Lecture 27- Antibiotics Flashcards Preview

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Flashcards in Lecture 27- Antibiotics Deck (11):
1

What is an antibiotic?

Antibiotics are derived from micro-organisms, other antibacterials are synthetic agents(eg sulphonamides), or a hybrid of the two.

2

What is selective toxicity?

Anti-bacterial drugs exploit the differences in the biochemistry and structure between mammalian cell and bacterial cell. Antibiotics target bacterial cells.

3

What are the two types of antibiotics?

  1. Bacteriostatic
  2. Bactericidal

 

4

How are bacteriostatic and bactericidal antibiotics different in their function?

Bacteriostatic

Prevent bacterial replication but do not kill them
Stop or slow growth so that immune system can kill the bacteria.
Examples- Sulphonamides

              - Tetracyclines

              - Chloramphenicol

              - Macrolides(erythromycin)

Bactericidal

- these kill bacteria

Examples are B-lactams such as - Penicillins  and Cephalosporins

Bactericidals are used where immunosuppresants are being used(organ transplant) as the immune system is compromised so the bacterial cells are not killed by it.

Also used in cancer and tuberculosis.

5

How do antibiotics work?

3 main mechanisms

1. Inhibition of bacterial cell wall synthesis(transpeptidases)

2. Inhibition of bacterial protein synthesis(ribosomal complex or tRNA assembly).

3. Inhibition of DNA synthesis (Folic acid pathway, DNA gyrase)

6

What happens in inhibition of bacterial cell wall synthesis?

  • Bacterial cell walls consist of peptidoglycan and amino-acid crooslinks.
  • B-Lactam antibiotics eg Penicillin inhibit the transpeptidase enzymes involved in cross-linking of the cell wall.

7

What happens in inhibition of protein synthesis?

Drugs act on the bacterial ribosome to inhibit protein synthesis with little effect on mammalian protein synthesis- example of selective toxicity.

Examples- Amphenicols, Tetracyclines

8

What happens in inhibition of DNA synthesis?

  • Antifolates
  • Bacterial cells require folic acid for nucleic acid synthesis.
  • Bacteria synthesise their folic acid from PABA, which is converted to folic acid and then to folinic acid.
  • Drugs compete with PABA to inhibit folic acid synthesis. Example- Sulphonamides

Trimethoprim is used in combination with sulphonamides. It DECREASES the chance for resistance.

Quinolones

Inhibit enzyme DNA gyrase required for replication

9

What are the main mechanisms of anti-biotic resistance?

  1. Change in site where drug acts.(eg methylation of ribosomal RNA receptor site for erythromycin)
  2. Reduced bacterial uptake or enhanced efflux of drug (eg tetracycline- lack of facilitated uptake transport).
  3. Bacteria produces an enzyme that inactivates the drug( eg B-Lactamase destroys Penicillin- its B-lactam ring). Resistance can be overcome by adding a B-lactamase inhibitor to the antibiotic. eg clavulanic acid= potent inhibitor 

Amoxycillin + clavulanic acid= Augmentin

10

What is MRSA?

MRSA is a super bug.

- a resistant bacteria

-multiplies very rapidly and causes infections eg skin infections, septicaemia, toxic shock syndrome and death.

Drug used to fight it- VANCOMYCIN but it is developing resistance to it now.

11

What are the factors involved in the choice of antibiotics?

1. Bacterial factors

2. Drug factors

3. Patient variables(host factors)