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83 Cards in this Set

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30s ribosome inhibitors
tetracyclines, aminoglycosides
chlortetracyclin, oxytetracycline, tetracycline, demecyclocyline, methacycline, doxycycline, minocycline, tigecycline
tetracycline MOA
reversibly binding to 30s ribosome (inhibit tRNA attached to the A site). Bacteriostatic. Broad spectrum, G+ and G-, anaerobes, rickettsiae, clamydia, vibrio, mycoplasma, spirochetes and some protozoa
tetracycline mechanisms of resistance
ribosome protection, increased efflux (active transport pump), impared influx, enzymatic inactivation
tetracycline resistant strains may be susceptible to
doxycycline, minocycline and tigecycline
Drug absorption
oral (doxycycline and minocycline are 95% absorbed)
factors affecting oral absorption
food (except for doxy and mino) divalent cations, dairy products, alkaline pH
Which tetracycline is IV only
Drug distribution
widely to tissues and body fluids, cross placenta and excreted in milk. Bound to and damage growing bones and teeth
metabolized in
eliminated by
except for
doxycycline and tigecyclin
which have long acting half lives
doxy, minocycline. Once daily dosing
clinical uses of tetracyclines
drug of choice for mycoplasma pneumoniae, chlamydiae, rickettsiae and some spirochetes
in combination can be used to treat
gastric and duodenal ulcer caused by helicobacter pylori
usually combined with
amino glycoside to treat plague, tularemia and brucellosis
preferred oral and IV
treatment of skin and intraabdominal infections
adverse reactions
GI effects (nausea and vomiting) pseudomembranous colitis. Damage on teeth and bone when given to pregnant women or children of young ages, discoloration in fetal teeth, deformity or growth inhibition of bones
What should not be given to counteract the GI symptoms
milk or antacids
more adverse reactions
liver tox, kidney tox, local tissue tox (venous thrombosis (IV)), photosensitization, vestibular reactions (dizziness, vertigo, nausea)
streptomycin, neomycin, kanamycin, amikacin, gentamicin, tobramycin, netilmicin
aminoglycosides MOA
irreversibly binding to 30s ribosome, interferes with proofreading process of mRNA, inhibits peptide-tRNA translocation from A to P site. Bactericidal
active against
G- and G+, not anaerobes
How is it administered
Poor GI absorption, usually IV/IM
eliminated by
rapid concentration dependant killing and great post antibiotic effect (once daily dosing)
clinical uses of aminoglycosides
often combined with a beta lactam antibiotic for the treatment of serious infections or infective endocarditis caused by enterococci eg with penicillin (synergistic effect)
tox of aminoglycosides
significant tox with > 5 days of use, ototox (irreversible), nephrotox (reversible). Monitoring serum conc. Is essential.
2nd line agent for tuberculosis, bubonic plague (yersinia pestis)
not safe for systemic use (extremely nephrotoxic), only used topically or orally
bacteria resistant to other aminoglycosides or tb (2nd line agent)
most often used aminoglycoside
interchangable with gentamicin, treat infections caused by pseudomonas aeruginosa
active against some bacteria that are resistant to gentamicin or tobramycin
structurally related to aminoglycosides, used IM solely to treat drug resistant gonorrhea in pt allergic to penicillin
aminoglycosides mechanism of drug resistance
plasmid encoded aminoglycoside modifying enzyme, altered ribosomal binding sites
50s ribosome inhibitors
macrolides, clindamycin, chloramphenicol, streptogramins, oxazolidinones
erythromycin, clarithromycin, azithromycin, thelothromycin, ketolides
macrolide MOA
bind to and inhibit 50s ribosomal subunit (inhibit translocation process)
macrolides effective against
G+, bacteriostatic or bactericidal at high conc.
obtained from streptomyces erythreus
semisynthetic derivitaves of erythromycin
clarithromycin and azithromycin
mechanism of resistance for macrolides
active efflux or decreased cell permeability. Hydrolyzed by esterases, modification of the ribosomal binding site (ribosomal protection). Chromosomal mutation by inducible or constitutive methylase
constitutive methylase productions confers resistance to
clindamycin and streptogramin (MLS type B resistance
which macrolide is destroyed by stomach acid
erythromycin and must be administered with enteric coating
more stable in stomach acid and better absorbed
clarithromycin and azithromycin
longest half life of macrolides
azithromycin 2-4 days once daiy dosing
how is azithromycin taken
empty stomach food affect absorption
which macrolides inhibit liver cytochrome p450 enzymes
erythromycin and clarithromycin
what does this do
icrease serum concentration of theophylline, oral anticoagulants, cyclosporin, carbamazepine and methylprednisolone
clinical uses of macrolides
diptheria, cornebacterial sepsis, erythrasma. Respiratory, neonatal, ocular or genital chlamydial infections, CAP, staph infections in penicillin allergig pt's.
DOC for chlamydia
erythromycin adverse reactions
GI intolerance, liver tox (acute cholestatis hepatitis)
describe the structure
semisynthetic 14 membered ring macrolide
How do ketolides work and what do they do
inhibit p450 enzymes, respiratory infections
side effects of ketolides
GI tox and severe liver failure
use of clindamycin
broad spectrum especially effective against anaerobes
Clindamycin MOA
inhibits bacterial protein synthesis by binding to the 23s rRNA of the 50S subunit
mechanism of resistance for clindamycin
mutation of the ribosomal site, modification of the binding site by a constitutively expressed methylase (MLS-type B resistance). Enzymatic inactivation
clinical uses of clindamycin
treat infections caused by bacteriods and other anaerobes associated with mixed infections. Recommended for prophylaxis of endocarditis in pts with valvular heart disease whoare undergoing dental procedures
adverse rxs of clindamycin
increased risk for diarrhea and colitis due to clostridium difficile
chloramphenicol MOA
binds to 50s ribosome (inhibits the peptidyltransferase reaction) bacteriostatic broad spectrum.
use of chloramphenicol
aerobic and anaerobic G+ and -
pharmakokinetics of chloramphenicol
inactivated in the liver via conjugation and excreted in urine. Dosage adjustment needed in pts with hepatic failure. Inhibit liver p450 enzymes (potential drug interactions)
mech of resistance
decrease drug permeability, production of plasmid encoded chloramphenicol acetyltransferase
clinical use of chloramphenicol
topically in the treatment of eye infections, alternative agent for treating meningitis in pts who are allergic to penicillin
side effects of chloramphenicol
aplastic anemia (irreversible), grey baby syndrome
quinupristin, dalfopristin
quinupristin and salfopristin moa
binds to 50s ribosomal subunit (bactericidal
quinupristin and salfopristin active against
g+ cocci including VRSA and VRE
pharmakokinetics of quinupristin and dalfopristin
inhibit cyp3a4 enzymes which metabolize warfarin, diazepam
quinpristin resistance
modification of binding site by a methylase (MLS-B type)
dalfopristin resistance
enzymatic inactivation
tox of quinupristin and dalfopristin
infusion related pain and arthralgiamyalgia syndrome (muscle pain)
linezolid MOA
inhibits protein synthesis by binding to the 23s rRNA of the 50s subunit (blocks initiation).. Bacteriostatic
linezolid use
G+ organisms. Reserved for treatment of multidrug resistant G+ bacteria ie MRSA VRE
major side effect
hamatologic toxicity
cheapest g-
gentamicin, tobramycin
expensive g-
imipenem-cilastatin, ceftriaxone
bactericidal protein synthesis inhibitors
streptogramins, aminoglycosides