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MMMD > W05_Antimicrobials I > Flashcards

W05_Antimicrobials I Flashcards

1
Q

class of drugs with the suffix -cillin?

A

penicillins

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2
Q

class of drugs with the suffix -penem?

A

carbapenems

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3
Q

class of drugs with the suffix -floxacin?

A

fluoroquinolones

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4
Q

class of drugs with the suffix -thromycin?

A

macrolides

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5
Q

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

A

aminoglycosides

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6
Q

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

A

cephalosporins

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7
Q

bactericidal drugs typically target which part of the bacteria?

A

cell wall/membrane integrity, DNA synthesis

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8
Q

bacteriostatic drugs typically target which part of the bacteria?

A

protein synthesis

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9
Q

what is the bacterial cell wall made of?

A

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

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10
Q

beta-lactams include which groups of drugs?

A

penicillins, cephalosporins, carbapenems, monolactams

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11
Q

what’s the MoA for beta-lactams?

A

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

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12
Q

what are 3 main mechanisms of antimicrobial resistance?

A

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

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13
Q

what’s beta-lactamase?

A

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

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14
Q

what’s clavulanic acid?

A

beta-lactamase inhibitor. used in amoxicillin-clavulanate.

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15
Q

what’s tazobactam?

A

beta-lactamase inhibitor. used in piperacillin-tazobactam.

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16
Q

how do beta-lactamases affect cephalosporins and carbapenems?

A

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

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17
Q

third-gen cephalosporins are what kind of antimicrobial?

A

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

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18
Q

note: carbapenems are still generally resistant to ESBLs.

A

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

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19
Q

what’s the MoA of MRSA resistance?

A

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

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20
Q

route for amoxicillin?

A

oral

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21
Q

route for ampicillin?

A

parenteral/IV

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22
Q

what kinds of bacteria is piperacillin used for?

A

gram-negative (broad)

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23
Q

what kinds of bacteria do cephalosporins target?

A

broad GN and GP. not good for anaerobes.

24
Q

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

A

cephalosporin

25
Q

MoA for vancomycin?

A

binds directly to D-Ala/D-Ala site

26
Q

what are side effects of vanco?

A

nephrotoxicity

27
Q

what type of bacteria does vanco affect?

A

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

28
Q

MoA for vancomycin-intermediately susceptible s.aureus resistance?

A

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

29
Q

MoA for vancomycin-resistant staphylococcus aureus resistance?

A

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

30
Q

what is DNA gyrase?

A

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

31
Q

what is DNA topoisomerase IV?

A

enzyme that ensures DNA is coiled again. parC and parE

32
Q

MoA of fluoroquinolones?

A

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

33
Q

how do bacteria develop resistance to fluoroquinolones?

A

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

34
Q

MoA of trimethoprim/sulfamethoxazole (septra)?

A

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

35
Q

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

A

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

36
Q

MoA of aminoglycosides?

A

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

37
Q

MoA of macrolides?

A

protein synthesis inhibitor

38
Q

MoA of clindamycin?

A

protein synthesis inhibitor

39
Q

MoA of tetracyclines?

A

protein synthesis inhibitor

40
Q

MoA of oxazolidinones?

A

protein synthesis inhibitor

41
Q

aminoglycosides are notorious for which side effect?

A

nephro and ototoxicity

42
Q

what is the post-antibiotic effect?

A

bactericidal effect continues after aminoglycoside levels are undetectable

43
Q

how do bacteria resist aminoglycosides?

A

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

44
Q

what are the three main macrolides?

A

azithromycin, clarithromycin, erythromycin

45
Q

what is clindamycin?

A

a “lincosamide”. it’s the only one. similar to the macrolides

46
Q

how do bacteria resist macrolides?

A

23S ribosomal RNA modification to prevent binding

47
Q

which tetracycline is used most often, practically?

A

doxycycline

48
Q

tetracyclines are active against which types of bacteria?

A

GP (including MRSA) and GN

49
Q

what is linezolid?

A

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

50
Q

what’s metronidazole?

A

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

51
Q

what’s the fungal equivalent of cholesterol?

A

ergosterol

52
Q

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

A

antifungal

53
Q

what’s amphotericin B? MoA?

A

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

54
Q

MoA of azoles?

A

preventing the conversion of lanosterol to ergosterol; cell membranes affected

55
Q

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

A

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

56
Q

what’s the fungal equivalent of PBP?

A

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

57
Q

MoA of echinocandins?

A

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

MMMD (62 decks)

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