Antimicrobials Flashcards
What are the 5 main methods on how anti-microbials work?
- inhibiting cell wall synthesis (B-lactams, vancomycin)
- inhibiting nucleic acid synthesis (fluoroquinolones, rifamycins)
- stopping metabolite production folate (trimethoprim, sulfonamides)
- inhibiting cell membrane synthesis (daptomycin)
- inhibiting protein synthesis (linezoid, tetracyclines, macrolides, aminoglycosides)
What is the difference between bactericidal and bacteriostatic agents?
Bactericidal
- means destroying, or killing bacteria
- works optimally when bacteria divides at USUAL rate so sometimes combining both will not work in patient’s favour
Bacteriostatic
- stopping divisions and replication of bacteria
- slowing the growth
- bacteria are still alive and rely on body’s usual mechanisms
Give some examples of penicillins, their mechanism and whether static or cidal
- amoxicillin and flucloxicillin
- mechanism: acts on cell wall
- bactericidal
Give some examples of ceflasporins, mechanism and whether static or cidal
- ceftriaxone, cephalexin
- acts on cell wall
- cidal
Give examples of quinolones, mechanism of action, whether static or cidal
- ciprofloxacin, levofloxacin
- DNA/RNA synthesis
- both static and cidal
Give examples of macrolides, mechanism of action, whether static or cidal
- erythromycin, clarithromycin
- inhibits protein synthesis
- static
Give examples of tetracycline, mechanism of action, static or cidal
- doxycycline
- inhibits protein synthesis
- static
Give examples of aminoglycosides, MOA, whether static or cidal
- gentamicin
- inhibits protein synthesis
- both
- requires monitoring
Give examples of glycopeptides, MOA, static or cidal
- vancomycin (needs monitoring)’
- acts on cell wall
- cidal
Give examples of carbopenams, MOA, static or cidal
- meropenem
- acts on cell wall
- cidal
How does antibiotic resistance develop?
- presence of beta lactam enzymes
- efflux pumps
- plasmid DNA can be passed from cell to cell
Why do we need to do drug monitoring?
- narrow therapeutic window
- maximize effect of antibiotic
- there is risk of toxicity
- examples: vancomycin and gentamicin
- need to do blood tests at a specified time
- for vancomycin, a level must be taken at every 4th dose as a minimum and must be taken an hour before next dose is due
What is the difference between time dependent and concentration dependent killing of bacteria?
- MIC (minimum inhibitory concentration) needed to kill bacteria
- time dependent: long half lives are beneficial, they spend longer at the binding sites (needs frequent dosing to be kept over MIC)
- concentration dependent: levels important, need a certain concentration at the binding sites
Why do we use antibiotics?
- short term management of bacterial infections
- prophylaxis in acute setting such as high risk procedures, but dont give unnecessary antibiotics
- long term prophylaxis: only give if suitable, local UHL guidelines, associated risks
- sometimes if giving antibiotics, you’ll kill all but the resistant ones, so they survive and produce an infection that’s even worse
What are combination antibiotics used for? Explain co-amoxiclav
- provide a synergistic effect
- examples: tazocin, co-trimoxazole
- co-amoxiclave: combo of clavulanic acid and amoxicillin
- clavulanic acid: inhibits effects of some B lactamase enzymes so amoxicillin can work better
- amoxicillin: acts on cell walls of bacteria in usual standard MOA