Flashcards in Sulfonamides, trimethoprim, fluoroquninolones, metronidazole Deck (12):
sulfonamides: mechanism and resistance. cidal/static
sulfonamides are PABA analogues. they inhibit dihydropteroate synthesis, which is an enzyme needed for folate synthesis. bacteriostatic.
resistance develops when the enzyme is altered, decr. uptake, or incr. PABA synthesis
gram positive, gram negative, nocardia, chlamydia. SMX or triple sulfides for simple UTI
hypersensitivity, hemolysis if G6PD deficient, nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus, displace other drugs, like warfarin, from albumin
inhibits folate synthesis by inhibiting dihydrofolate reductase. bacteriostatic.
used in combo with sulfonamides. causes a block of folate synthesis. used in combination for UTIs, shigella, slamonella, pneumocystis jirovecii treatment and prophylaxis, and toxoplasmosis prophylaxis
toxicity of trimethoprim
megaloblastic anemia, leukopenia, granulocytopenia.
fluoroquniolones mechanism and special considerations. cidal/static. resistance
inhibit DNA gyrase and topoisomerase IV. cidal. must not take with antacids. resistance via chromosome-encoded mutation in DNA gyrase, plasmid mediated resistance, or efflux pumps
gram negative rods of urinary and GI tracts (incl. some pseudomonas), Neisseria, some gram positive organisms
toxicity to fluoroquinolones
GI upsett, superinfections, rashes, headache, dizziness. tendonitis, tendon rupture, myalgias. contraindicated in pregnancy, nursing, and childhood because of possible cartilage damage. some cause prolonged QT intervals
metronidazole mechanism, cidal/static
free radical formation in the bacterial cell that damages DNA. bactericidal and antiprotozoal.
use of metronidazole
treats giardia, entamoeba, trichomonas, gardnerella vaginals, anaerobes. use with PPI and chlarithromycin for treatment of H. pylori