Lecture - Resp (Usher Antibiotics Intro)

Question 1

Basics

1. What even are antiobiotics?
   - what three ways can you give these bioavailable compounds?
2. They interefer with specific bacterial what?
3. Differential toxicity for bacterial cells
   - target shouldnt be present in what? or the target should be what?
4. Broad vs narrow spectrum of activity - what does this mean?

Answer 1

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Question 2

Overview of all (slide 6)

1. SO there are three types of anti-biotics - what are they?
2. In the cell wall synthesis ABs - what are the four types of ABs?
   - why do we target cell walls?
3. Nucleic acid synthesis - what are the 4 types of ABs here?
4. In the prtein synthesis, what are the two types of ABs?

Answer 2

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Question 3

What is the difference between a gram-positive cell wall and a gram-negative cell wall?

Answer 3

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Question 4

Okay, so with cell wall synthesis, how does it work?

Answer 4

So the penicillin-binding protein (transpeptidase) cross-links peptide side chains of peptidoglycan. So this matrix of peptidoglycan. Serine is in the active site and is important in the cross linking of these peptide chains

Question 5

B-lactams

1. What does the B-lactam ring of penicillin look like? Is this present in all beta lactams?

Answer 5

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Question 6

Classes of B-lactams

1. Classes differ in spectra of ____ and ______ to beta-lactamases
2. Multiple drugs within classes due to modifcation of what?
   - so these modifications affect what?
3. Maybe tell me the classes of the b-lactams?
4. What about allergy?
5. What step do B-lactams inhibit in the peptidoglycan synthesis?
   - bind _____ to the transpeptidase due to what type of bond with what?
   - inhibits what?

Answer 6

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Question 7

Glycopeptides! (still cell wall synthesis ABs)

1. These include what ABs?
2. What spectrum of bacteria do the glycopeptides work on?
   - whyyyyy?
   - can you give it orally? Why?
3. Glycopeptides bind to what? This inhibits the cross linking too

Question 8

Protein synthesis inhibitors

1. Bind to what in the ribosome functional sites?
2. How do you get differential selectivity here?
3. What are the two ABs in the 16s rna and what are the three in the 23 rna?

Answer 8

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Question 9

Nucleic acid synthesis

1. Which one is mainly effective against anaerobes?
2. What two ABs can have resistance developing by chromosomal mutation during therapy? SO what does that say about treatment and the use of these ABs?

Answer 9

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Question 10

Nucleic acid synthesis: ABs that target folate synthesis

1. Bacterial pathway for production of _________ acid
   - what is this an essential co-factor for?
2. Sulphoamides
   - these are structurally similar to what?
   - whereabouts in the synthesis of tetrahydrofolic acid pathway does this AB work?
   - they compete with what?
3. Trimethoprim
   - structurally similar to what?
   - competitive inhibitor of what?
4. DO we often use sulphoamides and trimethoprim on their own?

Answer 10

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Question 11

Nucleic acid synthesis: Fluoroquinolones

1. What’s an example of this AB?
2. How does it work?
   - what do type 2 topoisomerases normally do?
   - what is DNA supercoiling required for?
   - remodeling/unwinding of DNA is required for what?

Answer 11

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Question 12

Nucleic acid synthesis: Metronidazole

1. Makes what in the DNA?
2. It is a prodrug - what does that mean?
   - so what is it activated by and where is it found?
3. What spectrum does this ABs therefore cover?