Aminoglycosides and Antimicrobial Agents Flashcards
Aminoglycosides
Gentamicin, Tobramycin, Amikacin, Streptomycin, Neomycin
Aminoglycoside MOA
inhibit protein synt., intracellular, BIND IRREVERSIBLE TO 30S SUBUNIT (resistance opposite)
Aminoglycoside Kinetics
cidal, conc. dependent killing, antimicrobial effect continues after conc. not measurable for 1-3 hours.
Aminoglycosides
poor oral absorption, distribution to ECF, polar (enters cells through pores), poor CSF penetration, 99% unchanged by kidneys
Aminoglycoside Monitoring
peaks and troughs daily 6-14 hours post dose, hartford nomogram
Aminoglycoside ADR
ototoxicity, tinnitus, hearing loss, loss of balance, nephrotoxicity, respiratory paralysis
Mycobacteria
intracellular pathogens, slow growing, can be dormant, cell wall impermeable to many agents, combo therapy required
Tuberculosis
caused by mycobacterium tuberculosis, causes latent or active infection, 1/3 of world pop. infected
Latent TB
treatment allows for lesser chance to contract active infection, isoniazid for 9mo., rifampin x4mo.
Active TB
Rifampin, Isoniazid, pyrazinamide, ethambutol, lasts 6mo. but resistant strains could take up to two years to treat
1st line Antimycobacterials
Isoniazid, rifampin, pyrazinamide, ethambutol, streptomycin
2nd line Antimycobacterials
Ethionamide, cycloserine, amkacin, aminosallicylic acid, capreomycin, clofazimine, levofloxacin, ciprofloxacin, rifabutin, rifapentine
Isoniazid MOA
inhibits synt. of mycolic acids in cell wall, pro-drug, cidal, static in resting organisms. well absorbed, into CSF, metabolized in liver, out in urine, NO DOSAGE ADJUSTMENT IN RENAL IMPAIRMENT
Isoniazid ADE
neuropathy (give with B6 supplementation), hepatits, GI, CNS, Rash
Rifampin MOA
RNA polymerase inhibitor, cidal, staph, H. influenzae, neisseria, p450 inducer, excreted into bile