W5/L7 Flashcards

1
Q

What’s the broad target of penicillins?

A

Cell wall synthesis

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2
Q

What’s the MoA of penicillins?

A

They bind PBP transpeptidases to inhibit peptidoglycan synthesis

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3
Q

Why do mycoplasma have intrinsic penicillin resistance?

A

Their cell wall doesn’t have peptidoglycan

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4
Q

Why does pseudomonas have intrinsic penicillin resistance?

A

Via the chromosomal beta-lactamases they always produce

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5
Q

Why can’t penicillin G be given orally?

A

It’s acid labile

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6
Q

What’s the acid-stable form of penicillin G?

A

Penicillin V

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7
Q

What drug do we treat penicillin-resistant staph with?

A

Flucloxacillin

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8
Q

What’s another name for co-amoxyclav?

A

Augmentin

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9
Q

What is co-amoxyclav?

A

Ampicillin/amoxycillin + clavulanic acid

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10
Q

What is clavulanic acid?

A

A “suicide inhibitor” of beta-lactamases

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11
Q

What is the penicillin used for pseudomonas? Why?

A

Carbenicillin - it’s more resistant to beta-lactamases

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12
Q

Which generation of cephalosporins are indicated for bacterial meningitis & why?

A

3rd generation. They penetrate the BBB

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13
Q

What are the two mechanisms of cephalosporin resistance?

A

Reduced PBP binding affinity

Acquisition of a beta-lactam insensitive PBP

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14
Q

Which bacteria have intrinsic vancomycin resistance? Why?

A

Gram -‘ve cells, as the molecule is to large and charged to penetrate their wall

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15
Q

What’s the MoA of glycopeptides?

A

Binds the terminal D-Ala-D-Ala, of peptidoglycan, which prevents their cross linking

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16
Q

What’s the main glycopeptide?

A

Vancomycin

17
Q

What drug do we treat methicillin-resistant staph with?

A

Vancomycin

18
Q

What are two mechanisms of acquired vancomycin resistance?

A
  • Staph producing excess peptidoglycan

- Enterococci replacing the terminal- Ala with a -Lac to block binding