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Pathology > Microbiology - Antimicrobials 1 > Flashcards

Microbiology - Antimicrobials 1 Flashcards

1
Q

when do most antibiotics work?

A

when the cell is active i.e. when bacteria is dividing

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2
Q

what are the 3 selective targets for antimicrobials?

A
  • peptidoglycan layer of cell wall
  • inhibition of bacterial protein synthesis
  • DNA gyrase and other prokaryote enzymes
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3
Q

which antibiotics inhibit cell wall synthesis?

A

beta-lactams

glycopeptides

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4
Q

name some beta-lactam antibiotics

A

penicillin
cephalosporin
carbapenems
BROAD SPECTRUM

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5
Q

name some glycopeptides

A

vancomycin
teicoplanin
GRAM POSITIVE

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6
Q

describe the gram positive cell wall

A

thick peptidoglycan cell wall

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7
Q

describe the gram negative cell wall

A

thinner peptidoglycan cell wall
outer membrane conferring resistance to some antibiotics
can be more resisitant and harder to treat due to outer membrane

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8
Q

what is the moa of beta lactams?

A
  • inactivate enzymes involved in terminal stages of cell wall synthesis (transpeptidases/ pencillin binding proteins)
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9
Q

when are beta lactams ineffective?

A
  • if cell wall has already been formed

- ineffective against bacteria lacking peptidoglycan cell walls (mycoplasma, chlamydia)

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10
Q

when is penicillin used?

A

gram +ve, streptococci, clostridia

broken down by beta lactamase

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11
Q

when is amoxicillin used?

A 
broad spectrum (enterococci to gram -ve)
broken down by beta lactamase
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12
Q

when is flucloxacillin used?

A

staph aureus
not broken down by beta lactamase produced by SA
similar to penicillin
less reactive

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13
Q

when is piperacillin used?

A 
broad spectrum (pseudomonas, non-enteric gram -ve)
- broken down by beta lactamase
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14
Q

what does clavulanic acid used?

A

as part of co-amoxiclav

it is a beta lactamase inhibitor so protects penicillin from enzymatic breakdown

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15
Q

what is tazobactam made up of?

A

tazocin and piptazobactam

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16
Q

name some cephalosporins

A
  • cefuroxime
  • ceftriaxone
  • ceftazidime
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17
Q

what cover does cefuroxime provide?

A
  • stable to many beta lactamases made by gram -ve
  • similar cover to co-amox
  • less active against anaerobes (add metronidazole)
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18
Q

what cover does ceftriaxone provide?

A
  • associated with C difficile
  • treat meningitis
  • no cover against pseudomonas
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19
Q

what cover does ceftazidime provide?

A

pseudomonas

HAIs often

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20
Q

what antibiotics do you use in ESBL producing organisms that are resistant to cephalosporins?

A

carbapenems

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21
Q

name some carbapenems

A
  • meropenem
  • imipenem
  • ertapenem
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22
Q

what cover do carbapenems provide? when used?

A

broad spectrum

stable to ESBL enzymes

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23
Q

what are the key features of beta lactams?

A
  • relatively non toxic
  • renally excreted so dec dose if renal impairment
  • short half life
  • ## won’t cross BBB
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24
Q

when are glycopeptides used?

A

gram +ve

inhibit cell wall synthesis

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25
Q

what are important uses of glycopeptides?

A
  • MRSA infections

- C. difficile infections

26
Q

name the broad antibiotic categories that inhibit protein synthesis

A
  • aminoglycosides
  • tetracyclines
  • macrolides
  • chloramphenicol
  • oxazolidinones (linezolid)
27
Q

name some aminoglycosides

A
  • gentamicin
  • amikacin
  • tobramycin
28
Q

moa of aminoglycosides

A
  • bind to 30S ribosome subunit
  • rapid concentration dependent bactericidal
  • ototoxic and nephrotoxic so monitor levels
29
Q

which are active against pseudomonas?

A

gentamicin

tobramycin

30
Q

how do aminoglycosides react with beta lactams?

A

synergistic combination

used in endocarditis treatment, pneumonia

31
Q

what is the moa of tetracyclines?

A
  • reversibly bind to 30S ribosome unit
  • prevent binding of aminoacyl-tRNA to ribosomal acceptor site
  • inhibits protein synthesis
32
Q

what are tetracyclines active against?

A

chlamydia
rickettsia
mycoplasma

33
Q

what are the problems with tetracyclines?

A
  • now widespread resistance
  • deposited in growing bone (don’t give to children, pregnant women)
  • SE: photosensitivity rash
34
Q

name some macrolides

A

erythromycin
clindamyxin
clarithromycin
azithromycin

35
Q

moa of macrolides

A
  • bind to 50s subunit of ribosome
  • interfere with translocation
  • stimulate dissociation of peptidyl-tRNA
36
Q

what are macrolides used against?

A
  • active against campylobacter, legionella, pneumophilia
  • useful for staph/ strep in pen-allergic patients
  • little activity against gram-ve
37
Q

moa of chloramphenicol

A
  • binds to peptidyl transferase of 50S ribosomal subunit

- inhibits formation of peptide bonds during translation

38
Q

when is chloramphenicol used?

A

if pen- allergic, used for meningitis

eye preparations

39
Q

why is chlorampenicol rarely used?

A
  • risk of aplastic anaemia

- risk of grey-baby syndrome in neonates

40
Q

moa of oxazolidinones

A

binds to 23S component of 50S subunit

prevents formation of a functional 70S initiation complex

41
Q

what are oxazolidinones used against?

A

against gram +ve (MRSA, VRE)

not active against gram -ve

42
Q

what are the disadvantages of oxazolidinones?

A
  • expensive

- may cause thrombocytopaenia and optic neuritis

43
Q

what are the antibiotics that inhibit DNA synthesis?

A
  • quinolones/fluoroquinolones

- nitroimidazoles

44
Q

name some quinolones

A

ciprofloxacin
levofloxacin
moxifloxacin

45
Q

how do quinoloes work?

A

act on alpha unit of DNA gyrase

46
Q

what are the advantages of quinolones?

A

broad antibacterial activity

well absorbed orally (good bioavailability)

47
Q

what are the advantages of quinolones?

A

UTI
pneumonia
atypical pneuomina
bacterial gastroenteritis

48
Q

name some nitroimidazoles

A

metronidazole

tinidazole

49
Q

what is the moa of nitrioimidazoles

A

under anaerobic conditions, an active intermediate is produced
this causes DNA strand breakage

50
Q

uses of nitrioimidazoles

A

active against anaerobic bacteria

51
Q

what antibiotics inhibit RNA synthesis

A

rifampicin and rifabutin

52
Q

how do rifamycins work?

A
  • inhibit protein synthesis by binding to DNA-dependent RNA polymerase
53
Q

use of rifamycins

A

active against mycobacteria and chlamydia

54
Q

what are important things to remember with rifamycins?

A

interactions with other drugs metabolised in liver (e.g. OCP)
need to monitor LFTs
turns secretions orange

55
Q

which antibiotics interfere with cell membrane toxins?

A
  • daptomycin

- colistin

56
Q

name the antibiotics that inhibit folate metabolism

A
  • sulphonamides (e.g. sulphamethoxazole)

- diaminopyrimidines (e.g. trimethoprim)

57
Q

what is co-trimoxazole? when is it used?

A
  • sulphamethoxazole and trimethoprim
  • synergisitc action between 2 drug classes because they act on sequential steps in same pathway
  • used in PCP
58
Q

what are the different mechanisms of resistance?

A

BEAT

  1. Bypass antibiotic sensitive step
  2. Enzyme chemical modification/ inactivation of antibiotic (ESBLs)
  3. Accumulation reduced of antibiotic (Impaired uptake = doxycycline, enhanced efflux = flucytosine)
  4. Target modification or replacement (MRSA, flucloxicillin, macrolides)
59
Q

which antibiotics are affected by inactivation by microbes?

A

beta lactams
aminoglycosides
chloramphenicol

60
Q

which antibiotics are affected by microbes altering the target?

A 
beta lactams
macrolides
quinolones
rifampicin
chloramphenicol
linezolid
glycopeptides
61
Q

which antibiotics are affected by reduced accumulation?

A 
tetracyclines
beta lactams
aminoglycosides
quinolones
chloramphenicol
62
Q

which antibiotics are affected by the antibiotic sensitive step being bypassed?

A

trimethoprim

sulphonamides

Pathology (21 decks)

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