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Transplant Immunology and Pharmacology Flashcards

7 cards from real CCTC practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.

Read the first 7 Transplant Immunology and Pharmacology flashcards as text
  1. Which cytokine is primarily responsible for driving the differentiation of naive CD4+ T cells into Th17 cells?

    Answer: TGF-β combined with IL-6

    TGF-β combined with IL-6 drives naive CD4+ T cells toward the Th17 lineage, which produces IL-17 and contributes to certain rejection pathways.

  2. A transplant recipient on tacrolimus develops new-onset diabetes mellitus. What is the most likely mechanism?

    Answer: Direct pancreatic beta-cell toxicity reducing insulin secretion

    Tacrolimus causes direct pancreatic beta-cell toxicity that impairs insulin secretion, leading to post-transplant diabetes mellitus (PTDM).

  3. What is the mechanism by which belatacept prevents T-cell activation compared to calcineurin inhibitors?

    Answer: It inhibits the CD28-B7 costimulatory pathway

    Belatacept is a CTLA4-Ig fusion protein that blocks CD28-B7 costimulation, preventing the second signal required for full T-cell activation.

  4. Which HLA mismatch is most strongly associated with hyperacute rejection?

    Answer: Preformed donor-specific antibodies against HLA class I

    Preformed donor-specific antibodies (DSAs) against HLA class I antigens bind the graft endothelium immediately upon reperfusion, triggering complement activation and hyperacute rejection.

  5. A kidney transplant patient on mycophenolate mofetil (MMF) is started on ciprofloxacin. Which pharmacokinetic interaction is most concerning?

    Answer: Ciprofloxacin reduces enterohepatic recirculation of MPA, lowering drug exposure

    Fluoroquinolones alter gut flora that normally hydrolyze MPA-glucuronide conjugates, reducing enterohepatic recirculation and lowering mycophenolic acid (MPA) exposure by up to 30%.

  6. Which complement pathway is primarily activated by antibody-mediated rejection?

    Answer: Classical pathway via C1q binding to antigen-antibody complexes

    In antibody-mediated rejection, donor-specific antibodies form immune complexes on graft endothelium that bind C1q, activating the classical complement pathway.

  7. What is the primary reason sirolimus (rapamycin) is often avoided in the early post-transplant period for kidney recipients?

    Answer: It impairs wound healing and increases risk of lymphocele formation

    Sirolimus inhibits mTOR-dependent cell proliferation required for wound healing, increasing rates of wound complications and lymphocele formation in the early post-transplant period.