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28 Cards in this Set
- Front
- Back
What are some examples of aminoglycosides?
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Tobramycin, gentamycin, streptomycin
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How do aminoglycosides work?
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*protein synthesis inhibitors
*bind irreversibly to 30S subunit of ribosomes *interfere with fidelity of translation |
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T/F:
Aminoglycosides are usually cidal with a single unit. |
True
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What are some side effects of aminoglycosides?
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*may bind mitochondrial ribosomes
*renal damage *ototoxicity |
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How does resistance to aminoglycosides occur?
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*synthesis of de-activating enzymes
*drug requires oxidative metabolism to enter cell, so ineffective against anaerobes |
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What are some macrolides?
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Erythromycin, azithromycin, clarithromycin.
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How do macrolides work?
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*protein synthesis inhibitor
*bind reversibly to 50S subunit of ribosome *block peptide bond formation |
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Describe the killing ability of macrolides.
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*bacteriostatic
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What is a side effect of macrolide therapy?
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*gastric toxicity
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How does resistance to macrolides occur?
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Synthesis of enzymes that methylate the target (the 50S subunit)
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Name some tetracyclines.
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Tetracycline, doxycycline.
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How do tetracyclines work?
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*protein synthesis inhibitor
*bind reversibly to 28S ribosomal subunit *prevent recognition of tRNA |
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Are tetracyclines bacteriostatic or cidal?
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They are bacteriostatic except at very high doses.
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Would you co-administer tetracyclines and PCN?
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No - they are antagonistic b/c the bacteriostatic action of tetracyclines would provide phenotypic resistance against PCN.
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How does resistance to tetracyclines occur?
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Synthesis of de-activating enzymes and specific efflux pumps.
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What are the 2 mechanisms of actions for PCN's?
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*cell wall synthesis inhibitor
1.Increase autolysin activity 2.Prevent binding of lys or DAP to D-ala-D-ala; i.e. inhibits transpeptidases in peptidoglycan synthesis |
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What kind of genotypic resistance to PCN's exists?
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*synthesis of B-lactamases
*mutation of PBP |
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What kind of phenotypic resistance to PCN's exists?
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They are effective only against actively growing bacteria.
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How do rifampins work?
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*inhibit nucleic acid metabolism
*bind and inhibit RNA polymerase |
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What kinds of problems have been seen with rifampin therapy? What can be done to lessen these?
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*the target site is hypervariable, thus widespread resistance is a problem
*concommittant use of another drug can reduce the rate of effective mutation |
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How does vancomycin work?
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*cell wall synthesis inhibitor
*binds D-ala-D-ala peptidoglycan precursors and blocks polymerization *injures cytoplasmic membrane |
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How does resistance to vancomycin occur?
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Use of D-ala-lactate instead of D-ala-D-ala
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Name some fluoroquinolones.
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Ciprofloxacin, levofloxacin
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What is the mode of action of the fluoroquinolones?
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*inhibit nucleic acid metabolism
*bind and inhibit gyrases *prevents conformational changes in bacterial DNA |
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How does resistance to fluoroquinolones occur?
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Mutations in the gyrases.
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How do sulfonamides work?
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*inhibit nucleic acid metabolism
*block incorporation of PABA into folic acid |
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Are sulfonamides technically antibiotics or antimicrobials? What's the difference?
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They are antimicrobials in that they are not derived from a living source.
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What other drug are sulfonamides usually given with? Why?
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Trimethoprim, which inhibits DHF reductase. This means that 2 steps of the DHF pathway are blocked.
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