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Clinical Pathology > Intro to antibacterial agents > Flashcards

Intro to antibacterial agents Flashcards

1
Q

What is meant by bacteristatic?

A

Antibiotics that inhibit bacterial growth, ie protein synthesis inhibitors.

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2
Q

What is meant by bactericidal?

A

Antibiotics that kill bacteria, ie cell wall-active agents

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3
Q

What is the minimum inhibitory concentration?

A

Minimum concentration of antibiotic at which visible growth is inhibited.

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4
Q

What is antimicrobial synergism?

A

Activity of two antimicrobials given together is greater than the sum of their activity if given separately.

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5
Q

Give a clinical example of synergism.

A

β-lactam/aminoglycoside combination therapy of streptococcal endocarditis.

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6
Q

What are possible antibiotic targets?

A
  • Cell wall
  • Protein synthesis
  • DNA synthesis
  • RNA synthesis
  • Plasma membrane
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7
Q

What is the bacterial cell wall made of?

A

Peptidoglycan - Polymer of glucose-derivatives, N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)

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8
Q

Give example of antibiotics that inhibit cell wall synthesis.

A

β-lactams
Glycopeptides

(also cycloserine and fosfomycin)

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9
Q

Why are the beta-lactam antibiotics so-called?

A

Because they have a beta -lactam ring structure.

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10
Q

What was the first beta-lactam antibiotic?

A

Benzylpenicillin (penicillin G). Acid labile so must be delivered parenterally.

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11
Q

What was the first oral antibiotic?

A

Phenoxymethylpenicillin (penicillin V)

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12
Q

Describe the beta lactam ring

A

Four members - CCCN

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13
Q

How do beta lactams work?

A

Interfere with function of “penicillin binding proteins” - transpeptidases enzymes involved in the peptideoglycan cross-linking.

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14
Q

Give examples of classes of beta lactams.

A

Penicillins (relatively narrow spectrum), cephalosporins, carbapenems, monobactams (broad spectrum).

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15
Q

What kind of ribosomes do bacteria possess?

A

70s (30s+50s)

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16
Q

How do aminoglycosides such as gentamicin inhibit protein synthesis?

A
  • Bind to 30S ribosomal subunit

- Mechanism of action not fully understood

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17
Q

How to macrolides (erythromycin), lincosamides (clindamycin) and the streptogramins work?

A
  • Bind to 50S ribosomal subunit
  • Blockage of exit tunnel
  • Inhibit protein elongation
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18
Q

How do tetracyclines inhibit protein synthesis?

A
  • Bind to 30S ribosomal subunit
  • Inhibit RNA translation
  • Interfere with binding of tRNA to rRNA
19
Q

How do oxazolidinones inhibit protein synthesis?

A
  • Inhibits initiation of protein synthesis
  • Binds to 50S ribosomal subunit
  • Inhibits assembly of initiation complex
  • May also bind to 70S subunit
20
Q

How do trimethoprim and the sulfonamides inhibit DNA synthesis.

A
  • Inhibit folate synthesis - folic acid is a purine synthesis precursor
  • Trimethoprim inhibits dihydrofolate reductase
  • Sulfonamides inhibit dihydropteroate synthetase
21
Q

How do the quinolones and flouroquinolones (ciprofloxacin) inhibit DNA synthesis?

A

Inhibit one or more of two related enzymes -DNA gyrase and topoisomerase IV

Involved in remodelling of DNA during DNA replication
Supercoiling/strand separation

22
Q

How do RNA synthesis inhibitors like rifampicin work?

A
  • RNA polymerase inhibitor

- Prevents synthesis of mRNA

23
Q

How does the plasma membrane agent daptomycin work?

A
  • Cyclic lipopeptide
  • Inserts lipophilic tail into cell membrane resulting in depolarisation and ion loss
  • Effective in Gram-positives only
24
Q

What are the specific adverse effects associated with aminogylcosides?

A
  • Reversible renal impairment on accumulation

- Therapeutic drug monitoring indicated

25
Q

What are the main adverse effects of beta lactams?

A
  • Main problems are allergic reactions
  • Generalised rash 1-10%
  • Anaphylaxis approx. 0.01%
26
Q

What is the main adverse effect of linezolid?

A

Bone marrow depression

27
Q

What factors are responsible for the clinical features and transmissability of C.diff infection?

A

Combination of enterotoxin (A and B) and spore production.

28
Q

What is the assumed cause of C.diff infection?

A

Abolition of colonisation resistance (normal flora?).

29
Q

What is the designation of the hypervirulent strain of C.diff?

A

027

30
Q

What are the common precipitating antibiotics for C.diff?

A
  • Cephalosporins
  • Ciprofloxacin (esp. ribotype 027)
  • Clindamycin
    (may be precipitated by any antibiotic)
31
Q

What are the less common precipitating antibiotics for C.diff?

A
  • Benzylpenicillin
  • Aminoglycosides
  • Glycopeptides
  • Piperacillin-tazobactam
32
Q

What is empiric therapy?

A

Based on predicted susceptibility of likely pathogens and local policies.

33
Q

What is targeted therapy?

A

Based on predicted susceptibility on infecting orginisms and local policy.

34
Q

What is susceptibility-guided therapy?

A

Based on susceptibility testing results.

35
Q

What bacteria is flucloxacillin most commonly used for

A

S. aureus

36
Q

What bacteria is benzylpenicillin most commonly used for?

A

S. pyogenes

37
Q

What are cephalosporins used for?

A

Gram -ve

38
Q

What is metrindazole used for?

A

Anaerobes

39
Q

What is vancomycin used for?

A

Gram +ve - MRSA

40
Q

In what bodily fluid do beta lactams show good availability in the presence of inflammation?

A

CSF

41
Q

Which antibiotics do not show good availability in CSF?

A

Aminoglycosides and vancomycin

42
Q

Which antibiotics show good availability in urine?

A

Trimethoprim and β-lactams

43
Q

Which antibiotics show poor availability in urine?

A

MLS Abx

44
Q

What are the reasons for combining antibiotics?

A
  1. To increase efficacy
    • Synergistic combination may improve outcome
  2. To provide adequately broad spectrum
    • Single agent may not cover all required organisms
    • Empiric treatment of sepsis
  3. To reduce resistance
    • Organism would need to develop resistance to multiple agents simultaneously
    • Antituberculous chemotherapy

Clinical Pathology (65 decks)

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