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WEEK 18:
Bacterial targets for therapy:
| Question | Answer |
|---|---|
| features of antibiotics (3) | selective toxicity, ability to get to infection site, and ability to overcome bacterial resistances to kill/ stop them growing |
| antibiotics which target cell wall (2) | glycopeptide abx and betalactams |
| betalactam examples(4) | pinicillins, cephalosporins, carbapenems and monobactams |
| betalactams and glycopeptide abx are | bactericidal antibiotics (kill bacteria) which stop 'sheets' from joining in cell wall |
| glycopeptide abx example | vancomycin |
| co-amoxiclav | mixture of clavulanic acid (which inhibits B-lactamases) and amoxicillin used to treat pneumonia |
| beta lactamases | destroy B-lactams leading to resistance |
| flucloxacillin | type of penicillin resistant to B-lactamases on their own and is used to treat septic arthritis and cellulitis |
| antibiotics which inhibit protein synthesis (3) | aminoglycosides, tetracyclines, and macrolides |
| aminoglycoside mechanism of action | interrupt bacterial protein synthesis by inhibiting ribosomal function in mRNA and tRNA |
| suffix for aminoglycosides | end with y/icin (eg gentamicin) |
| tetracyclines mechanism of action | inhibit bacterial protein synthesis by interrupting tRNA (end in 'line') and are active against gram +/- bacteria but their use is limited due to bacterial resistance |
| doxycycline | a bacteriostatic type of tetracycline |
| macrolides mechanism of action | inhibit protein synthesis by interrupting ribosomal function eg clarithromycin |
| clarithromycin | type of macrolide with a similar antibacterial spectrum to penicillin so can be given to individuals with a penicillin allergy |
| bacteriostatic | stop bacteria from growing |
| bactericidal | kill bacteria |
| antibiotics which stop bacteria DNA synthesis (3) | sulphonamides, trimethoprim and quinolones |
| mechanisms of action for sulphonamides and trimethoprim | sulphonamides block thymidine and purine synthesis by inhibiting microbial folic acid synthesis while trimethoprim prevents reduction of dihydrofolate to tetrahydrofolate |
| trimethoprim | bacteriostatic used to treat UTIs |
| quinolones suffix | acin eg ciprofloxacin |
| quinolones mechanism of action | bactericidal and bacteriostatic antibiotics which inhibit DNA replication by inhibiting DNA gyrase |
| sulfamethoxazole | type of sulphonamide which inhibits dihydropteroate synthase |
| adverse effects of quinolones (3) | lengthens QT interval, lower seizure threshold in patients with epilepsy and tendon damage risk especially in patients taking steroids |
| what should guide antibiotic choice (2) | empirical treatment (what bacteria is usually present in this disease?), and specimen guided treatment (what has been grown) |
| antimicrobial resistance (AMR) | occurs when microorganisms change in ways which make medications used to treat them ineffective |
| antibiotic resistance | occurs when bacteria change in response to the use of antibiotics used to treat them making them ineffective |
| MDR | multidrug resistance |
| resistance to antibiotics can be the result of (4) | impaired/ altered permeability of bacterial cell envelope (so struggle to enter), alteration of target site (change binding site), and specific enzymes can destroy antibiotics eg B-lactamases |
| how is resistance transferred between bacteria (3) | transduction (DNA introduced/ transferred via bacteriophage (virus)), conjugation (bacterium plasmids containing resistance factor is directly passed to another bacterium), and transformation (pick up DNA fragments) |
Created by:
kablooey
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