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Bact: stupid drugs
Drugs
Question | Answer |
---|---|
drugs that alter the bacteria cell wall | fosfomycin, cycloserine, vancomycin, bacitracin, B lactams |
how does fosfomycin work | binds covalently to muramic acid synthesizing enzyme to inhibit synthesis of Muramic |
how are bacteria developing fosfomycin resistance | decreased uptake |
how does cycloserine work? | inhibits synthesis of D-ala D-ala |
how are bacteria becoming resistant to cycloserine | decreased uptake |
how does vancomycin work | binds D-ala D-ala and prevents transglycosylation |
how are bacteria becoming resistant to vancomycin | they alter D-ala D-ala to make it D-ala-D lactate |
who is especially resitant to vancomycin | enterococcus |
how does bacitracin work | blocks dephosphyorylation of lipid carriers |
what does bacitracin and vancomycin work against | Gram + |
how does b lactams work | inhibits PBP which carry out crosslinking, it inhibits transpeptidation |
are B-lactams bacteriocidal or bacteriostatic | cidal |
what does the b lactam ring mimic | the D-ala D-ala of the peptidoglycan precursor |
how do b lactams differ | different side chains same nucleus |
who are two b-lactamase inhibitors | clavulanic acid and sulbactam |
What drugs work on cell membrane | polymyxin |
how does polymyxin work | cationic detergent that binds LPS |
how is polymyxin applied | topical kills even non-dividing gram neg bacteria |
what drugs work on the DNA structure | nitrofuantoin adn metronidazole |
how do drugs that work on the DNA structure function | the nitro group is reduced by a nitroreductase and makes a reactive species that cleaves DNA |
nitrofurantoin and metroniadazole are only effective against? | anaerobes |
what drugs alter DNA synthesis | quinolones, fluoroquinolones |
how do drugs that alter DNA synthesis work? | inhibits DNA gyrase, topoisomerase II blocks DNA supercoiling |
how are bacteria resistant to quinolones | alter target |
what drugs alter RNA synthesis | Rifamycins |
how does rifamycin work | blocks RNA polmerase |
how does resistance to rifamycin work | alter B subunit of RNA polymerase |
drugs that alter protein synthesis are static or cidal | static |
what drugs affect the 50S ribosomal unit | chloramphenicol, macrolides (azithromycin, erythromycin, clarithromycin), lincosamides |
how do choramphenicols work | bind reversibly to exit tunnel of 50s |
how do the macrolides work (erythro, azithro, clarithro) | block translocation and elongation |
how does resistance develope to macrolides | alter target |
how do lincosamides work | binds 50S and blocks peptide bond formation |
how does tetracyclin work | stops tRNA from binding |
who should not get tetracyclin | pregnant women and children (bone seeking) |
how have bacteria become resistant to tetracyclin | decreased uptake increased efflux |
how do aminoglycosides work | bind irreversibly to 30S |
what is special about aminoglycosides | they are bacteriocidal |
when are aminoglycosides useful | anerobic conditions |
how are bacteria becoming resistant to aminoglycosides | alter target, inactivate the drug, decrease uptake |
how does bactrim work | inhibits thymine synth via blockage of dihydropteroate synthetase |
is bactrim static or cidal | static |
how has resistance developed to bactrim | alter target, decrease uptake, increase level of target enzymes |
how does trimethoprim work | inhibits thymine synth |
how are bacteria becoming resistant to trimethoprim | increase level of targer or alter target |
what does isoniazid do | inhibits mycolic acid synthesis |
when is mycolic acid important | M. Tb |
prblem with isoniazid | hepatotoxic |