Immunosuppressants & Organ Rejection Prevention

1. Which immunosuppressant increases the risk of opportunistic infections like CMV and PCP?

All immunosuppressants equally increase risk

Only calcineurin inhibitors

Only corticosteroids

MTOR inhibitors only

2. A patient receiving sirolimus reports joint pain and delayed wound healing post-transplant. What is the likely mechanism?

MTOR inhibition impairs growth factor signaling and tissue repair

Sirolimus causes direct connective tissue damage

Sirolimus triggers rheumatoid arthritis

Sirolimus depletes synovial fluid

3. Which immunosuppressant combination is most commonly used as maintenance therapy after solid organ transplant?

Calcineurin inhibitor, mycophenolate, and corticosteroid

Two calcineurin inhibitors plus azathioprine

MTOR inhibitor monotherapy

Antibody induction only

4. A transplant patient develops hyperkalemia while on an ACE inhibitor and tacrolimus. What is the mechanism?

Tacrolimus reduces renal potassium excretion and impairs aldosterone secretion

ACE inhibitors cause direct hyperkalemia independent of immunosuppression

Both drugs promote potassium reabsorption in the proximal tubule

Tacrolimus increases dietary potassium absorption

5. What is the mechanism of action of fingolimod in preventing transplant rejection?

Sphingosine-1-phosphate receptor modulator that traps lymphocytes in lymph nodes

Direct T cell depletion via antibody

Inhibition of calcineurin and IL-2 production

Blockade of B7-CD28 costimulation

6. A liver transplant recipient on triple immunosuppression develops a skin lesion suspicious for squamous cell carcinoma. What is the underlying risk?

Chronic immunosuppression increases skin cancer risk

Calcineurin inhibitors are directly carcinogenic

Corticosteroids cause UV sensitivity

MTOR inhibitors promote malignant transformation

7. Which immunosuppressant should be avoided or used cautiously in patients with TPMT deficiency?

Azathioprine

Tacrolimus

Sirolimus

Prednisone

8. A patient develops leukopenia and macrocytic anemia while on azathioprine. What is the mechanism?

Azathioprine inhibits purine synthesis, reducing lymphocyte proliferation

Azathioprine directly damages bone marrow stem cells

Azathioprine causes hemolysis

Azathioprine depletes B12 stores

9. Belatacept is a costimulation blocker. What T cell interaction does it interrupt?

CD28-B7 costimulatory signal

TCR-MHC interaction

IL-2 receptor signaling

Fas-FasL apoptotic pathway

10. A kidney transplant patient on tacrolimus develops tremor, headache, and confusion. What is the most likely diagnosis?

Tacrolimus neurotoxicity from elevated trough levels

Acute rejection episode

Opportunistic brain infection

Medication non-compliance

11. Which immunosuppressant class works by blocking the IL-2 receptor on T cells?

Calcineurin inhibitors

Monoclonal antibodies

Mammalian target of rapamycin (mTOR) inhibitors

Corticosteroids

12. Graft-versus-host disease (GVHD) occurs after bone marrow transplant. How do immunosuppressants prevent this?

By eliminating donor T cells and suppressing immune activation

By promoting graft acceptance without any immune suppression

By increasing regulatory T cells only

By blocking antibody production exclusively

13. A patient develops hypertension, hyperglycemia, and osteoporosis after transplant. Which immunosuppressant is most likely responsible?

Mycophenolate mofetil

Prednisone

Azathioprine

Belatacept

14. What is the primary advantage of using induction therapy with anti-lymphocyte antibodies in transplant recipients?

Reduces early acute rejection and allows lower maintenance doses

Eliminates the need for all other immunosuppressants

Prevents chronic rejection indefinitely

Reverses established acute rejection episodes

15. A patient on sirolimus develops proteinuria and elevated creatinine. Which mechanism explains this?

MTOR inhibition impairs glomerular filtration

Sirolimus is nephrotoxic at therapeutic levels

Sirolimus causes direct podocyte injury

MTOR inhibition promotes thrombotic microangiopathy

16. Basiliximab is a monoclonal antibody used in transplant rejection prevention. When should it be administered?

Intraoperatively and on postoperative day 4

Only if acute rejection occurs

Weekly for 12 weeks after transplant

Continuously via central line infusion

17. Which medication requires therapeutic drug monitoring with trough levels?

Prednisone

Azathioprine

Tacrolimus

Sirolimus

18. A transplant patient on mycophenolate mofetil (MMF) develops diarrhea and leukopenia. What is the most likely cause?

MMF selectively inhibits inosine monophosphate dehydrogenase in lymphocytes

MMF causes direct gastrointestinal toxicity

MMF reduces platelet production

MMF activates complement cascade

19. Cyclosporine and tacrolimus are both calcineurin inhibitors. What is their primary mechanism?

Inhibit T cell proliferation by blocking IL-2 production

Deplete B cells through complement activation

Block costimulatory signals on dendritic cells

Inhibit protein synthesis in all lymphocytes

Immunosuppressant Quiz: Can You Prevent Rejection?

1. Which immunosuppressant increases the risk of opportunistic infections like CMV and PCP?

2.

What first name or nickname would you like us to use?

2. A patient receiving sirolimus reports joint pain and delayed wound healing post-transplant. What is the likely mechanism?

3. Which immunosuppressant combination is most commonly used as maintenance therapy after solid organ transplant?

4. A transplant patient develops hyperkalemia while on an ACE inhibitor and tacrolimus. What is the mechanism?

5. What is the mechanism of action of fingolimod in preventing transplant rejection?

6. A liver transplant recipient on triple immunosuppression develops a skin lesion suspicious for squamous cell carcinoma. What is the underlying risk?

7. Which immunosuppressant should be avoided or used cautiously in patients with TPMT deficiency?

8. A patient develops leukopenia and macrocytic anemia while on azathioprine. What is the mechanism?

9. Belatacept is a costimulation blocker. What T cell interaction does it interrupt?

10. A kidney transplant patient on tacrolimus develops tremor, headache, and confusion. What is the most likely diagnosis?

11. Which immunosuppressant class works by blocking the IL-2 receptor on T cells?

12. Graft-versus-host disease (GVHD) occurs after bone marrow transplant. How do immunosuppressants prevent this?

13. A patient develops hypertension, hyperglycemia, and osteoporosis after transplant. Which immunosuppressant is most likely responsible?

14. What is the primary advantage of using induction therapy with anti-lymphocyte antibodies in transplant recipients?

15. A patient on sirolimus develops proteinuria and elevated creatinine. Which mechanism explains this?

16. Basiliximab is a monoclonal antibody used in transplant rejection prevention. When should it be administered?

17. Which medication requires therapeutic drug monitoring with trough levels?

18. A transplant patient on mycophenolate mofetil (MMF) develops diarrhea and leukopenia. What is the most likely cause?

19. Cyclosporine and tacrolimus are both calcineurin inhibitors. What is their primary mechanism?