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Microbiology > Antimicrobials 1 > Flashcards

Antimicrobials 1 Flashcards

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1
Q

Gram positive vs. Gram negative

A

Gram positive = Thick peptidoglycan layer - catches Gram stain - purple
Gram negative = Thin peptidoglycan layer + outer LPS membrane - pink

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2
Q

What is the MoA of B-lactams?

A

B-lactam ring binds and inactivates transpeptidases that form cross links between peptidoglycan monomers in cell wall - weak cell wall = lysis
BACTERICIDAL to rapidly dividing daughter cells forming cross-links only - not active on stable cell walls already formed

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3
Q

Which bacteria lack a cell wall?

A

Mycoplasma, chlamydia, RIckettsia (B-lactams don’t work)

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4
Q

What are the 6 main types of penicillin? (B-lactam 1)

A

SA resistant:

  • (Benzyl)penicillin - still most potent but narrow spectrum - Gram positive only but not S aureus
  • Amoxicillin - broader spectrum to some Gram negs (E coli) but not S aureus
  • Piperacillin - even broader spectrum (covers Pseudomonas + more Gram negs) but not S aureus

SA sensitive: (new approaches)

  • Flucloxacillin - similar spectrum to penicillin + mainstay against S aureus
  • Co-amoxiclav = amoxicillin + clavulinic acid (B-lactamase inhibitor)
  • Tazocin = piperacillin + tazobactam (B-lactamase inhibitor)
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5
Q

What does SA produce that makes it resistant to B-lactams?

A

B-lactamase - degrades B-lactam ring that binds transpeptidase

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6
Q

Why is flucloxacillin favoured over Co-amox/Tazocin in difficult to access infections?

A

E.g. deep skin infections with lots of necrotic tissue, osteomyelitis
Don’t have to get 2 drugs into infection

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7
Q

3 generations of cephalosporins

B-lactams 2

A

1st gen - Cephalexin
2nd gen - cefuroxime
3rd gen - cefotaxime, ceftriaxone, ceftazidime

  • All stable to B-lactamases but not ESBLs
  • Increasing activity against Gram negatives, reducing activity against Gram positives
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8
Q

What happens to cephalosporin activity from 1st to 3rd generation?

A

Gram negative activity increases

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9
Q

Cephalosporin in meningitis

A

Ceftriaxone

Gram negative cocci

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10
Q

Cephalosporin for Pseudomonas

A

Ceftazidime

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11
Q

Cephalosporin with similar cover to co-amoxiclav but favoured as one drug

A

Cefuroxime

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12
Q

Needs to be combined with metronidazole to cover anaerobes

A

Cefuroxime (cef + met)

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13
Q

Carbapenems

B-lactams 3

A
  • Stable to ESBLs but now carbapenemases are a problem

- Reserved for high-risk mutli-drug resistance bacteria - most powerful B-lactams

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14
Q

3 types of B-lactam

A

Penicillins
Cephalosporins
Carbapenems

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15
Q

Inhibit cell wall synthesis

A

B-lactams

Glycopeptides

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16
Q

MoA of glycopeptides

A

Lodge into cell wall to physically block transpeptidases forming cross links - weak cell = lysis
BACTERICIDAL to daughter cells again

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17
Q

Two examples of glycopeptides

A

Vancomycin

Teicoplanin

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18
Q

Glycopeptide indications

A
  • Gram positive only. Very large molecules that can’t get through outer membrane of Gram negative (except Neisseria)
  • Used in tricky MRSA and C difficile infections
  • Nephrotoxic - monitor levels
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19
Q

Inhibitors of protein synthesis

A

Bind 30S: Aminoglycosides, tetracyclines
Bind 50S: Macrolides, chloramphenicol
Bind 23S: Linezolid

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20
Q

What is unusual about the aminoglycosides?

A

All inhibitors of protein synthesis are bacteriostatic (prevent division) except aminoglycosides (bactericidal)
Mechanism unknown

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21
Q 
AminoGlycoside
Binds 30S
Pseudomonas
Ototoxic + nephrotoxic
B-lactam synergy
Gram negatives
A

Gentamicin

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22
Q 
Tetracycline
Binds 30S
Bacteria without cell wall + MRSA
Deposit in bone - teeth staining, enamel hypoplasia
Bad rash in sunlight
A

Doxycyline

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23
Q

Binds 50S
Mild staph + strep infections in penicillin allergic
Atypical pneumonias (Legionella, Mycoplasma)
Campylobacter gastroenteritis

A

Macrolides (erythromycin, clarithromycin, azithromycin)

- New-old (newer agents longer half-life so better in paediatrics)

24
Q

Binds 50S
2nd line meningitis
Risk of aplastic anaemia
Grey baby syndrome

A

Chloramphenicol

25
Q

Binds 23S component of 50S
Really really active for Gram positive organisms
Expensive
Thrombocytopenia + optic neuritis

A

Linezolid

26
Q

Inhibitors of DNA synthesis

A

Fluoroquinolones

Nitroimadazoles

27
Q

Act on DNA gyrase
Older agents good for Gram negs (Pseudomonas), newer agents good for Gram pos
Well absorbed orally

A

Fluoroquinolones (ciprofloxacin, levofloxacin, moxifloxacin)

28
Q

Cover pseudomonas

A

Ciprofloxacin
Gentamicin
Colistin
Ceftazidime

29
Q

Breaks bacterial DNA strands
Excellent anaerobe + protozoal (e.g. Giardia) cover
Pure anaerobe infection rare so usually combined with other Abx

A

Nitroimidazoles (metronidazole)

30
Q

Intra-abdominal infection on surgical ward

A

Cef + Met
Cefuroxime (covers Gram positive and Gram negative aerobes)
Metronidazole (covers anaerobes)
~> Together work to cover bowel flora organisms

31
Q

Inhibit RNA synthesis

A

Rifamycins (Rifampacin)

32
Q

Binds RNA polymerase
Mycobacteria + Chlamydia
Turns secretions orange (check if compliant)
Never used as single agent - resistance - multi-drug therapy
Very broad spectrum but limited use

A

Rifampicin

33
Q

Cell membrane toxins

A

Daptomycin

Colistin

34
Q

Inhibit folate metabolism (needed for DNA synthesis)

A

Sulphonamides (sulphamethoxazole)

Diaminopyrimidines (nitrofurantoin)

35
Q

Tx for community acquired UTI

A

Trimethorprim

36
Q

Tx for PCP

A

Co-trimoxazole (Sulphamethoxazole + Trimethorprim)

Synergy - act on sequential stages of folate metabolism

37
Q

Anaerobes

A

Metronidazole

38
Q

Meningitis

A

Ceftriaxone

39
Q

Bacteriostatic vs. bacteriocidal

A 
Bacteriostatic = Prevents growth (replication)
Bactericidal = Kills bacteria
40
Q

4 mechanisms of antibiotic resistance

A

Modification of Abx
Modification of Abx target
Reduced Abx accumulation (efflux or impaired uptake)
Bypassing Abx sensitive step
(Most bacteria will employ more than 1 mechanism)

41
Q

4 types of B-lactamase (Abx modification)

A
  1. Abx modification
    Early B-lactamases (break down penicillins)
    ESBLs (break down cephalosporins, inhibited by clavulonic acid)
    AmpC (break down cephalosporins, not inhibited by clavulonic acid)
    Carbapenemases (all B-lactamases)
42
Q

Main resistance mechanism in pencillin resistant Pneumococci (e.g. PR S
pneumoniae) and MRSA

A
  1. Altered targets
    Slightly different mechanisms
    - MRSA: MecA encodes novel penicillin binding protein
    - PR S pneumoniae: Mutations in PBP genes
43
Q

Why can penicillin be used in bacterial sore throat?

A

Group A Strep bacteria (pyogenes, B, C or G hamolytic) not affected by resistance - just pneumoniae

44
Q

Mechanism / examples for B-lactams

A

Inhibit cell wall synthesis
Binds PBP to inhibit transpeptide cross links
Pencillins, Cephalosporins, Carbapenems

45
Q

Mechanism / examples of glycopeptide

A

Inhibit cell wall synthesis
Sit in cell wall to physically block transpeptide cross links
Vancomycin, teicoplanin

46
Q

Mechanism / examples of aminoGlycosides

A

Block protein synthesis
Inhibit 30S ribosome
Gentamicin

47
Q

Mechanism / examples of tetracyclines

A

Block protein synthesis
Inhibit 30S ribosome
Doxycycline

48
Q

Mechanism / examples of macrolides

A

Block protein synthesis
Inhibit 50S ribosome
Mycins

49
Q

Mechanism of chloramphenicol

A

Block protein synthesis

Inhibit 50S ribosome

50
Q

Linezolid

A

Block protein synthesis

Inhibit 23S of 50S ribosome

51
Q

Mechanism / examples of fluoroquinolones

A

Inhibit DNA synthesis
Act on DNA gyrase
Floxacins

52
Q

Mechanism / example of nitroimidazole

A

Inhibit DNA synthesis
Breaks DNA strands
Metronidazole

53
Q

Mechanism / example of rifamycins

A

Inhibit RNA synthesis

Rifampicin

54
Q

Mechanism / example of sulphonamides

A

Inhibit folate synthesis

Sulphamethoxazole

55
Q

Mechanism / example of diaminopyrimidines

A

Inhibit folate synthesis

Trimethoprim

Microbiology (19 decks)

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