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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

class 1 AND CLASS 2 AND CLASS 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Class 1 reaction:

A

produce ATP & simple carbon compounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

class 2 reactions:

A

use energy & class 1 compounds to make small molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

class 3 reactions

A

convert small molecules into macromolecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

antibiotics that target class 2 reactions: characteristics

A

folate biosynthetic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

antibiotics that target class 3 reactions: characteristics

A

particularly good target as differ between bacteria & host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

antibiotics mostly target what class of reactions?

A

3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

folate is essential for making?

A

DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why cant bacteriaget folate from their diet?

A

dont have any folate transporters, but they still need it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

drug sensitivity to drug binding may be different

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

antibiotic trimethoprim

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

bacteria static

A

bacteria can’t make DNA, therefore they stop growing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

broad spectrum antibiotic target

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

why are sulphonamides used very rarely?

A

have side effects that cause a lot of severe skin reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
mechanism of penicilin
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
location of protein synthesis:
ribosomes
27
mRNA carries instructions to?
ribosome
28
tRNA brings correct sequence of?
amino acids to ribosome
29
bacterial ribosomes vs human ribosomes
bacteria- 50S & 30S human- 60S % 40S - Mechanics of making proteins are different
30
tetracyclines
prevent tRNA bindig to the ribosome ( A site)
31
chloramphenicol
inhibits transpeptidation-causing premature termination of peptide chain
32
aminogylcosides
disrupt codon : anticodon-misreading of message antibiotics against gram negative bacteria (narrow spectrum)
33
macrolides
disrupt translocation (moving on of used tRNA)
34
tetracylines, chloramphenicol & macrolides are broad or narrow
broad spectrum
35
ways to interfere with nucleic acid synthesis:
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
bacteriocidal
kill bacteria
37
bacteriostatic
inhibit growth
38
antimicrobial tip the balance in favour of the immune system by?
weakening microorganisms, stopping them from growing
39
anti-viral drugs target?
different stages of the viral replication cycle
40
antiviral drug targets
attachments pentration uncoating replication of nucleic acid release assembly synthesis of protein coats
41
antimicrobial stewardship requires that we use?
anti-microbials only when truly necessary
42
bacterial antibiotic resistance can be:
innate or acquired
43
vertical transfer?
by next gen
44
horizontal transfer?
by plasmids
45
resistance mechanisms
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
anti-viral drugs are often used in?
combination to reduce the emergence of reistance