Renal pharm Flashcards

1
Q

What gout drug does not work for gout if pt has CKD? why?

A

Probenecid.

b/c it acts on OAT transporters in tubules, which are not functioning in CKD.

probenecid competitively binds to OAT (organic anion transporter), which means uric acid stays in the urine

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2
Q

Kidney transplantation:

  • 3 signal approaches to immunosuppression
  • drugs for each
A

All about APC-T cell interaction:

  1. Calcineurin inhibitors–stop IL2 generation
    - Cyclosporine (cyclophilin)
    - Tacrolimus (FKBP)
  2. mTOR inhibitors–stop IL2 response in target cell
    - Sirolimus
  3. DNA transcription inhibitors
    - Azathioprine (6-MP)
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3
Q

Cyclosporine and Tacrolimus for kidney transplant:

-biggest side effect

A

nephrotoxicity for both

but Sirolimus is not nephrotoxic

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4
Q

name some nephrotoxic drug groups

A
  • Calcineurin inhibitors
  • NSAIDs
  • aminoglycosides
  • Vancomycin
  • Acyclovir, gancyclovir
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5
Q

sirolimus:

side effect specific to kidney transplant

A

lymphocele

-can cause ureteric compression

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6
Q

Hirsutism: which drug’s side effect?

(transplantation drug)

A

Cyclosporine

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7
Q

Sirolimus

  • biggest side effect
  • next major side effect
A
  1. Hyperlipidemia
  2. bone marrow suppression (anemia, leukopenia, thrombocytopenia)

(cyclosporine and tacrolimus also can cause HL)

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8
Q

MMF

-major side effects

A
  1. bone marrow suppression (leukopenia, anemia, thrombocytopenia)
  2. opportunistic infections (esp CMV, and also bacterial UTI)
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9
Q

kidney transplant pt on MMF:

watch out esp for what infection?

A

CMV infection

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10
Q

hyperlipidemia and bone marrow suppression in transplant pt

what drug?

A

Sirolimus

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11
Q

what drug increases toxicity of azathioprine?

A

Allopurinol

-both act on purine synthesis pathway. XO inhibitors decrease metabolism of metabolites (and AZA) into uric acid.

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12
Q

Azathioprine

-major side effects

A
  • bone marrow suppression
  • also toxicity can increase if allopurinol is taken
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13
Q

Prednisolone

  • mech
  • time to effect
A
  • inhibit transcription of NK-kB, a pro inflammatory TF
  • reduces T and B cell proliferation
  • works by binding to a steroid response element that is a TF itself, so takes 8 hours. (transcription, protein synthesis)
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