Chloramphenicol – mechanism and toxicity MCQs With Answer

Chloramphenicol – mechanism and toxicity MCQs With Answer

Chloramphenicol is a broad‑spectrum antibiotic that inhibits bacterial protein synthesis by binding the 50S ribosomal peptidyl‑transferase center. B.Pharm students must master its mechanism of action, pharmacokinetics (excellent CSF penetration, hepatic glucuronidation), resistance (plasmid‑encoded chloramphenicol acetyltransferase, efflux), and serious toxicities such as dose‑related reversible bone marrow suppression, unpredictable idiosyncratic aplastic anemia, and gray baby syndrome in neonates due to immature glucuronidation. This concise, keyword‑rich introduction prepares you to apply clinical reasoning about indications, monitoring, and management of adverse effects. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. What is the primary mechanism of action of chloramphenicol?

  • Inhibition of DNA gyrase
  • Inhibition of peptidyl transferase on the 50S ribosomal subunit
  • Disruption of cell wall synthesis by inhibiting transpeptidase
  • Blocking 30S ribosomal initiation complex formation

Correct Answer: Inhibition of peptidyl transferase on the 50S ribosomal subunit

Q2. Chloramphenicol binds primarily to which ribosomal component?

  • 16S rRNA of the 30S subunit
  • 23S rRNA of the 50S subunit (peptidyl‑transferase center)
  • L30 protein of the 50S subunit
  • Initiation factors IF1 and IF2

Correct Answer: 23S rRNA of the 50S subunit (peptidyl‑transferase center)

Q3. Which statement explains chloramphenicol’s association with aplastic anemia?

  • It causes predictable dose‑dependent destruction of mature neutrophils only
  • It induces idiosyncratic, often irreversible bone marrow stem cell damage
  • It triggers autoimmune hemolysis due to RBC membrane disruption
  • It chelates iron leading to ineffective erythropoiesis

Correct Answer: It induces idiosyncratic, often irreversible bone marrow stem cell damage

Q4. The major enzymatic resistance mechanism to chloramphenicol is:

  • Methylation of 23S rRNA by Erm methylase
  • Acetylation by chloramphenicol acetyltransferase (CAT)
  • Plasmid‑encoded beta‑lactamase
  • Production of aminoglycoside‑modifying enzymes

Correct Answer: Acetylation by chloramphenicol acetyltransferase (CAT)

Q5. Gray baby syndrome occurs primarily because neonates have:

  • Enhanced renal clearance of chloramphenicol
  • Immature hepatic glucuronidation leading to drug accumulation
  • Upregulated chloramphenicol acetyltransferase activity
  • Increased blood‑brain barrier exclusion of the drug

Correct Answer: Immature hepatic glucuronidation leading to drug accumulation

Q6. Chloramphenicol’s antibacterial spectrum includes:

  • Only Gram‑positive cocci
  • Primarily mycobacteria
  • Broad spectrum: many Gram‑positives, Gram‑negatives, anaerobes and rickettsiae
  • Only obligate intracellular organisms

Correct Answer: Broad spectrum: many Gram‑positives, Gram‑negatives, anaerobes and rickettsiae

Q7. One important clinical use of chloramphenicol historically has been:

  • First‑line therapy for uncomplicated urinary tract infections
  • Empiric outpatient therapy for community‑acquired pneumonia
  • Alternative therapy for severe meningitis when other agents are contraindicated
  • Topical treatment of fungal skin infections

Correct Answer: Alternative therapy for severe meningitis when other agents are contraindicated

Q8. Which pharmacokinetic property of chloramphenicol explains its use in meningitis?

  • Poor oral absorption
  • Extensive protein binding preventing CNS entry
  • Excellent cerebrospinal fluid (CSF) penetration
  • Rapid renal excretion of unchanged drug

Correct Answer: Excellent cerebrospinal fluid (CSF) penetration

Q9. The principal metabolic pathway for chloramphenicol in adults is:

  • Renal filtration of unchanged drug
  • Hepatic glucuronidation
  • Acetylation by N‑acetyltransferase in the gut
  • Oxidation by monoamine oxidase

Correct Answer: Hepatic glucuronidation

Q10. Which of the following best describes chloramphenicol’s hematologic toxicities?

  • Only reversible neutropenia that resolves despite continued therapy
  • Both dose‑related reversible bone marrow suppression and idiosyncratic aplastic anemia
  • Exclusively hemolytic anemia in G6PD deficiency
  • Only thrombocytosis without clinical consequence

Correct Answer: Both dose‑related reversible bone marrow suppression and idiosyncratic aplastic anemia

Q11. A classic laboratory finding in drug‑induced aplastic anemia from chloramphenicol is:

  • Hypercellular bone marrow with megaloblastic changes
  • Pancytopenia with hypocellular (aplastic) marrow
  • Isolated high reticulocyte count with normal hemoglobin
  • Leukocytosis with left shift

Correct Answer: Pancytopenia with hypocellular (aplastic) marrow

Q12. The first step in managing suspected chloramphenicol‑induced aplastic anemia is:

  • Continue drug and start corticosteroids
  • Immediate discontinuation of chloramphenicol and supportive care
  • Switch to a higher dose to overcome resistance
  • Administer penicillin to prevent secondary infection

Correct Answer: Immediate discontinuation of chloramphenicol and supportive care

Q13. Chloramphenicol can cause clinically significant drug interactions by:

  • Inducing CYP450 enzymes and lowering other drug levels
  • Inhibiting hepatic enzymes and increasing levels of coadministered drugs
  • Chelating divalent cations and reducing absorption of fluoroquinolones
  • Accelerating renal secretion of anticoagulants

Correct Answer: Inhibiting hepatic enzymes and increasing levels of coadministered drugs

Q14. The primary route of elimination for chloramphenicol metabolites is:

  • Fecal excretion of unchanged drug
  • Renal excretion of glucuronide metabolites
  • Exhalation via the lungs
  • Sequestration in adipose tissue

Correct Answer: Renal excretion of glucuronide metabolites

Q15. Which monitoring is essential during prolonged chloramphenicol therapy?

  • Weekly liver ultrasound
  • Periodic complete blood counts (CBCs) to detect marrow suppression
  • Daily blood glucose measurements
  • Weekly audiometry

Correct Answer: Periodic complete blood counts (CBCs) to detect marrow suppression

Q16. Chloramphenicol is generally considered to be:

  • Bactericidal against most Gram‑positive organisms
  • Bacteriostatic against many organisms but can be bactericidal for some strains
  • Only fungistatic
  • Antiviral at therapeutic doses

Correct Answer: Bacteriostatic against many organisms but can be bactericidal for some strains

Q17. The enzyme that inactivates chloramphenicol by acetylation is abbreviated as:

  • CAT (chloramphenicol acetyltransferase)
  • TMP (trimethoprim reductase)
  • MDR1 (multidrug resistance protein 1)
  • G6PD (glucose‑6‑phosphate dehydrogenase)

Correct Answer: CAT (chloramphenicol acetyltransferase)

Q18. The binding of chloramphenicol to the bacterial ribosome is best described as:

  • Irreversible covalent modification of ribosomal proteins
  • Reversible inhibition of the peptidyl transferase activity
  • Competitive inhibition of aminoacyl‑tRNA synthetase
  • Allosteric activation of ribosomal RNA

Correct Answer: Reversible inhibition of the peptidyl transferase activity

Q19. Cross‑resistance between chloramphenicol and macrolides is:

  • Common because both methylate 23S rRNA
  • Uncommon because resistance mechanisms differ; acetylation causes chloramphenicol resistance
  • Absolute; resistance to one always confers resistance to the other
  • Dependent on porin mutations only

Correct Answer: Uncommon because resistance mechanisms differ; acetylation causes chloramphenicol resistance

Q20. In which patient population is chloramphenicol especially contraindicated?

  • Healthy adults with uncomplicated skin infections
  • Neonates due to risk of gray baby syndrome
  • Patients with mild hypertension
  • Adults taking low‑dose aspirin

Correct Answer: Neonates due to risk of gray baby syndrome

Q21. The idiosyncratic aplastic anemia associated with chloramphenicol is:

  • Clearly dose‑related and predictable
  • Unpredictable and not clearly dose‑related
  • Preventable by coadministration of folic acid
  • Limited to patients with hepatic failure

Correct Answer: Unpredictable and not clearly dose‑related

Q22. The pathophysiology of gray baby syndrome primarily involves:

  • Immune‑mediated vasculitis
  • Accumulation of unmetabolized drug due to immature liver conjugation
  • Excessive urinary losses of electrolytes
  • Blockade of peripheral dopamine receptors

Correct Answer: Accumulation of unmetabolized drug due to immature liver conjugation

Q23. The exact molecular target within the 50S subunit is often cited as:

  • Peptidyl‑transferase center in 23S rRNA
  • Decoding center in 16S rRNA
  • L7/L12 ribosomal protein complex
  • Ribosomal exit tunnel in 5S rRNA

Correct Answer: Peptidyl‑transferase center in 23S rRNA

Q24. By inhibiting peptidyl transferase, chloramphenicol directly prevents:

  • Peptide bond formation between amino acids during elongation
  • Initiation complex assembly at the start codon
  • Termination factor binding at stop codons
  • Amino acid charging of tRNA by synthetases

Correct Answer: Peptide bond formation between amino acids during elongation

Q25. An early hematologic sign of dose‑related chloramphenicol toxicity is:

  • Elevated platelet count
  • Decreased reticulocyte count and mild anemia
  • Marked eosinophilia
  • Polycythemia

Correct Answer: Decreased reticulocyte count and mild anemia

Q26. Definitive therapy for severe chloramphenicol‑induced aplastic anemia may include:

  • High‑dose chloramphenicol to outcompete the toxic metabolite
  • Hematopoietic stem cell (bone marrow) transplantation in selected cases
  • Long‑term oral iron supplementation alone
  • Topical steroids

Correct Answer: Hematopoietic stem cell (bone marrow) transplantation in selected cases

Q27. Chloramphenicol primarily blocks which phase of protein synthesis?

  • Initiation by preventing 30S assembly
  • Elongation by inhibiting peptidyl transferase activity
  • Termination by blocking release factors
  • Post‑translational protein folding in the cytosol

Correct Answer: Elongation by inhibiting peptidyl transferase activity

Q28. Plasmid‑mediated chloramphenicol resistance is most commonly found in which organisms?

  • Gram‑negative Enterobacteriaceae carrying CAT genes
  • Mycobacterium tuberculosis strains only
  • Obligate anaerobes that lack plasmids
  • Fungal pathogens

Correct Answer: Gram‑negative Enterobacteriaceae carrying CAT genes

Q29. Therapeutic drug monitoring for chloramphenicol is:

  • Never useful and not available
  • Occasionally used in neonates or severe toxicity to guide dosing
  • Mandatory for all outpatient prescriptions
  • Only used to detect bacterial resistance

Correct Answer: Occasionally used in neonates or severe toxicity to guide dosing

Q30. If chloramphenicol is contraindicated in bacterial meningitis, a commonly used alternative is:

  • Topical mupirocin
  • Third‑generation cephalosporin (e.g., ceftriaxone or cefotaxime)
  • Oral metronidazole monotherapy
  • Antifungal amphotericin B

Correct Answer: Third‑generation cephalosporin (e.g., ceftriaxone or cefotaxime)

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