Lecture 27 Flashcards Preview

Medsci 204 > Lecture 27 > Flashcards

Flashcards in Lecture 27 Deck (9):

What is the difference between bacteriostatic and bactericidal?

A bacteriostatic compound just inhibits growth of the bacteria allowing the immune system to overcome the infection while a bactericidal compound will actually kill the bacteria


What are the three main mechanisms of antibiotics?

Inhibition of bacterial cell wall synthesis (transpeptidases)
Inhibition of bacterial protein synthesis (ribosomal complex or tRNA assembly)
Inhibition of DNA synthesis/replication (folic acid, DNA gyrase)


How do antibiotics inhibit bacterial cell wall synthesis?

Bacterial walls are made up of peptidoglycans which has amino acid sugar cross links
beta-lactam antibiotics such as penicillin inhibit the transpeptidase enzyme involved in forming the cross links so their is a failure to form the cell wall


How do antibiotics target protein synthesis?

Drugs such as chloramphenicol, tetracycline, erythromycin and aminoglycosides act on the bacterial ribosome 70S to inhibit bacterial protein synthesis, do not act on mammalian 80S ribosomes so are selectively toxic


How do antibiotics target DNA synthesis?

Folic acid is required to synthesize pyrimidines for DNA synthesis, bacteria synthesize there own floate from para-aminobenzoic acid (PABA) while in humans it is dietary
Sulphonamides are analogs of PABA and compete with it to inhibit folic acid synthesis
Alternatively quinolones can be used to target bacterial DNA gyrase enzyme (which is a unique bacterial enzyme required for replication)


Why is cotrimoxazole more effective as an antibiotic than just sulphonamides?

Cotrimoxazole has both sulphonamides and Trimethoprim which is another compound which inhibits dihydrofolate reductase which is another compound along the folate synthetic pathway allowing for a higher antibacterial activity for there to be less chance of antibiotic resistance developing


What are the main mechanisms of antibiotic resistance?

Change in the site where the drug acts (methylation of ribosomal RNA receptor site for erythromycin)
Reduced bacterial uptake, or enhanced efflux of drug (tetracycline- lack of facilitated uptake transport)
Bacteria produces and enzyme which inactivates the drug (beta-lactamase)


How can beta-lactamase resistance be overcome?

Addition of a beta lactamase inhibitor such as clavulanic acid


What controls the choices of which antibiotic to use?

Bacterial factors including the type of organism, source of organism, host details and community information
Drug Factors including likely efficacy, route of administration, adverse effects profile, dosing frequency, palatability and stability, cost
Patient variables such as site of infection, drug allergies, underlying illness, other drug therapies, age and pregnancy status