Lecture 4 Flashcards

1
Q

selective toxicity

A

kill or inhibit the growth of a microorgansim without harming host cells

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2
Q

antibiotic

A

natural antibiotic

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3
Q

antimicrobial

A

man-made antibiotic

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4
Q

bacteriostatic

A

inhibit growth

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5
Q

bacteriocidial

A

killing

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6
Q

which type of antibiotic is used when host defenses can be counted on?

A

bacteriostatic

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7
Q

which type of antibiotic is used druing invasive infection: bacteremia, meningitis, endocarditis

A

bactericidal

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8
Q

which type of antibiotic would you use with an immunocompromised patient?

A

bactericidal because you can’t count on the immune system to help

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9
Q

antibiotic synergism

A

combination of two antibiotics with enhanced bactericidal activity when used together

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10
Q

antibiotic antagonism

A

combination of antibiotics in which one interferes with the activity of the other

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11
Q

broad spectrum

A

effective against a large variety of bacteria

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12
Q

narrow spectrum

A

effective against only a small subset of bacteria

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13
Q

advantage + disadvantage of broad spectrum

A

A: increased likelihood of effectiveness against a bacterial infection of unknown etiology
D: increased likelihood of disrupting the patients normal microbiota

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14
Q

advantage + disadvantage of narrow spectrum

A

A: avoids disruption of the normal microbiota
D: must have the specific disease causing bacteria identified in order to choose the correct antibiotic

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15
Q

order: narrow broad extended expanded

A

increasing specificity:

narrow expanded broad extended

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16
Q

True or False: antibiotics do not cause resistance

A

TRUE

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17
Q

sensitive (S)

A

infection may be treated with dosage regimen of an antimicrobial agent recommended

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18
Q

intermediate (I)

A

Infection may be treated in body sites where the drug are physiologically concentrated or when a high dosage of drug can be used

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19
Q

resistant (R)

A

resistant isolated are not inhibited by the usually achieved concentrations of the antimicrobial

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20
Q

True or false: antibiotics are only useful for treating bacterial infections.

A

TRUE

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21
Q

empiric theory

A

treatment while waiting for lab results (broad spectrum)

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22
Q

targeted theory

A

refined treatment (narrow spectrum)

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23
Q

antibiotic prophylaxis

A

prevent rather than treat the disease (pre-surgery, immunocompromised, exposure)

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24
Q

5 mechanisms of antibiotic resistance

A
  1. breakdown of antibiotic
  2. chemical modification of antibiotic
  3. alteration of traget
  4. altered permeability, decreased influx or increased efflux
  5. lack of target
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25
Q

minimum inhibitory concentration MIC

A

lowest concentration of antibiotic that inhibits growth

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26
Q

minimum bactericidal concentration MBC

A

lowest concentration of antibiotic that kills 99.9%

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27
Q

3 tests for antibiotic susceptibility

A
  1. Disk diffusion/ Kirby-Bauer test
    - circle of inhibition
  2. E-test
    - strip of inhibition
  3. Broth culture
    - dilutions
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28
Q

B-lactams example

A

penicillins, cephalosporins, cephamycins, carbapenems, monobactams

29
Q

B-lactams target

A

cell wall synthesis (bactericidal)

30
Q

glycopeptides example

A

vancomycin

31
Q

glycopeptides target

A

cell wall synthesis

32
Q

polypeptides example

A

bacitracin, polymixins

33
Q

polypeptides target

A

cell wall synthesis

34
Q

aminoglycosides target

A

protein sysnthesis

35
Q

what antibiotics target cell wall synthesis

A

b-lactams
glycopeptides
polypeptides

36
Q

macrolides target

A

protein synthesis

37
Q

tetracyclines target

A

protein synthesis

38
Q

chloramphenicol target

A

protein synthesis

39
Q

antibiotics that target protein synthesis

A

aminoglycosides, macrolides, tetracyclines, chloramphenicol

40
Q

quinolines target

A

nucleic acid synthesis

41
Q

rifampin target

A

nucleic acid synthesis

42
Q

metronidazole target

A

nucleic acid synthesis

43
Q

antibiotics that target nucleic acid synthesis

A

quinolones, rifampin, metronidazole

44
Q

antibiotics that target folic acid synthesis

A

sulfonamides, trimethoprim

45
Q

sulfonamides target

A

folic acid synthesis

46
Q

trimethoprim target

A

folic acid synthesis

47
Q

cell wall active antibiotics

A

disrupt peptidoglycan synthesis

48
Q

what is effective against actively dividing bacteria?

A

cell wall active antibiotics

49
Q

what is effective against resting and actively dividing bacteria?

A

membrane active antibiotics

50
Q

membrane active antibiotic

A

disrupts r interferes with membrane integrity/synthesis

51
Q

what is the mechanism of action for b-lactams?

A

antibiotics bind the active site in transpeptidases/penicilin bindind protein used in peptidoglycan synthesis

52
Q

what 4 ways can a bacteria be resistant to b-lactams?

A
  1. altered transpeptidases
  2. altered outer-membrane permeability
  3. presence of efflux pumps
  4. chemical modification of antibiotic (b-lactamase)
53
Q

true or false: resistance to one typically means bacteria will be resistant to the entire class

A

true

54
Q

how does vancomycin affect bacteria?

A

vancomycin binds to the peptide chains and prevents them form interacting properly with transpeptidase
- cross links can’t form-> cell death

55
Q

what confers vaancomycin resistance?

A

the last D-ala residue is replaced by D-lactate so vancomycin can’t bind
- cross links form and cell wall is successfully made

56
Q

how does bacitracin affect bacteria?

A

interferes with dephosphorylation in cycling of lipid carrier that transfers peptidoglycan subunits to the growing cell wall

57
Q

tetracyclines: bacteriostatic or bactericidal

A

bacteriostatic

58
Q

aminoglycosides: bacteriostatic or bactericidal

A

bactericidal

59
Q

macrolides: bacteriostatic or bactericidal

A

bacteriostatic

60
Q

tetracycline inhibits

A

30S subunit, therefore a protein synthesis inhibitor

61
Q

aminoglycoside inhibit

A

30S subunit, therefore a protein sysnthesis inhibitor **

*oxygen dependent and therefore only effective against aerobic organisms

62
Q

macrolides inhibit

A

50S subunit therefore a prtn synthesis inhibitor

63
Q

used as an alternate for individuals with penincilin allergy

A

macrolides

64
Q

nucleic acid synthesis inhbitors: bacteriostatic or bactericidal

A

bactericidal

65
Q

Quinolones inhibit…

A

DNA replication, recombination, and repair by affecting bacterial DNA topoisomeraste type II (gyrase) or topoisomerase type IV
NUCLEIC ACID SYNTHESIS

66
Q

rifampin, rifabutin inhibit…

A

binds to DNA-dependent RNA polymerase and inhibits initiation of RNA synthesis
NUCLEIC ACID SYNTHESIS

67
Q

metronidazole

A

NUCLEIC ACID SYNTHESIS

reduced by bacteria to create toxic compounds that damage DNA

68
Q

what do antimetabolites target?

A

folate metabolism

69
Q

block separate steps in folate metabolism and are synergistic when use together

A

sulfonamides

trimethoprim