

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15
Q

What is medium dose glucocorticoid therapy?

A

7.5mg- 30mg prednisone/ prednisoe equivalent per day

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16
Q

What is high dose glucocorticoid therapy?

A

30-100mg prednisone/ prednisoe equivalent per day

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17
Q

What is very high dose glucocorticoid therapy?

A

Greater than 100mg prednisone/ prednisoe equivalent per day

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18
Q

What is pulse glucocorticoid therapy?

A

Greater than 250mg for a day, or a few days prednisone/ prednisoe equivalent per day

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19
Q

What class of drug is Cyclosporine?

A

Calcineurin inhibitor

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20
Q

What immunity is inhibited by Cyclosporine?

A

T-cell mediated immunity especially involved in:

1) Transplant rejection (kidney)
2) Autoimmunity

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21
Q

What is the MOA of cyclosporine?

A

1) Complexes with CYCLOPHILIN in cytoplasm
2) Complex with CALCINEURIN
3) Complex prevents dephosphorylation of NFAT
4) NFAT cannot translocate to nucleus
5) NO IL-2, the T-cell growth factor

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22
Q

What are the clinical indications for Cyclosporine?

A

1) Prophylaxis for transplantation

2) GVHD

23
Q

What is the major toxicity associated with Cyclosporine?

A

Nephrotoxicity
Neurtoxicity
Skin cancer
Hirsutism

24
Q

What is the interaction between Grapefruit and Cyclosporine?

A
  • Grapefruit juice inhibits cytochrome p450

- Increases blood concentrations of Cyclosporine increasing toxicity

25
Q

What type of drug is Tacrolimus?

A

Calcineurin inhibitor (like Cyclosporin)

26
Q

What is the MOA of Tacrolimus?

A

1) Complexes with CYCLOPHILIN in cytoplasm
2) Complex with CALCINEURIN
3) Complex prevents dephosphorylation of NFAT (transcription factor in nucleus)
4) NFAT cannot translocate to nucleus
5) NO IL-2, the T-cell growth factor

27
Q

How does Tacrolimus differ from Cyclosporine?

A

Easier to measure blood levels with Tacrolimus

28
Q

What is the major clinical indication for Tacrolimus?

A

Prophylaxis for transplant rejection

29
Q

What class of drug is Azathioprine?

A

Purine antimetabolite

30
Q

What is the MOA of Azathioprine?

A

1) Metabolized to 6-mercaptopurine
2) 6-MP is metabolized further
3) Metabolites incorporate into DNA and block de novo purine synthesis

31
Q

What is unique about lymphocytes that makes Azathioprine specific?

A

Lymphocytes don’t have a pruine salvage pathway

*Thus, blocking de novo kills lymphocytes

32
Q

What are the clinical indications for Azathioprine?

A

1) Prevent transplant rejection
2) Severe RA
3) Glucocorticoid resistant autoimmune disease

33
Q

What are the adverse effects associated with Azathioprine?

A

1) Myelosuppression–monitor with CBC

2) Hepatotoxicity–monitor with liver enzymes

34
Q

What type of drug is Mcyphenolate Mofetil?

A

Purine antimetabolite

35
Q

What is the MOA of Mycophenolate Mofetil?

A

1) Prodrug
2) Metabolized to MPA (active)
3) Inhibits IMP required for de novo synthesis of pruine

*Results in killing lymphocytes

36
Q

What are the clinical indications for Mycophenolate Mofetil?

A

1) Prophylaxis for transplant rejection
2) SLE

*Commonly given with glucocortiocoid and calcineurin inhibitor

37
Q

What adverse effects of Mycophenolate Mofetil?

A

1) Myelosuppression
2) GI upset
3) CMV infections
4) TERATOGENIC

38
Q

What class of drug is Sirolimus?

A

Antimetabolite

39
Q

What is the MOA of Sirolimus?

A

mTOR inhibitor

40
Q

What are the clinical indications for Sirolimus?

A

1) Transplant prophylaxis

2) Renal transplant that can’t tolerate nephrotoxicity of other drugs

41
Q

What class of drug is Antithymocyte Globulin?

A

Biological

42
Q

What is the MOA of Antithymocyte Globulin?

A

1) Binds T-cell CD markers
2) Depletes circulating T-cells via:
- Complement activation
- Inhibition of T-cell activation

43
Q

What are the clinical indications for Antithymocyte Globulin?

A

1) Induction immunosuppression

2) Treatment of acute transplant rejection

44
Q

What adverse reaction is highly associated with Antithymocyte Globulin?

A

1) Cytokine storm (treated with glucocorticoids)

2) Serum sickness

45
Q

What class of drug is Muromonab-CD3?

A

Biological

46
Q

What is the MOA of Muromonab-CD3?

A

Anti-CD3 antibody (T-cell CD marker)

1) Initiates complement mediated lyisis
2) Prevention T-cell activation

47
Q

What are the clinical indications for Muromonab-CD3?

A

Reverse glucocorticoid-resistant organ transplant

48
Q

What is a drawback to Muromonab-CD3?

A

Mouse-antibody; body will generate antibodies generated against Muromonab-CD3

Can only be used once

49
Q

What complications are associated with Muromonab-CD3?

A

1) Cytokine storm with administration

2) Potentially fatal adverse reactions including anaphylaxis

50
Q

What are the three anti-TNF-a biologicals?

A

1) Infliximab
2) Adalimumab
3) Etanercept

51
Q

What is Infliximab?

A

Part mouse and part human anti-TNF-a antibody

52
Q

What is Adalimumab?

A

Recombinant IgG1 anti-TNF-a antibody

53
Q

What is Entercept?

A

TNF-a receptor fused to Fc IgG1

54
Q

How are the anti-TNF-a biologicals clinically used?

A

Autoimmune diseases

Pharmacology for Amjad (64 decks)

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