Antibiotics Flashcards

1
Q

What is the most common mechanism of antibiotic activity

A

Effects on cell wall integrity
- Interferes with cell wall synthesis

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2
Q

How do beta lactams work

A

Target serine proteases and penicillin binding proteins
- Inhibits assembly and degrade cell wall

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3
Q

Four different beta lactams

A
  • Penicillin
  • Cephalosporin
  • Monobactams
  • Carbapenems
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4
Q

What is commonly associated with Clostridium difficile infections?

A

3rd generation/broad spectrum cephalosporins

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5
Q

Penicillin effective against mostly…

A

Gram +

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6
Q

Cephalosporins mostly effective against…

A

G- with each generation, but also some G+

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7
Q

Monobactams mostly effective against

A

Aerobic G-

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8
Q

Carbapenems mostly effective against

A

G+, G-, anaerobes

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9
Q

Glycopeptides/vancomycin

A

Targets cell wall
- Targets G+

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10
Q

Lipopeptides/daptomycin

A

Cell membrane inhibitor
Disruption of ionic concentration gradiet of the cell membrane
- Targets G+

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11
Q

Polypeptides

2 types

A

Cell membrane target
Bacitracin: topical, G+
Polymyxins/colistin: topical or IV, G-

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12
Q

Antimycobacterial

2 types

A

Inhibit mycolic acid synthesis in cell wall
Isoniazid and ethambutol

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13
Q

Prokaryotic ribosomes are made up of what?

A

30s and 50s subunits on the mRNA that lead to translation of genetic message

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14
Q

What are the 3 antibiotics that target the 30s ribosomal subunit

A
  • Aminoglycosides
  • Tetracycline
  • Glycylcycline
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15
Q

The six antibiotics that target the 50s ribosomal subunit

A
  • Macrolides
  • Lincosamide
  • Chloramphenicol
  • Oxazolidinone
  • Streptogramins
  • Ketolides
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16
Q

Aminoglycosides

A

30s
- Almost always used with cell wall synthesis inhibitors
- Anaerobes are usually resistant
- GNR, some GP, mycobacteria

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17
Q

Tetracyclines

A

30s
- G+, G-, mycoplasma, chlamydiae, rickettsiae
- Not give to <8 yo children, preg women
- Food decreases absorption

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18
Q

Glycylcyclines

A

30s
- Similar to tetracyclines
- More against G-, anaerobes, rapid growing mycobacteria

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19
Q

Macrolides

A

50s
- Aerobic and anaerobic G+ cocci

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20
Q

Lincosamides

A

50s
- G+ cocci, anaerobes
- C. difficile diarrhea

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21
Q

Chloramphenicol

A

50s
- G+, G-, anaerobes, chlamydiae, mycoplasma, rickettsiae
- Aplastic anemia risk, backfire against human protein synthesis

22
Q

Oxazolidinones

A

50s
- Aerobic G+, mycobacteria, anaerobes

23
Q

Streptogramin

A

50s
- G+, anaerobes

24
Q

Ketolides

A

50s
- Similar to erythromycins from macrolides
- - G+ cocci

25
Q

What was the first effective systemic antimicrobial used in the US in the 1930s

A

Essential metabolite antimicrobials

26
Q

Sulfonamides

A

Essential metabolite inhibitor

27
Q

Trimethoprim

A

Essential metabolite inhibitor

28
Q

Inhibitors of DNA replication

A

Quinolones/fluoroquinolones

29
Q

Interfere with DNA transcription

A

Rifampin

30
Q

Causes breaks in DNA

A

Metronidazole

31
Q

Drug of choice for bacterial vaginosis

A

Metronidazole

32
Q

Group at the heart of multi drug antibiotic resistance

A

ESKAPE
- ENFA
- STAU
- KLPN
- ACBA
- PSAE
- Enterobacter species

33
Q

Multi drug resistance

A

Resistance to at least 1 in 3 or more antimicrobial categories

34
Q

Extensively drug resistant

A

Resistance in at least one in ALL but 1-2 antimicrobial categories

35
Q

Pan drug resistant

A

Resistant to everything

36
Q

Preventing resistance

A

Vaccination
Infection control
Protect food supply
Antibiotic responsibility
Screening, treatment, education

37
Q

Intrinsic mechanisms of antimicrobial resistance

A

Impermeability barriers
Biofilms
Drug efflux
Enzyme inactivation or degradation

38
Q

Horizontal gene transfer: transformation

A

Parts of DNA taken up by bacteria from outside environment

39
Q

Horizontal gene transfer: conjugation

A

Cell to cell contact between two bacteria and transfer plasmids

40
Q

Horizontal gene transfer: transduction

A

Bacteria specific viruses transfer DNA between 2 closely related bacteria

Bacteriophag

41
Q

Intrinsic antimicrobial resistance: impermeability barriers

A
  • LPS
  • Can reduce the number of porins or change sructure to reduce affinity for antibiotics
42
Q

Intrinsic antimicrobial resistance: biofilms

A

Motile bacteria attached to substrate
- Decreased penetration of antibiotic
- Slowed bacterial growth

43
Q

Intrinsic antimicrobial resistance: drug efflux

A

Pumps that transport the antibiotic back out of the cell

44
Q

Intrinsic antimicrobial resistance: enzyme inactivation/degradation

A

Self explanatory

45
Q

Fourextrinsic antimicrobial resistance mechanisms

A

Efflux
Target site modification
Antibiotic alteration
Enzymatic inactivtion

46
Q

How to combat beta lactam antibiotics

A
  • Making enzyme beta lactamase
  • alter antibiotic target site
  • alter porin channels
47
Q

How to combat glycopeptides

A
  • Alter antibiotic target site
48
Q

How to combat aminoglycosides

A
  • Alter antibiotic target site
  • Modify antibiotic
  • Alter porin channels
49
Q

How to combat quinolones

A
  • Alter antibiotic binding site
  • efflux
50
Q

What is MIC?

A

Minimum inhibitory concentration that visibly inhibits growth of the test organism