Antibiotics - Morris Flashcards

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1
Q

How does MRSA acquire resistance?

A

Acquires SCCmecA
Produces altered PBPs
Beta lactamase inhibitor wont make a difference

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2
Q

Piperacillin - and Pip tazo spectrum of activity

A

Piperacillin = broad gram negative

PipTazo - Broad gram neg and anaerobes

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3
Q

Gut anaerobes are known for making

A

Beta lactamase

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4
Q

3rd gen Cephalosporins considered

A

Extended spectrum Beta lactams

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5
Q

Which carbapenem is very resistant to Pseudomonas?

A

Ertapenem!

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6
Q

Greatest value of the cephalosporins?

A

Effective against ESblactamases

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7
Q

Staph aureus resistant first due to

A

a beta lactamase

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8
Q

Mechanism of action of Vanco - (hint) how is it different from the beta lactams

A
  • Binds directly D-ala D-ala
  • Skips the PBPs -
  • prevents crosslinking
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9
Q

Because of the size and shape of vanco what can’t it bind to?

A

Gram negative cell walls

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10
Q

what are some of the toxicities of Vanco?

A

Renal failure, nephrotoxic

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11
Q

VISA - vancomycin intermediately susceptible Staph - mechanism

A

Thickened cell wall

reduced access of vanco

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12
Q

VRSA-

A

Alteration of the D-ala to D-Lac

preventing binding prevent crosslinking

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13
Q

DNA gyrase is a …(type 2 Top)

A

Topoisomerase 2
- A tetramer
GryA GyrB 2 subunits each
works ahead of the replication fork

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14
Q

Topoisomerase 4 made up of (Type 2 top)

A

ParC and ParE

Works AFTER the replication fork

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15
Q

In Gram negatives the FQs target mainly…

A

DNA gyrase - GyrA especially

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16
Q

in Gram positives the FQs target

A

Topoisomerase 4 - Esp ParC

17
Q

Moderate level of resistance to FQs occurs when

A

GyrA is mutated in Gram negs

ParC is mutated in Gram pos

18
Q

High level resistance to FQs occurs when

A

Both enzymes mutated

19
Q

FQ resistance can also be mediated by

A
  • Efflux pumps (on outer cell membrane)

- Gram negatives have porins to reduce accumulation of the drug (also on cell membrane)

20
Q

TMP-SMX are

A

Bacteriostatic

block folic acid metabolism (S before T)

21
Q

Drugs classified as protein synthesis inhibitors

A
Macrolides
Aminoglycosides
Tetracyclines
Clindamycin
Oxazolidinones
22
Q

Aminoglycosides notorious for there

A

Nephro and OTOtoxicity

23
Q

Aminoglycosides - mechanism of action

A

Bind 30S ribosome
AND
CIDAL - make cell leaky by binding Mg and Ca
They also have a post-antibiotic effect

24
Q

Which bacteria are most resistant to aminoglycosides?

A

Gram positives - thick cell wall hard to penetrate

25
Q

Mechanisms of resistance to aminoglycosides?

A

Efflux, reduce entry

Modify the 30S ribosome prevent binding

26
Q

Mechanism of action of Clindamycin and Macrolides?

A

Bind 50S ribosome - are bacteriostatic

27
Q

Unique feature of Clindamycin

A

Has anaerobic activity

28
Q

Mechanisms of resistance to Clindamycin and Macrolides?

A

Modify the subunit

29
Q

Side Effects of Clindamycin and Macrolides

A

GI intolerance

30
Q

Tetracyclines - mechanism of action

A

Bind 30S subunit

31
Q

Linezolid is a

A

Oxazolidinone -

Binds 50S

32
Q

Spectrum of activity of Linezolid?

A

Gram positives includes MRSA and VRE

NOT gram negatives

33
Q

Side effects of Linezolid?

A

Neutropenia, Neuropathy

34
Q

Metronidazole MOA

A

Produces toxic radicals
Bacteriacidal
ONLY against Anerobes -