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96 Cards in this Set

  • Front
  • Back
Two mechanisms for ketolides
bind 50 S ribosome
block ribosome assembly
dna gyrase inhibitors
quinolones
nalidixic acid class
quinolone
cipro class
quinolone
sparfloxacin class
quinolone
gatifloxacin class
quinolone
rna synthesis inhibitors
rifamycins
tetracycline mechanism
bind to the 30 S ribosomal subunit
aminoglycoside mechanism
bind to the 30 S ribosomal subunit
aminocyclitol mechanism
bind to the 30 S ribosomal subunit
spectinomycin class
aminocyclitol
streptomycin class
aminoglycoside
neomycin class
aminoglycoside
amikacin class
aminoglycoside
netilimicin class
aminoglycoside
erythromycin class
macrolide
clarithromycin class
macrolide
azithromycin class
macrolide
dirithiromycin class
macrolide
troleandomycin class
macrolide
macrolide mechanism
bind 50 S subunit
ketolide mechanism
bind 50 S subunit
oxazolidinone mechanism
bind 50 S subunit
streptogramin B mechanism
bind 50 S subunit
strepogramin A mechanism
bind 50 S subunit
chloramphenicol mechanism
bind 50 S subunit
lincosamide mechanism
bind 50 S subunit
14-member ring with ester and two sugars
macrolide
14-member ring with ester and one sugar and one ketone
ketolide
telithromycin class
ketolide
linezolid class
oxazolidinones
19 membered ring with lactone and six membered ring with N
streptogramin B
24 membered ring with lactone, conjugated double bonds, two five membered rings
streptogramin A
quinupristin class
streptogramin B
dalfopristin class
streptogramin A
clindamycin class
lincosamide
methenamine decomposes to
formadehyde
two UTI treatments
Methenamine and Nitrofurantoin
4:5 with S in ring
penicillin
4:6
cephalosporin
4:5 without S in ring
Carbapenem
4
monobactam
imipenem class
carbapenem
meropenem class
carbapenem
aztreonam class
monobactam
two sugars with peptide backbone and large rings with aromatic rings
vanco
4 cell wall synthesis inhibitors with b-lactams
penicillins
cephalosporins
carbapenems
monobactams
cell wall synthesis inhibitors without b-lactams
vanco
bacitracin
large polypeptide ring with D and L amino acids, a peptide tail with lipophilic amine
bacitracin
fosfomycin class
cell wall synthesis inhibitor, pyruvyltranferase inhibitor
pyruvyltranferase inhibitor
fosfomycin
clavulinic acid class
non-antibiotic, beta-lactamase inhibitor
sulbactam class
non-antibiotic, beta-lactamase inhibitor
tazobactam class
non-antibiotic, beta-lactamase inhibitor
prolonged QT interval, liver tox, phototox, no antacids
quinolones
prevents renal metabolism of carbapenems
cilastin
nephrotox and deafness
aminoglycosides
just prolonged QT
macrolides
Ca injection pain
tetracyclines
bone/teeth disposition
tetracyclines
teeth yellowing, no antacids / milk
tetracyclines
MTT chain can inhibit Vit K
cephalosporins
cause disulfiram rx with alcohol
cephalosporins
non-compatible with rifabutin
macrolides
non-compatible with chloramphenicol
macrolides
non-compatible with aminoglycosides
polymixins
synergistic with aminoglycosides
penicillins and cephalosporins
with you can't mix macrolides and rifabutin
increases metabolism (of what?)
with you can't mix macrolides and chloramphenicol
similar 50 S binding sites
with you can't mix aminoglycosides and polymixins
respiratory paralysis and renal dysfunction
three mechanisms of resistance
1) influx / efflux
2) metabolism
3) target alteration
primary cause(s) of resistance for quinolones
influx / efflux and target alteration, QRDR
primary cause(s) of resistance for tetracyclines
decreased intake (1)
primary cause(s) of resistance for aminoglycosides
metabolism; phophorylation and acteylation of OH and amine groups
primary cause(s) of resistance for macrolides
all three; decreased intake, alcohol acetylation, single 50 S residue
primary cause(s) of resistance for chloramphenicol
metabolism; OH acetylation
primary cause(s) of resistance for lincosamides
metabolism; OH acetylation and no cross-resistance with macrolides
primary cause(s) of resistance for penicillins and cephalosporins
metabolism and target alteration (PBP)
have all three mechanisms of resistance
macrolides
four groups with acetylate OH groups (mechanism 2)
aminoglycosides, macrolides, chloramphenicol and lincosamides
only this type of bacteria make LPS
gram (-)
portion of LPS which elicits a fever
Lipid A
resist killing by white blood cells and grow very, very slowly
acid-fast bacteria
does not allow prediction of cell wall type
morphology (rod or sphere)
poke holes in the cell membrane
polymixins
quinolone removed from market and used only in hospitals
trovafloxacin
two Fs increase this ADR
phototoxicity
associated with increased pulled achilles tendons esp. in elderly and more so if used with steroids
fluoroquinolones
bioavailability of ALL quinonlones with greatly decreased with
antacids; COOH form salts with Ca and Mg
binds to 50 S and inhibits translocation
erythromycin (macrolides) and clindamycin
binds to 50 S and inhibits peptidyl transferase
chloramphenicol
bind to 30 S and inhibit binding of aminoacyl-tRNA
tetracyclines and aminoglycosides
cause misreading of mRNA
aminoglycosides
chelate metals which results in insoluble complexes at neutral pH
tetracyclines
why tetracyclines hurt when injected
insoluble Ca complexes
most common side effect of aminoglycosides
nephrotoxicity