Understanding aminoglycosides — potent bactericidal antibiotics used for serious gram‑negative and some gram‑positive infections — is crucial for B. Pharm students. This concise overview explains aminoglycoside mechanism (irreversible binding to the 30S ribosomal subunit causing misreading of mRNA and inhibited protein synthesis), pharmacokinetics (renal elimination, concentration-dependent killing, post-antibiotic effect), common agents (gentamicin, amikacin, streptomycin, tobramycin) and major toxicities, especially ototoxicity (cochlear and vestibular hair‑cell damage mediated by reactive oxygen species and genetic susceptibility). Emphasis is placed on monitoring, prevention, and resistance mechanisms. Now let’s test your knowledge with 30 MCQs on this topic.
Q1. Which of the following best describes the primary mechanism of action of aminoglycosides?
- Reversible inhibition of the 50S ribosomal subunit
- Irreversible binding to the 30S ribosomal subunit causing misreading of mRNA
- Inhibition of folate synthesis by blocking dihydropteroate synthase
- Disruption of bacterial cell wall by inhibiting peptidoglycan cross-linking
Correct Answer: Irreversible binding to the 30S ribosomal subunit causing misreading of mRNA
Q2. Aminoglycosides are most active against which type of bacteria?
- Anaerobic gram-positive cocci
- Aerobic gram-negative bacilli
- Intracellular organisms like Chlamydia
- Fungal pathogens
Correct Answer: Aerobic gram-negative bacilli
Q3. The entry of aminoglycosides into gram-negative bacteria relies on which process?
- Energy-independent passive diffusion through porins
- Oxygen-dependent active transport across the inner membrane
- Endocytosis mediated by lipoteichoic acid
- Facilitated diffusion via efflux pumps
Correct Answer: Oxygen-dependent active transport across the inner membrane
Q4. Which aminoglycoside is classically used for drug-resistant tuberculosis and targets the 30S subunit?
- Gentamicin
- Streptomycin
- Neomycin
- Tobramycin
Correct Answer: Streptomycin
Q5. Aminoglycoside killing is best characterized as:
- Time-dependent killing with no post-antibiotic effect
- Concentration-dependent killing with a significant post-antibiotic effect
- Bacteriostatic and dependent on protein synthesis inhibition only
- Dependent solely on maintaining trough levels above MIC
Correct Answer: Concentration-dependent killing with a significant post-antibiotic effect
Q6. Which monitoring parameter correlates most closely with aminoglycoside toxicity risk?
- Peak plasma concentration
- Trough plasma concentration
- Time above MIC
- Area under the curve (AUC) only
Correct Answer: Trough plasma concentration
Q7. A common pharmacokinetic property of aminoglycosides is:
- Hepatic metabolism with biliary excretion
- Extensive tissue binding in adipose tissue
- Renal elimination by glomerular filtration
- High oral bioavailability
Correct Answer: Renal elimination by glomerular filtration
Q8. Which mechanism is a major bacterial resistance strategy against aminoglycosides?
- Production of beta-lactamases
- Modification of the 30S ribosome by methyltransferases
- Increased porin expression
- Synthesis of alternate folate pathways
Correct Answer: Modification of the 30S ribosome by methyltransferases
Q9. Aminoglycoside ototoxicity primarily affects which cells in the inner ear?
- Stria vascularis epithelial cells
- Inner and outer hair cells of the cochlea and vestibular hair cells
- Spiral ganglion neurons only
- Endothelial cells of cochlear vessels
Correct Answer: Inner and outer hair cells of the cochlea and vestibular hair cells
Q10. Which clinical sign is most suggestive of cochlear (auditory) ototoxicity?
- Vertigo and loss of balance
- Tinnitus and high-frequency hearing loss
- Peripheral neuropathy with paresthesia
- Renal tubular acidosis
Correct Answer: Tinnitus and high-frequency hearing loss
Q11. Which factor increases the risk of aminoglycoside-induced ototoxicity?
- Young age and rapid drug clearance
- Concomitant use of loop diuretics and renal impairment
- Short duration of therapy with low cumulative dose
- Concurrent administration of beta-lactam antibiotics
Correct Answer: Concomitant use of loop diuretics and renal impairment
Q12. The mitochondrial A1555G mutation is clinically important because it:
- Confers resistance to aminoglycosides in bacteria
- Predisposes patients to aminoglycoside-induced hearing loss
- Protects renal tubular cells from toxicity
- Enhances aminoglycoside renal clearance
Correct Answer: Predisposes patients to aminoglycoside-induced hearing loss
Q13. Which aminoglycoside is commonly used topically and is highly nephrotoxic if given systemically?
- Amikacin
- Neomycin
- Gentamicin
- Tobramycin
Correct Answer: Neomycin
Q14. For serious gram-negative infections, what dosing strategy often reduces nephrotoxicity while maintaining efficacy?
- Multiple daily low-dose administration
- Once-daily (extended-interval) high-dose administration
- Continuous intravenous infusion over 72 hours
- Oral administration with activated charcoal
Correct Answer: Once-daily (extended-interval) high-dose administration
Q15. Aminoglycosides exhibit synergistic bactericidal activity when combined with which class for enterococcal endocarditis?
- Fluoroquinolones
- Glycopeptides
- Beta-lactams
- Sulfonamides
Correct Answer: Beta-lactams
Q16. Which laboratory test is most useful to detect early cochlear damage from aminoglycosides?
- Serum creatinine measurement
- Pure tone audiometry, especially high-frequency testing
- Urinalysis for proteinuria
- Complete blood count
Correct Answer: Pure tone audiometry, especially high-frequency testing
Q17. Which statement about aminoglycoside trough and peak levels is correct?
- High peaks increase toxicity; troughs are irrelevant
- Peaks correlate with efficacy; high troughs correlate with toxicity
- Troughs correlate with efficacy; peaks correlate with toxicity
- Neither peak nor trough monitoring is clinically useful
Correct Answer: Peaks correlate with efficacy; high troughs correlate with toxicity
Q18. Which adverse effect besides ototoxicity is a major concern with aminoglycosides?
- Hepatotoxicity leading to jaundice
- Nephrotoxicity causing acute tubular necrosis
- Severe cardiotoxicity with arrhythmias
- Bone marrow suppression with pancytopenia
Correct Answer: Nephrotoxicity causing acute tubular necrosis
Q19. Which practice can help reduce aminoglycoside ototoxicity in clinical use?
- Prolonging therapy duration whenever possible
- Co-administering loop diuretics routinely
- Therapeutic drug monitoring and avoiding high troughs
- Using oral formulations for systemic infections
Correct Answer: Therapeutic drug monitoring and avoiding high troughs
Q20. The primary molecular event by which aminoglycosides cause bacterial death is:
- Inhibition of cell wall synthesis leading to lysis
- Production of defective proteins that disrupt bacterial membranes
- Blocking DNA gyrase and causing DNA breaks
- Inhibition of folate metabolism required for nucleotide synthesis
Correct Answer: Production of defective proteins that disrupt bacterial membranes
Q21. Aminoglycosides are ineffective against anaerobic bacteria primarily because:
- Anaerobes have thick cell walls impermeable to drugs
- Uptake of aminoglycosides requires oxygen-dependent transport absent in anaerobes
- Anaerobes possess intrinsic 30S methylation rendering drugs inactive
- Aminoglycosides are inactivated by stomach acid before reaching anaerobes
Correct Answer: Uptake of aminoglycosides requires oxygen-dependent transport absent in anaerobes
Q22. Which aminoglycoside is preferred for Pseudomonas aeruginosa infections?
- Tobramycin
- Streptomycin
- Neomycin
- Linezolid
Correct Answer: Tobramycin
Q23. Which cellular process in cochlear hair cells contributes to aminoglycoside ototoxicity?
- Inhibition of mitochondrial protein synthesis leading to reactive oxygen species
- Activation of nuclear DNA repair mechanisms
- Increased synthesis of myelin in auditory nerves
- Enhanced glutathione production protecting hair cells
Correct Answer: Inhibition of mitochondrial protein synthesis leading to reactive oxygen species
Q24. Which dosing adjustment is most appropriate in a patient with reduced renal function?
- Increase dose and shorten dosing interval
- Decrease dose or extend dosing interval based on creatinine clearance
- Continue standard dosing because aminoglycosides are hepatically cleared
- Switch to oral aminoglycoside to reduce toxicity
Correct Answer: Decrease dose or extend dosing interval based on creatinine clearance
Q25. Aminoglycoside-modifying enzymes confer resistance by:
- Altering cell wall porins to prevent entry
- Phosphorylating, acetylating, or adenylating the drug molecule
- Methylating human mitochondrial ribosomes only
- Cleaving the drug into inactive metabolites via beta-lactamase-like action
Correct Answer: Phosphorylating, acetylating, or adenylating the drug molecule
Q26. In therapeutic drug monitoring for gentamicin, typical target peak and trough levels for serious infections are approximately:
- Peak 0.5–1 mcg/mL; trough <0.1 mcg/mL
- Peak 5–10 mcg/mL; trough <2 mcg/mL
- Peak 50–100 mcg/mL; trough 20–30 mcg/mL
- Peak and trough values are not measured clinically
Correct Answer: Peak 5–10 mcg/mL; trough <2 mcg/mL
Q27. Which clinical scenario should raise immediate concern for aminoglycoside ototoxicity?
- New onset tinnitus during gentamicin therapy
- Transient mild nausea after a single dose
- Stable hearing with mild headache
- Decrease in blood pressure unrelated to dosing
Correct Answer: New onset tinnitus during gentamicin therapy
Q28. Which drug interaction markedly increases the risk of ototoxicity when combined with aminoglycosides?
- ACE inhibitors such as lisinopril
- Loop diuretics such as furosemide
- Oral antidiabetics like metformin
- Topical corticosteroids for dermatitis
Correct Answer: Loop diuretics such as furosemide
Q29. Which statement about amikacin is true?
- It is least useful for resistant gram-negative infections
- It is designed to resist many aminoglycoside-modifying enzymes
- It is primarily eliminated by hepatic metabolism
- It has no ototoxic potential
Correct Answer: It is designed to resist many aminoglycoside-modifying enzymes
Q30. Which preventive measure is experimental but studied to reduce aminoglycoside ototoxicity?
- Co-administration of iron supplements to increase ROS
- Use of antioxidants or iron chelators to reduce reactive oxygen species
- Increasing dosing frequency to maintain constant levels
- Combining with other ototoxic drugs for protective effect
Correct Answer: Use of antioxidants or iron chelators to reduce reactive oxygen species
I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.
Mail- Sachin@pharmacyfreak.com