Antibiotics and Antibiotic resistance Flashcards Preview

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Flashcards in Antibiotics and Antibiotic resistance Deck (40)
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1
Q

Define Antibiotic

A

A substance produced by a micro-organism (or a similar substance produced wholly or partly by chemical synthesis) which at low concentrations kills or inhibits the growth of other micro-organisms

2
Q

How are Antibiotics normally taken?

A

Used Systemically, meaning inside the body

3
Q

Define Selective Toxicity

A

Affects only the microbe

Affects the microbe much more than patient

4
Q

Define Bactericidal (C)

A

Kills and/or lyses bacterial cell

5
Q

Define Bacteriostatic (S)

A

Inhibits growth -reversible effect

6
Q

What are the targets for Antibiotics?

A

METABOLIC REACTIONS
CELL WALL
CELL MEMBRANE

7
Q

Why can target sites of the Antibiotics be a problem?

A

Besides the Cell wall, all of the targets are in the host as well as the microbe

8
Q

How does Sulphonamides (S) antibiotic effect the cell?

A

By inhibiting Folate metabolism

9
Q

How does Fluoroquinolones(C) antibiotic effect the cell?

A

By inhibiting DNA synthesis causing cell death

10
Q

How does Rifampicin (C) antibiotic effect the cell?

A

By inhibiting RNA synthesis (transcription), causing cell death

11
Q

How do Tetracyclines(S) and Chloramphenicol (S) antibiotic effect the cell?

A

By inhibiting Protein synthesis (translation)

12
Q

In the cell wall what are the two processes that Antibiotics target and what Antibiotics target these?

A

Synthesis
•Cycloserines(S)

Stability / integrity
•ß-lactams (C)
•Vancomycin(C)

13
Q

In the Cell Membrane, what are the two processes that Antibiotics target and what Antibiotics target these?

A

Stability / integrity
•Polymyxins(C)
•Polyenes(C)

14
Q

What is the difference between Folate metabolism in bacteria and in Mammalian cells?

A

Bacteria synthesise folic acid whereas humans obtain folic acid from diet

15
Q

How does Sulphonamides affect Folate Metabolism?

A

It inhibits the enzyme which activates the process between Para-Aminobenzoic acid and Dihydrofolic acid, preventing the conversion

16
Q

How does Trimethoprim affect Folate Metabolism?

A

It inhibits the enzyme which activates the process between Dihydrofolic acid and Trimethoprim, preventing the conversion

17
Q

How is Bacterial DNA coiled?

A

Activating gyrase

18
Q

Define Anti-gyrase

A

The process in which super-coiling in bacterial DNA is prevented

19
Q

What does Rifampicin do in the bacterial cell?

A

Prevents production of mRNAInhibits transcription

20
Q

How does Tetracycline Inhibit protein synthesis (translation)?

A

By acting on the 30s ribosome unit

21
Q

How does Chloramphenicol Inhibit protein synthesis (translation)?

A

By acting on 50s ribosome unit

22
Q

Define ß-LACTAMS

A

This is a group of Antibiotics which within their chemical structures contain a ß-Lactam ring.

Includes Penicillins and cephalosporins

23
Q

What does B-Lactams do?

A

Inhibit final stage of peptidoglycan assembly (cross-linking)

Bind irreversibly to transpeptidase

Induce autolytic enzymes

24
Q

In B-Lactams what does the R group do?

A

Gives properties such as acid resistance, membrane transport or resistance to ß-lactamase

25
Q

What is the Role of Vancomycin?

A

Binds to D-Ala-D-Ala on peptidoglycan side chain

Block transpeptidation

26
Q

What is the role of Polymyxin

A

Disrupts bacterial cell membranes

27
Q

Why are Antifungal drugs hard to produce?

A

Fungi are eukaryotes with similar structure function to humans & animals.

Harder to find unique targets

Difficult to treat

28
Q

Why are Anti viral drugs hard to produce?

A
  • Viruses use the host cells own metabolic processes to replicate
  • Even harder to treat as the target is the host.
29
Q

What is the problem with Nucleoside analogues and give examples

A

Toxic to host too

Ganciclovir

Zidovudine(AZT)

30
Q

What is the two different Antibiotic resistance?

A

Natural/Innate Resistance and Acquired Resistance

31
Q

Define Natural/Innate Resistance

A

Variations in the structure of cell envelope/cell wall

Altered binding sites/enzymatic inactivation

Efflux mechanism

32
Q

Define Acquired Resistance

A

Mutation

Adaptation

Gene Transfer (plasmids, transposons)

33
Q

Where the Genes that are responsible for Antibiotic Resistance located?

A

Chromosome or on plasmid

34
Q

Define Exclusion

A

Envelope impervious to antibiotic

Gram-negative bacterial Outer Membrane

35
Q

Define Excretion

A

Tetracycline efflux pump, removal of Tetracycline

36
Q

Define Alter targets

A

Structure of ribosome (methylation of ribosomal RNA), polymerases and gyrases

Modify metabolic pathway -sulphonamides

37
Q

Define Destroy antibiotic

A

B-lactamases open B-lactam ring

38
Q

Define Modify antibiotic

A

–Phosphorylation -Streptomycin

–Acetylation –Chloramphenicol

39
Q

What are the causes of Antibiotic Resistance?

A
  • Over-prescribing
  • Non-compliance
  • Indiscriminate use of antibiotics e.g supplement feeds in agriculture
40
Q

What ways can we overcome Antibiotic resistance?

A
  • Identification of the pathogen
  • Selection of the antimicrobial agent appropriate for the pathogen
  • Is the organism resistant to the prescribed antibiotic
  • Drug combinations (penicillin + clavulanic acid)