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Pharm Spring Exam 2 > Tansplant Drugs > Flashcards

Tansplant Drugs Flashcards

1
Q

Classes of immunosuppressives

A

Glucocorticoids, cyototoxic antimetabolites, calcineurin and mTOR inhibitors, anti-cytokine/cytokine receptor Ab’s, Anti T and B cell therapy, costimulation pathway inhibitors

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2
Q

Allograft Immune response

A

Antigens from transplanted organ are presented to host T-Cells

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3
Q

TNF-alpha

A

produced by helper T Cells, macrophages, NK cells

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4
Q

Glucocorticoid mechanism of action

A

Inhibit expression of pro-inflammatory mediators

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5
Q

Cytotoxic antimetabolite mechanism of action

A

Inhibit clonal expansion of lymphocyte population

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6
Q

Calcineurin and mTOR inhibitors mechanism of action

A

Inhibit lymphocyte signalling

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7
Q

IL2 receptor Ab’s mechanism of action

A

Neutralize cytokines and cytokine receptors

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8
Q

T cell depletor mechanism of action

A

Depletes T Cells (no shit)

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9
Q

Belatacept mechanism of action

A

Blockade of costimulation

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10
Q

Glucocorticoid uses

A

Graft vs host, RA, SLE, asthma, MS, allergic reactions, BLOCKS CYTOKINE STORM CAUSED BY MUROMANAD-CD3

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11
Q

Glucocorticoid toxicity

A

Growth suppression, avascular bone necrosis, osteopenia, risk of infection, cataracts, impaired healing, hyperglycemia, htn, DIABETEOGENIC WHEN COMBINED WITH CALCINEURIN INHIBITORS

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12
Q

Azathioprine mechanism of action

A

Purine antimetabolite, inhibits DNA, RNA synthesis

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13
Q

Azathioprine adverse effects

A

Immunosuppression, myelosuppression, toxicity in GI mucosa, bone marrow due to suppression of proliferating cells

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14
Q

Azathioprine pharmacology

A

Azathioprine is cleaved into 6-mercatopurine in liver, RBC’s, taken up by lymphocytes, converted into 6-thio-GTP and 6-thio-dGTP, which are incorporated into RNA, DNA

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15
Q

Azathioprine disposition

A

PO, well absorbed, hepatic, RBC metabolism, renal excretion

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16
Q

Azathioprine DDI’s

A

Decrease dose with allopurinol, exacerbation of myelosuppression with ACE inhibitors because they decrease EPO.

17
Q

Mycophenolate Mofetil Mechanism of action

A

Inhibits IMP dehydrogenase, an important part of the guanine biosynthesis pathway. Selectively targets B and T cells, which depend on de novo purine sythesis.

18
Q

Mycophenolate Mofetil pharmacology

A

Hydrolized in liver to active metabolite - mycophenolic acid

19
Q

Mycophenolate Mofetil use

A

Prevent rejection of kidney transplants, used with calcinuerin inhibitors and glucocorticoids, and in autoimmune disease.

20
Q

Mycophenolate Mofetil ADME

A

Metabolized to glucoronide derivative in liver, excreted in urine

21
Q

Mycophenolate Mofetil DDI’s

A

Tacrolinus impairs glucoronidation, decrease dose. Plasma levels elevated in renal insufficiency

22
Q

Mycophenolate Mofetil Toxicity

A

Luekopenia, Diarrhea, vomiting, teratogenic,

23
Q

Cyclosporine, Tacrolimus mechanism of action

A

Calcinuerin Inhibitors - IL-2 production inhibition

24
Q

IL-2

A

Promotes clonal expansion, activation, and differentiation of mature T-Cells

25
Q

Calcinuerin

A

Calcinuerin is induced as a consequence of T-Cell receptor activation, and promotes T-Cell expansion and differentiation by intracellular signalling

26
Q

Sirolimus mechanism of action

A

Prevents T-cell activation and proliferation by inhibiting protein synthesis

27
Q

Cyclosporine uses

A

Transplant rejection prevention, RA, psoriasis in immunocompromised, IBD, endogenous uveitis, nephrotic syndrome

28
Q

Cyclosporine ADME

A

PO/IV (different PO preparatations are NOT interchangeable), CYP3A, >25 metobolites, excreted in feces

29
Q

Cyclosporine Toxicity

A

Renal Dysfunction, HTN - common in renal and universal in cardiac transplants, diabetogenic with glucocorticoids

30
Q

Cyclosporine DDI’s

A

CYP3A inhibition or induction has a major effect - monitor blood levels. Renal dysfunction when combined with NSAIDS or sirolimus

31
Q

Tacrolimus ADME

A

PO/IV - must be individually dosed to patient. Variable/incomplete GI absorbtion. Extensive CYP3A Metabolism, fecal excretion

32
Q

Tacrolimus toxicity

A

Nephrotoxic, htn, diabetogenic, especially w/glucocorticoids

33
Q

Tacrolimus DDI’s

A

CYP3A inhibition or induction has a major effect - monitor blood levels. Renal dysfunction when combined with NSAIDS- MONITOR BLOOD LEVELS

34
Q

Sirolimus mechanism of action

A

binds to and inhibitos mTOR, a kinase that is key in cell cycle progression at G1-S. DOES NOT INHIBIT CALCINEURIN. Inhibits T-Cell activation and proliferation

35
Q

Sirolimus ADME

A

PO, CYP3A - highly variable bioavailability, monitor blood levels (consistently with or without food.) Fecal excretion. T 1/2 62 hours

36
Q

Sirolimus toxicity

A

Not renal toxic. Dose dependent htn, increase in serum cholesterol, triglycerides, lymphocoele, myelosupression,

37
Q

Sirolimus DDI’s

A

CYP3A inhibition or induction has a major effect - monitor blood levels. Aggravates renal toxicity WITH CYCLOSPORINE.

Pharm Spring Exam 2 (1 decks)

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