Overview of Antimicrobials Flashcards
MOA - disrupt cell wall production
- B-lactam: PCN, Cephalosporins, Carbapenems (workhorses)
- Monobactams (Aztreonam)
- Glycopeptides (Vanco)
MOA - inhibit DNA synthesis
- FQ
2. Metronidazole
MOA - destabilize cell membranes (ice pick puncturing balloon)
- cyclic lipopeptides
MOA - destabilize cell wall & cell membrane
- lipoglycopeptides
MOA - inhibit protein synthesis
50S ribosome
- macrolides (Azithro)
- lincosamides (Clindamycin)
- oxazolidinones (Linezolid)
- pleuromutilins
30S ribosome
- aminoglycosides (AG)* - Genta, Tobra
- tetracyclines (TTC) - Doxy
- glycylcyclines
MOA - inhibit folic acid synthesis
- TMP-SMX
3 general mechanisms of Abx resistance
- decrease intracellular [drug]
- drug inactivation by enzymes (Beta lactamases)
- abx target modification - decreased affinity for PBP (old key, new deadbolt), DNA topoisomerase mod, rRNA methylation
Bolded bactericidal vs. bacteriostatic
When is bactericidal preferred?
Bactericidal: b-lactam, FQ
Bacteriostatic: TTC, macrolides
-cidal agents preferred if host is compromised or host defense do not operate well
What is concentration-dependent killing?
Increased drug concentration increases bactericidal effects.
Large, infrequent doses enhance efficacy and minimize toxicity. Think of a tsunami.
e.g. AG, FQ, glycopeptides, lipoglycopeptides
What is post-antibiotic effect?
Short exposure to abx prevent microbe from growing even after abx has been removed.
What is time-dependent killing?
Drug is effective as long as concentration is > MIC.
Small frequent doses or continuous infusion.
e.g. b-lactam
Abx active against intracellular organisms
- FQ
2. Macrolides
Anti-anaerobic abx
- Clindamycin
- Metronidazole
- PO Amox/Clav
- IV ampicillin/sulbactam & pip/taz
- all carbapenems
“Bioequivalent” Abx
- FQ
- TTC
- Metronidazole
Abx renal excretion
- b-lactam (most)
- monobactam
- glycopeptide
- cyclic lipopeptides/lipoglycopeptides
- AGs
- FQs (split excretion)
- TTC/glycylcyclines (split excretion)
- Oxazolidinones (split excretion)