Antibacterial Drugs Flashcards

1
Q

Name the key benefit and downside of antibiotics

A

+ allow for more invasive procedures

- bacteria can become resistant after time

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2
Q

What is the difference between gram-positive and gram-negative bacteria?

A

Gram-negative:
- lipid outer layer, 2 periplasms, small peptidoglycan layer

gram-positive
- thicc peptidoglycan layer, periplasm, membrane

Name comes from biological assay, peptidoglycan gives a stronger result therefore thicker peptidoglycan wall -> gram pos

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3
Q

What is the difference between bacteriostatic and bactericidal drugs?

A

static:
requires immunocompetent host
non-life threatening
for uncomplicated infections

cidal:
deep-seated infection
life-threatening

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4
Q

Define MIC and MBC and how they are calculated?

A

Minimal inhibitory concentration and minimal bactericidal concentration
Calculated with Dilution test:
-serial dilution of antimicrobial drug
- incubate on plate
- last conc to not have any growth = MBC
- last conc to not show visible growth = MIC

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5
Q

What is a broad spectrum antibiotic (as opposed to a narrow spectrum antibiotic)

A

Treats many types of bacteria, not specific

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6
Q

What are the 3 types of antimicrobial therapy?

A
  • Definitive Drug therapy: antibiotics prescribed based on Organism identity and susceptibility
  • Empiric therapy: “this other person had the same thing and reacted well to this”
  • prophylactic therapy: use of antimicrobial agent to prevent infection
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7
Q

How do Penicillin and Aminoglycoside synergize when given as an antibiotic treatment?

A

Aminoglycoside is a protein synthesis inhibitor, but it can’t reach the ribosomes because of the cell wall

Penicillin inhibits the cell wall but doesn’t do anything else

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8
Q

What are the 5 major mechanisms of bacterial resistance?

A
Decreased entry
enhanced efflux
Bypass pathway
Altered target site
Enzymatic Degradation
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9
Q

True/False? We only have a few antibiotic drugs because we don’t need that many

A

False, bacteria become resistant and don’t respond to them anymore

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10
Q

True/False? A resistant bacterium can transmit antibacterial resistance to another bacterium

A

True

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11
Q

Which of the gram types of bacteria is easier to treat and why?

A

Gram-positive, because its cell membrane is much simpler and doesn’t contain many enzymes that could interfere with antibiotics

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12
Q

How is the periplasm of bacterial cell walls formed?

3 thick steps

A

1) peptidoglycan units (made up of MurNAc and GlcNAc, which each have L-Lysine and D-alanine residues) are phosphorylated by Bactoprenol IN CYTOPLASM
2) Bactoprenol flips the peptidoglycan unit into the periplasm and pops off (to repeat the process)
3) Penicillin-Binding protein (PBP) polymerizes the peptidoglycan units and crosslinks their L-lys and D-ala residues together

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13
Q

What do all beta lactams have in common?

A

square carbonyl-N ring

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14
Q

What is a beta-lactamase and what is its problem?

A

They open the beta-lactam ring making them ineffective

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15
Q

What is NDM-1?

A

Gene that confers resistance to all beta-lactam antibiotics in Canada

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16
Q

What is the poster child for glycopeptides?

A

Vancomycin

17
Q

How do beta-lactams function?

A

They bind PBP and inhibit the crosslinking of peptidoglycan units

18
Q

How do glycopeptides function?

A

They bind to the amino acids of the peptidoglycan unit and prevent more amino acids from being added as well as preventing cross-linking

19
Q

How does Bacitracin work?

A

By inhibiting the shuttle pump from hydrolysing phosphate bonds, it can’t incorporate peptidoglycan units into periplasm

20
Q

How do lipopeptides such as colistin (polymyxin) and daptomycin work?

A

Disrupts the CYTOPLASMIC MEMBRANE and punches a hole, K+ spills out and causes cell death

Effective against gram- bacteria, but toxic (used as last resort)

21
Q

What class of drugs are D-Cycloserine and Fosfomycin and what are their respective mechanisms of action?

A

Intracellular inhibitors

Fosfomycin: mimics PEP and inhibits conversion of glcNAc to MurNAc

D-cycloserine: mimics D-alanine and prevents synthesis of D-alanine from L-alanine

22
Q

How do aminoglycosides function?

A

They diffuse through porins in the outer membrane of gram- bacteria, then through active transport of the inner cytoplasmic membrane

Bind to ribosomal 30S subunit

23
Q

What is the cause for the postantibiotic effect of aminoglycosides?

A

Irreversible binding to 30S ribosome

Intracellular drug accumulation persists after plasma levels decline

24
Q

What do tetracyclines bind to?

A

30S ribosomal subunit

25
Q

What are all protein synthesis inhibitors susceptible to?

A

Decreased influx/increased efflux

Change in 30S/50S

26
Q

Which 3 enzymes degrade aminoglycosides (among others)?

A

N-acetyltransferases (AACs)
O-adenylyltransferases (ANTs)
O-phosphotransferases (APHs)

27
Q

Is it possible to overcome bacterial resistance? How or how not?

A

Yes, with library screening to identify new/unexpected synergies

eg loperamide potentiates minocycline

28
Q

What do topoisomerase inhibitors do?

A

Cause supercoiling of bacterial DNA during cell division

29
Q

Name the 4 antimycobacterial drugs included in the First-line cocktail for tuberculosis

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

30
Q

What does Isoniazid do?

A

Inhibits synthesis of Mycolic acid

*Part of TB first line cocktail

31
Q

What does Pyrazinamide do?

A

Inhibits synthesis of Mycolic acid

*Part of TB first line cocktail

32
Q

What does Ethambutol do?

A

Inhibits synthesis of Arabinogalactan

*Part of TB first line cocktail

33
Q

Name 4 Beta-lactam cell wall synthesis inhibitors

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

34
Q

Name the type of non-beta lactam cell wall synthesis inhibitor we learned in class and its example

A

Glycopeptides (vancomycin)

35
Q

Name the class of cell membrane disruptors learned in class

A

Lipopeptides

36
Q

How does Rifampicin work?

A

Inhibits DNA-dependent RNA polymerase

*Part of TB first line cocktail