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38 Cards in this Set
- Front
- Back
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what is the mechanism of action of vancomycin
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it targets the D-Ala-D-Ala of the peptidoglycan pentapeptides and binds to the cell wall subunit preventing it from crosslinking and elongation
DOESNT GO AFTER PBP |
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what is the spectrum of activity of Vancomycin
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no gram negative activity because it is too large to go through the pores
bactericidal against staph/strep and beta lactam resistant bacteria bacteriastatic against enterococci |
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what are the pharmacokinetics of vancomycin
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excreted unchanged renally
poor oral absorbtion not dialyzable by normal HD well distributed to total body water |
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what are the pharmacodynamics
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concentration independent
as you increase concentration get faster and more killing till about 1mg/L |
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what is the most important factor when correlating drug exposure w/ clinical outcome
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time above MIC
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what is the importance of Cmax in vancomycin and beta lactams
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Cmax is not important because a high concentration is not going to give proportional returns on how fast and how much bacteria you kill what's really important is to MAKE SURE TROUGH CONCENTRATION IS ABOVE A CERTAIN THRESHOLD
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how does vancomycin compare to beta lactams in treating MSSA
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beta lactams better at fighting MSSA
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should vancomycin be used as the primary mode of therapy
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no high incidence of failur
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what are the clinical indications for Vancomycin
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beta lactam hypersensitivity
beta lactam resistant pathogens |
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what are some of the beta lactam resistant pathogens
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MRSA
PRSP (penicillin resitant S. pneumonia) these two resist by altering the penicilling binding proteins which are the target for Beta lactams MRSE Ampicillin resistant enterococcus |
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what are the clinical indications you may see in the hospital for vancomycin
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gunshot
skin infections IV line/catheter infections endocarditis (infection/inflammation of heart valves) surgical prophylaxis bacterial meningitis antibiotic associated diarrhea |
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how can antibiotic associated diarrhea occur
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when you got to the hospital and get a broad spectrum antibiotic it will change the ecology of your natural flora allowing for Clostridium difficile to have a more favorable environment to proliferate
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how can you treat antibiotic associated diarrhea
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give vancomycin orally, this isn't usually done due to its poor oral absorption but in this case it is given orally because we want the drug to stay in the gut and not get absorbed
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why should vancomycin be used over cephalosporins for surgical prophylaxis
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due to the increasing prevelance of MRSA
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what are the adverse events of vancomycin
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infusion related reactions
red man/neck syndrome blood dyscrasias (neutropenia etc) ototoxicity nephrotoxicity |
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what are the infusion related reactions caused by vancomycin
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fever, chills, phlebitis (inflammation of the veins)
this is due to vancomycin reaching a high concentration therefore can't give vancomycin as a bolus or give it to reach high concentrations during surgery |
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why does vancomycin cause redman/neck syndrome
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this can be circumvented by giving vancomycin slowly for atleast an hour so the body can adapt to it. this must be done preanesthesia unlike cephalosporins which can be given w/ anesthesia
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what is the prevelance of nephrotoxicity
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it has low prevelance when vancomycin is given alone but high when given w/ other nephrotoxic drugs such as ferosemid/aminoglycosides/cyclosporins
it has been shown that as duration of admin of vancomycin increases the higher the probability of nephrotoxicity occuring |
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what is the mechanism of resistance of vancomycin and where was it first found
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the target site is altered, instead of D-Ala-D-Ala it will become D-Ala-D-LACTATE which is not recognized by vancomycin
this was first found in ENTEROCOCCUS (resistant to all known antibiotics) and is plasmid mediated |
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what is the synthetic derivative of vancomycin
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telavancin
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what is the mechanism of Aminoglycosides
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bind to 30s ribosome subunit and decrease initiation and protein synthesis
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are aminoglycosides bactericidal or bacteristatic
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bactericidal
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what are aminoglycosides active against
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gram negative bacteria
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in what conditions will aminoglycosides have poor activity
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low pH enivironment (acidic urine, adbdominal abscess)
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what are the clinical indications for aminoglycosides
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gram negative infections
synergy vs gram positive organisms (enterococcus tuberculosis) mycobacterium tuberculosis |
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what is the first line of treatment for Mycobacterium tuberculosis
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streptomycin
2nd line: amikacin, kanamycin |
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how can AG be used to treat gram positive organisms
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since the drugs work with two different mechanisms and since the AG has a hard time getting to the site of action pairing it with a CELL WALL ACTIVE AGENT will weaken the cell wall and allow AG to get to the site of action
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what are the pharmacokinetics of AG
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highly polar cations
poorly absorbed from GI tract (b/c so polar) |
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how can AG be used in Intestinal decontamination
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AG will sit in intestine and will decrease likely hood for infection.
AG CAN'T BE USED FOR SYSTEMIC INFECTION |
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can AG be used to treat bacterial meningitis
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no, due to poor penetration therefore can't give enough drug via IV to treat it so have to put drug directly in CSF
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how are AG eliminated
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renally via glomerular filtration
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how are AG metabolized
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they are not metabolized to a significant extent
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what is the relationship b/t drug concentration and antimicrobial effect for AG
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concentration dependent killing (higher concentration kills organisms faster)
peak serum concentration (Cmax):MIC optimized @ 10:1 |
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what are the major forms of toxicity for AG
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nephrotoxicity
ototoxicity neuromuscular blockade |
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how does nephrotoxicity occur when using AG
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AG accumulates in the lysosomes of the renal proximal tubule cells and binds to phospholipidases this results in reduced lysosomal function which triggers events causing necrosis of tubular cells
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what are the monitoring parameters for nephrotoxicity when using AG
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AG concentrations
urine input and output BUN/SCr |
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what are the forms of ototoxicity
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auditory
vestibular |
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what are the mechanisms of resistance for AG
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decreased AG uptake
ribosomal target modifcation AG modifying enzymes |
