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MD2001 Week 7 > Princicples of Antimicrobial Chemotherapy > Flashcards

Princicples of Antimicrobial Chemotherapy Flashcards

1
Q

Define chemotherapy.

A

The use of chemicals to inhibit the growth of invading organisms or cancerous cells.

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2
Q

What did Ehrlich discover?

A

Discovered and established the concept of selective toxicity.

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3
Q

What did Ehrlich discover that killed trypanosomes?

A

Salvarsan.

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4
Q

What did Ehrlich discover about resistance?

A

Trypanosomes could become resistant. Trypanosomes resistant to one agent remained susceptible to others.

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5
Q

What did Domagk discover?

A

Prontosil- a red dye that inhibited bacteria.

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6
Q

What was Domagk’s achievement?

A

Developed the concept of rational design of anti-bacterials.

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7
Q

What did Florey and Chain recognise?

A

The value of penicillin as a treatment of bacterial infection.

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8
Q

What is selective toxicity?

A

Drugs intended to be toxic to invading organism/cancerous cells but be relatively harmless to host cells.

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9
Q

What does selective toxicity depend on?

A

The existence of biochemical differences between the target group of cells and the host.

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10
Q

How are aminoglycosides an example of selective toxicity?

A

They have a very narrow therapeutic index thus the dose that causes toxicity is very close to the TD.

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11
Q

What are examples of anti-tuberculosis drugs?

A

Isoniazid and pyrazinamide.

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12
Q

What may tuberculosis patients develop when treated with anti-tb drugs?

A

Hepatoxicity

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13
Q

What is hepatotoxicity?

A

The medical term for damage to the liver caused by a chemical.

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14
Q

What are examples of beta lactam and cephalosporin class drugs?

A

Penicillin G, flucloxacillin and tazobactam.

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15
Q

What are examples of glycopeptide class drugs?

A

Vancomycin and teicoplanin.

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16
Q

What are examples of cyclic peptide drugs?

A

Bacitracin and polymyxin.

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17
Q

What are examples of phosphoric acid class drugs?

A

Fosphomycin

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18
Q

What are examples of lipopeptide class drugs?

A

Daptomycin

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19
Q

Where are peptidoglycans present?

A

They make up the cell wall of bacteria and do not occur in eukaryotes.

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20
Q

What are the strands of peptidoglycans made up of?

A

N-acetylclucosamine and N-acetlymuramic acid dimers.

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21
Q

What forms the cross links between the peptidoglycan strands?

A

The peptide side chains of the amino acids form a latticework of cross links.

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22
Q

Which drugs prevent peptidoglycan cross-linking?

A

Penicillin G, flucloxacillin, tazobactam and vancomycin.

23
Q

What are the early penicillins?

A

Penicillins g and v.

24
Q

What are the beta lactamase resistant penicillins?

A

Methicillin, oxacillin, nafcillin, cloxacillin and dicloxacillin.

25
Q

What is the penicillin most commonly used in the UK?

A

Flucloxocillin.

26
Q

What are the broad spectrum penicillins?

A

Ampicillin and amoxicillin.

27
Q

What can broad spectrum penicillins be used against?

A

Gram negative bacteria.

28
Q

What are the extended spectrum penicillins?

A

Carbenicillin, ticarcillin, azlocillin and piperacillin.

29
Q

Where does cephalosporium acremonium comes from?

A

Fungus.

30
Q

How do cephalosporins work?

A

In the same mechanisms as penicillins.

31
Q

How is cephalexin given?

A

Orally.

32
Q

How is cefuroxime and cefotaxime given?

A

Parenterally.

33
Q

How are cephalosporins classified?

A

By generation (1st, 2nd and 3rd).

34
Q

What are examples of bacterial folate antagonists?

A

Sulphonamides and trimethoprim.

35
Q

How do sulphonamides and trimethoprim work?

A

They act through an inhibition of the folate pathway in bacteria.

36
Q

Why are bacteria susceptible to bacterial folate antagonists?

A

Bacteria must make their own supply of folate, but humans do not.

37
Q

Which enzyme do sulfonamides interfere with?

A

Dihydropteroate synthetase.

38
Q

Which enzyme do trimethoprims interfere with?

A

Dihydrofolate reductase.

39
Q

What are examples of aminoglycosides?

A

Streptomycin, kanamycin, neomycin and gentamycin.

40
Q

How do aminoglycosides work?

A

Form ionic bonds at CSM and diffuse into cytoplasm and bind to bacterial ribosomes.

41
Q

How do aminoglycosides inhibit protein synthesis in bacteria?

A

They bind to ribosomes: at the interface between the assembled 30s and 50s subunits or directly to the subunits.

42
Q

How do aminoglycosides actions result in the inhibition of protein synthesis?

A

Misreading of mRNA.

43
Q

What is the action of tetracyclines?

A

They prevent attachment of the tRNA to the acceptor site on the mRNA-ribosomal complex.

44
Q

How are tetracyclines different to aminoglycosides?

A

They are only weakly bound to the ribosomes.

45
Q

What property affects the activity of individual tetracyclines?

A

Their solubility in the lipid membrane of the bacteria.

46
Q

What is the action of chloramphenicol, erythromycin and clindamycin?

A

Prevent the addition of new AAs to the growing peptide chain by binding ribosomes.

47
Q

What does the actions of chloramphenicol, erythromycin and clindamycin prevent?

A

Association of the peptidyl-transferase with the AA and no peptide bond is formed.

48
Q

What specifically might erythromycin prevent?

A

Translocation of the ribosome down the mRNA template.

49
Q

What are fluoroquinolones?

A

Synthetic antibiotics.

50
Q

What are broad spectrum agent examples of fluoroquinolones?

A

Ciprofloxacin, ofloxacin and norfloxacin.

51
Q

What are narrower spectrum drug examples of fluoroquinolones?

A

Nalidixic acid.

52
Q

How do fluoroquinolones act?

A

By inhibiting bacterial DNA Topoisomerase II also known as DNA gyrase.

53
Q

What does DNA gyrase (topoisomerase II) do?

A

This enzyme catalyses the introduction of negative supercoil DNA permitting transcription and replication.

54
Q

What is the use of fluoroquinolones defined by?

A

The spectrum of activity and by pharmacokinetics.

MD2001 Week 7 (10 decks)

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