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74 Cards in this Set

  • Front
  • Back
___ binds 23S subunit of 50S, prevents formation of initiation complex
time dep bacteristatic
some PAE
oxazoladinones (Linezolid)
___ bind 30S, prevent binding of aminoacyl tRNA to A-site -->
time dep Bacteristatic
some PAE
___ bind 30S, interfere with initiation complex and cause misreading of mRNA ->
concentration dependent bactericidal
significant PAE
___ binds 50S, inhibits peptidyl transferase elongation of peptide
time dep bacteristatic
some PAE
___, ___, ___, and ___ bind 50S and inhibit translocation (also worded as: they inhibit the peptidyl transferase reaction)
all time dep bacteristatic w/ PAE except one
macrolides (erythromycin)
lincosamines (clindamycin)- bind A and P sites of 50S
Type B streptogramins
Ketolides (telithromycin)-concentration dep bactericidal, sig PAE
binding of chloramphenicol may inhibit binding of which other two drugs due to close proximity of binding site
clindamycin and
what is the general MOA for oxazoladinones
type III
time dependent- moderate to prolonged PAE
name an oxazoladinone
name five bugs sensitive to linezolid
enterococcus faecalis
enterococcus faecium
staph epidermidis
staph haemolyticus
staph pneumoniae
specific MOA of linezolid
prevents formation of 70S by binding 23S rRNA of 50S subunit -> prevents formation of initiation complex for protein synthesis
linezolid- oral absorption?
yup, good
bug's mechanism of resistance to linezolid
mutations of 23S RNA prevent binding of linezolid
three adverse effects of linezolid
thrombocytopenia, anemia, myelosuppression
what is the general MOA of tetracyclines
bacteriostatic- type III
time dependent
moderate to prolonged PAE
all tetracyclines
drugs with more lipophilic substituents (minocycline and doxycycline) are most active by...
what is the specific MOA of tetracyclines
binds 30S -> prevents binding of aminoacyl-tRNA during protein synthesis
how do tetracyclines get through the outer membrane of gram neg bacteria?
through the plasma membrane?
how is this different in mammalian cells
outer- passive diffusion through porin channel
inner- active transport
mammalian- lack the active transport system required
tetracyclines- oral absorption?
adequate but incomplete
name three ways bugs become resistant to tetracyclines
1. decreased influx or acquisition of an energy-dependent efflux mechanism
2. ribosome protecting proteins
3. enzymatic inactivation of drug
is hypersensitivity to tetracyclines common
Name some adverse effects of tetracyclines (7)
1. GI: pseudomembranous enterocolitis
2. perm tooth discoloration in pregnant women and kids <8
3. IV admin -> venous thrombosis
4. IM admin -> painful local irritation
5. renal toxicity
6. hepatic toxicity
7. photosensitivity
general MOA of aminoglycosides
bactericidal type I ->
conc dependent
significant PAE
what group of bugs is susceptible to aminoglycosides
gram neg
aminoglycosides specific MOA
bind 16S part of 30S -> irreversibly inhibiting protein synthesis- interfere w/ formation of initiation complex; misreading mRNA code; premature termination
with aminoglycosides, a PAE persists even after serum concentration has fallen below...
the MIC
how do aminoglycosides get through the outer membrane?
the plasma membrane?
Name 4 things that inhibit passage through plasma membrane
outer- passive diffusion
inner- active transport

1. divalent cations
2. hyperosmolarity
3. lowered pH
4. anaerobic conditions
aminoglycosides- oral absorption?
accumulations in CSF?
excretion by kidney?
IM or IV absorption
oral absorption- poor
low accumulation in CSF
rapid excretion by kidney
rapid IM and IV absorption
there is ___ activity of aminoglycosides in the presence of beta-lactam antibiotics
enhanced (synergism)
Name two ways bugs gain resistance to aminoglycosides
1. acquisition of inactivating enzymes (acetylases, adenylases, phosphorylases- plasmid encoded)
2. if drug fails to permeate the inner bacterial membrane
Name 5 adverse effects of aminoglycosides
1. ototoxicity
2. nephrotoxicity
3. curare-like NM block (-> resp paralysis, tx w/ Ca and neostigmine)
4. nerve dysfunction
5. allergic skin reax and contact dermatitis
is chloramphenicol used in the US
no- but we have to learn about it anyway :)
it's used in other countries because of very low cost
what is the general MOA of chloramphenicol
bacteriostatic type III
time dependent
moderate to prolonged PAE
when do you use chloramphenicol
only when benefits outweigh the risks of potential toxicities
what is the specific MOA of chloramphenicol
binds reversibly to 50S -> prevents binding of aminoacyl-tRNA to A site -> inhibits peptidyl transferase step of protein synthesis elongation
how does chloramphenicol get into cell
facilitated diffusion
chloramphenicol- oral absorption?
gets into CSF?
cross placenta?
half life correlated w/?
good oral absorption
gets into CSF
crosses placenta
half life related to plasma bilirubin concentrations (requires hepatic function for later secretion in urine)
name two mechanisms of resistance to chloramphenicol
1. decreased membrane permeability (influx)
2. chloramphenicol acetyl transferase (plasmid encoded)
Name five adverse effects of chloramphenicol
1. direct bone marrow toxicity due to dose-related normocytic anemia, due to erythroid suppression
2. allergic reax resulting in idiosyncratic blood dyscrasia
3. inhibits mammalian 80S
4. Gray Baby syndrome (inadequate glucuronic acid conjugation after inadequate renal secretion)
5. inhibits P450
streptogramins type B
MLS antibiotics
what was recently added to the MLS antibiotics
ketolides (MLKS?)
what is the general MOA of macrolides
type III bacteriostatic ->
time dependent
moderate to prolonged PAE
which two macrolides have broader spectrum due to modifications
macrolide specific MOA
bind 50S and inhibit translocation of protein synthesis
if erythromycin is inactivated by gastric acid, where is it absorbed?
still in the upper small intestine
what does insertion of the azo group into the lactone ring provide azithromycin
increased bioavailability and stability -> requires only once a day dose instead of 3x per day
which macrolides are eliminated by liver?
which are eliminated through renal and non-renal mechanisms?
erythromycin and azithromycin- liver
clarithromycin- renal and non-renal mechanisms (clarithromycin uses the kidney)
name four mechanisms of resistance to macrolides
1. efflux via ATP dependent pump (except clindamycin)
2. make a methylase that modifies ribosomal target (=MLSb determinants- resistance to whole MLS group)
3. hydrolysis by esterases
4. mutation of 23S
which two macrolides inhibit hepatic enzymes
erythromycin (p450) and clarithromycin
general mechanism of action of lincosamides
bacteriostatic type III
time dependent
moderate to prolonged PAE
___ is a congener of lincomycin that has improved pharmacokinetics and less toxicity

(for those of us who didn't major in English...
congener = n. A member of the same kind, class, or group. )
bugs susceptible to clindamycin
gram positive cocci
specific MOA of clindamycin
binds the P and A sites in 50S and suppresses protein synthesis
clindamycin- oral absorption?
bone penetrance?
cross placenta?
reaches CNS?
good oral absorption
gets into bone
crosses placenta
DOES NOT get into CNS
how do bugs get resistance to clindamycin
MLSb induced ribosomal methylation

*not a substrate for efflux pump*
name 3 adverse effects of clindamycin
1. GI
2. inhibited neuromuscular transmission
3. skin rashes (esp in HIV patients)
type B streptogramin
= streptogramin B (quinupristin) + streptogramin A (dalfopristin)
general MOA of type B streptogramins
bacteriostatic type III
time dependent
moderate to prolonged PAE
type B streptogramins are semisynthetic derivatives of the naturally occurring ___
type B streptogramins effective against...
inactive against...
often reserved for ... and ...
good for gram pos cocci
bad for gram neg's
reserved for vancomycin resistant E. faecium or multi-drug-resistant Gram positives
mechanism of action of streptogramin B
quinupristin binds 50S -> inhibits translocation; occupies same site as macrolides
mechanism of action of streptogramin A
dalfopritin binds near quinupristin and induces conformation change in 50S -> enhancing binding of quinupristin
administration of type B streptogramins?
t 1/2?
elimination by?
IV only!
short half life
biliary excretion
name two mechanisms of resistance to type B streptogramins
1. active transport efflux and acetyltransferases against streptogramin A
2. MLSb ribosome methylation and lactonases
name three adverse effects of type B streptogramins
1. infusion related pain and phlebitis at site of infusion
2. arthralgias
3. myalgias
ketolide general mechanism of action
bacteriocidal type I
concentration dependent
significant PAE
specific MOA of telithromycin
binds 50S like the macrolides do
telithromycin is especially useful for
drug-resistant respiratory infections
pneumococcus: community acquired pneumonia, acute sinustitis, acute exacerbations of chronic bronchitis, tonsillitis/pharyngitis
name four drugs whose concentrations are increased by telithromycin inhibiting p450
name five commonly reported adverse effects of telithromycin