Antibiotics and antifungals COPY Flashcards
What are the main classes of antibiotic drugs?
- Sulphonamides 2. Trimethoprim 3. Fluoroquinolones 4. Rifamycins 5. Macrolides 6. Glycopeptides 7. Carbapenems, cephalosporins, penicillins 8. Polymyxins 9. Lipopeptide
What are the 4 main steps in prokaryotic protein synthesis? What drugs target each step?
- Nucleic acid synthesis - sulphonamides, trimethoprim 2. DNA replication - fluoroquinolones 3. RNA synthesis - rifamycins 4. Protein synthesis - macrolides
What drugs are used to treat fungal infections and how do they work?
- Azoles(e.g. fluconazole) - inhibit ergosterol production (in fungal CM) 2. Polyenes(e.g. amphotericin) - bind to ergosterol and make pores in CM
What mechanisms are commonly used by bacteria to become resistant to drugs?
- 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
How do sulphonamides work?
Targets DHOp synthase to inhibit NA synthesis
How does trimethoprim work?
Targets DHF reductase to inhibit NA synthesis
How do macrolides work?
Target ribosomes to inhibit protein synthesis
How do fluoroquinolones work?
Target DNA gyrase/topoisomerase IV to inhibit DNA synthesis
How do rifamycins work?
Target RNA polymerase to inhibit RNA synthesis
How do glycopeptides work?
Target pentapeptide to inhibit peptidoglycan synthesis
How do carbapenems, cephalosporins + penicillins work? WHat group of drugs are they?
Target transpeptidase enzyme involved in PtG incorporation into cell wall. The group of drugs they are is beta-lactams
How do polymyxins work?
Target LPS to disrupt Gm-ve CMs
How does lipopeptide work?
Disrupts Gm+ve cell walls
How is tuberculosis treated?
- RNA-polymerase inhibitor - rifampicin 2. Mycolic acid synthesis inhibitors 3. Pyrazinamide - reduces availability of ribosomes required for protein translation
What are mycobacteria?
- 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