Flashcards in Overview of Antimicrobials Deck (18)
MOA - disrupt cell wall production
1. B-lactam: PCN, Cephalosporins, Carbapenems (workhorses)
2. Monobactams (Aztreonam)
3. Glycopeptides (Vanco)
MOA - inhibit DNA synthesis
MOA - destabilize cell membranes (ice pick puncturing balloon)
1. cyclic lipopeptides
MOA - destabilize cell wall & cell membrane
MOA - inhibit protein synthesis
1. macrolides (Azithro)
2. lincosamides (Clindamycin)
3. oxazolidinones (Linezolid)
1. aminoglycosides (AG)* - Genta, Tobra
2. tetracyclines (TTC) - Doxy
MOA - inhibit folic acid synthesis
3 general mechanisms of Abx resistance
1. decrease intracellular [drug]
2. drug inactivation by enzymes (Beta lactamases)
3. 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.
Abx active against intracellular organisms
3. PO Amox/Clav
4. IV ampicillin/sulbactam & pip/taz
5. all carbapenems
Abx renal excretion
1. b-lactam (most)
4. cyclic lipopeptides/lipoglycopeptides
6. FQs (split excretion)
7. TTC/glycylcyclines (split excretion)
8. Oxazolidinones (split excretion)
Abx hepatic excretion (memorize these so you don't have to know renal)
4. All Macrolides*
MUST KNOW THE STARRED
What anti-anaerobic abx would you use if above the diaphragm, such as the oropharynx?