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Blood, Lymph, Immune, Bone > Immunosuppressants > Flashcards

Immunosuppressants Flashcards

1
Q

What is the MOA for Glucocorticoids?

A

they bind to the Glucocorticoid receptor and the glucocorticoid response element (GRE) and regulates transcription

This leads to decreased circulating lymphocyte levels and suppresses some subsets of T cells and antigen stimulation of T cell proliferation (T-cell production, IL2 production) and inhibits the function of phagocytes

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2
Q

what is the clinical use for glucocorticoids?

A

prevent rejection (prophylaxix)

at high doses you can treat acute rejection episodes

GVHD

and autoimmune diseases (acute glomerular nephritis, autoimmune hemolitic anemia)

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3
Q

Glucocorticoids

Adverse Effects

A

Endo: decreased hormone release

eye: glaucoma/cataracts

moon facies

buffalo hump

easy bruising

poor wound healing

Muscle wasting

renal system (fluid retention, electrolyte imbalances)

reduced fertility

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4
Q

One of the most serious adverse effects of glucocorticoid use:

A

Osteoperosis

d/t increased bone resorption and decreased bone formation

decreased calcium absorption from gut

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5
Q

Names of Glucocorticoids

A

Prednisone

Methylprednisolone

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6
Q

Calcineurin inhibitors

MOA

A

Calcineurin inhibitors

decrease IL-2 transcription

Cyclosporine binds to cyclophillin

Tacrolimus binds to FKBP.

NFAT-P isn’t dephosphorylated which is required for interleukin synthesis

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7
Q

Calcineurin inhibitors

route of administration

metabolism

A

IV or oral

CYP450 3A

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8
Q

Calcineurin inhibitors

Clinical Usage

A

Calcineurin inhibitors

allograft transplantation (not effective in ongoing or acute rejection)

GVHD (used in combination with Methotrexate)

Psoriasis

RA

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9
Q

Calcineurin inhibitors

Black Box Warning

A

Calcineurin inhibitors

Skin cancer

increased risk of infection

nephrotoxicity

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10
Q

Calcineurin inhibitors

what causes acute nephrotoxicity?

A

Calcineurin inhibitors cause acute nephrotoxicity thru vasoconstriction of afferent and efferent glomerular arterioles

the amount of vasoconstriction is dose related and usually reversible

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11
Q

Calcineurin inhibitors

names

A

Calcineurin inhibitors:

Cyclosporine

Tacrolimus

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12
Q

What are the cardiologic effects of Calcineurin inhibitors?

What effect does it have on K+?

A

Calcineurin inhibitors cause a moderate increase in

BP.

Calcineurin inhibitors can cause hyperkalemia because of the reduced efficiency of urinary K+ secretion. Can be life threatening with concurrent administration of an ACEi

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13
Q

Sirolimus

Black Box

A

Sirolimus

Liver and lung transplants

can also cause hypokalemia, thrmbocytopenia, anemia, leukopenia, GI effects, edema, hypertension

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14
Q

Sirolimus

Metabolism

Half-Life

A

Sirolimus

CYP450 3A and P-glycoprotein

(use caution if coadministered with cyclosporine and tacrolimus)

60 hours

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15
Q

Sirolimus

MOA

A

Sirolimus

suppresses cytokine mediated T-Cell proliferation.

Binds to FKBP and forms a complex. This complex binds and blocks mTOR.

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16
Q

Azathioprine

MOA

A

Azathioprine

inhibits DNA synthesis during the S phase

azathioprine is converted to 6-MP which decreases the purine nucleotide pool which is needed for DNA replication (required in general but especially after antigen stimulation)

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17
Q

Azathioprine

what type of cells are most sensitive?

A

Azathioprine

proliferating cells (stimulated lymphoid cells) are most sensitive

T-Cells

but azathioprine depresses both cell mediated and antibody mediated reactions

18
Q

Azathioprine

route of administration:

metabolism

A

Azathioprine

Oral

Metabolized by CYP450

inactivation is by Xanthine oxidase

19
Q

Azathioprine

Black Box

A

Azathioprine

Increased risk of neoplasia (mutagenic)

can also cause GI toxicity at higher doses and Bone Marrow suppression (leukopenia is common)

20
Q

Cyclophosphamide

MOA

A

Cyclophosphamide

prevents cell division by cross-linking DNA strands and decreasing DNA synthesis

21
Q

Cyclophosphamide

clinical usage

A

Cyclophosphamide

immunosuppression is off-lable

used as an anticancer agent

22
Q

Methotrexate

MOA

A

Methotrexate

irreversibly binds to and inhibits dihydrofolate reductase (DHFR)

23
Q

Methotrexate

Clinical Usage

A

Methotrexate

GVHD (extensively)

RA

Psoriasis

24
Q

Methotrexate

Adverse Reactions

A

Pregnancy category X

Hepatotoxicity

Death

Induces Lung Disease

25
Q

Mycophenolate mofetil

MOA

A

Mycophenolate mofetil

noncompetitive inhibitor of IMPDH (important for guanine synthesis)

selectively inhibits T and B lymphocyte proliferation

26
Q

Mycophenolate mofetil

Clinical Usage

A

Mycophenolate mofetil

administered with glucocorticoids

maintenance of immunosuppression

(has mostly replaced azathioprine for maintenance immunosuppression following organ transplants)

27
Q
A
28
Q

Mycophenolate mofetil

Black Box

A

Mycophenolate mofetil

Malignancies

Pregnancy (Category D)

may also cause bone marrow depression and GI upset

29
Q

Anti-Thromocyte globulin (ATG)

MOA

A

Anti-Thromocyte globulin (ATG)

purrified gamma globulin from the serum of rabbits immunized with human thymocytes

cytotoxic antibodies against T lymphocytes

30
Q

Anti-Thromocyte globulin (ATG)

Clinical Usage:

A

Anti-Thromocyte globulin (ATG)

Acute rejection episodes

Steroid resistant rejections

31
Q

Anti-Thromocyte globulin (ATG)

Adverse effects

A

allergic type reactions

local pain and erythema

32
Q

Muromonab-CD3 (OKT3)

MOA

A

Muromonab-CD3 (OKT3)

monoclonal Ab directed against CD3 on surface of human thymocytes and mature T cells causing the internalization of T cell receptor

33
Q

Muromonab-CD3 (OKT3)

Clinical Usage

A

Muromonab-CD3 (OKT3)

acute organ transplant rejection

depletion of donor bone marrow of T-cells prior to transplant (Minimise GVHD)

34
Q
A
35
Q

Muromonab-CD3 (OKT3)

Adverse effects

A

Muromonab-CD3 (OKT3)

Allergic responses

Chills

Fever

Wheezing

Cytokine storm

36
Q

What is a cytokine storm?

A

Cytokine storm

common to many antibody drugs that target lymphocytes, results from activation of T cells and release of T cell cytokines before the antibody-coated T cells can be cleared by macrophages.

It typically occurs after the first few doses and the symptoms dissipate as T cells are eliminated

premedicate with glucocorticoids, diphenhydramine, acetaminophen

37
Q

Daclizumab and Basiliximab

MOA

A

Daclizumab and Basiliximab

monoclonal antibodies to part of IL-2 receptor (CD25)

IL-2 antagonist but the mechanism isn’t well understood

Daclizumab- Humanized IgG1

Basilizimab- chimeric mouse-human IgG1

38
Q

Daclizumab and Basiliximab

Clinical usage

A

Daclizumab and Basiliximab

prophylasis against acute rejection

used in combination with cyclosporin and corticosteroids

39
Q

Rho (D) immune globulin

Clinical usage

A

Rho (D) immune globulin

administered to pregnant women to prevent alloimmunization of Rh (-) mothers who may potentially have a fetus who is Rh (+)

40
Q

What is the most common immunosuppressant for acute renal allograft rejection?

A

High dose corticosteroids are the first line therapy for acute renal allograft rejection. 2nd is Anti-T cell antibody therapy

41
Q

What is the prophylaxis treatment for GVHD?

A

methotrexate + cyclosporine

42
Q

What is the treatment for GVHD?

A

glucocorticoids are the most effective treatment option

2nd line agents include: cyclosporine, tacrolimus, antithymocyte globulin

Blood, Lymph, Immune, Bone (13 decks)

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