W05_Antimicrobials I

Question 1

class of drugs with the suffix -cillin?

Answer 1

penicillins

Question 2

class of drugs with the suffix -penem?

Answer 2

carbapenems

Question 3

class of drugs with the suffix -floxacin?

Answer 3

fluoroquinolones

Question 4

class of drugs with the suffix -thromycin?

Answer 4

macrolides

Question 5

class of drugs with the suffix -micin or -mycin?

Answer 5

aminoglycosides

Question 6

class of drugs with the prefix -cef/-ceph?

Answer 6

cephalosporins

Question 7

bactericidal drugs typically target which part of the bacteria?

Answer 7

cell wall/membrane integrity, DNA synthesis

Question 8

bacteriostatic drugs typically target which part of the bacteria?

Answer 8

protein synthesis

Question 9

what is the bacterial cell wall made of?

Answer 9

peptidoglycan (NAG + NAM, plus PBP transpeptidase). NAG/NAM linked via their D-Ala residues

Question 10

beta-lactams include which groups of drugs?

Answer 10

penicillins, cephalosporins, carbapenems, monolactams

Question 11

what’s the MoA for beta-lactams?

Answer 11

the beta-lactam ring binds to the PBP transpeptidase of the cell wall, and prevent crosslinking. thus, cell wall disrupted and bacteria dies.

Question 12

what are 3 main mechanisms of antimicrobial resistance?

Answer 12

drug inactivation/modification;
alteration of target site;
reduced drug accumulation at target site;
alteration of metabolic pathway (less common)

Question 13

what’s beta-lactamase?

Answer 13

an enzyme that chops up the beta-lactam rings and inactivate the drug

Question 14

what’s clavulanic acid?

Answer 14

beta-lactamase inhibitor. used in amoxicillin-clavulanate.

Question 15

what’s tazobactam?

Answer 15

beta-lactamase inhibitor. used in piperacillin-tazobactam.

Question 16

how do beta-lactamases affect cephalosporins and carbapenems?

Answer 16

these are usually naturally resistant to the enzymatic breakdown (ring protected by large side groups)

Question 17

third-gen cephalosporins are what kind of antimicrobial?

Answer 17

extended-spectrum beta-lactam. note that ESBL (lactamase) are growing to deactivate these drugs

Question 18

note: carbapenems are still generally resistant to ESBLs.

Answer 18

these are broad-spectrum drugs with less resistance. use cautiously

Question 19

what’s the MoA of MRSA resistance?

Answer 19

a gene (SCCmecA) that alters the PBP so that beta-lactams can’t bind.

Question 20

route for amoxicillin?

Answer 20

oral

Question 21

route for ampicillin?

Answer 21

parenteral/IV

Question 22

what kinds of bacteria is piperacillin used for?

Answer 22

gram-negative (broad)

Question 23

what kinds of bacteria do cephalosporins target?

Answer 23

broad GN and GP. not good for anaerobes.

Question 24

if a patient is allergic to penicillin, you can give what other type of drug, with 5% chance of another allergy?

Answer 24

cephalosporin

Question 25

MoA for vancomycin?

Answer 25

binds directly to D-Ala/D-Ala site

Question 26

what are side effects of vanco?

Answer 26

nephrotoxicity

Question 27

what type of bacteria does vanco affect?

Answer 27

GP. (because its shape and size can't bind GN cell walls)

Question 28

MoA for vancomycin-intermediately susceptible s.aureus resistance?

Answer 28

cell walls thickened, so vanco can't penetrate deeply to get to the cell wall precursors

Question 29

MoA for vancomycin-resistant staphylococcus aureus resistance?

Answer 29

D-Ala changed to D-Lac. vanco can't bind no mo.

Question 30

what is DNA gyrase?

Answer 30

topoisomerase II, an enzyme that introduces DNA negative supercoiling during synthesis. gyrA and gyrB

Question 31

what is DNA topoisomerase IV?

Answer 31

enzyme that ensures DNA is coiled again. parC and parE

Question 32

MoA of fluoroquinolones?

Answer 32

locks DNA topoisomerases in place. causes DNA cleavage. gyrA in GN. parC in GP.

Question 33

how do bacteria develop resistance to fluoroquinolones?

Answer 33

DNA mutation of one or two topoisomerases; efflux pumps; altered GN porins (that don't let the antimicrobial in)

Question 34

MoA of trimethoprim/sulfamethoxazole (septra)?

Answer 34

blocks 2 steps of folic acid metabolism, so no cell synthesis

Question 35

patients with neutropenia should be given with type of antimicrobial (static or cidal)?

Answer 35

cidal - they can't fight the static bacteria, so that's less useful

Question 36

MoA of aminoglycosides?

Answer 36

protein synthesis inhibitor. note that aminoglycosides also make the cell membrane leaky. combined, these are CIDAL drugs, not static! only work on GN.

Question 37

MoA of macrolides?

Answer 37

protein synthesis inhibitor

Question 38

MoA of clindamycin?

Answer 38

protein synthesis inhibitor

Question 39

MoA of tetracyclines?

Answer 39

protein synthesis inhibitor

Question 40

MoA of oxazolidinones?

Answer 40

protein synthesis inhibitor

Question 41

aminoglycosides are notorious for which side effect?

Answer 41

nephro and ototoxicity

Question 42

what is the post-antibiotic effect?

Answer 42

bactericidal effect continues after aminoglycoside levels are undetectable

Question 43

how do bacteria resist aminoglycosides?

Answer 43

GP cell walls are too thick; drug modification to prevent entry/binding; reduce entry, increase efflux

Question 44

what are the three main macrolides?

Answer 44

azithromycin, clarithromycin, erythromycin

Question 45

what is clindamycin?

Answer 45

a "lincosamide". it's the only one. similar to the macrolides

Question 46

how do bacteria resist macrolides?

Answer 46

23S ribosomal RNA modification to prevent binding

Question 47

which tetracycline is used most often, practically?

Answer 47

doxycycline

Question 48

tetracyclines are active against which types of bacteria?

Answer 48

GP (including MRSA) and GN

Question 49

what is linezolid?

Answer 49

oxazolidinone. bacteriostatic. used against GP (including MRSA and VRE).

Question 50

what's metronidazole?

Answer 50

accepts electrons to make free radicals. thus, only bactericidal to anaerobes. and some parasites

Question 51

what's the fungal equivalent of cholesterol?

Answer 51

ergosterol

Question 52

polyenes, azoles, and echinocandins are classes for which type of agents?

Answer 52

antifungal

Question 53

what's amphotericin B? MoA?

Answer 53

polyene antifungal. binds and disrupts ergosterol to cause leaky membrane. also affects human cells - nephrotoxicity.

Question 54

MoA of azoles?

Answer 54

preventing the conversion of lanosterol to ergosterol; cell membranes affected

Question 55

what kinds of drug interactions should you consider with azole usage?

Answer 55

it inhibits a p450-dependent enzyme. take caution here.

Question 56

what's the fungal equivalent of PBP?

Answer 56

1,3-beta-glucan synthase. (binds D-glucose together to make the wall)

Question 57

MoA of echinocandins?

Answer 57

inhibit 1,3-beta-glucan synthase. to prevent cell wall formation like a beta-lactam