Antibiotics and antifungals COPY Flashcards

1
Q

What are the main classes of antibiotic drugs?

A
  1. Sulphonamides 2. Trimethoprim 3. Fluoroquinolones 4. Rifamycins 5. Macrolides 6. Glycopeptides 7. Carbapenems, cephalosporins, penicillins 8. Polymyxins 9. Lipopeptide
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2
Q

What are the 4 main steps in prokaryotic protein synthesis? What drugs target each step?

A
  1. Nucleic acid synthesis - sulphonamides, trimethoprim 2. DNA replication - fluoroquinolones 3. RNA synthesis - rifamycins 4. Protein synthesis - macrolides
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3
Q

What drugs are used to treat fungal infections and how do they work?

A
  1. Azoles(e.g. fluconazole) - inhibit ergosterol production (in fungal CM) 2. Polyenes(e.g. amphotericin) - bind to ergosterol and make pores in CM
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4
Q

What mechanisms are commonly used by bacteria to become resistant to drugs?

A
  1. Changes to target - change DNA gyrase 2. Hyperproduction - make more DHFR enzyme 3. Additional target - make diff. DHFR enzyme 4. Destruction enzymes - B-lactamases 5. Alter permeation - increase efflux mechanisms
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5
Q

How do sulphonamides work?

A

Targets DHOp synthase to inhibit NA synthesis

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6
Q

How does trimethoprim work?

A

Targets DHF reductase to inhibit NA synthesis

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7
Q

How do macrolides work?

A

Target ribosomes to inhibit protein synthesis

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8
Q

How do fluoroquinolones work?

A

Target DNA gyrase/topoisomerase IV to inhibit DNA synthesis

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9
Q

How do rifamycins work?

A

Target RNA polymerase to inhibit RNA synthesis

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10
Q

How do glycopeptides work?

A

Target pentapeptide to inhibit peptidoglycan synthesis

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11
Q

How do carbapenems, cephalosporins + penicillins work? WHat group of drugs are they?

A

Target transpeptidase enzyme involved in PtG incorporation into cell wall. The group of drugs they are is beta-lactams

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12
Q

How do polymyxins work?

A

Target LPS to disrupt Gm-ve CMs

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13
Q

How does lipopeptide work?

A

Disrupts Gm+ve cell walls

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14
Q

How is tuberculosis treated?

A
  1. RNA-polymerase inhibitor - rifampicin 2. Mycolic acid synthesis inhibitors 3. Pyrazinamide - reduces availability of ribosomes required for protein translation
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15
Q

What are mycobacteria?

A
  • Gram positive w/more complex outer wall - Wall contains a PtG-arabinogalactan polymer that binds mycolic acids, pore forming proteins and a number of extractable lipids - Gives bacteria a ‘waxy’ outer layer - E.g. mycobacteria tuberculosis, mycobacteria leprae
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16
Q

What does bacitracin do

A

•Bacitracin inhibits bactoprenol regeneration preventing PtG transportation

17
Q

Describe structure of mycolic bacteria, and what other types of bacteria are there

A

Mycolic Bacteria

  • Outer mycolic acid layer
  • E.g. Mycobacterium Tuberculosis

other types : gram negative and positive

18
Q

Describe process of bacteria l protein synthesis

A

1.Nucleic Acid Synthesis

Dihydropteroate (DHOp)

  • Produced from paraaminobenzoate (PABA)
  • Converted into dihydrofolate (DHF)

Tetrahydrofolate (THF)

  • Produced from DHF by DHF reductase
  • THF ® Important in DNA synthesis

2.DNA replication

DNA gyrase

•Topoisomerase ® releases tension

3.RNA synthesis

RNA polymerase

  • Produces RNA from DNA template
  • Differ from eukaryotic RNA polymerase

4.Protein synthesis

Ribosomes

  • Produce protein from RNA templates
  • Differ from eukaryotic ribosomes
19
Q

Describe the process of bacterial cell wall synthesis

A

1.Peptidoglycan (PtG) synthesis

  • A pentapeptide is created on N-acetyl muramic acid (NAM)
  • N-acetyl glucosamine (NAG) associates with NAM forming PtG

2.PtG transportation

•PtG is transported across the membrane by bactoprenol

3.PtG incorporation

•PtG is incorporated into the cell wall when transpeptidase enzyme cross-links PtG pentapeptides

20
Q

List the causes of antibiotic resistance

A

Unnecessary prescription,Livestock farming,Lack of regulation,

Lack of development(Very few antibiotics in recent years)

21
Q

Mechanism of antibiotic resistance

A

•Desctruction enzymes(b-lactamases hydrolyse C-N bond of the b-lactam ring)

Additional target(Bacteria produce another target that is unaffected by the drug[•E Coli produce different DHF reductase enzyme making them resistant to trimethoprim])

Alterations in target enzymes(Alteration to the enzyme targeted by the drug. Enzyme still effective but drug now ineffective[•S Aureus - Mutations in the ParC region of topoisomerase IV confers resistance to quinolones])

Hyperproduction

•Bacteria significantly increase levels of DHF reductase(e.g.Coli produce additional DHF reductase enzymes making trimethoprim less effective)

Alterations in drug permeation(.Reductions in aquaporins & increased efflux systems[•Primarily of importance in gram –ve bacteria])

NOTE:

Difference between ‘Additional target’ and ‘Alterations in target enzymes’ is that in the former we still have the first enzyme working but another has been added which is unaffected by the drug; and in the latter, there is a replacement , withthe replacement being unaffected by the drug

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