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106 Cards in this Set
- Front
- Back
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differentiate antibacterial, antimicrobial, and antibiotic
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antibacT = exclusively against bacT
antimicrobial = other microorganisms as well as bacT antibiotic = made by microorganism that suppresses another organism |
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what are the 4 essentials for successful antibacT therapy?
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drug must contact bug
"" be in high enough concentration (MIC) "" present for enough time bug must be sensitive to drug |
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what are 2 ways of acquired resistance?
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mutation (maybe too low of conc then natural selection)
R-Factor resistance (genetically acquired w/o ever seeing the drug) |
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what are 3 resistance mechanisms?
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membrane plugs
ribosomal blockade enzymatic digestion |
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what is ribosomal blockade?
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protein produced can inhibit the abx from binding to the ribosome (ribosome decoy to bind w/ abx)
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T/F you want to restrict prophylactic abx therapy
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TRUE
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T/F media may cause apparent resistance in vitro if impurities are there which might nullify the effects of the drug being tested.
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true.
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what happens in the MAJORITY of combined antimicrobial drug interactions?
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one or the other dominates so drug a + drug b = drug a alone
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what is: bacteriostatic + bacteriostatic = bacteriocidal
an example of? |
synergy
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what is potentiation?
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not quite sure look it up.
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T/F combination drugs can prevent OR cause development of resistant strains
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true.
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T/F combination drugs have reduced specificity
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true.
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what's the most common cause of failure of antimicrobial therapy?
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duration of tx too short!!
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T/F fever usually implies bacterial or viral infection.
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FALSE
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name 3 organisms with unpredictable sensitivity
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E. coli
klebsiella coag(+) staph |
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T/F if possible, use a bacteriostatic as opposed to a -cidal.
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FALSE
use cidal |
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what is maximized in time vs concentration dependant activity? which is dosed more frequent?
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conc = maximized the cmax/MIC ration
time = maximize the time period when C > MIC TIME is more frequent! |
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T/F an advantage to combination therapy is in life-threatening septicemia.
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true.
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see slides 43-45 if it's needed to know.
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ok.
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when is prophylactic (anticipatory) antimicrobial therapy indicated?
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high risk patients eg diabeties or immunosuppressed patients
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what are 5 predisposing factors to nosocomial infection?
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age
severity of disease duration of hosp stay use of invasive support systems previous antimicrobial use |
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define colonization resistance
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tendency of normal gut flora to suppress the pathogenic bugs within gut-mediated by factors produced by the normal organisms.
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what's the most common nosocomial infection in SA practice? 2 others?
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klebsiella
resistant e. coli and serratia |
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what're the 2 most common nosocomial infections in LA practice?
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salmonella
aminoglycoside resistant gram (-) |
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see slides 55-56 for wound classifications.
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ok.
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why do you want to administer an antimicrobial at the end of surgery?
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anesthesia and stress immunosuppresses
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how long postsurgically do you want to give antimicrobials
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no longer than 1-3 days
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how long do you want to use glucocorticoids with antimicrobials? why not longer?
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less than 7 days generally
they delay containment of infection and destruction of microbe |
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T/F broad specture abx get gram + and - AND possibly protozoa, rickettsia etc.
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true.
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T/F bacteriostatics inhibit bacterial growth and replication at any dose
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false.
at HIGH dose can be bacteriocidal. |
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read the static/cidal stuff on slides 5-6
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ok.
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what are 4 mechs of antibacterial action?
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cell wall synth
cell membrane protein synth nucleic acid/intermediary metabolism |
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what 5 body parts can be toxified by abx?
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neuro
nephro hepato entero marrow |
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T/F cell wall blockers are usually bacteriostatic.
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FALSE. cidal.
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when do you want to give cell wall blockers?
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when host defenses are suppressed.
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T/F bacteriocidals can be inhibited by bacteriostatics AND require active multiplication to work
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true.
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what's the mechanism for penicillin and what's it's spectrum?
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blocks peptidoglycan crosslinking..
mostly gram (+) |
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what are 4 toxicity issues with penicillins?
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allergies
gut flora in pocket pets CNS toxicity superinfections in gut |
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what can enhance a penicillins penetration in common scenarios?
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inflammation! so you might be able to use it at the beginning but not later.
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what does the clav in clavamox do?
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it allows the amoxicillin to be used where it would normally be inhibited by blocking b-lactamase.
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T/F penicillins are often combined in a syringe with aminoglycosides
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false
not compatible in vitro! |
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which synthetic penicillin is resistant to penicillinase?
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cloxacillin.
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which synthetic penicillin is effective against proteus and pseudomonas, is given IV only and is sketchy to use in cats?
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carbenicillin.
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maybe check out all the synthetic penicillins real quick. slides 14-18ish.
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ok.
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T/F cephalosporin mechanism of action is very similar to penicillin and are primarily bacteriostatic.
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FALSE. first part true but are mainly bacterioCIDAL.
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what's the spectrum of cephalosporin relative to pen?
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broader (gets - and +)
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what's the difference between 2nd/3rd gen cephalosporins and the 1st gen?
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more gram - activity
improved b-lactamase activity |
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what's the toxicity of cephalosporins?
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local rxns at injection site
kidney |
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cephalosporins:
1) best absorption 2) dose frequency 3) liver |
1) parenteral best, oral poor
2) BID/TID cuz short 1/2 life 3) hepatic biotransformation |
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what do bacitracin and vancomycin do?
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cell-wall active antimicrobials
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see slide 31.
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ok.
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what's the mechanism and spectrum for tetracyclines?
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inhibits tRNA binding at 30s ribosomal subunit
very broad spectrum (+ and -) |
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talk about the 4 toxicities of tetracyclines
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GI = direct and suprainfection
CV = collapse! bone/teeth renal = esp. with expired preparations |
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tetracycline:
1) acid/base behavior 2) distribution 3) excretion 4) placenta action |
1) act as weak acid
2) good distribution 3) renal, some biliary 4) yes |
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why aren't polymyxins used systemically?
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toxicities
kidney, neuro and local allergic |
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how do you administer polymixins and how is it excreted?
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topically/intramamm/intrauterine
renally |
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what are the 2 categories of protein synth inhibitors?
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bacteriostatic and bacteriocidal
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T/F PS inhibitors can enhance or antagonize each other
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true.
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see slide 40
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ok.
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what is the mechanism of chloramphenicol?
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inhibits peptide chain elongation and inhibits fxn of 50s ribosomal subunit
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what's the spectrum and stremf of chloramphenicol?
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bacteriostatic!
broad spec so gram (-) too. |
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what are 4 common apps of chloramphenicol?
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salmonella
brain abscess bacT meningitis intraocular |
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what's the big no-no for chloramphenicol?
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food animals
hella toxic to humans. |
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what's the most important thing about human chloramphenicol toxicity?
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NON DOSE DEPENDANT. 1 molecule can do it.
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what is the solubility for chloramphenicol and who cares?
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very lipid soluble = wide distribution
can accumulate if impaired metabolism condition. |
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what can chloramphenicol do to other drugs?
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inhibits CP450 so other drug metab goes down.
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what is florfenicol? what's the use?
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fluorinated relative
food animal respiratory dz remember phenicols are bacTSTATIC |
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how do macrolides work, what's their spectrum?
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inhibit ribosome synth
narrow specrum (mainly gram +) |
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what are 2 toxicities with macrolides?
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local injection rxn
horses get GI disturbances |
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what pH do macrolides work at? what's the downside here?
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best at high pH cuz they are organic bases.
ion trapping in milk and tissue concentrations higher than serum |
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what's the mech of lincosamide?
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inhibits transfer of tRNA on 50s ribosomes
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what drug should you think with anaerobes?
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clindamycin
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what' the spectrum for lincosamides?
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gram + not gram - really
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what are 2 toxicities of lincosamides?
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fatal colitis in horses
skel muscle paralysis in high concentrations |
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what are azalides like azithromycin and clarithromycin?
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better than macrolides longer oral absorption longer half life broader spec and higher tissue concentrations
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what do azalides get?
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gram positive and anaerobes AND myco
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what's the spectrum and use for aminoglycosides?
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+ and - but use for severe gram - infection
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what's the problem with aminoglycosides?
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rapid resistance and can't be given orally.
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when do you NOT want to use aminoglycosides?
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poor oxygenation like an abcess
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what kind of synergistic combination do you use aminoblycosides with?
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with b-lactam drugs
but NOT in the same syringe? |
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EXAM QUESTION!!!!!
what is the toxicity of aminoglycosides? is it reversible? |
NEPHROTOXICITY!!!!! after one dose.
proximal tubular necrosis. YES it's reversible. |
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what other toxicity besides kidney do aminoglycosides do?
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cranial nerve 8 = deafness and ataxia
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T/F aminoglycosides chelate sodium
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FALSE they chelate calcium.
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T/F aminoglycosides are very polar with poor gut absorption and do NOT go to the brain.
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true.
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read up on aminoglycosides he seems to like them.
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ok.
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what's the normal dosing regiment for aminoglycosides.
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once a day
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what is the rationale for once-daily dosing?
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post antibiotic effect (PAE)
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which is associated with toxicity, peak or trough?
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trough!!!
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look at the 4 rationales in more detail. slide 17-21
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ok.
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what 4 things is the post-antibiotic effect dependent upon and what is it extended by?
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organism
previous peak concentration exposure time neutrophil phagocyte activity extended by b-lactams |
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T/F when the same daily dose is given as a bolus, a higher ratio is achieved
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true.
whatever that means. |
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T/F uptakeinto renale tubule cells and inner ears is saturated at a high dose.
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false
at LOW serum levels. LOW. |
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what are you trying to maximize with a single dose strategy?
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peak under the curve x MIC
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how do you monitor for aminoglycosides and whats the max recommended dosing interval?
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serum creatinine initial and weekly
over 48 hrs not good. |
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um see slide 24 of lecture 14
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ok.
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what's a big interaction with aminoglycosides?
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penicillin! they inactivate each other.
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what's the mechanism of action of quinolones?
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inhibit DNA gyrase
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what 2 drugs are quinolones antagonized by and 1 synergist?
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antag = chloramphenicol and rifampin
syn = aminoglycosides |
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quinolones:
spectrum primary use 2 toxicities 2 no goes |
gram negative
resistant UTIs hepatic and GI no in growing or pregnant |
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what is nalidixic acid?
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neurotoxic and prevents use of quinolones in dogs and cats.
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what are the floxacins?
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newer quinolones, less toxic, more potent
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how does rifampin work?
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interferes w/ RNA synth
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what's rifampin's spectrum?
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antibacterial, antichlamydial, antiviral, TB, enhances antifungals
resistant staph and some gram (-) |
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what does rifampin toxicity look like? 4 things.
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orange bodily secretions
G.I. effects Rash increase in liver enzymes |
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rifampin:
absorption site solubility/boundedness distribution exretion |
GI absorb
lipid and mostly bound great distribution hepatic excretion |
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azalides like azithromycin
relative compare to erythromycin spectrum |
a) related to macrolides
b) better absorption than erythromycin, longer life and broader spec, and higher tissue levels c) gram + aerobes like staph/strep and anaerobes and myco |
