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D&D Unit 3 > Antibacterial Agents: Cell Wall Synthesis Inhibition > Flashcards

Antibacterial Agents: Cell Wall Synthesis Inhibition Flashcards

1
Q

What are the different stages of bacterial cell wall synthesis?

A

1: cell wall subunits assembly (in CYTOSOL)
2: Linear polymerization of subunits (CELL MEMBRANE)
3: Cross-linking of peptidoglycan polymers (CELL WALL)

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2
Q

What is the mechanism of action for penicillins?

A

Stage 3 - Cell wall synthesis inhibition

Bactericidal

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3
Q

Describe resistance to penicillins

A
  • Penicillinase production via plasmid in presence of penicillin — Problem w/ MSSA
  • Alterations in penicillin-binding proteins – MRSA
  • Inability to penetrate outer membrane of g(-) bacteria —- Pen G can’t
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4
Q

Describe the absorption of penicillins

A
  • Moderately strong acids, highly water-soluble

Pen G: IM/IV (poor oral)

Pen V: good po

Dicloxacilin: good po

Amoxicillin: good po

Piperacillin + Beta-lactamase inhibitor: IV only

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5
Q

Describe the distribution of Penicillins

A
  • Distribute throughout body water — penetrate into cells/tissues poorly (b/c it’s ionized at physiological pH)
  • Can enter inflamed tissues or membranes (CSF, joints, eyes)
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6
Q

Describe the elimination of penicillins

A

90% renal excretion

t1/2 = <1-2 hrs

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7
Q

What are narrow spectrum penicillins used for? (E.g. Pen G and V)

A

G(+) cocci = staph, strep, enterococcus

G(-) cocci = Neisseria

Anaerobes

NOT (!!!!) MSSA, MRSA

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8
Q

What are penicillinase resistant penicillins used for? (E.g. Dicloxacilin)

A

MSSA skin infections

NOT(!!!!) MRSA

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9
Q

Other than penicillinase-resistant antibiotics, all other PCNs are susceptible to penicillinase unless they are combined with what?

A

A beta-lactamase inhibitor!!

Amoxicillin-clavulanate

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10
Q

What are extended spectrum penicillins used for? (E.g. amoxicillin)

A

G(-) RODS = E.coli

G(+) COCCI = staph, strep, enterococcus (less so than Pen G and V)

NOT (!!) MRSA or MSSA

NOT Klebsiella or E.coli (TEM-1)

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11
Q

What are antipseudomonal penicillins used for? (E.g. Piperacillin/Ticarcilin + Beta-lactamase inhibitor)

A

G(+) COCCI = strep, staph, entero

MSSA

E.Coli, Klebsiella

Pseudomonas, bacteroides, anaerobes!!

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12
Q

What are potential adverse rxns to penicillins?

A
  • Anaphylaxis (Type 1, rare)

- Rash (common)

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13
Q

What are potential adverse rxns to narrow spectrum PCNs?

A

Convulsions at very high doses

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14
Q

What are potential adverse rxns to extended spectrum PCNs?

A
  • Diarrhea

- Superinfection (CDAD)

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15
Q

What is the mechanism of action for cephalosporins?

A

Stage 3 - Cell wall synthesis inhibition

Bactericidal

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16
Q

How do cephalosporins differ from PCNs G and V?

A
  • Broader spectrum vs g(-) bacteria
  • Less susceptibility to beta-lactamases
  • Less cross-reactivity in penicillin sensitive patients
17
Q

Describe the absorption of cephalosporins

A

1st gen: Cephalexin (po), Cefazolin (IV only)

2nd gen: Cefaclor (po), Cefuroxime (po, IV)

3rd gen: Cefdinir (po), Ceftriaxone (good CNS penetration!!!)

18
Q

Describe the distribution of cephalosporins

A
  • Penetrate well into most tissues/fluids (includes placenta)
  • Not the case for brain and CSF
  • However, 3rd generation can do CNS penetration
19
Q

Describe the excretion of cephalosporins

A
  • Via kidneys!

- Dose adjustment required w/ renal insufficiency (makes sense) — except w/ ceftriaxone

20
Q

What are 1st generation cephalosporins used for? (E.g. Cephalexin, Cefazolin)

A

G(+) COCCI

MSSA

G(-) RODS = E. Coli, Klebsiella

21
Q

What are 2nd generation cephalosporins used for? (E.g. Cefaclor, Cefuroxime)

A

G(+) COCCI => less than 1st gen

MSSA

RODS

Bacteroides fragilis (anaerobes)

22
Q

What are 3rd generation cephalosporins used for? (E.g. Cefdinir, Ceftriaxone)

A

Expanded g(-) RODS (E.colis, klebsiella)

good G(+) cocci — ceftriaxone

moderate pseudonomas

Ceftriaxone –» N. gonorrhoeae

23
Q

What are adverse rxns associated w/ cephalosporins?

A
  • Generally well-tolerated due to high toxicity

1) Allergy/hypersensitivity: anaphylaxis, rashes, nephritis
2) GI distress: nausea, vomiting, diarrhea
3) Superinfection w/ 2nd and 3rd gen
4) Can intensify anticoag warfarin! w/2nd gen

24
Q

What is the mechanism of action for Vancomycin?

A
  • Stage 2: cell wall synthesis inhibition
  • Blocks glycopeptide elongation by binding to D-alanyl-D-alanine part of cell wall precursor

Bactericidal

25
Q

Which bacteria are shown to be resistant to Vancomycin?

A

S. Aureus (VRSA)

Enterococci (VRE)

B/c these bacteria do not have a D-ala-D-ala peptide

26
Q

Describe the absorption of Vancomysin

A

bad PO

IV use!

27
Q

How is vancomycin excreted from the body?

A

Via the kidneys

Remember dosage adjustment may be needed w/ renal probs

28
Q

What is vancomysin used for?

A

G(+) Cocci => S. aureus, Staph, Strep, Entero

Anaerobes => C. Diff (but metronidazole is first choice…)

29
Q

What are adverse rxns associated w/ Vancomycin?

A
  • Usually related to dosing and/or route of admin

1) Chills, fever, rash
2) Nephrotoxicity
3) Ototoxicity

30
Q

Describe the mechanism of action for carbapenems

A
  • STAGE 3: CW synthesis inhibitor

- Beta-lactamase resistant

31
Q

How are carbapenems administered?

A

Parenterally (IV only)

32
Q

Describe the distribution of carbapenems

A

Good into CSF

33
Q

How are carbapenems excreted?

A

Via kidneys

increase t1/2 if renal failure

34
Q

What are carbapenems used for?

A
  • Reserved for multiple drug resistant organisms
  • Used when aminoglycosides and cephalosporins don’t work
G(-) rods
G(+) cocci
Pseudomonas
C perf
MSSA, not MRSA
35
Q

What are the adverse rxns associated w/ carbapenems?

A

N/v, diarrhea, rash

Seizures, rarely

D&D Unit 3 (12 decks)

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