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Undeleted > Antimicrobial agents > Flashcards

Antimicrobial agents Flashcards

1
Q

what do cidal vs. static AMs do

A

cidal - act on cell wall, membrane or DNA

static - inhib protein synthesis

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2
Q

when were majority of AMs invented

A

40s and 50s

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3
Q

naming for penicillin

A

-cillin

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4
Q

naming for cephalosporins

A

Ceph- or cef-

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5
Q

naming for carbapenems

A
  • penem
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6
Q

naming for fluoroquinilones

A

-floxacin

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7
Q

naming for macrolides

A

-thromycin

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8
Q

naming for aminoglycocides

A

-micin or mycin

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9
Q

what is ideal AM

A
  • kills infection
  • safe
  • no SE
  • ignores bystanders
  • no resitance
  • cheap
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10
Q

what type of agent do you need it neutropenic

A

cidal - satics won’t kill

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11
Q

how is cell wall held together

A

NAG and NAM sugars with a d-ALA d-ALA cross link

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12
Q

what is the d-ALA crosslink called

A

transpeditidase - penicillin binding protein -PBP

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13
Q

what are the 3 b-lactam AMs

A
  1. penicillin
  2. cepahlosporins
  3. carbapenems
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14
Q

what is major toxicity of B-lactams

A

allergy

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15
Q

what gives a B-lactam a wider spectrum

A

longer and more complex side chains

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16
Q

what is MOA of B-lactams

A

irreversibly bind to transpeptidase and prevent peptidoglycan cross-linking

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17
Q

3 main mech of resistance

A
  1. drug inactivation or modification
  2. alteration of target site
  3. reduced drug accumulation at target site
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18
Q

what is uncommon resistance

A

alteration of metabolic pathways

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19
Q

what is B-lactam resistance

A

B-lactamase - cleaves the B-lactam rings so it can’t bind to the PBP site

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20
Q

what ABs are used to counter B-lactamases

A

clavulanic and tazobactam - inhib B-lactamases - not actually AM themselves

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21
Q

what 2 AM classes are naturally resistant to B-lactamases

A

cephalosporin and carbapenem - especially extended spectrum - many side chains

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22
Q

what are ESBLs

A

extended spectrum B-lactamases - resistance that has further developed

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23
Q

what are useful against ESBL

A

carbapenems

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24
Q

what is MOA of MRSAs

A

changes in the PBP so that the B-lactams can’t bind - due to SCCmecA genes

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25
Q

what is main drug of choice for streps

A

penicillin - amoxicillin (oral) ampicillin (IV)

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26
Q

what do most cephalosporins cover well

A

most Gr+ and Gr-, but not anaerobes

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27
Q

what cephalosporins is good for anaerobes

A

3rd gen

28
Q

what is broadest spectrum B-lactams

A

carbapenems, but not many available

29
Q

how to test for penicillin alergy

A

skin test to rule out Type 1 sensitivity

30
Q

what is chance of cephalosporin allergy if allergic to penicilin

A

5%

31
Q

MOA of vancomycin

A

Binds directly to d-ALA and prevents peptidoglycan crosslinking

32
Q

what is vancomycin able to target

A

Gr+ - can’t bind Gr- because of large size

33
Q

what is vancomycin problems

A

weak AM and not well tolerated so dosing is an issue

34
Q

2 mechs of resisitance to vancomycin

A

VISA - Vanco Intermediate susceptable SA - thickened cell wall so can’t get in as well
VRSA - Vanco Resisitant SA - alteration of d-ALA to d-LAC to prevent binding

35
Q

what is responsible for DNA supercoiling

A

DNA gyrase (topoisomerase 2) - introduces negative supercoiling

36
Q

what does topoisomerase 4 do?

A

similar to DNA gyrase, but does not cause DNA towrap around itself

37
Q

where do topoisomerase 2 and 4 work

A

2 (gyrase) works ahead of the fork and 4 works after the fork

38
Q

what is the most overused AM

A

fluroquinolones (FQs)

39
Q

what is FQ MOA

A
  1. DNA are separated when supercoiling and create a pocket
  2. FQ binds in pocket and stabilizes
  3. prevents uncoiling
  4. broken bits of DNA are repaired in a disorganized manner
40
Q

what are Gr - and + targets in FQs

A

+ topoisomerase 4

- DNA gyrase

41
Q

what causes moderate restance to FQ

A

mutation in primary target (topoismoerase)

42
Q

what causes high level resistance in FQ

A

second mutation in the target

43
Q

what are 3 mech of FQ resistance

A
  1. altered target (above)
  2. efflux pumps push out FQ
  3. altered porin (Gr- only) that don’t allow FQ in
44
Q

what is MOA of sulfonamides and trimethoprim

A

block folate synthesis at 2 sites which is needed for DNA production - static, with a touch of cidal

45
Q

where does bacterial protein synthesis occur

A

ribosome - has a large 50S subunit and smaller 30S subunit

46
Q

5 classes of protein syn inhibitors

A
  1. aminoglycosides
  2. macrolides
  3. clindamycin
  4. tetracyclins
  5. oxazolidinones
47
Q

what is major problems with aminoglycosides

A

nephro and ototoxicity

48
Q

MOA of aminoglycosides

A
  1. bind to 30S subunit
  2. also bind to outer membrane and displace Mg and Ca
  3. leaky cell
  4. cidal and static
49
Q

mechanisms of resistance in aminoglycosides

A
  1. in safe doses can’t cross Gr+ wall
  2. modification of drug by bact enzymes so can’t cross wall
  3. modify the ribosome to prevent binding
50
Q

MOA of macrolides and clindamycin

A

bind to 50S subunit and are cidal

51
Q

MOA of resistance in macrolides and clindamycin

A

modification of 23S subunit to prevent binding

52
Q

what is MOA of tetracyline

A

bind to 30S subunit and are static

53
Q

use of tetracyline

A

active against a wide variety of bact and MRSA

54
Q

what class is linzolid

A

oxazolidinone

55
Q

MOA of linzolid

A

bind to 50S subunit and are static

56
Q

what is range of linzolid

A

very active agains + and no -

57
Q

MOA of metronidazole (-flagel)

A

in bact it accepts electrons and causes free radicals - cidal

58
Q

range of metronizaole

A

anaerobes only

59
Q

3 main classes of anti fungals

A
  1. polyenes
  2. azoles
  3. echinocandins
60
Q

MOA of polyenes

A

amphoceterin B binds to ergosterol in membrane and causes leaks

61
Q

what is prob with polyenes

A

also binds cholesterol

  • fever, rigors
  • nephrotoxitiy
62
Q

2 ways to avoid polyene toxiticy

A
  1. slow infusion

2. bind with liposomes - expensive

63
Q

MOA of azoles

A

inhib enzyme which converts lanosterol to ergosterol

- altered membrane and slowed growth

64
Q

major issue with azoles

A

CYP450 inhibitor

65
Q

what is mech of resistance in azoles

A

the usual suspects

66
Q

MOA of echinocandins

A

inhib. 1,3-B glucan synthase and therefore inhib cell wall formation- fungal version of B-lactams

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