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59 Cards in this Set
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- Back
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name the 9 classes of drugs that are protein synthesis inhibitors
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1. aminoglycosides
2. tetracycline's 3. glycylcyclin's 4. macrolides 5. lincosamides 6. chloramphenicol 7. streptogramins 8. oxazolidinones 9. mupirocin |
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the protein synthesis inhibitors are bactericidal or bacteriostatic
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bacteriostatic except aminoglycosides and mupirocin
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aminoglycosides binds to ____
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both 30 and 50s subunits
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what binds 30s subunits?
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tetracycline's and spectinomycin
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what binds 50s subunits?
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macrolides, chloramphenicol, streptogramins, lincosamides
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what does linezolid do?
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prevents formation of 70s
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what does mupirocin do?
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binds tRNA
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how does aminoglycosides work?
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1. prevents initiation meth-t-RNA from binding
2. binds to interface b/w 30 and 50s subunits 3. enhances early breakdown of ribosomal unit |
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how does tetracyclines work?
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1. bind 30s subunit to prevent t-RNA from binding to A site
2. prevent elongation of peptide 3. binding reversible, when drug gone synthesis resumes |
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how does macrolides work?
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1. bind 50s subunit
2. interferes with transfer of peptide t-RNA complex from site A to P site 3. prevents elongation |
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how does ketolides work?
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1. bind 50s subunit
2. interferes with initiation complex 3. interferes with transfer of peptide t-RNA complex from site A to P site 4. prevents elongation |
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how does lincosamides work?
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1. bind 50s subunits
2. interferes with initiation complex 3. site very close to macrolides & chloramphenicol 4. precents elongation |
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whats special lincosamides?
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it can sterically inhibit other drugs binding to their site, do not use together.
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how does chloramphenicol work?
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1. bind 50s subunit
2. inhibits bond formation between peptide and new amino acid 3. binding reversible |
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name the 2 streptogramins
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dalfopristin and quinupristin
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what ribosomal subunit does streptogramins bind to?
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bind 50s subunit
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how does dalfopristin work?
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prevents peptide bond formation (inhibits peptidyltransferase, early termination)
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how does quinupristin work?
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inhibits t-RNA synthesis (inhibits elongation, early termnation)
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how does linezolid work?
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binds specific 23s ribosomal DNA on 50s subunit preventing formation of functional 70s ribosomal unit
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how dose mupirocin work?
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1. inhibit isoleucyl-t-RNA synthase
2. prevents incorporation of isoleucine into proteins |
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whats special about mupirocin?
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there is no cross tolerance with other antibiotics b/c of its specific MOA
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name some aminoglycosides
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amikacin, gentamicin, netilmicin, tobramycin, streptomycin
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what kind of bacteria is aminoglycoside effective against?
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gram- bacilli, aerobic bacteria
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are aminoglycosides bactericidal or bacteriostatic?
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bactericidal
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aminoglycosides are ______ dependent killing
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concentration
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how are aminoglycosides eliminated?
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glomerular filtration
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what are its indications?
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used in combination in serious infections, sepsis, pneumonia, endocarditis
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why is aminoglycoside combined with B-lactam?
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to increase bacterial uptake
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what are some of its toxicities?
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nephrotoxicity, ototoxicity, neuromuscular blockade
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how do aminoglycosides cause nephrotoxicity?
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accumulated in proximal tubule, inhibits prostaglandin synthesis
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in aminoglycosides, nephrotoxicity incidence is related to what?
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age, total dose, females>males, duration of treatment
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what drugs will potentiate ototoxicity of aminoglycosides?
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cisplatin, cyclosporine, other nephrotoxins
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under what conditions will aminoglycoside cause ototoxicity
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prolonged adminsitration, increase dose
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what other agents will enhance the ototoxicity of aminoglycosides?
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ethacrynic acid, furosemide, cisplatin, etc
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what are the proposed mechanisms that aminoglycosides can cause ototoxicity?
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1. calcium hypothesis: interferes w/ Ca channel in hair cells
2. free radical hypothesis: they interact w/ Iron to form superoxide and hydroxyl free radicals 3. NMDA hypothesis: they interact w/ NMDA receptors and glutamate to cause excitotoxicity |
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how dose aminoglycosides cause neuromuscular blockade? what is it contraindicated in?
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blocks presynaptic release of Ca++, this is contraindicated in myasthenia gravis
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how does aminoglycoside resistance develop?
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1. plasmid acquired, aminoglycoside modifying enzymes
2. altered transport into bacteria 3. altered ribosome |
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what bacteria are tetracyclines effective against?
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gram+ and gram- anaerobes, aerobes, rikettsia, chlamydia, lyme's disease
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are tetracyclines bacteriostatic and bactericidal?
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bacteriostatic
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what are the routes of adminstration for tetracyclines?
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oral and IV
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how does tetracyclines enter bacteria?
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by diffusion and active transport
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what things will impaire absorption of tetracycline?and how?
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milk and antacids.
chelate divalent cations |
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T/F
tetracyclines enters CNS, crosses placenta, found in breast milk |
true
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how are tetracyclines excreted
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glomerular filtration, some biliary excretion
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list the toxicities of tetracyclines? (7)
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1. GI disturbances
2. Photosensitivity 3. Super-infections (Pseudomembranous colitis due Clostridium difficile) 4. Effects on bone and teeth 5. Renal and hepatic toxicity 6. Vestibular disturbances 7. Hypersensitivity reactions |
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how is tetracycline resistance developed? (3)
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1. Plasmid mediated – addition of active efflux transporters
2. Ribosomal produced protection protein displaces tetracycline's 3. Increased enzymatic inactivation |
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how are tigecyclines administered? and how is it excreted?
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iv
excreted in bile and urine unchanged |
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what are tigecyclines indicated for?
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Complicated skin, skin structure and inta-abdominal infections, effective in other tetracycline resistant organisms
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what are the toxicities of tigecycline?
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similar to tetracycline
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name some macrolides
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erythromycin, clarithromycin, azithromycin
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what are macrolides effective against?
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gram+, cocci and bacilli, chlamydia, legionella
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macrolides are inactivated by ____
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acid
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how are macrolides excreted?
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billiary
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T/F
macrolides crosses placenta, crosses BBB |
false, it corsses placenta, but not BBB
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list the toxicities of macrolides
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1. cholestatic hepatitis
2. sensitivity reactions 3. GI distrubances 4. tinnitus, hearing loss, reversible |
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what are the toxicities of erythromycin?
and of erythromycin and clarithromycin? |
QT prolongation with antihistamines, ketoconazole
inhibit CYP3A4 |
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what is clarithromycin used for?
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H.pylori and mycobacterium avium-intracellulare
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what is azithromycin used for?
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H.influenzae and mycobacterium avium-intracellulare
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how does macrolides resistance develop?
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1. active transport out of bacteria
2. decreased binding to ribosome 3. increased metabolism 4. 50s ribosomal mutations |
