Antimicrobials Flashcards

Week 2

1
Q

Phase I clinical trial

A

Test on healthy volunteers for safety and dose-ranging

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2
Q

Phase II clinical trial

A

Test on patients to assess efficacy, effectiveness and safety

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3
Q

Phase III clinical trial

A

Assess efficacy, effectiveness and safety

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4
Q

Narrow spectrum antimicrobial

A

Antimicrobial effective against a limited number of bacterial genera

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5
Q

Broad spectrum antimicrobial

A

Antimicrobial effective against a large number of bacterial genera

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6
Q

Give some features of the ideal antibiotic

A
  • selective toxicity
  • bacterialcidal
  • slows emergence of resistance
  • narrow spectrum of activity
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7
Q

Why is a narrow spectrum of activity ideal?

A

Doesn’t encourage resistance developing over many generas

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8
Q

4 ways to classify anti-bacterial agents

A
  1. Bacterialcidal or bacteriostatic
  2. Spectrum of activity
  3. Chemical structure
  4. Targets/selective toxicity
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9
Q

Ribosomes of bacteria

A

70s

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10
Q

Ribosomes of eukaryotes

A

80s

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11
Q

What can bacteria synthesise on their own which humans need to take in?

A

Folic acid/folate

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12
Q

Why enzyme involved in folic acid synthesis do humans also have

A

DHPS

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13
Q

2 kinds of beta-lactam antibiotics

A

penicillins

chepalosporins

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14
Q

What do beta-lactams inhibit?

A

The enzymes PBPs (penicillin binding proteins) which are required for transpeptidation of cell wall

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15
Q

Transpeptidation =

A

the last step in cross-linking of peptidoglycan cell wall

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16
Q

3 antibiotic classes that work on cell wall synthesis =

A

penicillins
cephalosportins
glycopeptides

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17
Q

broad spectrum penicillin

A

amoxicillin

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18
Q

most common glycopeptide

A

vancomycin

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19
Q

Vancomycin is only active against what type of bacteria?

A

Gr+ (MRSA)

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20
Q

Glycopeptides MoA

A

Bind to cell wall subunit and prevent incorporation of unit

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21
Q

Classes of antibiotics which inhibit protein synthesis

A
  • macrolides
  • aminoglycosides
  • tetracyclins
  • chloramphenicol
  • lincosamides
  • puromycin
  • fusidic acid
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22
Q

Macrolides

A

50S inhibitors

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23
Q

Tetracyclins

A

30S inhibitors

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24
Q

Aminoglycosides

A

30S inhibitors

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25
Q

Classes which disrupt nucleic acid synthesis

A

Quinolones

Rifamycins

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26
Q

Quinolones

A

Inhibit DNA replication

27
Q

Classes of antimetabolites

A

Sulfonamides

Trimethoprim

28
Q

Which pathway do antimetabolites distrupt?

A

formation of dihydrofolic acid.

29
Q

Sulfonamides MoA

A

Inhibit PABA

30
Q

Trimethoprim MoA

A

Inhibits DHPS

31
Q

Which antimetabolite inhibits an enzyme found in humans?

A

trimethoprim

32
Q

Class of antibiotics which acts as a detergent on plasma membrane

A

Polmyxins

33
Q

Ex narrow spectrum antibiotics

A

Macrolides
Vancomycin
penG

34
Q

Ex broad-spectrum antibiotics

A

Aminoglycosides
2nd and 3rd gen cephalosporins
quinolones
some synthetic penicillin

35
Q

Narrow spectrum penicillin

A

benzyl penicillin

36
Q

suffix of macrolides

A
  • thromycin
37
Q

Bacteriostatic or bacteriocidal: aminoglycosides

A

both

38
Q

What kind of bacteria are aminoglycosides best for?

A

Gr- aerobes

39
Q

What can be used with an aminoglycoside to treat Gr+ infections like staph endocarditis

A

Beta-lactam

40
Q

Ex of aminoglycodies

A

gentamicin
neomycin
streptomycin
tobramycin

41
Q

Side effects of aminoglycodies

A

ototoxicity
nephrotoxic
inhibit Ach release (contraindicated in MG)

42
Q

Use of tetracylines

A

Acne, community acquired pneumonia, intracellular pathogens, MRSA

43
Q

Side effects of tetracyclines

A

Phototoxicity
tinnitus
permanent teetch discoloration and delayed bone growth
nephrotoxic and hepatotoxic

44
Q

Ex of macrolides

A

erythormycin, azithromycin, clarithromycin

45
Q

Bacteriostatic or bacteriocidal: macrolides

A

bacteriostatic

46
Q

Spectrum of macrolides

A

Narrow. Gr+ aerobic, Gr- aerobic

47
Q

Some uses of macrolides

A

Resp infections, STIs, H.pylori

48
Q

DOC in pregnancy

A

amoxicillin

49
Q

Bacteriostatic or bacteriocidal: cephalosporins

A

bacteriocidal

50
Q

name 2 drugs that can have cross-reactivity (hint = they have a similar chemical structure)

A

penicillins and cephalosporins

51
Q

DOC for MRSA

A

Vancomycin

52
Q

What drug does sulfonamides increase plasma conc of?

A

Warfarin

53
Q

2 antibiotics which need to be metabolised by liver first

A

Sulfonamides

Trimethoprim

54
Q

Bacteriostatic or bacteriocidal: sulfonamides

A

Bacteriostatic (cidal when with TMP)

55
Q

Bacteriostatic or bacteriocidal: trimethoprim

A

Bacteriostatic (cidal when with smx)

56
Q

Trimethoprim contraindications

A

pregnancy and children (teratogenic and bone marrow suppression)

57
Q

Stages of antibiotic resistance/sensitivity

A

sensitive
intermediate
resistance

58
Q

What does ‘intermediate’ mean in terms of antibiotic resistance

A

higher dose of antibiotic needed

59
Q

Minimum inhibitory concentration =

A

Minimum conc below which bacterial growth is not inhibited (need to be above MIC)

60
Q

innate resistance

A

bacteria lacks a suitable target or is impermeable to the drug

61
Q

acquired resistance

A

resistance acquired via mutation or gene transfer

62
Q

Major mechanisms of bacterial resistance:

A
  • modify target
  • limit access (reduce penetration, increase efflux)
  • bypass pathway
  • enzymatic inactivation
63
Q

S.aureus developed resitance to beta-lactams in 2 ways=

A

beta-lactamases

alter PBP so beta-lactam can’t fit

64
Q

Ex of mechanisms which can cause multi-drug resistance

A

efflux pumps