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Aminoglycosides

Created: 17/10/2005

 

AMINOGLYCOSIDES

Gentamicin
Neomycin
Streptomycin
Netilmicin
Amikacin
Kanamycin
Tobramycin

Mechanism of action

  • Aminoglycosides are bactericidal
  • Initial site of action is the outer bacterial cell membrane
  • Antibiotic molecules create fissures in the cell membrane
  • Bind to the 30s ribosome and inhibit bacterial protein synthesis
  • NB Aminoglycoside uptake into bacteria cells is active. Anaerobes have less energy available for this uptake, so aminoglycosides are less active against anaerobes
  • NB Exhibit rapid concentration-dependent killing action

Indications

  • Gram-negative sepsis

  • Complicated skin, bone or soft tissue infection
  • Complicated UTI
  • Septicemia
  • Peritonitis
  • Severe pelvic inflammatory disease
  • Endocarditis
  • Mycobacterium infection
  • Neonatal sepsis

Distribution

  • Poorly absorbed from GI tract
  • Primarily distributed in EC fluid – tissue concentration is much less than in plasma
  • Exception is urine, otic perilymph and renal cortical tissue

Excretion

  • Excreted unchanged (ie not metabolised) into the urine by glomerular filtration
  • Plasma half-life 2-3 hrs (much higher with renal impairment and in elderly)
  • NB half-life in renal cortex approx 100hrs, half-life in patients with renal dysfunction 30-60 hrs

Side effects and Drug Interactions

  • Nephrotoxiticy
    • Usually reversible
    • Caused by renal cortical accumulation, binding to the brush border of the tubular epithelium resulting in proximal convoluted tubular cell degeneration and sloughing
    • NB Risk Factors for Nephrotoxicity
    • Modifiable - diuretics, IVcontrast exposure, hypovolaemia, ACE inhibitors, NSAIDs, other nephrotoxic medications
    • Non-modifiable – age, renal dysfunction
  • Ototoxity
    • Usually irreversible
  • Neuromuscular blockade
  • Parasthesia
  • Peripheral neuropathy
  • Hypersensitivity reactions

ArticleDate:20051017
SiteSection: Article
 
   
    
                                            



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