Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bacto > plenary 3 antibacterials > Flashcards

plenary 3 antibacterials Flashcards

1
Q

antibiotics definition

A

microbial metabolites which can kill or inhibit the growth of susceptible bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does the therapeutic use of ABs depend on

A

their selective toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

at therapeutic levels ABs have either

A

bacteriostatic or bacteriocidial effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does bacteriostatic mean

A

inhibits the growth of bacteria, allowing the host immune defenses to eliminate the infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does bacteriocidal mean

A

cause irreperable damage and bacterial cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

name some bacteriostatic antimicrobials

A
  • tetracyclines
  • chloramphenicol
  • macrolides
  • sulfonamides
  • trimetoprim
  • nitrofurans
  • lincosamides
  • rifampicins
  • novobiocin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

name some bacteriocidal antimicrobials

A
  • beta lactam ABs
  • polypeptides
  • aminoglycosides
  • quinolines
  • bacitracin
  • vancomycin
  • nitroimidazoles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

modes and sites of action for antibacterial drugs

A
  • inhibition of cell wall synthesis
  • inhibition of cell membrane function
  • inhib. protein synthesis
  • inhib DNA dependant RNA polymerase
  • inhib DNA gyrase
  • disrupt DNA structure
  • Inhibit DNA synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which inhibit cell wall synthesis

A
  • beta lactam abs
  • bacitracin
  • vancomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which inhibit cell wall funct

A

polypeptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which inhibit protein synthesis at 30S

A
  • aminoglycosides

- tetracyclines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which inhibit protein synthesis at 50S

A
  • chloramphenicol
  • macrolides
  • lincosamides
  • nitrofurans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which inhibit DNA dependant RNA polymerase

A

rifampicins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which inhibit DNA gyrase

A
  • quinolones

- novobiocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

which disrupt DNA structure

A

nitroimidazoles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which inhibit DNA synthesis

A
  • sulfonamides

- trimethoprim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cell wall inhibitors

A
  • penicillins
  • cephalosporins
  • vancomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

penicillins mechanism of action

A

block polypeptide synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are penicillins active against

A

only against actively growing cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

are penicillins active against Gr-

A

mainly Gr+ but some Gr-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

are penicillins sensitive to acids

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how are penicillins eliminated

A

by renal excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

penicillins half life

A

short

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

penicllins solubility in lipids

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

penicillins IC conc

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how are bact becoming resistant to penicillins

A
  • beta-lactamase enzymes

- lack of penicillin binding protein receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

which microbacteria do cephalosporins come from

A

cephalosporin acremonium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

are cephalosporins Gr-

A

mainly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

resistance to cephalosporins

A
  • structural
  • modification of binding site
  • beta-lactamase enzyme
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

as we incr generations what happens to the spectrum of cephalosporins

A

it increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

generation one cephalosporins

A

Gr+ rods, Gr- cocci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

2nd generation cephalosporins

A

wider spectrum, lactamase stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

3rd generation cephalosporins

A

more wider spectrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

4th generation cephalosporins

A

very broad spectrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

against which type is vancomycin

A

only against Gr+ bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

polymyxins mechanism of action

A

they do damage to the cell membrane funct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

two parts of polymyxins

A

hydrophobic and hydrophilic parts

38
Q

what do polymyxins do when they bind to the cell membrane phospholipids

A

they cause structural disorganisation, permeability damage and cell lysis

39
Q

polymyxins are selectively toxic to which type of gram bact

A

gr-

40
Q

do polymyxins act on multiplying cells

A

yes, both resting and multiplying

41
Q

resistance to polymyxins

A

rare

42
Q

aminoglycosides mechanism of action

A

inhibition of protein synthesis

43
Q

aminoglycosides are active against which types of bacteria

A

Gr- bact, mycobacteria

44
Q

adverse effects aminoglycosides

A

ototoxic and nephrotoxic

45
Q

aminoglycosides resistance

A
  • binding site
  • anaerobic bact
  • inactivating enzymes
  • pH - active in alkaline enviro
46
Q

tetracyclines mechanism of action

A

inhibition of binding of tRNA

47
Q

spectrum tetracyclines

A

wide

48
Q

resistance tetracyclines

A
  • inhibition of transport

- efflux

49
Q

where do we see a cross resistance in the tetracyclines group

A

between tetracyclines

50
Q

chloramphenicol mechanism of action

A

inhibition of protein synthesis

51
Q

which enzymes do the chloramphenicol group inhibit

A

peptidyl-transferase - inhibit transpeptidation

52
Q

spectrum chloramphenicols

A

wide

53
Q

are chloramphenicols lipid soluble

A

yes

54
Q

resistance chloramphenicols

A

chloramphenicol-acetylase

55
Q

macrolides mechanism of action

A

inhibition of binding of tRNA to ribosomes

56
Q

are macrolids lipid soluble

A

yes

57
Q

macrolides act on which type of bacteria

A

mainly Gr+ and some Gr-

58
Q

macrolids resistance

A

structural, modification of binding site, cross resistance

59
Q

lincosamides mechanism of action

A

inhibition of peptidyl transferase

60
Q

which bact do lincosamides act on

A

mainly Gr- aerobic and anaerobic, mycoplasma

61
Q

quinolines mechanism of action

A

inhibition of superhelix of DNA

62
Q

which enzyme in particular do quinolines inhibit

A

DNA-gyrase

63
Q

which types of bact do quinolines act on

A

both Gr+ and Gr-

64
Q

quinolines resistance

A
  • transport
  • obligate anaerobes
  • modification of gyrase
65
Q

rifampins mechanism of action

A

inhibition of RNA replication

66
Q

rifampins inhibit which enzyme in particular

A

DNA dependant RNA polymerase

67
Q

rifampins spectrum

A

wide

68
Q

rifampins resistance

A

mutation results in alteration of enzyme

69
Q

bc resistance is common how is rifampin usually used

A

in combo therapy

70
Q

sulfonamides mechanism of action

A

interfere with biosynthesis of folic acid and prevent synthesis of purine nucleotides

71
Q

what do sulfonamides produce to stop folic acid production

A

functional analogues of PABA to compete for enzyme-> forming non funct folic acid analogues

72
Q

which type of bact do sulfonamides act on

A

mainly Gr+

73
Q

sulfonamides resistance

A
  • metabolic changes
  • inactivating enzymes
  • exogenous folic acid
74
Q

at which enzyme do sulfonamides stop folic acid synthesis

A

pteridine synthetase

75
Q

at which enzyme do trimethoprims stop folic acid synthesis

A

dihydrofolate reductase

76
Q

under what conditions are nitrofurans most active

A

anaerobic conditions

77
Q

what are the unstable reduction products that nitrofurans produce able to cause

A

strand breakage in bacterial DNA

78
Q

when are nitrofurans usually used

A

in local treatment and treatment of UTIs

79
Q

ntiroimidazoles’ reactive metabolites can do what

A

damage bacterial DNA

80
Q

nitroimidazoles act on what types of bact

A
  • anaerobes and microaerophiles

- Gr- and Gr+

81
Q

why shouldnt nitroimidazoles be used in lab animals

A

theyre carcinogenic

82
Q

resistance to antibacterials can occur as a result of

A
  • enzymatic drug inactivation
  • modification of binding sites
  • decr IC accumulation
  • alteration in metabolism
83
Q

types of resistance

A
  • innate
  • acquired
  • cross resistance
  • multiresistant bact strains
84
Q

whats innate resistance

A

chromosonally encoded, relates to general physio of bacterial cell

85
Q

whats acquired resistance

A

can arise from a mutation or transfer of genetic material encoding, resistance genes

86
Q

whats cross resistance

A

a single mechanism confers resistance to multiple antimicrobial agents, commonly seen with closely related antimicrobial agents

87
Q

methods of antimicrobial susceptibility testing

A
  • disc diffusion method
  • broth-dilution method
  • E-test
88
Q

factors affecting the zone of inhibition

A
  • the size of the inoculum
  • the test medium
  • the antimicrobial agent and its conc
  • incubation conditions
89
Q

susceptible diameter

A

> 20mm

90
Q

moderately susceptible diameter

A

15

91
Q

resistant

A

<15mm

92
Q

principles of antibiotic therapy

A
  • targeted Ab treatment necessary
  • most effective ab
  • correct dosage
  • correct treatment time
  • tissue conc must exceed effective conc at site of infection

Bacto (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions