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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
what is main drug of choice for streps
penicillin - amoxicillin (oral) ampicillin (IV)
26
what do most cephalosporins cover well
most Gr+ and Gr-, but not anaerobes
27
what cephalosporins is good for anaerobes
3rd gen
28
what is broadest spectrum B-lactams
carbapenems, but not many available
29
how to test for penicillin alergy
skin test to rule out Type 1 sensitivity
30
what is chance of cephalosporin allergy if allergic to penicilin
5%
31
MOA of vancomycin
Binds directly to d-ALA and prevents peptidoglycan crosslinking
32
what is vancomycin able to target
Gr+ - can't bind Gr- because of large size
33
what is vancomycin problems
weak AM and not well tolerated so dosing is an issue
34
2 mechs of resisitance to vancomycin
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
what is responsible for DNA supercoiling
DNA gyrase (topoisomerase 2) - introduces negative supercoiling
36
what does topoisomerase 4 do?
similar to DNA gyrase, but does not cause DNA towrap around itself
37
where do topoisomerase 2 and 4 work
2 (gyrase) works ahead of the fork and 4 works after the fork
38
what is the most overused AM
fluroquinolones (FQs)
39
what is FQ MOA
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
what are Gr - and + targets in FQs
+ topoisomerase 4 | - DNA gyrase
41
what causes moderate restance to FQ
mutation in primary target (topoismoerase)
42
what causes high level resistance in FQ
second mutation in the target
43
what are 3 mech of FQ resistance
1. altered target (above) 2. efflux pumps push out FQ 3. altered porin (Gr- only) that don't allow FQ in
44
what is MOA of sulfonamides and trimethoprim
block folate synthesis at 2 sites which is needed for DNA production - static, with a touch of cidal
45
where does bacterial protein synthesis occur
ribosome - has a large 50S subunit and smaller 30S subunit
46
5 classes of protein syn inhibitors
1. aminoglycosides 2. macrolides 3. clindamycin 4. tetracyclins 5. oxazolidinones
47
what is major problems with aminoglycosides
nephro and ototoxicity
48
MOA of aminoglycosides
1. bind to 30S subunit 2. also bind to outer membrane and displace Mg and Ca 3. leaky cell 4. cidal and static
49
mechanisms of resistance in aminoglycosides
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
MOA of macrolides and clindamycin
bind to 50S subunit and are cidal
51
MOA of resistance in macrolides and clindamycin
modification of 23S subunit to prevent binding
52
what is MOA of tetracyline
bind to 30S subunit and are static
53
use of tetracyline
active against a wide variety of bact and MRSA
54
what class is linzolid
oxazolidinone
55
MOA of linzolid
bind to 50S subunit and are static
56
what is range of linzolid
very active agains + and no -
57
MOA of metronidazole (-flagel)
in bact it accepts electrons and causes free radicals - cidal
58
range of metronizaole
anaerobes only
59
3 main classes of anti fungals
1. polyenes 2. azoles 3. echinocandins
60
MOA of polyenes
amphoceterin B binds to ergosterol in membrane and causes leaks
61
what is prob with polyenes
also binds cholesterol - fever, rigors - nephrotoxitiy
62
2 ways to avoid polyene toxiticy
1. slow infusion | 2. bind with liposomes - expensive
63
MOA of azoles
inhib enzyme which converts lanosterol to ergosterol | - altered membrane and slowed growth
64
major issue with azoles
CYP450 inhibitor
65
what is mech of resistance in azoles
the usual suspects
66
MOA of echinocandins
inhib. 1,3-B glucan synthase and therefore inhib cell wall formation- fungal version of B-lactams

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