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Phar 504 > Transplant Therapeutics > Flashcards

Transplant Therapeutics Flashcards

1
Q

What are the two types of transplantation

A

thoracic and abdominal

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2
Q

What organs are transplanted in thoracic

A

heart and lung

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3
Q

What organs are transplanted in abdominal

A

Liver, small bowel, kidney, pancreas

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4
Q

What are the overall goals of immunosupression

A

improve graft survival, improve patient survival, maintain good Quality of life

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5
Q

What are the three pathways to immunosuppression

A

depletion of lymphocytes, diversion of lymphocyte traffic, blocking of lymphocyte proliferation and response

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6
Q

What are the four phases of immunosuppression

A

desensitization (prn), induction, maintenance, rejection (prn)

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7
Q

When are induction drugs used

A

utilized in peri-operative period

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8
Q

What drug is universally administered to all patients in the induction phase

A

methylprednisolone

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9
Q

What antibody agents deplete lymphocytes in the induction phase

A

thymoglobulin, Atgam, Alemtuzumab

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10
Q

What antibody agents are non lymphocyte depleting in the induction phase

A

Basiliximab

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11
Q

What is the pharmacology of corticosteroids

A

decrease cytokine gene expression, redistribute T-cells from circulation to lymphoid tissue, decrease inflammation

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12
Q

What is the dosing for corticosteroids that is most commonly used

A

250mg-1000mg IVPB, followed by a steroid taper or IV MP

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13
Q

How long are lymphocytes suppressed after steroids are given

A

24 hours

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14
Q

T/F: If prednisone by mouth is greater than 30mg it may be split between every 6 hours to minimize ADRs

A

False: If prednisone by mouth is greater than 50 mg it may be split to every 12 hours to minimize ADRs

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15
Q

What are ADRs of corticosteroids

A

hyperglycemia, high blood pressure/fluid retention, leukocytosis

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16
Q

Which immunosuppresants are polyclonal antibodies, what type are they

A

thymoglobulin and Atgam, IgG

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17
Q

What is the MOA of polyclonal antibodies, what is the result

A

polyspecific binding to T cell leads to opsonization and elimination, T-cell depletion

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18
Q

How is Thymoglobulin and Atgam dosed, which drug causes longer and greater T-cell depletion

A

Thymoglobulin: 1.5mg/kg IV for 3-7 days, Atgam: 10-15mg/kg for 3-days, thymoglobulin

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19
Q

T/F: Due to their nature polyclonal antibodies can cause a depletion in other cells, lymphoproliferative disease, and even trigger T cell activation

A

True

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20
Q

What are the ways to limit infusion reactions and cytokine release for polyclonal antibodies

A

Pre-medicate (acetaminophen and diphenhydramine), prolong the infusion rate, infuse via central access

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21
Q

What lab level is monitored when using polyclonal antibodies, what is the goal

A

Absolute lymphocyte count (ALC), less than 200 cells/ul

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22
Q

Which immunosuppressants are monoclonal antibodies

A

Basiliximab and Alemtuzumab

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23
Q

What is the MOA of basilximab

A

Acts as IL-2 receptor antagonist to CD25 protein found on the alpha chain on the surface of an activated T cell, blocks signal 3 and T-cell proliferation

24
Q

What is the dosing for basiliximab

A

20mg IVPB on Day 0 and Day4

25
Q

How is Alemtuzumab different from Basiliximab, what is the MOA

A

binds nearly all T and B lymphocytes, targets CD52 leading to antibody- dependent lysis following cell surface binding

26
Q

What is the dosing for Alemtuzumab

A

single 30mg dose on Day 0

27
Q

T/F: Maintenance drugs are for lifelong immunosuppresion and are administered in the post-transplant period

A

True

28
Q

What calcineurin inhibitors is used more often, what is the other medication used

A

Tacrolimus, cyclosporine

29
Q

What antimetabolite is used most often, what is the other medication used

A

Mycophenolic acid, azathiprine

30
Q

T/F: For CNIs formulations are not interchangeable and errors can lead to graft failure

A

True

31
Q

What does tacrolimus complex with to inhibit calcineurin, what does cyclosporine complex with

A

FKBP-12, cyclophilin

32
Q

T/F: CNI’s inhibt transcription directly

A

False: CNIs inhibit calcineurin -> inhibit IL-2 synthesis -> prevention of T-cell proliferation

33
Q

What are the three formulations for tacrolimus

A

Prograf (immediate release), Astagraf-XL (extended release), Envarsus- XR (extended release with the best bioavailability)

34
Q

How is prograf dosing converted when switched to Astagraf

A

1:1, total dose per day is the same but instead of twice a day it’s once a day

35
Q

How is Prograf dosing converted when switched to Envarsus

A

1:0.8, total dose per day is reduced by 20 percent once a day due to the better bioavailability

36
Q

When would a patient receive CNIs IV, what is the danger of this formulation

A

bone marrow transplant patients with severe Mucositis, high risk of nephrotoxicity

37
Q

What CNI route of administration is used via NG tube, where is it made

A

Suspension, compounded in the pharmacy

38
Q

What are key guidelines for giving tacrolimus sublingual

A

can only administer immediate release (Prograf) and decrease the dose by 50%

39
Q

What CYP3A4 induces will decrease the levels of CNIs

A

Phenytoin and carbamazepine, rifampin, Nafcillin

40
Q

What CYP3A4 inhibitors will increase the levels of CNIs

A

ketoconazole and fluconazole, erythromycin and clarithromycin, dilitizaem and verapmil, ritonavir

41
Q

What are ADRs of CNIs

A

Nephrotoxicity, neurotoxicity, electrolytes, diabetes, hypertension

42
Q

What is the acute nephrotoxicty caused by CNIs, chronic

A

reduced GFR/ reversible, interstitial fibrosis and scarring/irreversible

43
Q

Why is diabetes more likely when taking CNIs

A

lowered insulin secretion via direct Beta-cell toxicity or DNA inhibition (dose dependent)

44
Q

What CNI should pediatric patients less than 5 receive

A

cyclosporine

45
Q

When should tacrolimus be switched over to cyclosporine

A

For patients with Diabetes, hair loss, tremors/falls

46
Q

T/F: When IMS agents are changed they should be checked everyday

A

False: Check levels 7 days after change and then monthly

47
Q

What are the antimetabolites

A

azathioprine and mycophenolic acid

48
Q

What is the MOA of azathioprine

A

inhibition of de novo purine synthesis (adenine and guanine), incorporation into DNA; all through conversion to 6-MP

49
Q

What enzyme is responsible for inactivating and action steps for 6-MP, why must it be screen for before using azathioprine

A

TPMT, slow inactivation of 6MP can lead to accumulation of myelosuppressive metabolites leading to death

50
Q

What is the mycohphenolic acid MOA

A

only inhibits the DeNovo pathway inhibiting synthesis of guanosine in active T cells, inhibits inosine 5’ monophosphate dehydrogenase (IMPDH)

51
Q

What drug should be avoided when taking azathioprine

A

Allopurinol

52
Q

T/F: For Antimetabolites dose adjustments are based on side effects

A

True

53
Q

What drug has two peaks and a trough, what drug inhibits enterohepatic recirculation that causes this effect

A

MPA, cyclosporine a

54
Q

What is a main side effect of MPA

A

diarrhea and nausea

55
Q

What drugs are is more likely to cause a cytokine storm due to their mechanism of action

A

Thymoglobulin and Atgam

56
Q

Which of CNIs causes the most problems with hypertension

A

Cyclosporine

57
Q

What are the major side effects of Tacrolimus

A

Alopecia and diarrhea

Phar 504 (34 decks)

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