Intro to antimicrobial drugs Flashcards

1
Q

principles antimicrobial chemotherapy

A

drugs should be toxic to invading microorganisks but not to the host
need to exploit biochemical differences between pathogen & host
gram positive bacteria easily treated by antibiotics

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2
Q

bacterial metabolism have 3 main stages of metabolism that we can target:

A

class 1 AND CLASS 2 AND CLASS 3

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3
Q

Class 1 reaction:

A

produce ATP & simple carbon compounds

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4
Q

class 2 reactions:

A

use energy & class 1 compounds to make small molecules

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5
Q

class 3 reactions

A

convert small molecules into macromolecules

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6
Q

antibiotics that target class 1 reactions: characteristics

A

similar to host reactions, multiple pathways to produce energy
-kill the host instead of the bacteria

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7
Q

antibiotics that target class 2 reactions: characteristics

A

folate biosynthetic pathway

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8
Q

antibiotics that target class 3 reactions: characteristics

A

particularly good target as differ between bacteria & host

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9
Q

antibiotics mostly target what class of reactions?

A

3

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10
Q

folate is essential for making?

A

DNA

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11
Q

folate to thymidylate for making DNA (process)

A

Foltate converted into dihydrofolate, which is reduced into tetrahydrofolate which is a cofactor to make thymidylate

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12
Q

why cant bacteriaget folate from their diet?

A

dont have any folate transporters, but they still need it

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13
Q

synthesis of folate is a very good target for antibiotics why?

A

because every bacteria needs to make folate.
If we hit synthesis with sulphonamide, that will hurt the bacteria but not the human

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14
Q

The enzyme, dihydrofolate reductase is structurally different in bacteria & in humans. therefore?

A

drug sensitivity to drug binding may be different

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15
Q

antibiotic trimethoprim

A

inhibits the bacterial form of the enzyme & not the human form

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16
Q

bacteria static

A

bacteria can’t make DNA, therefore they stop growing

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17
Q

broad spectrum antibiotic target

A

many different types of bacteria (gram positive &negative)
-but can cause antibiotic resistant bacteria

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18
Q

why are sulphonamides used very rarely?

A

have side effects that cause a lot of severe skin reactions

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19
Q

sulphonamides + trimethoprim can be used for a super folate inhibition in very severe infections such as:

A

pneumocytis (type of lung infection that you can get in HIV patients)

20
Q

role of pepidoglycans:

A

Make up cell wall, which forms a ‘string bag’ around bacterial cells
Supports underlying plasma membrane
Together comprise the bacteria envelope

21
Q

structure of peptidogylcan

A
  • tetrapeptide side chains & peptide cross-links
  • linking is catalysed by these enzymes called transpeptidase and carboxypeptidase
22
Q

penicilin is a really good antibiotic against? (what bacteria?

A

gram-positive bacteria

23
Q

class 3 reaction example

A

peptidodylcans & protein synthesis

24
Q

cell wall provides?

A

mechanical strength that allows bacteria to survive environmental conditions that alter osmotic pressures

25
Q

mechanism of penicilin

A

inhibit the transpeptidase and carboxypeptidase enzymes by bonding with them, stopping the activity of the enzymes, which means that the peptide cross links can’t form, weakening the cell wall
-if the cell wall is weak, then the cell will break down & die in response to environmental change

26
Q

location of protein synthesis:

A

ribosomes

27
Q

mRNA carries instructions to?

A

ribosome

28
Q

tRNA brings correct sequence of?

A

amino acids to ribosome

29
Q

bacterial ribosomes vs human ribosomes

A

bacteria- 50S & 30S
human- 60S % 40S
- Mechanics of making proteins are different

30
Q

tetracyclines

A

prevent tRNA bindig to the ribosome ( A site)

31
Q

chloramphenicol

A

inhibits transpeptidation-causing premature termination of peptide chain

32
Q

aminogylcosides

A

disrupt codon : anticodon-misreading of message
antibiotics against gram negative bacteria (narrow spectrum)

33
Q

macrolides

A

disrupt translocation (moving on of used tRNA)

34
Q

tetracylines, chloramphenicol & macrolides are broad or narrow

A

broad spectrum

35
Q

ways to interfere with nucleic acid synthesis:

A

Inhibiting synthesis of nucleotides
Altering base-pairing properties of DNA template
Inhibiting DNA or RNA polymerase
Inhibiting DNA gyrase (uncoils supercoiled DNA to allow transcription)
Fluroquinolones- inhibit the enzyme DNA gyrase

36
Q

bacteriocidal

A

kill bacteria

37
Q

bacteriostatic

A

inhibit growth

38
Q

antimicrobial tip the balance in favour of the immune system by?

A

weakening microorganisms, stopping them from growing

39
Q

anti-viral drugs target?

A

different stages of the viral replication cycle

40
Q

antiviral drug targets

A

attachments
pentration
uncoating
replication of nucleic acid
release
assembly
synthesis of protein coats

41
Q

antimicrobial stewardship requires that we use?

A

anti-microbials only when truly necessary

42
Q

bacterial antibiotic resistance can be:

A

innate or acquired

43
Q

vertical transfer?

A

by next gen

44
Q

horizontal transfer?

A

by plasmids

45
Q

resistance mechanisms

A

Production of enzymes that inactivate drug e.g. beta lactamases
Alteration of drug binding site e.g. penicillin
Reduction of drug update by bacterium e.g. tetracyclines
Alteration of enzyme pathways e.g. trimethoprim (dihydrofolate reductase)

46
Q

anti-viral drugs are often used in?

A

combination to reduce the emergence of reistance