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28 Cards in this Set

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