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MICABI - Exam 1


aminoglycosides (8) Streptomycin; Neomycin; Kanamycin; Tobramycin; Paromomycin; Gentamicin; Netilmicin; Amikacin
aminoglycosides commonly used systemically (3) Tobramycin; Gentamicin; Amikacin
aminoglycoside mechanism of action They interact with the 30S subunit of the ribosome and block protein synthesis; Aminoglycosides get into bacteria through porin proteins and electron transport (energy-dependent)
aminoglycoside concentrations aminoglycosides are known to be rapidly bactericidal and this killing effect depends on the concentration of the drug (shoot for 5-6x MIC for Cmax)
resistance mechanisms for aminoglycosides (3) 1) ribosomal resistance (mycobacteria); 2) resistance due to decreased drug uptake (anaerobes); 3) resistance caused by aminoglycoside modifying enzymes (**most important clinically) - strains will show higher MICs than strains of same species w/o upregul
aminoglycoside spectrum potent against gram negatives (enterococcus varies); not very active against gram positives except staph
aminoglycosides with beta-lactams results in synergy (common for endocarditis)
aminoglycoside with chloramphenicol results in antagonism
aminoglycoside PK very polar - poorly absorbed orally (1%) so given IV; distributed poorly but accumulate in high levels in kidneys; not metabolized - excreted unchanged
aminoglycosides toxicities (3) 1) neuromuscular blockade; 2) ototoxicity; 3) nephrotoxicity
aminoglycoside toxicity mechanism drug enters cell lysosome, inhibits mitochondrial function and Na/K ATPase, cell swells and ruptures
aminoglycoside toxicity time course only observable after 5-7 days of therapy
aminoglycoside toxicity reversibility nephrotoxicity usually reversible after D/C; ototoxicity not always reversible (depends on extent of damage; vestibular damage usually permanent)
aminoglycoside toxicity - comparisons among them for ototoxicity netilmicin the least toxic; rest are equal
aminoglycoside toxicity - comparisons among them for nephrotoxicity Gentamicin>tobramycin>amikacin>netilmicin
concentrations at risk for oto/nephrotoxicity with aminoglycosides > 2 mg/L (gentamicin/tobramycin) or 8-10 (amikacin)
Gentamicin specifics used to treat serious infection of gram negative bacilli. Most gentamicin-resistant strains are cross resistant to tobramycin but are susceptible to amikacin. It is more nephrotoxic than tobramycin, but roughly equivalent in ototoxic potential.
Tobramycin specifics similar to gentamicin except that it is much less active against enterococci, Tobramycin is not active against mycobacteria.
Amikacin specifics Resistant to most of the aminoglycoside modifying enzyme; broadest spectrum of activity; use should be limited to severe infections by strains suspected of being resistant to gentamicin and tobramycin
Netilmicin specifics newest of the aminoglycosides in the market. More resistant to aminoglycoside modifying enzyme and less toxic than gentamicin.
Kanamycin specifics given orally to kill the bowl flora prior to intestinal surgery.
Neomycin specifics very nephrotoxic, and is no longer administered parenterally. The primary use is in the topical treatment of superficial infection of the skin and eye
Streptomycin specifics role has declined; can used in combination with a penicillin to treat bacterial endocarditis due to S. viridans and enterococcus; still used for tuberculosis and other uncommon infections (plague, brucellosis…).
Paromomycin specifics used only for treating intestinal amebiasis.
Created by: Krafty