WorksheetsNephrotoxic drugs
Total questions: 8
Worksheet time: 16mins
An elderly patient with heart failure is prescribed furosemide and gentamicin. After several days, he develops acute kidney injury. Which best explains the mechanism of toxicity in this case?
Crystal deposition in distal tubules
Additive tubular injury and reduced renal perfusion
Immune-mediated inflammation of the interstitium
Increased efferent arteriole vasodilation lowering GFR
A 65-year-old woman develops acute kidney injury within 5 days of starting NSAIDs for arthritis. Which mechanism is most likely responsible?
Afferent arteriole vasoconstriction due to prostaglandin inhibition
Efferent arteriole vasodilation due to angiotensin II blockade
Mitochondrial dysfunction in proximal tubular cells
Precipitation of drug crystals in renal tubules
A patient on methotrexate therapy presents with reduced urine output and flank pain. Urinalysis shows crystal deposition. Which preventive strategy would have been most effective?
Administering high-dose vitamin C
Ensuring adequate hydration and urine alkalinisation
Using angiotensin receptor blockers instead of methotrexate
Reducing methotrexate dose gradually
Which of the following best explains why older adults with multiple comorbidities are at increased risk of drug-induced nephrotoxicity?
Higher tubular transporter activity increases drug uptake
Larger renal reserve allows more drug exposure
Reduced GFR, and altered pharmacokinetics
Enhanced hepatic clearance compensates for renal impairment
In rhabdomyolysis-induced kidney injury, which mechanism contributes most to acute tubular obstruction?
Formation of myoglobin casts in distal tubules
Afferent arteriole vasodilation increasing hydrostatic pressure
Autoimmune attack on tubular basement membrane
Excess bicarbonate reabsorption causing alkalosis
A patient taking ACE inhibitors and NSAIDs develops acute kidney injury. What is the main reason for this interaction?
Both drugs cause tubular necrosis through oxidative stress
Both drugs inhibit renal autoregulation of GFR
Both drugs increase renal clearance of creatinine
Both drugs reduce urine concentration ability
Aminoglycosides (e.g., gentamicin) cause nephrotoxicity primarily through:
Crystal deposition in the tubules
Tubular cell toxicity and acute tubular necrosis
Alteration of glomerular hemodynamics
Induction of immune-mediated inflammation
How does therapeutic drug monitoring (TDM) help in preventing nephrotoxicity?
By replacing renal function tests
By ensuring drug concentrations remain in the therapeutic range
By preventing dehydration
By blocking immune-mediated kidney injury
