Antibiotics Flashcards
(28 cards)
Definition: Concentration of abx needed to inhibit bacterial growth; lowest concentration of antibiotic that completely inhibits growth
Minimum inhibitory concenration
Definition: the serum concentration of an antimicrobial achieved with optimal dosing
Breakpoint
Def: The MIC inhibits the growth of the bacterium
Bacteriostatic
Def. The MIC to inhibit and kill bacterium are close
Bacteriocidal
What are the bacteriostatic drugs?
Lincosamides, macrolides, chloramphenicol, tetracyclines, sulfonamides, trimethoprim (BUT NOT TMS!). LMCTST (lewd mothers call teachers stupid taints).
What are the concentration dependent drugs?
Flroroquinolones, aminoglycosies, metronidazole; azitrhomycin and tetracyclines have mixed
What are the time dependent?
B-lactames, macrolides, lincosamides, tetracycline, chloramphenicol, potentiated sulfonamides
What abx inhibit cell wall synthesis?
Beta lactams (penicillins, cephalosporins, penems), vancomycin
Amoxicillin: Spectrum? Where does it get high concenrtation? Metabolism? Excretion?
Spectrum - Excellent G+ (staph, strep, enterococci), some G-, Proteus, anaerobes. High conc - kidney, liver, lung. Meta: hydosis of the b-lactam ring. Renal tubule excretion
Cephasporins: Spectrum? Distribution? Metabolism? Excretion?
Excellent against Gram +, proteus, klebsiella –> as generations advance get increase G- activity and less resistance. Distribution: blood, urine, bile, pleural, bone. Metabolism - cefotaxime deacetylaction. Excretion - renal
Carbapenems: Spectrum? Excretion?
G+ and -, anaerobes; renal elimination
Vancomycin: Spectrum? Where does it get high concenrtation? Metabolism? Excretion?
Gram + only, tissues/fluids, no metabolism, renally excreted
Protein synthesis inhibitors:
30S and 50s
30s - aminoglycosides and tetracycline
50s - chloramphenicl, macrolides and lincosamides
Aminoglycosides: Spectrum? Where does it get high concenrtation? Metabolism? Excretion?
Gram - infections, poor in CNS and respiratory tissue, no metabolism, renal excretion. 30s!
Chloramphenicol: Where does it get high concenrtation? Metabolism? Excretion? Possible SE?
Distribution: CNS, eye, tissue. Metabolism - glucoronidations in the liver. Renal metobolite excretions. SE: Reversible BM suppression. 50s!
MOA of Fusidic acid?
Inhibits protein synthesis
Lincosamine: Spectrum? Where does it get high concenrtation? Metabolism?
Gram + mostly, distribution high in the liver, kidney, GI, brain, low in the CSF; metbolized in the liver. 50s!
Macrolides: Spectrum? Where does it get high concenrtation? Metabolism? Excretion?
Gram +, tissue concentration better than fluid - does not cross the BBB. Metabolized in the liver - cyp 450 enzyme inducers can result in treatment failure. Excreted in the bile and feces. 50s!
Tetracyclines: Spectrum? Where does it get high concenrtation? Metabolism? Excretion?
Broad (+/-, rickettsia). Penetrates brain, spinal fluid and prostate; renal and fecal excretion
What drugs inhibit nucleic acid synthesis/function?
Nitrofurantion, nitroimidazoles, fluoroquinolones, rifampin
Nitroimidazoles: Spectrum? Where does it get high concenrtation? Metabolism? Excretion?
Anaerobic* and protozoal infections; high distribution in tissue; metabolism - liver oxidation and glucoronide formation. Eliminated in the urine. Metronidazole!
FQs: MOA?Spectrum? Where does it get high concenrtation? Metabolism? Excretion?
MOA - bind the DNA gyrase. Gram - and some gram +, distrubuted in fluids and tissue; Metabolism - enrofloxacin is de-ethulated to cipro. Excreted renal.
Rifampin: MOA? SE?
Binds DNA-dependent RNA polymerase. Hepatotoxicity.
What drug(s) cause damage to the cell membrane?
Polymixins and detergents