Therapeutics: DIN 1

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  1. Where is the most common area for drug induced kidney injury?
  2. What drugs damage the Tubules?
    • Aminoglycosides
    • Radiologic contrast media
    • Cisplatin (Platinol) and Carboplatin (Paraplatin)
    • Amphotericin B (Fungizone)
  3. What are the AGs that cause DIN and in what order are they nephrotoxic to the tubules?
    Neomycin > gentamicin & tobramycin > amikacin > streptomycin & netilmicin
  4. What is the MOA of aminoglycoside induced DIN?
    • Proximal tubule epithelial damage
    • Leads to obstruction of tubular lumen and back-leakage of glomerular filtrate
  5. What presentation is characteristic of aminoglycoside induced DIN?
    • Gradual increase in SCr and decrease in CrCl after 6-10 days of therapy
    • Non-oliguric decreases in K and Mg may also occur
  6. What are the predisposing factors for Aminoglycoside induced nephrotoxicity?
    • Dehydration
    • Hypotension
    • Pre-existing renal insufficiency
    • Increased age
    • Shock
    • G- bacteremia
    • Liver disease
    • Obstructive jaundice
    • Poor nutrition
    • Hypoalbuminemia
    • K or Mg deficiencies
  7. What other drugs should you not administer concomitantly with Aminoglycosides due to risk of nephrotoxicity?
    • Amphotericin B
    • Vancomycin
    • Diuretics
    • CSA
    • Contrast Dye
    • Cisplatin
    • NSAIDs
  8. What dosing recommendations should be made to avoid aminoglycoside nephrotoxicity?
    • Trough should not be > 2mg/L
    • Watch large doses and prolonged therapy
  9. What non-dosing practices can you use to prevent aminoglycoside nephrotoxicity?
    • Maintain Hydration and hemodynamic stability
    • D/C other nephrotoxic agents
    • Caution use of QD dosing
    • D/C if SCr is > 0.5 mg/dL
    • Limit time on therapy and dose size
  10. What are the 1st generation Iodinated contrast dyes?
    • Ioxaglate (Hexabrix)
    • Iothalamate (Conray)
    • Diatrizoate (Cystografin)
  11. What are the 2nd generation Iodinated contrast dyes?
    • Iohexol (Omnipaque)
    • Ioversol (Optiray)
    • Iopamidol (Isovue)
  12. Are 1st generation contrasts dyes considered ionic or non-ionic?
  13. Are 2nd generation contrasts dyes considered ionic or non-ionic?
  14. Are 1st generation contrasts dyes considered hyperosmolar or low osmolar?
  15. Are 2nd generation contrasts dyes considered hyperosmolar or low osmolar?
    Low Osmolar
  16. What are the risk factors for Contrast nduced nephrotoxicity?
    • Renal insufficiency (SCr >1.5, eGFR < 60)
    • Diabetes
    • Dehydration
    • CV disease (HF, MI)
    • Age >70
    • Myeloma
    • HTN
    • Hyperuricemia
    • Large volume contrast
    • Multiple contrast examinations within a short time interval
  17. Metformin with Contrast dye can cause what adverse reaction?
    Lactic acidosis
  18. When should you start stop Metformin when contrast dye is going to be used?
    • Stop: at time or before or procedure
    • Start: 48 hours after procedure and after evaluation of kidney function
  19. What is the MOA of Cisplatin and Carboplatin in DIN?
    • Binds cellular proteins and forms sulfhydryl groups
    • Disrupts cell enzyme activity
    • Uncouples oxidative phosphorylation
    • Creates reactive O2 intermediates
  20. What are the risk factors for developing DIN from Carboplatin and Cisplatin?
    • Increased age
    • Dehydration
    • AGs
    • Alcohol abuse
    • Renal irradiation
  21. What type of damage occurs due to Cisplatin and Carboplatin?
    Proximal tubule damage
  22. What is the clinical presentation for Cisplatin or Carboplatin DIN?
    • SCr peaks 10-12 days after therapy
    • Should go down after 21 days
    • Can cause irreversible chronic renal failure
    • Damage is cumulative from treatments
    • Low K, Ca, Mg
  23. What is Amfostine used for?
    Pretreatment for Cisplatin and Carboplatin to reduce myelosupression, ototoxicities, Neuro and nephro-toxicities
  24. What is the dose for Amifostine for Carboplatin, Cisplatin pretreatment?
    • 910 mg/m^2
    • Give 30 minutes before cisplatin
  25. Describe the MOA of Amfostine:
    • Organic thiophosphate
    • Chelates platins
  26. Is Cisplatin/Carboplatin therapy reversible
    • May be
    • Cumulative toxicity may not be
  27. What is the MOA of Amphotericin B in DIN?
    • Direct tubular epithelial damage
    • Increase tubular permeability and necrosis
    • Arterial vasoconstriction
    • Ischemic damage
  28. What is the clinical presentation of Amphotericin B caused DIN?
    • Increased SCr and BUN
    • Decreased K, Na and Mg
    • Impaired urine concentrating abilities
  29. What are the risk factors for Amphotericin B caused DIN?
    • Baseline renal insufficiency
    • High average daily dose, or rapid infusion
    • Diuretics, volume depletion
    • Concomitant nephrotoxic drugs (i.e. cyclosporine)
  30. What are the liposomal amphotericin B formulations?
    • Amphotec
    • Abelcet
    • Ambisome
  31. What ways can you prevent Amphotericin B DIN?
    • Limit cumulative dose
    • Avoid concomitant nephrotoxins
    • Hydrate w/ 1 IV NS or high Na diet
    • Use liposomal formulations
  32. What can cause Tubular epithelial damage through osmotic nephrosis?
    • Mannitol
    • LMW Dextran
    • Radio contrast dye
    • Propylene glycol
    • Immune globulin
  33. What are the mechanisms of osmotic nephrosis?
    • Form vacuoles and causes swelling
    • Leads to necrosis and proximal tubular epithelial damage
  34. Osmotic dieresis/volume depletion can increase nephrotoxicity of what drugs?
    • NSAIDs
    • ACEIs
    • CSA
  35. How can you prevent osmotic nephrosis?
    • Limit dose of offending agent
    • Avoid dehydration
    • Watch concomitant diuretics
  36. What drugs can cause hemodynamically medicated AKI?
    • ACEIs/ARBs
    • NSAIDs
    • Cyclospirne (CSA) or Tacrolimus
Card Set:
Therapeutics: DIN 1
2014-05-03 04:43:01
Therapeutics DIN
Therapeutics: DIN 1
Therapeutics: DIN 1
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