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Clinical Pharmacy 2 > Renal Transplantation > Flashcards

Renal Transplantation Flashcards

1
Q

What are the benefits of renal transplantation?

A
  • not life saving (like liver, lung or heart transplant)
  • survival benefit
  • improved QOL
  • cost saving (after first year post transplant)
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2
Q

What are the advantages of a living donor vs a deceased donor?

A
  • graft survival is longer (20 years minimum vs 13 years minimum)
  • there is not as much of a wait time for a living donor
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3
Q

What are the types of living kidney donors?

A
  1. direct donation
  2. kidney paired exchange
  3. altruistic, non directed
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4
Q

What are the types of deceased kidney donors?

A
  1. neurological determination of death
  2. donation after cardiac death
  3. medical assistance in dying
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5
Q

What does a patient all have to go through as part of the recipient evaluation?

A
  • tranplant nephrologist
  • blood group, HLC typing, HLC cross matching, HLA antibody screening
  • infection screening: TB, HBV, HCV, HIV, CMV, EBV, BK
  • imaging: CXR, U/S
  • cardiac evaluation
  • vascular disease screen
  • psychiatry assessment
    (approx. 9 months in MB)
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6
Q

What is evaluated when matching donors to recipeints?

A
  • HLA: human leukocyte antigens

- HLA are the markers on most cells that help to identify self from foreign

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7
Q

Class 1 HLA does what?

A
  • stimulates T killer cells
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8
Q

Class 2 HLA does what?

A
  • stimulates T helper cells, macrophages, B cells
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9
Q

Typical matching is between what?

A
  • A, B, DR and DQ types
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10
Q

The degrees of ________ is directly related to the degree of immunologic risk?

A
  • HLA disparity
  • – the closer the match, the less immunosuppression that the person will have to have over time- the closest match a person will have will likely be their sibling
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11
Q

What sensitizing events can lead to an anti-HLA antibody?

A
  • pregnancy, blood transfusions, previous transplant

- increased difficultly in finding a match in these cases

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12
Q

What is a PRA panel screening?

A
  • this is the degree of transplantability
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13
Q

What is cross matching between a donor and a recipient?

A
  • testing for HLA antibodies that can cause severe rejection and graft loss
  • positive cross match here is bad - the recipients cells are able to recognize and attack the donor cells
  • there is an increased risk of rejection
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14
Q

What happens when a person develops HLA antibodies after a transplant?

A
  • there is an increased risk of graft loss in this case- often this is a result of non-conplaiance and under immunosuppression
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15
Q

How is immunosuppression achieved?

A
  • depletion of lymphocytes, depletion of antibodies
  • blocking of the lymphocyte response
    (non-depleting monoclonal antibody IL-2 receptor antagonists, calcineurin inhibitors, antiproliferative agents, mTOR inhibitors)
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16
Q

What medications are used at the time of transplant to reduce the risk of acute injection- what is this referred to as?

A
  • induction therapy
  • can use wither DEPLETING ABS (anti-thrymocyte: thyroglobulin) or NONDEPLETING ABS (IL-2 receptor:basiliximab)
  • also add on corticosteroids here- prednisone or methylprednisone
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17
Q

What drugs fall under the class of calcineurin inhibitors?

A
  • cyclosporin

- tacrolimus

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18
Q

What drugs fall under the class of antiproliferatives?

A
  • azathoprine
  • mycophenolate mofetil
  • mycophenolate sodium
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19
Q

What drug is considered to be a rapamycin derivative?

A
  • sirolimus
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20
Q

What is the MOA of tacrolimus?

A
  • inhibits earlt in T cell activation and clonal expansion
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21
Q

What is the MOA of mycophenolate mofetil?

A
  • it works to decrease the T cell proliferation
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22
Q

What is the MOA of prednisone?

A
  • sequesters and inhibits lymphocytes
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23
Q

Should use THREE drugs in combination for immunosuppression- what are they?

A
  1. T cell communication
  2. Antiproliferatives
  3. Prednisone
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24
Q

What are the T cell communication drugs? (calcineurin inhibitors)

A
  • cyclosporine

- tacrolimus

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25
Q

What are the anti proliferative agents?

A
  • azathioprine
  • mycophenolate
  • sirolimus
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26
Q

What is the calcineurin inhibitor that cause more diabetes?

A

tacrolimis

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27
Q

What CNI causes hair loss? Which one causes hair growth?

A
  • hair loss: tacrolimis

- hair growth: cyclosporin

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28
Q

Diarrhea will cause an ____ drug level due to the pumping out of the drug

A

increased

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29
Q

What are the adverse drug reactions that come fro CNIs?

A
  • increased blood glucose
  • increased blood pressure
  • increased lipids
  • increased K
  • decreased Mg
  • decreased P
  • increased UA
  • tremor, nephro and hepatotoxicity, gingival hyperplasia
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30
Q

What CNI is a stronger inhibitor of cyp 3A4?

A
  • CSA > TAC
31
Q

What is the effect that a CNI will have on p-glycoprotein?

A
  • both substrate and an inhibitor
  • diarrhea can be caused by sloughing of intestinal endothelium -> loss of pgp -> increased CNI levels
  • other medications may use the pgp pathway
32
Q

What are some of the medications that will inhibit or increase the levels of CNIs?

A
  • azoles
  • macrolides
  • non DHP CCBs
  • grapefruit juice
  • ritonovir/protease inhibitors
33
Q

What are some of the medications that will induce or decrease the levels of CNIs?

A
  • rifampin, phenytoin, carbamazepine, phenobarbital, St. John’s Wort
34
Q

What is the effect from the interaction between cyclosporin and nifedipine/phenytoin?

A
  • gum hyperplasia
35
Q

What is the effect of the interaction between statins, dig and caspofungin?

A
  • decreased clearance
36
Q

What is the interaction between cyclosporine and colchicine?

A
  • increased myopathy and hepatotoxicity
37
Q

What is the interaction between warfarin and cyclosporin?

A
  • decreased INR and CSA levels
38
Q

What is the interaction between K sparing diuretics and cyclosporine?

A
  • hyperkalemia
39
Q

What are the 2 statins here that are okay to use with CSA?

A
  • fluvastatin and pravastatin
40
Q

What are the main drug interactions with tacrolimis?

A
  • K sparing diuretics (cause hyperkalemia)
  • metoclopramide (increased tacrolimis exposure)
  • statins (TAC/atorvastatin might be okay)- but NEVER use atorvastatin 80
41
Q

What is considered to be the “safer” NOAC to use with CNIs?

A
  • apixaban- safer compared to warfarin
42
Q

What drugs have additive nephrotoxicity when added onto cyclosporine and tacrolimus?

A
  • NSAIDs, ACEI/ARB, aminoglycosides
43
Q

What additive medication helps CNIs be renal sparing?

A
  • CCBs - this is because they cause afferent vasodilation
44
Q

What are the adverse DIs associated with sirolimus?

A
  • increased lipids
  • proteinuria
  • delayed wound healing
  • anemia
  • hypertension
  • caution in liver and lung transplant - hepatic artery stenosis, bronchial anastomotic dehiscence
45
Q

What is a big drug interaction that is associated with sirolimus?

A
  • cyclosporine: space CSA four hours before sirloins

- — if taken together will have increased sirloins concentrations

46
Q

What are the medications that will increase SIR concentrations?

A
  • azoles (single fluconazole dose has minimal effects)
  • macrolides
  • non DHP CCBs
  • ritonavir/protease inhibitors
  • grapefruit juice
47
Q

What are the medications hat will decrease SIR concentrations?

A
  • rifampin
  • phenytoin
  • carbamazepine
  • phenobaribital
  • St. John’s Wort
48
Q

What drugs are considered to be anti-poliferative agents?

A
  • azathioprine and mycophenolate
49
Q

What are the AEs associated with AZA?

A
  • bone marrow suppression, hepatotoxicity
50
Q

what are the AEs associated with mycophenolate?

A
  • leukopenia, GI intolerance (GI effects here are severe- people will sometimes be unable to leave their homes because of diarrhea)
51
Q

NEVER use AZA and _____ together due to severe bone marrow suppression

A

allopurinol

52
Q

What are other DIs associated with AZA?

A
  • allopurinol
  • ACE inhibitors (profound neutropenia)
  • warfarin(decreased INR)
53
Q

What are the drug interactions associated with mycophenolate?

A
  • anitbiotics (may change enterohepatic recirculation, may change trough level but not necessarily overall exposure)
  • cholestyramine (prevents reabsorption via enterohepatic recirculation, significant decrease in MPA concentration)
  • PPIs (decreases MPA levels, use lowest dose possible)
  • antacids (dose separated by 2 hours minimum)
  • iron preps (dose seperation not required)
54
Q

What is mycophenolate dependent on for absorption?

A
  • dependent on pH for absorption- mycophenolate is pH dependent with its absorption - not based on chelation so this is why you need to space out antacids and not iron preps
55
Q

What are the most common AE associated with corticosteroids?

A
  • increaed lipids, increased BG, increased bp, sleep disturbances, increased appetite/weight, moos swings, osteoporosis, acne, fluid retention
56
Q

What is a monitoring parameter for cyclosporine levels?

A
  • want to ensure that the trough level (winning 30 minutes pre-dose)
    • high variability of cyclosporine trough levels
  • target level depends on time since transplant and is individual to each patient
  • usual maintenance target range: 50-150 mcg/L
57
Q

Trough levels of tacrolimis should correspond to what?

A
  • to AUC/drug exposure

- target range in reference: 6-8 mcg/L

58
Q

What is the target drug range for sirolimus?

A

AUC/drug exposure

  • target level depends on time since transplant and is individual to each patient
  • usual maintenance range: 6-10 mcg/L
59
Q

What is the monitoring parameter associated with mycophenolate?

A
  • these levels are not routinely done - wide inter-individual variability in MPA exposure
  • no single time point here accurately reflects exposure
  • some centres do trough levels in setting of toxicity or absorption concerns (target and dose adjustments are unclear)
60
Q

Glucose control in these patients helps to ____ the TGs

A

decrease

61
Q

What are the main reasons for dyslipidemia?

A
  • CKD
  • age
  • lifestyle: diet, smoking, exercise
  • prednisone
  • cyclosporine
62
Q

What immunosuppressent is there no interaction with statins?

A
  • tacrolimis
63
Q

What immunosuppressants have the most reports of myopathy?

A
  • combination of CSA with a statin, there are a few with tacrolimis and sirolimus
64
Q

What is the incidence of pneumocystis jiroveci?

A
  • PJP has significant morbidity and mortality in solid organ transplant patients (mortality up to 50%)
  • associated with periods of higher immunosupression (eg. first 3-12 months post-transplant)
  • tx: co-trimoxazole 15-20 mg TMP/kg/day
  • – 1600/3200 (2 DS tabs) q8h
65
Q

Who is at the highest risk of CMV?

A
  • when the donor has had CMV before and the recipient has not – more likely to get it this way
66
Q

What is the prophylaxis treatment for CMV?

A
  • valganciclovir 900 mg for 6 months
67
Q

What are the problems associated with BK virus and renal transplantation?

A
  • polyomavirus- reactive and replciate in an immunosuppressed state
  • may lead to bk nephropathy and graft failure
  • routine screening for BK viremia and graft dysfunction
  • NO GOOD TX- switch to cyclosporin to reduce immunosuppression
68
Q

What is the impact that an infection from EBV has on kidneys?

A
  • common virus in the general population
  • associated with a development of post transplant lymphoproliferative disorder
  • lower immunosuppressive therapy!
69
Q

What are the complications associated with UTIs and kidney transplants?

A
  • can led to sepsis, graft dysfunction and failure
70
Q

What are the risk factors associated with UTIs?

A
  • females, advanced age history if UTIs pre transplant, prolonged use of a catheter, indwelling device, polycycstic kidney disease
71
Q

Should UTIs be prophylaxed for?

A
  • yes! there is benefit in the first 3 months

- TMPSMX is preferred over cipro

72
Q

What are some of the common complications associated with renal transplantation?

A
  • anemia (surgical blood loss, time for new kidney to start expo production
  • analgesia- chronic pain
  • decreased bone density due to steroid use
  • increased blood pressure
  • increased cholesterol (esp wit sirolimus use)
  • increased cancer risk
  • diabetes onset (with steroid use this is difficult to control)
  • depression
  • cataracts (due to steroid use)
  • exercise
73
Q

What drug is known to be teratogenic, and what should be done if someone is planning on getting pregnant?

A
  • mycophenolate is known to be teratogenic
  • switch women to azathioprine if planning on conceiving
  • – recommend for women and men!

Clinical Pharmacy 2 (18 decks)

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