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Infectious Disease > 2.3.3 Antibacterial Chemotherapy I > Flashcards

2.3.3 Antibacterial Chemotherapy I Flashcards

1
Q

Describe the structure and function of the bacterial cell wall

A
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2
Q

Describe the multiple sites of inhibition by antibacterial agents

A
  1. Cell wall synthesis (ICWS)
  2. Membrane integrity
  3. Protein synthesis
  4. Nucleic acid synthesis
  5. Nucleic acid integrity
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3
Q

Explain the mechanisms of resistance to ICWS

A
  1. No cell wall, no activation of murein hydrolases, metabollically inactive
  2. Inaccessible PBPs - Gram neg or MRSA (structural change of PBP)
  3. B-lactamase production (major mechanism of resistance, plasmid-mediated)
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4
Q

Explain the role of the ß-lactam ring in the pharmacokinetics and pharmacodynamics of ICWS

A

The beta-lactam ring allows the antibiotic to mimic D-ala-D-ala structure of the peptidoglycan cell wall. This mimicry allows for covalent binding of PBPs which ultimately disrupts transpeptidation necessary for constructing the peptidoglycan cell wall

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5
Q

Describe the role of transpeptidases/penicillin binding proteins (PBP) and murein hydrolases (autolysins)

A

PBP allows for the transpeptidation reaction necessary for construction the peptidoglycan cell wall

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6
Q

Describe the chemotherapeutic spectrum of penicillins

A

Primarily gram +

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7
Q

Describe the unique properties and indications for use of other ß-lactams

A
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8
Q

Name the anti-pseudomonal penicillins

A

Ticarcillin, piperacillin, mezlocillin

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9
Q

Name the extended spectrum penicillins

A

Ampicillin, amoxacillin, ticarcillin, piperacillin, mezlocillin

(increased gram - activity)

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10
Q

What are the 2 main types of penicilin?

A

Pen G and Pen V

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11
Q

Name the anti-staphylococcal penicillins

A

Nafcillin, isoxazolyl penicillins (ox-,clox-)

(beta-lactamase resistant)

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12
Q

What are the two adverse effects of penicillin?

A
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13
Q

What is true about cephalosporins in comparison to penicillins?

A

Poor oral absorption

More renal toxicity

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14
Q

What are the general trends b/t the cephalosporin generations?

A
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15
Q

Which cephalosporins belong to each of the four generations?

A
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16
Q

What are the adverse effects of cephalosporin?

A

Local irritation

Renal toxicity - enhanced by aminoglycosides

Cefotetan – disulfrim effect -> bleeding and platelet disorders

17
Q

What are the monobactams and carbapenems? Give some characteristics.

A
18
Q

How does vancomycin differ from penicillin in its MOA?

A

Vancomycin inhibits transglycosylation by binding directly to the D-ala-D-ala of cell walls being synthesized

Penicillin - inhibits PBPs blocking transpeptidation

19
Q

What is the MOA of fosfomycin?

A

Inhibits cytoplasmic step in cell well precursor synthesis

20
Q

Know this chart

A
21
Q

What is the target of bacterial protein synthesis?

A

Targeting of 70S ribosome of bacteria (either the 30S or 50S subunit)

22
Q

What is the target of tetracycline?

A

Reversible binding of 30S ribosome

23
Q

What are the adverse effects of tetracyclines?

A

GI irritation, superinfections, impaired liver function, photosensitization, and calcium chelation

24
Q

What is the major mechanism of resistance to tetracyclines?

A

Efflux pumps

Another mechanism: altered ribosomal proteins or RNA are secondary mechanisms

25
Q

What is unique about tigecycline?

A

Not effected by the efflux pump (effective in bugs that have developed resistance to tetracyclines through efflux pumps)

26
Q

Name the macrolide antibiotics

A

Erythromycin, clarithromycin, azithromycin

27
Q

What is the target of the protein synthesis inhibitors?

A
28
Q

What are some pharmacokinetic characteristics of macrolides?

A
29
Q

What are the clinical uses and adverse effects of macrolide abx?

A
30
Q

What are the mechanisms of resistance to macrolide abx?

A

Altered (methylated) rRNA

Efflux pump

Esterase which hydrolyzes erythromycins (enterovacteriaceae)

31
Q

What is unique about azithromycin in comparison to other macrolides?

A

Extended half-life (2-4 days)

32
Q

What is unique about telithromycin?

A
33
Q

What is the MOA of aminoglycosides and their pharmacokinetics?

A
34
Q

What type of cell killing model is demonstrated by aminoglycosides?

A

Concentration-dependent (size of punch)

35
Q

What is the clinical usage of aminoglycosides?

A

non-resistant gram neg infections (E. coli, proteus, Pseudomonas)

36
Q

What are the main adverse effects of aminoglycosides?

A

Nephrotoxicity, ototoxicity, neuromuscular blockade

37
Q

What happens when aminoglycosides are administered alone?

A

Resistance emerges rapidly

38
Q

What is a good mneumonic for AGs?

A

“Mean” (aminoglycoside) GNATS caNNOT kill anaerobes.

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

Nephrotoxicity, Neuromuscular blockade, Ototoxicity, Teratogen

Infectious Disease (40 decks)

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