1. AMINOGLYCOSIDES Streptomycin* Gentamicin* Tobramycin* Amikacin Kanamycin Neomycin(topical) * most commonly used Antibacterial Spectrum Bactericidal ( exclusive for aerobic G- bacteria ) M. Tuberculosis ( streptomycin & amikacin ) Not effective against G+ & anaerobes

2. AMINOGLYCOSIDES ( Cont. ) Pharmacokinetics Polycations ( highly charged ) Poorly absorbed from GIT ( parenteral or topical ) No distribution to most cells, including CNS Only 10 % bind of the drug bind to plasma protein No significant metabolic breakdown Excreted unchanged in urine ( glomerular filtration) Half- life 2-3 hrs

3. AMINOGLYCOSIDES ( Cont. ) Mechanism of action Inhibit protein synthesis ( 30 s subunit ) Bactericidal Inhibition of cell wall synthesis increases their entrance into cells ( synergism ) eg.: Piperacillin or ceftazidime + gent. or tobra. Against P.aeruginosae

4. Clinical Use T.B ( streptomycin, i.m ) P. Aeruginosa infections ( other than UTI’s ) an aminoglycoside+ piperacillin or an aminoglycoside+ ceftazidime (p.aeruginosa UTI’s, ciprofloxacin preferred) Brucellosis in combination with a tetracycline( severe cases) Topical Creams, ointments or solution for infected burns, wounds or skin lesions. Ear & eye drops and ointments

5. Adverse Effects Ototoxicity & nephrotoxicity ( directly related to serum conc. ) Neuromuscular blockade ( very high dose ) Special problems with AGS use : Narrow toxic- therapeutic ratio Monitoring of serum levels