L20: Antibiotics Flashcards

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1
Q

Antibiotic vs antimicrobial

A
  • Antibiotic: produced in nature

- Antimicrobial: synthetic

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2
Q

Bacteriostatic vs bactericidal. In which pt groups are each best suited?

A
  • Bacteriostatic: inhibit growth of bacteria, but don’t kill – used in pts with good immune system when host defenses can be counted on
  • Bactericidal: kill bacteria – used during invasive infections (bacteremia, meningitis, endocarditis etc.) and in pt who is immunocompromised
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3
Q

What is antibiotic synergism?

A
  • Combination of antibiotics with enhanced bactericidal activity when used together
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4
Q

What is antibiotic antagonism?

A
  • Combination of antibiotics in which one interferes with the activity of the other
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5
Q

Advantages and disadvantages of broad and narrow-spectrum antibiotics

A
  1. ) Broad-spectrum: effective against large variety of bacteria
    - Advantage: increased likelihood of effectiveness against bacterial infection of unknown etiology
    - Disadvantage: increased likelihood of disrupting pts normal microbiota
  2. ) Narrow-spectrum: effective against only a small subset of bacteria
    - Advantage: avoid disruption of normal microbiota
    - Disadvantage: must have disease causing bacterium(a) identified
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6
Q

Spectrum of antibiotic activity

A
  • Narrow spectrum, expanded, broad, extended
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7
Q

Do antibiotics cause resistance?

A
  • No!!!! They select against selective bacteria and for resistant bacteria, allowing for survival of bacterial that have gained rare mutation/genetics
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8
Q

From a clinical lab, what are ranges of antibiotic resistance that will show up on a lab report

A
  1. ) S: sensitive – treat with dosage of antimicrobial recommended
  2. ) I: intermediate – treat directly in body sites where drug are physiologically concentrated or when high dosage can be used
  3. ) R: resistant – not inhibited by usually achieved concentration
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9
Q

Empiric vs targeted antibiotic therapy. What is the difference?

A
  • Empiric: treatment while waiting for lab results (broad spectrum)
  • Targeted: treatment as lab results dictate (narrow spectrum)
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10
Q

Mechanisms of antibiotic resistance by bacteria

A
  1. ) Breakdown of antibiotic
  2. ) Chemical modification of antibiotic
  3. ) Alteration of target
  4. ) Altered permeability (decreased influx / increased efflux)
  5. ) Lack of target
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11
Q

What is MIC/MBC in terms of antibiotic testing?

A
  • MIC = minimum inhibitiory concentration – level of antimicrobial concentration that inhibits growth (bacteriostatic)
  • MBC = minimum bactericidal concentration – level of antimicrobial concentration that kills 99.9% of bacteria
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12
Q

How to determine MIC?

A
  • Disk-diffusion assay (Kirby-Bauer test)
  • E-test (newer)
  • Broth culture (determines MIC and MBC)
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13
Q

Difference between a cell wall active and membrane active antibiotic

A
  1. Cell wall active: disrupts peptidoglycan synthesis and therefore is only active against dividing bacteria
  2. Membrane active: disrupts membrane integrity/synthesis and therefore is active against resting and actively dividing bacteria
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14
Q

Classes of antibiotics (and examples) targeting cell wall synthesis. Are these effective against static bacterial infections?

A
  1. ) Beta-lactams: penicillins, cephalosporins, cephamycines, carbapenems, monobactams
  2. ) Glycopeptides: vancomycin
  3. ) Polypeptides: bacitracin, polymixins
    - ineffective against static bacterial infections, only against actively dividing bacteria
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15
Q

Classes of antibiotics/specific examples targeting protein synthesis.

A
  1. ) Aminoglycosides: gentamicin, kanamycin
  2. ) Macrolides: erythromycin, azithromycin (z-pak)
  3. ) Tetracyclines/doxycycline
  4. ) Chloramphenicol
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16
Q

Classes of antibiotics/specific examples targeting nucleic acid synthesis

A
  1. ) Quinolones: ciprofloxacin, levofloxacin
  2. ) Rifampin (specific), rifabutin (specific)
  3. ) Metronidazole
17
Q

Classes of antibiotics/specific examples targeting folic acid synthesis

A
  1. ) Sulfonamides

2. ) DHFR inhibitor: trimethoprim

18
Q

Mechanism of beta-lactam action – bacteriostatic or bactericidal?

A
  • Beta-lactams bind to transpeptidases (penicillin binding proteins-PBPs) covering reactive serine site and prevent cross-linking of peptidoglycan sheets
  • Bacteriostatic
19
Q

How can bacteria become resistant to beta-lactams?

A
  1. ) Alter transpeptidase (eg. To have decreased affinity for antibiotic)
  2. ) Alter outer-membrane permeability
  3. ) Presence of efflux pumps
  4. ) Chemical modification of antibiotic (eg. Via beta-lactamase)
20
Q

Someone is being treated with penicillin, which is not combatting his or her infection. The patient is switched to a cephalosporin medication. Is this good or bad?

A
  • Resistance to a specific antibiotic typically confers resistance to that entire class. Pt should be placed on a different class of antibiotic
21
Q

Mechanism of vancomycin (a glycopeptide class of antibiotic) – bacteriostatic or bactericidal?

A
  • Binds to two D-ala residues on end of pentapeptide chain in peptidoglycan and prevents them from interacting with transpeptidase that cross-links them causing cell death. Will only work on cells that are actively dividing.
  • Bacteriostatic
22
Q

How can bacteria become resistant to vancomycin?

A
  • 5th D-ala residue is replaced with D-lactate so vancomycin cannot bind
23
Q

Mechanism of action of bacitracin (a polypeptide class of antibiotic) – bactericidal or bacteriostatic?

A
  • Interferes with dephosphorylation of bactoprenol, which is the lipid carrier that transfers peptidoglycan subunits to growing cell wall. This prevents it from recycling to inner membrane leaflet
  • Bacteriostatic
24
Q

Mechanism of action of tetracycline/doxycycline – is it bacteriostatic/bactericidal? Broad or narrow spectrum?

A
  • Bacteriostatic, broad spectrum, binds 30S subunit
25
Q

Mechanism of action of macrolides – is it bacteriostatic/bactericidal?

A
  • binds 50S subunit – good alternative to individuals with penicillin allergy
  • bacteriostatic
26
Q

Mechanism of action of quinolones – bactericidal or bacteriostatic?

A
  • inhibits DNA replication, recombination and repair by affecting bacterial topoisomerase/aka gyrase
  • bactericidal
27
Q

Mechanism of action of rifampin/rifabutin – is it bactericidal or bacteriostatic?

A
  • binds to DNA-dependent-RNA polymerase and inhibits initiation of RNA synthesis
  • bactericidal
28
Q

Mechanism of action of metronidazole – is it bactericidal or bacteriostatic?

A
  • reduced by bacteria to form toxic compound that damages DNA
  • bactericidal
29
Q

Mechanism of action of sulfonamides – bacteriostatic or bactericidal?

A
  • Blocks step in folic acid synthesis, folic acid used for purine and thymidine synthesis
  • Bacteriostatic
30
Q

Mechanism of action of DHFR inhibitor (trimethoprim) – bacteriostatic or bactericidal?

A
  • blocks step in folic acid synthesis, folic acid used for purine and thymidine synthesis
  • bacteriostatic