Pharmacology Quiz: Corticosteroids And Immunosuppression
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Corticosteroids And ImmunosuppressionQuestion 1 of 20

A patient is being converted from a chronic daily dose of 20 mg of hydrocortisone to a therapeutically equivalent anti-inflammatory dose of dexamethasone. (Accepted dose equivalency: 20 mg hydrocortisone = 5 mg prednisone = 0.75 mg dexamethasone).

Compared to the hydrocortisone regimen, what is a primary clinical consequence of switching to the equivalent dose of dexamethasone?

Reduced overall anti-inflammatory effect due to lower bioavailability.
A greater degree and duration of HPA axis suppression.
Less impact on glucose metabolism and fluid retention.
A significantly increased mineralocorticoid activity.
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Pharmacology Quiz

Pharmacology Quiz: Corticosteroids And Immunosuppression

Practice Corticosteroids And Immunosuppression in Pharmacology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

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This quiz focuses on Corticosteroids And Immunosuppression, giving you a quick way to practice the rules, question types, and explanations that matter most for Pharmacology.

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Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

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Question 1

A patient is being converted from a chronic daily dose of 20 mg of hydrocortisone to a therapeutically equivalent anti-inflammatory dose of dexamethasone. (Accepted dose equivalency: 20 mg hydrocortisone = 5 mg prednisone = 0.75 mg dexamethasone).

Compared to the hydrocortisone regimen, what is a primary clinical consequence of switching to the equivalent dose of dexamethasone?

  1. Reduced overall anti-inflammatory effect due to lower bioavailability.
  2. A greater degree and duration of HPA axis suppression. (correct answer)
  3. Less impact on glucose metabolism and fluid retention.
  4. A significantly increased mineralocorticoid activity.
Explanation: Dexamethasone has a very long biological half-life (~36-72 hours) compared to hydrocortisone (~8-12 hours). While the doses are equivalent in terms of anti-inflammatory effect, the prolonged duration of action of dexamethasone leads to more profound and sustained suppression of the hypothalamic-pituitary-adrenal (HPA) axis. Dexamethasone has potent glucocorticoid activity but virtually no mineralocorticoid activity, so fluid retention (D) would be less of an issue. It has a greater, not lesser, impact on glucose metabolism (C). Bioavailability is not the primary differentiating factor here (A).

Question 2

A 45-year-old renal transplant recipient, whose immunosuppression was recently changed from tacrolimus to sirolimus due to calcineurin inhibitor-induced nephropathy, presents with a 4-week history of dyspnea on exertion and a persistent, dry cough. His oxygen saturation is 92% on room air. A chest X-ray shows bilateral interstitial infiltrates.

This patient's presentation is most suggestive of a serious, non-infectious pulmonary complication specifically associated with which of his medications?

  1. Prednisone
  2. Mycophenolate mofetil
  3. Tacrolimus
  4. Sirolimus (correct answer)
Explanation: When you encounter pulmonary complications in transplant patients, you need to distinguish between infectious causes (common due to immunosuppression) and drug-specific adverse effects. This case presents a classic non-infectious pulmonary toxicity pattern. The patient's bilateral interstitial infiltrates, dry cough, and dyspnea developing after switching to sirolimus points directly to sirolimus-induced pneumonitis. This is a well-recognized, potentially serious adverse effect of mTOR inhibitors like sirolimus, occurring in 5-15% of patients. The mechanism involves inflammatory infiltration of lung tissue, creating the interstitial pattern seen on chest imaging. Choice A (Prednisone) is incorrect because corticosteroids typically suppress inflammation and would be more likely to predispose to infections rather than cause interstitial pneumonitis. Choice B (Mycophenolate mofetil) can cause GI toxicity and bone marrow suppression but is not associated with this specific pulmonary syndrome. Choice C (Tacrolimus) was actually discontinued due to nephrotoxicity, and calcineurin inhibitors don't typically cause interstitial lung disease. The timing is crucial here - the patient was recently switched to sirolimus, and symptoms developed over four weeks, which fits the typical onset pattern for sirolimus pneumonitis. Study tip: Remember that mTOR inhibitors (sirolimus, everolimus) have a unique side effect profile including pneumonitis, delayed wound healing, and hyperlipidemia - effects not seen with other immunosuppressants. When you see interstitial lung disease in a transplant patient on sirolimus, always consider drug-induced pneumonitis before assuming infection.

Question 3

A 72-year-old man with a history of a remote duodenal ulcer is being started on therapy for metastatic prostate cancer, which includes high-dose dexamethasone. Concurrently, his orthopedic surgeon has prescribed celecoxib for severe osteoarthritis pain.

The combination of these two medications significantly increases the patient's risk for which adverse event, warranting prophylactic intervention?

  1. Acute kidney injury
  2. Severe myelosuppression
  3. Thromboembolic events
  4. Gastrointestinal bleeding (correct answer)
Explanation: When you encounter questions about drug combinations and adverse events, focus on how each medication's mechanism amplifies shared risks, especially in vulnerable patient populations. Dexamethasone (a corticosteroid) and celecoxib (a COX-2 selective NSAID) both independently increase gastrointestinal bleeding risk through different mechanisms. Dexamethasone reduces the protective gastric mucus barrier and delays ulcer healing, while celecoxib decreases prostaglandin E2 production, which normally protects the gastric mucosa. When combined, these effects are synergistic, not just additive. This patient's history of duodenal ulcer makes him particularly high-risk, as the protective mechanisms are already compromised. The combination creates a perfect storm warranting prophylactic proton pump inhibitor therapy. Looking at the incorrect options: (A) Acute kidney injury could theoretically occur with celecoxib alone, but the combination doesn't significantly amplify this risk compared to GI bleeding. (B) Severe myelosuppression isn't associated with either dexamethasone at these doses or celecoxib - this would be more relevant with chemotherapeutic agents. (C) Thromboembolic events can occur with corticosteroids, but celecoxib (unlike some other NSAIDs) doesn't significantly increase this risk, and it's not the primary concern requiring immediate prophylaxis. Remember this pattern: corticosteroid + NSAID = high GI bleeding risk, especially in elderly patients with ulcer history. Always consider prophylactic PPI therapy for this combination, and watch for questions testing synergistic adverse effects rather than simple drug interactions.

Question 4

A patient with severe asthma is treated with a 14-day course of oral prednisone, starting at 40 mg daily. The physician instructs the patient to taper the dose over the final 7 days of the course rather than stopping it abruptly.

The primary pharmacological reason for this gradual dose reduction is to allow for the recovery of which physiological process?

  1. Endogenous cortisol production by the adrenal cortex. (correct answer)
  2. Pro-inflammatory cytokine synthesis by immune cells.
  3. Glucocorticoid receptor sensitivity in target tissues.
  4. Insulin secretion by pancreatic beta cells.
Explanation: Administration of exogenous corticosteroids for more than 2-3 weeks suppresses the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus reduces CRH production, the pituitary reduces ACTH production, and the adrenal cortex atrophies and ceases to produce endogenous cortisol. Abrupt withdrawal of the exogenous steroid can cause acute adrenal insufficiency, as the atrophied glands cannot mount a response. A gradual taper allows the HPA axis to recover its function and resume normal cortisol production. Rebound inflammation (B) is a clinical concern, but the critical physiological reason for the taper is preventing adrenal crisis.

Question 5

A 6-month-old infant who received a heart transplant is on an immunosuppressive regimen including high-dose corticosteroids. The infant's mother reports a recent visit from a cousin who developed a rash and was diagnosed with chickenpox the next day.

What is the most urgent concern for this infant?

  1. Risk of developing Reye's syndrome from the varicella infection.
  2. Risk of disseminated varicella infection with visceral involvement. (correct answer)
  3. Risk of post-herpetic neuralgia following the primary infection.
  4. Risk of bacterial superinfection of the cutaneous lesions.
Explanation: The infant is severely immunocompromised due to the transplant and high-dose corticosteroid therapy. Primary infection with varicella-zoster virus (chickenpox) in such a patient can be life-threatening. Instead of a typical self-limited rash, they are at high risk for disseminated disease, which involves visceral organs like the lungs (pneumonia), liver (hepatitis), and brain (encephalitis), and carries a high mortality rate. This is the most immediate and severe risk. Reye's syndrome is associated with aspirin use during viral illness. Post-herpetic neuralgia follows zoster (shingles), not primary varicella. Bacterial superinfection is a risk, but less urgent than visceral dissemination.

Question 6

A 62-year-old male with newly diagnosed multiple myeloma is initiated on a treatment regimen that includes high-dose dexamethasone (40 mg daily for 4 days). The patient has a past medical history significant for well-controlled type 2 diabetes mellitus and hypertension.

Which of the following adverse effects is most likely to require immediate and significant medical intervention within the first week of therapy?

  1. Development of posterior subcapsular cataracts.
  2. Marked hyperglycemia requiring insulin therapy. (correct answer)
  3. Avascular necrosis of the femoral head.
  4. Significant reduction in bone mineral density.
Explanation: High-dose corticosteroids like dexamethasone have potent metabolic effects, including causing insulin resistance and increasing gluconeogenesis. In a patient with pre-existing diabetes, this almost invariably leads to severe, acute hyperglycemia that requires close monitoring and often initiation or significant intensification of insulin therapy. The other options are serious long-term complications of chronic corticosteroid use that would not manifest acutely within the first week of treatment.

Question 7

A 28-year-old woman with lupus nephritis is treated with mycophenolate mofetil (MMF) 1.5 g twice daily. After several months of therapy, she complains of persistent, watery diarrhea, significant abdominal cramping, and fatigue. Her complete blood count shows a new normocytic anemia and mild leukopenia.

These clinical and laboratory findings are most characteristic of toxicity affecting which two organ systems by the therapeutic agent?

  1. Renal and neurologic
  2. Hepatic and dermatologic
  3. Gastrointestinal and hematopoietic (correct answer)
  4. Cardiovascular and musculoskeletal
Explanation: Mycophenolate mofetil has two major dose-limiting toxicities: gastrointestinal (diarrhea, vomiting, cramping) and hematopoietic (leukopenia, anemia, thrombocytopenia). The patient's presentation of severe diarrhea and cramping combined with anemia and leukopenia is a classic picture of MMF toxicity. The other organ systems listed are not the primary sites of MMF's common adverse effects.

Question 8

A 52-year-old postmenopausal woman is diagnosed with polymyalgia rheumatica and is expected to require treatment with prednisone 15 mg daily for at least one year. A baseline DEXA scan reveals osteopenia (T-score -1.8). She is counseled to take supplemental calcium and vitamin D.

In addition to calcium and vitamin D, which intervention is most strongly recommended to mitigate a major long-term risk of her steroid therapy?

  1. Initiation of a weekly oral bisphosphonate. (correct answer)
  2. Regular screening with serum parathyroid hormone levels.
  3. A low-impact exercise regimen such as swimming.
  4. Annual monitoring of 24-hour urine calcium excretion.
Explanation: Long-term corticosteroid use is a leading cause of secondary osteoporosis. For a postmenopausal woman with pre-existing osteopenia starting a dose of prednisone ≥7.5 mg/day for an anticipated duration of >3 months, pharmacologic prophylaxis is indicated to prevent glucocorticoid-induced osteoporosis and fractures. An oral bisphosphonate (e.g., alendronate, risedronate) is the first-line recommended agent. While lifestyle modifications like exercise are beneficial, they are not sufficient. Monitoring PTH or urine calcium are not standard primary prevention strategies in this context.

Question 9

A 6-year-old child is undergoing induction chemotherapy for acute lymphoblastic leukemia (ALL), which includes intermittent high-dose dexamethasone. The child is scheduled for a well-child visit with their pediatrician, and their immunization record indicates they are due for the MMR (measles, mumps, rubella) and varicella vaccines.

What is the most appropriate action regarding the administration of these vaccines?

  1. Administer both vaccines as scheduled to maintain the immunization schedule.
  2. Administer the MMR vaccine but hold the varicella vaccine due to higher risk.
  3. Withhold both vaccines as they are contraindicated during this period. (correct answer)
  4. Administer inactivated versions of both the MMR and varicella vaccines.
Explanation: The patient is profoundly immunosuppressed due to both the ALL itself and the intensive chemotherapy regimen, including high-dose corticosteroids. The MMR and varicella vaccines are live attenuated vaccines. Administering live vaccines to a severely immunocompromised individual is absolutely contraindicated because it can lead to disseminated, life-threatening infection from the vaccine-strain virus. Both must be withheld until the patient's immune system has recovered, typically several months after completing chemotherapy. There are no inactivated versions of the MMR or varicella vaccines.

Question 10

A 55-year-old female lung transplant recipient, maintained on tacrolimus, mycophenolate mofetil, and a low-dose prednisone taper, presents with a two-week history of non-productive cough, progressive dyspnea, and low-grade fever. A chest CT reveals diffuse ground-glass opacities. Bronchoalveolar lavage is performed, and a silver stain of the fluid is positive.

Given these findings, the patient's symptoms are most likely caused by an infection with which pathogen?

  1. Streptococcus pneumoniae
  2. Influenza A virus
  3. Pneumocystis jirovecii (correct answer)
  4. Mycobacterium tuberculosis
Explanation: This patient's presentation—subacute onset of dyspnea, cough, fever, and diffuse ground-glass opacities on imaging—in the context of profound T-cell immunosuppression (especially from tacrolimus) is classic for Pneumocystis jirovecii pneumonia (PJP). The positive silver stain on the BAL fluid is a key diagnostic finding for PJP. While the other pathogens can cause pneumonia in immunosuppressed hosts, the clinical syndrome and diagnostic findings strongly point to PJP, a well-known opportunistic infection in this population, often occurring if prophylaxis is missed or ineffective.

Question 11

A 44-year-old renal transplant recipient presents with a gradually rising serum creatinine one year after transplantation. An allograft biopsy is performed. Histopathology reveals viral cytopathic changes within the tubular epithelial cells and a positive immunohistochemical stain for the SV40 large T antigen.

This finding is most indicative of nephropathy caused by the reactivation of which virus, a known complication of the patient's immunosuppressive state?

  1. Cytomegalovirus (CMV)
  2. Epstein-Barr virus (EBV)
  3. Herpes simplex virus (HSV)
  4. BK polyomavirus (correct answer)
Explanation: When you encounter a renal transplant patient with rising creatinine and viral cytopathic changes, you need to consider opportunistic infections that arise from immunosuppression. The key diagnostic clue here is the positive immunohistochemical stain for SV40 large T antigen, which is pathognomonic for a specific virus. BK polyomavirus (D) is the correct answer because it's the only virus among the choices that contains the SV40 large T antigen. BK virus belongs to the polyomavirus family and shares antigenic properties with SV40. This virus commonly causes polyomavirus-associated nephropathy (PVAN) in immunocompromised patients, particularly renal transplant recipients. The characteristic presentation includes gradually rising creatinine, tubular epithelial cell damage with viral inclusions, and positive SV40 T antigen staining. Cytomegalovirus (A) can cause nephritis in transplant patients, but it produces characteristic owl's eye inclusions and tests positive for CMV antigens, not SV40 T antigen. Epstein-Barr virus (B) primarily causes post-transplant lymphoproliferative disorder rather than direct nephropathy, and it has its own specific antigenic markers. Herpes simplex virus (C) rarely causes significant nephropathy in transplant recipients and would stain positive for HSV antigens. Remember this pattern: when you see a renal transplant patient with nephropathy and positive SV40 T antigen staining, think BK polyomavirus. This specific immunohistochemical marker is virtually diagnostic for BK virus reactivation, making it a high-yield association for pharmacology exams covering immunosuppression complications.

Question 12

A 34-year-old male with moderate-to-severe Crohn's disease that has been refractory to conventional therapy is being considered for treatment with infliximab. His medical history is notable for travel to Southeast Asia five years ago.

Prior to initiating infliximab, which of the following screening protocols is most critical to prevent a potentially fatal infectious complication?

  1. Serologic testing for Hepatitis C virus and HIV.
  2. Stool testing for Clostridioides difficile toxin.
  3. Tuberculin skin test or interferon-gamma release assay. (correct answer)
  4. Serum antibody titers for varicella-zoster virus.
Explanation: Infliximab is a tumor necrosis factor-alpha (TNF-α) inhibitor. TNF-α is crucial for granuloma formation and containment of Mycobacterium tuberculosis. Administration of a TNF-α inhibitor can lead to the reactivation of latent tuberculosis infection (LTBI), which can be life-threatening. Therefore, screening for LTBI with either a tuberculin skin test (TST) or an interferon-gamma release assay (IGRA) is mandatory before starting therapy. While other infection screenings are important in immunosuppressed patients, the risk of TB reactivation with TNF-α inhibitors is a specific and major concern requiring universal screening.

Question 13

A 55-year-old female lung transplant recipient, maintained on tacrolimus, mycophenolate mofetil, and a low-dose prednisone taper, presents with a two-week history of non-productive cough, progressive dyspnea, and low-grade fever. A chest CT reveals diffuse ground-glass opacities. Bronchoalveolar lavage is performed, and a silver stain of the fluid is positive.

Given these findings, the patient's symptoms are most likely caused by an infection with which pathogen?

  1. Streptococcus pneumoniae
  2. Influenza A virus
  3. Pneumocystis jirovecii (correct answer)
  4. Mycobacterium tuberculosis
Explanation: This patient's presentation—subacute onset of dyspnea, cough, fever, and diffuse ground-glass opacities on imaging—in the context of profound T-cell immunosuppression (especially from tacrolimus) is classic for Pneumocystis jirovecii pneumonia (PJP). The positive silver stain on the BAL fluid is a key diagnostic finding for PJP. While the other pathogens can cause pneumonia in immunosuppressed hosts, the clinical syndrome and diagnostic findings strongly point to PJP, a well-known opportunistic infection in this population, often occurring if prophylaxis is missed or ineffective.

Question 14

A 62-year-old male with newly diagnosed multiple myeloma is initiated on a treatment regimen that includes high-dose dexamethasone (40 mg daily for 4 days). The patient has a past medical history significant for well-controlled type 2 diabetes mellitus and hypertension.

Which of the following adverse effects is most likely to require immediate and significant medical intervention within the first week of therapy?

  1. Development of posterior subcapsular cataracts.
  2. Marked hyperglycemia requiring insulin therapy. (correct answer)
  3. Avascular necrosis of the femoral head.
  4. Significant reduction in bone mineral density.
Explanation: High-dose corticosteroids like dexamethasone have potent metabolic effects, including causing insulin resistance and increasing gluconeogenesis. In a patient with pre-existing diabetes, this almost invariably leads to severe, acute hyperglycemia that requires close monitoring and often initiation or significant intensification of insulin therapy. The other options are serious long-term complications of chronic corticosteroid use that would not manifest acutely within the first week of treatment.

Question 15

A 70-year-old female patient is being treated with high-dose prednisone for giant cell arteritis. Three weeks into therapy, her daughter reports that the patient has become increasingly irritable, sleeps only 2-3 hours per night, and has started expressing paranoid thoughts that her neighbors are spying on her. The patient is agitated and has disorganized speech during the clinic visit.

What is the most appropriate initial step in managing this patient's new-onset symptoms?

  1. Initiate a high-potency antipsychotic such as haloperidol.
  2. Discontinue prednisone immediately due to severe neurotoxicity.
  3. Reduce the prednisone dose to the lowest effective level possible. (correct answer)
  4. Add a benzodiazepine to manage agitation and insomnia.
Explanation: The patient is exhibiting classic signs of steroid-induced psychosis, a known dose-dependent neuropsychiatric side effect of corticosteroids. The primary and most definitive management is to reduce the corticosteroid dose as much as the underlying inflammatory condition allows. While antipsychotics or benzodiazepines may be used as adjuncts for severe symptoms, they are not the primary treatment; dose reduction is. Abruptly discontinuing prednisone for a condition like giant cell arteritis is dangerous and could lead to disease relapse and permanent vision loss.

Question 16

A 28-year-old woman with lupus nephritis is treated with mycophenolate mofetil (MMF) 1.5 g twice daily. After several months of therapy, she complains of persistent, watery diarrhea, significant abdominal cramping, and fatigue. Her complete blood count shows a new normocytic anemia and mild leukopenia.

These clinical and laboratory findings are most characteristic of toxicity affecting which two organ systems by the therapeutic agent?

  1. Renal and neurologic
  2. Hepatic and dermatologic
  3. Gastrointestinal and hematopoietic (correct answer)
  4. Cardiovascular and musculoskeletal
Explanation: Mycophenolate mofetil has two major dose-limiting toxicities: gastrointestinal (diarrhea, vomiting, cramping) and hematopoietic (leukopenia, anemia, thrombocytopenia). The patient's presentation of severe diarrhea and cramping combined with anemia and leukopenia is a classic picture of MMF toxicity. The other organ systems listed are not the primary sites of MMF's common adverse effects.

Question 17

A 58-year-old liver transplant recipient maintained on tacrolimus presents for a routine follow-up. He complains of a new tremor in his hands, persistent headache, and notes his home blood pressure readings are consistently elevated. Laboratory tests reveal a blood glucose of 180 mg/dL (fasting) and a serum creatinine of 1.9 mg/dL (baseline 1.2 mg/dL).

This constellation of findings is most consistent with which of the following?

  1. Subtherapeutic levels of tacrolimus leading to graft rejection.
  2. Supratherapeutic levels of tacrolimus leading to systemic toxicity. (correct answer)
  3. An opportunistic cytomegalovirus (CMV) infection.
  4. Development of post-transplant lymphoproliferative disorder (PTLD).
Explanation: The patient's symptoms and lab findings—neurotoxicity (tremor, headache), hypertension, nephrotoxicity (rising creatinine), and hyperglycemia—are all hallmark toxicities of calcineurin inhibitors like tacrolimus. This clinical picture strongly suggests that the drug levels are too high (supratherapeutic). Subtherapeutic levels would risk rejection, often presenting with rising liver enzymes in this patient. While CMV and PTLD are risks, they do not typically present with this specific combination of multi-system toxicities directly attributable to the drug.

Question 18

A 66-year-old male with dermatomyositis was treated with high-dose prednisone, resulting in good control of his rash and initial improvement in muscle strength. After 4 months of therapy, he presents with worsening difficulty climbing stairs and rising from a chair. His rash remains quiescent. A physical exam confirms progressive, symmetric proximal muscle weakness. Laboratory testing reveals a normal serum creatine kinase (CK) level.

What is the most likely cause of the patient's new-onset muscle weakness?

  1. A flare of his underlying dermatomyositis.
  2. Development of steroid-induced myopathy. (correct answer)
  3. Hypokalemia secondary to corticosteroid therapy.
  4. Disuse atrophy from prolonged inactivity.
Explanation: This is a classic presentation of steroid-induced myopathy. It is characterized by the insidious onset of painless, symmetric proximal muscle weakness, typically occurring after prolonged exposure to high-dose corticosteroids. A key distinguishing feature is a normal or near-normal serum CK level. In contrast, a flare of inflammatory myositis (like dermatomyositis) would be associated with a significantly elevated CK. While hypokalemia can cause weakness, it's less likely to be the primary cause of this progressive picture. Disuse atrophy is possible but less likely to be the main driver than the direct toxic effect of the steroids.

Question 19

A 45-year-old renal transplant recipient, whose immunosuppression was recently changed from tacrolimus to sirolimus due to calcineurin inhibitor-induced nephropathy, presents with a 4-week history of dyspnea on exertion and a persistent, dry cough. His oxygen saturation is 92% on room air. A chest X-ray shows bilateral interstitial infiltrates.

This patient's presentation is most suggestive of a serious, non-infectious pulmonary complication specifically associated with which of his medications?

  1. Prednisone
  2. Mycophenolate mofetil
  3. Tacrolimus
  4. Sirolimus (correct answer)
Explanation: When you encounter pulmonary complications in transplant patients, you need to distinguish between infectious causes (common due to immunosuppression) and drug-specific adverse effects. This case presents a classic non-infectious pulmonary toxicity pattern. The patient's bilateral interstitial infiltrates, dry cough, and dyspnea developing after switching to sirolimus points directly to sirolimus-induced pneumonitis. This is a well-recognized, potentially serious adverse effect of mTOR inhibitors like sirolimus, occurring in 5-15% of patients. The mechanism involves inflammatory infiltration of lung tissue, creating the interstitial pattern seen on chest imaging. Choice A (Prednisone) is incorrect because corticosteroids typically suppress inflammation and would be more likely to predispose to infections rather than cause interstitial pneumonitis. Choice B (Mycophenolate mofetil) can cause GI toxicity and bone marrow suppression but is not associated with this specific pulmonary syndrome. Choice C (Tacrolimus) was actually discontinued due to nephrotoxicity, and calcineurin inhibitors don't typically cause interstitial lung disease. The timing is crucial here - the patient was recently switched to sirolimus, and symptoms developed over four weeks, which fits the typical onset pattern for sirolimus pneumonitis. Study tip: Remember that mTOR inhibitors (sirolimus, everolimus) have a unique side effect profile including pneumonitis, delayed wound healing, and hyperlipidemia - effects not seen with other immunosuppressants. When you see interstitial lung disease in a transplant patient on sirolimus, always consider drug-induced pneumonitis before assuming infection.

Question 20

A 72-year-old man with a history of a remote duodenal ulcer is being started on therapy for metastatic prostate cancer, which includes high-dose dexamethasone. Concurrently, his orthopedic surgeon has prescribed celecoxib for severe osteoarthritis pain.

The combination of these two medications significantly increases the patient's risk for which adverse event, warranting prophylactic intervention?

  1. Acute kidney injury
  2. Severe myelosuppression
  3. Thromboembolic events
  4. Gastrointestinal bleeding (correct answer)
Explanation: When you encounter questions about drug combinations and adverse events, focus on how each medication's mechanism amplifies shared risks, especially in vulnerable patient populations. Dexamethasone (a corticosteroid) and celecoxib (a COX-2 selective NSAID) both independently increase gastrointestinal bleeding risk through different mechanisms. Dexamethasone reduces the protective gastric mucus barrier and delays ulcer healing, while celecoxib decreases prostaglandin E2 production, which normally protects the gastric mucosa. When combined, these effects are synergistic, not just additive. This patient's history of duodenal ulcer makes him particularly high-risk, as the protective mechanisms are already compromised. The combination creates a perfect storm warranting prophylactic proton pump inhibitor therapy. Looking at the incorrect options: (A) Acute kidney injury could theoretically occur with celecoxib alone, but the combination doesn't significantly amplify this risk compared to GI bleeding. (B) Severe myelosuppression isn't associated with either dexamethasone at these doses or celecoxib - this would be more relevant with chemotherapeutic agents. (C) Thromboembolic events can occur with corticosteroids, but celecoxib (unlike some other NSAIDs) doesn't significantly increase this risk, and it's not the primary concern requiring immediate prophylaxis. Remember this pattern: corticosteroid + NSAID = high GI bleeding risk, especially in elderly patients with ulcer history. Always consider prophylactic PPI therapy for this combination, and watch for questions testing synergistic adverse effects rather than simple drug interactions.