Thioguanine MCQs With Answer offers B. Pharm students a focused, clinically oriented review of thioguanine pharmacology, mechanism of action, metabolism, toxicities and monitoring. This concise set emphasizes key concepts: conversion to 6‑thioguanine nucleotides, activation by HGPRT, modulation by TPMT, myelosuppression, hepatotoxicity (including veno‑occlusive disease), drug interactions and therapeutic uses in hematologic malignancies. Questions target pharmacokinetics, resistance mechanisms, genetic testing, adverse‑effect management and safe prescribing principles. Designed to strengthen exam readiness and clinical reasoning, these MCQs integrate biochemical pathways with practical monitoring strategies and safety precautions. Now let’s test your knowledge with 30 MCQs on this topic.
Q1. Which pharmacologic class does thioguanine belong to?
- Alkylating agent
- Antimetabolite (thiopurine)
- Topoisomerase inhibitor
- Monoclonal antibody
Correct Answer: Antimetabolite (thiopurine)
Q2. The primary cytotoxic effect of thioguanine is due to incorporation of its metabolites into which macromolecule?
- Carbohydrates
- Lipids
- DNA
- Collagen
Correct Answer: DNA
Q3. Which enzyme is responsible for initial activation of thioguanine into thioguanine nucleotides?
- Xanthine oxidase
- Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)
- CYP3A4
- Thiopurine methyltransferase (TPMT)
Correct Answer: Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)
Q4. Thiopurine methyltransferase (TPMT) primarily affects thioguanine therapy by:
- Increasing renal excretion of the drug
- Methylating and inactivating metabolites, altering toxicity and efficacy
- Enhancing incorporation into RNA only
- Activating thioguanine to an active nucleotide
Correct Answer: Methylating and inactivating metabolites, altering toxicity and efficacy
Q5. A patient with inherited TPMT deficiency receiving standard thioguanine doses is at highest risk for:
- Hypertension
- Severe myelosuppression
- Hypoglycemia
- Peripheral neuropathy
Correct Answer: Severe myelosuppression
Q6. The most common and clinically significant adverse effect of thioguanine requiring routine monitoring is:
- Renal failure
- Myelosuppression (neutropenia, anemia, thrombocytopenia)
- Cardiac arrhythmia
- Ototoxicity
Correct Answer: Myelosuppression (neutropenia, anemia, thrombocytopenia)
Q7. Which hepatic complication is classically associated with thioguanine use?
- Portal hypertension due to nodular regenerative hyperplasia / veno‑occlusive disease
- Acute viral hepatitis
- Cholestatic jaundice from bile duct obstruction
- Autoimmune hepatitis
Correct Answer: Portal hypertension due to nodular regenerative hyperplasia / veno‑occlusive disease
Q8. Thioguanine is most commonly indicated in which of the following conditions?
- Chronic myeloid leukemia as a single agent
- Acute myeloid leukemia as part of combination chemotherapy
- Type 2 diabetes mellitus
- Bronchial asthma
Correct Answer: Acute myeloid leukemia as part of combination chemotherapy
Q9. What is the usual route of administration for thioguanine in clinical practice?
- Oral
- Intravenous only
- Intramuscular only
- Topical
Correct Answer: Oral
Q10. Compared with mercaptopurine, thioguanine’s interaction with allopurinol (xanthine oxidase inhibitor) is generally:
- Markedly increased causing severe toxicity
- Less pronounced because xanthine oxidase is not the major pathway
- Causes immediate hepatic failure
- Results in complete inactivation of thioguanine
Correct Answer: Less pronounced because xanthine oxidase is not the major pathway
Q11. Essential baseline and ongoing monitoring for a patient on thioguanine should include:
- Complete blood count (CBC) and liver function tests (LFTs)
- Fasting blood glucose only
- Chest X‑ray every week
- Urinalysis only
Correct Answer: Complete blood count (CBC) and liver function tests (LFTs)
Q12. Which of the following is a contraindication or major precaution for thioguanine therapy?
- Pregnancy due to teratogenic risk
- History of controlled hypothyroidism
- Corrected vitamin D deficiency
- Well-controlled seasonal allergies
Correct Answer: Pregnancy due to teratogenic risk
Q13. The active cytotoxic metabolites of thioguanine are collectively called:
- 6‑thioguanine nucleotides (6‑TGNs)
- 7‑methylguanine derivatives
- Thiouracil fragments
- Azathioprine metabolites
Correct Answer: 6‑thioguanine nucleotides (6‑TGNs)
Q14. A common mechanism of cellular resistance to thioguanine is:
- Upregulation of HGPRT activity
- Decreased activity of HGPRT (reduced activation)
- Increased drug accumulation in the nucleus
- Enhanced incorporation into DNA
Correct Answer: Decreased activity of HGPRT (reduced activation)
Q15. Therapeutic drug monitoring of thioguanine can involve measurement of:
- Serum creatinine only
- 6‑thioguanine nucleotide (6‑TGN) concentrations in red blood cells
- Plasma glucose
- Serum albumin levels
Correct Answer: 6‑thioguanine nucleotide (6‑TGN) concentrations in red blood cells
Q16. Intracellular 6‑TGN persistence implies that dose interruptions may still lead to:
- Immediate elimination of toxicity
- Prolonged myelosuppression after stopping therapy
- Instant return to normal liver histology
- Increased renal clearance
Correct Answer: Prolonged myelosuppression after stopping therapy
Q17. When combining thioguanine with other myelosuppressive agents, the primary clinical concern is:
- Synergistic renal toxicity
- Additive or synergistic myelosuppression
- Loss of antitumor activity of both drugs
- Enhanced protein binding leading to hypoalbuminemia
Correct Answer: Additive or synergistic myelosuppression
Q18. Before initiating thioguanine therapy, genotyping or phenotyping for which enzyme is recommended to reduce risk of severe toxicity?
- CYP2D6
- Thiopurine methyltransferase (TPMT)
- Glucose‑6‑phosphate dehydrogenase (G6PD)
- Butyrylcholinesterase
Correct Answer: Thiopurine methyltransferase (TPMT)
Q19. The cytotoxicity of thioguanine primarily causes cell death by:
- Inhibiting microtubule polymerization
- Incorporation into DNA causing strand breaks and apoptosis
- Blocking acetylcholine release
- Chelating essential ions in the bloodstream
Correct Answer: Incorporation into DNA causing strand breaks and apoptosis
Q20. Thioguanine tablets should be dispensed with counseling to avoid which patient behavior?
- Taking with a high‑calcium meal
- Missing routine blood tests and LFT monitoring
- Using with topical creams
- Regular exercise during therapy
Correct Answer: Missing routine blood tests and LFT monitoring
Q21. Which statement about thioguanine pharmacokinetics is accurate?
- It is mainly eliminated unchanged in urine without metabolism
- It undergoes intracellular conversion to active nucleotides and extensive metabolism
- It is a large protein‑bound biologic with no intracellular activity
- It is administered intravenously exclusively due to poor oral absorption
Correct Answer: It undergoes intracellular conversion to active nucleotides and extensive metabolism
Q22. Methylation of thioguanine metabolites by TPMT results in:
- Formation of inactive methylated metabolites that reduce 6‑TGN formation
- Direct activation to more potent DNA‑incorporated nucleotides
- Immediate renal excretion of the active drug
- Increased risk of pulmonary fibrosis
Correct Answer: Formation of inactive methylated metabolites that reduce 6‑TGN formation
Q23. Which supportive therapy is commonly considered for severe neutropenia caused by thioguanine?
- Granulocyte colony‑stimulating factor (G‑CSF)
- High‑dose insulin
- Oral iron supplementation only
- Topical antibiotics
Correct Answer: Granulocyte colony‑stimulating factor (G‑CSF)
Q24. Chronic hepatic toxicity from thioguanine may present clinically as:
- Progressive jaundice, portal hypertension and splenomegaly
- Acute pancreatitis with elevated lipase only
- Isolated rhinorrhea and sinusitis
- Hyperthyroidism symptoms
Correct Answer: Progressive jaundice, portal hypertension and splenomegaly
Q25. Which of the following best describes thioguanine’s effect on purine synthesis?
- It directly donates purine bases for DNA synthesis
- It disrupts de novo purine synthesis and causes incorporation of false nucleotides
- It enhances purine salvage exclusively without cytotoxicity
- It only affects pyrimidine metabolism
Correct Answer: It disrupts de novo purine synthesis and causes incorporation of false nucleotides
Q26. Use of thioguanine in inflammatory bowel disease (IBD) is limited primarily because of:
- High risk of hepatotoxicity including nodular regenerative hyperplasia
- Lack of any immunosuppressive effect
- Rapid renal accumulation causing nephritis
- Inability to be absorbed from the GI tract
Correct Answer: High risk of hepatotoxicity including nodular regenerative hyperplasia
Q27. Which laboratory value change is an early indicator of thioguanine toxicity that requires prompt action?
- Falling white blood cell and neutrophil counts
- Gradual rise in hemoglobin
- Decreased serum uric acid within normal range
- Stable platelet count
Correct Answer: Falling white blood cell and neutrophil counts
Q28. Increased TPMT activity in a tumor cell would most likely result in:
- Enhanced formation of 6‑TGN and greater cytotoxicity
- Increased methylation of the drug leading to reduced therapeutic effect
- Immediate cell lysis from osmotic shock
- Complete prevention of drug absorption in the gut
Correct Answer: Increased methylation of the drug leading to reduced therapeutic effect
Q29. Which clinical action is recommended before starting thioguanine to minimize severe toxicity?
- Assess TPMT activity or genotype
- Administer a test dose of high intensity radiation
- Start concurrent high‑dose allopurinol without monitoring
- Discontinue all vaccines permanently
Correct Answer: Assess TPMT activity or genotype
Q30. Which symptom is a possible manifestation of thioguanine‑induced mucosal toxicity?
- Mucositis and oral ulcers
- Decreased visual acuity only
- Chronic dry skin without inflammation
- Isolated hair thinning with no mucosal signs
Correct Answer: Mucositis and oral ulcers
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