Micro - Rx.
Terms
undefined, object
copy deck
- 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 -
T/F:
Aminoglycosides are usually cidal with a single unit. - True
- What are some side effects of aminoglycosides?
-
*may bind mitochondrial ribosomes
*renal damage
*ototoxicity - 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.
- *bacteriostatic
- 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.