W05_Antimicrobials I Flashcards
class of drugs with the suffix -cillin?
penicillins
class of drugs with the suffix -penem?
carbapenems
class of drugs with the suffix -floxacin?
fluoroquinolones
class of drugs with the suffix -thromycin?
macrolides
class of drugs with the suffix -micin or -mycin?
aminoglycosides
class of drugs with the prefix -cef/-ceph?
cephalosporins
bactericidal drugs typically target which part of the bacteria?
cell wall/membrane integrity, DNA synthesis
bacteriostatic drugs typically target which part of the bacteria?
protein synthesis
what is the bacterial cell wall made of?
peptidoglycan (NAG + NAM, plus PBP transpeptidase). NAG/NAM linked via their D-Ala residues
beta-lactams include which groups of drugs?
penicillins, cephalosporins, carbapenems, monolactams
what’s the MoA for beta-lactams?
the beta-lactam ring binds to the PBP transpeptidase of the cell wall, and prevent crosslinking. thus, cell wall disrupted and bacteria dies.
what are 3 main mechanisms of antimicrobial resistance?
drug inactivation/modification;
alteration of target site;
reduced drug accumulation at target site;
alteration of metabolic pathway (less common)
what’s beta-lactamase?
an enzyme that chops up the beta-lactam rings and inactivate the drug
what’s clavulanic acid?
beta-lactamase inhibitor. used in amoxicillin-clavulanate.
what’s tazobactam?
beta-lactamase inhibitor. used in piperacillin-tazobactam.
how do beta-lactamases affect cephalosporins and carbapenems?
these are usually naturally resistant to the enzymatic breakdown (ring protected by large side groups)
third-gen cephalosporins are what kind of antimicrobial?
extended-spectrum beta-lactam. note that ESBL (lactamase) are growing to deactivate these drugs
note: carbapenems are still generally resistant to ESBLs.
these are broad-spectrum drugs with less resistance. use cautiously
what’s the MoA of MRSA resistance?
a gene (SCCmecA) that alters the PBP so that beta-lactams can’t bind.
route for amoxicillin?
oral
route for ampicillin?
parenteral/IV
what kinds of bacteria is piperacillin used for?
gram-negative (broad)
what kinds of bacteria do cephalosporins target?
broad GN and GP. not good for anaerobes.
if a patient is allergic to penicillin, you can give what other type of drug, with 5% chance of another allergy?
cephalosporin
MoA for vancomycin?
binds directly to D-Ala/D-Ala site
what are side effects of vanco?
nephrotoxicity
what type of bacteria does vanco affect?
GP. (because its shape and size can’t bind GN cell walls)
MoA for vancomycin-intermediately susceptible s.aureus resistance?
cell walls thickened, so vanco can’t penetrate deeply to get to the cell wall precursors
MoA for vancomycin-resistant staphylococcus aureus resistance?
D-Ala changed to D-Lac. vanco can’t bind no mo.
what is DNA gyrase?
topoisomerase II, an enzyme that introduces DNA negative supercoiling during synthesis. gyrA and gyrB
what is DNA topoisomerase IV?
enzyme that ensures DNA is coiled again. parC and parE
MoA of fluoroquinolones?
locks DNA topoisomerases in place. causes DNA cleavage. gyrA in GN. parC in GP.
how do bacteria develop resistance to fluoroquinolones?
DNA mutation of one or two topoisomerases;
efflux pumps;
altered GN porins (that don’t let the antimicrobial in)
MoA of trimethoprim/sulfamethoxazole (septra)?
blocks 2 steps of folic acid metabolism, so no cell synthesis
patients with neutropenia should be given with type of antimicrobial (static or cidal)?
cidal - they can’t fight the static bacteria, so that’s less useful
MoA of aminoglycosides?
protein synthesis inhibitor. note that aminoglycosides also make the cell membrane leaky. combined, these are CIDAL drugs, not static! only work on GN.
MoA of macrolides?
protein synthesis inhibitor
MoA of clindamycin?
protein synthesis inhibitor
MoA of tetracyclines?
protein synthesis inhibitor
MoA of oxazolidinones?
protein synthesis inhibitor
aminoglycosides are notorious for which side effect?
nephro and ototoxicity
what is the post-antibiotic effect?
bactericidal effect continues after aminoglycoside levels are undetectable
how do bacteria resist aminoglycosides?
GP cell walls are too thick;
drug modification to prevent entry/binding;
reduce entry, increase efflux
what are the three main macrolides?
azithromycin, clarithromycin, erythromycin
what is clindamycin?
a “lincosamide”. it’s the only one. similar to the macrolides
how do bacteria resist macrolides?
23S ribosomal RNA modification to prevent binding
which tetracycline is used most often, practically?
doxycycline
tetracyclines are active against which types of bacteria?
GP (including MRSA) and GN
what is linezolid?
oxazolidinone. bacteriostatic. used against GP (including MRSA and VRE).
what’s metronidazole?
accepts electrons to make free radicals. thus, only bactericidal to anaerobes. and some parasites
what’s the fungal equivalent of cholesterol?
ergosterol
polyenes, azoles, and echinocandins are classes for which type of agents?
antifungal
what’s amphotericin B? MoA?
polyene antifungal. binds and disrupts ergosterol to cause leaky membrane. also affects human cells - nephrotoxicity.
MoA of azoles?
preventing the conversion of lanosterol to ergosterol; cell membranes affected
what kinds of drug interactions should you consider with azole usage?
it inhibits a p450-dependent enzyme. take caution here.
what’s the fungal equivalent of PBP?
1,3-beta-glucan synthase. (binds D-glucose together to make the wall)
MoA of echinocandins?
inhibit 1,3-beta-glucan synthase. to prevent cell wall formation like a beta-lactam
