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47 Cards in this Set
- Front
- Back
MOA of quinolones
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Inhibit DNA gyrase
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MOA of sulfonamides
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Inhibit dihydropteroate synthase
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Anemia caused by trimethoprim
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Megaloblastic anemia
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Reason fluoroquinolones are contraindicated in children and pregnancy
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Cartilage damage
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Anti-microbials that cause hemolysis in G6PD-deficient patients
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Sulfonamides
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Anti-biotic frequently used for chronic UTI prophylaxis
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TMP-SMX
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Antimetabolites selectively toxic to microorganisms b/c they interfere w/ folic acid synthesis
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Sulfonamides and trimethoprim
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Antimicrobials that have a common chemical nucleus resembling PABA
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sulfonamides
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Reason for the use of 3 separate sulfonamides (triple sulfa)
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B/C of solubility limitation it is used to reduce the likelihood that any one drug will preipitate
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Drug that is structurally similar to folic acid; a weak base that gets trapped in acidic environments, reaching high concentrations in prostatic and vaginal fluids
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Trimethoprim
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Bacterial topoisomerase responsible for negative supercoiling of dsDNA that balances the positive supercoiling of DNA replication, acts as a "swivel", preventing damage to the DNA strand
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DNA gyrase
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Bacterial topoisomerase initiatingdecatenation, the mechanism by which 2 daughter DNA molecules are separated at the conclusion of DNA replication
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Topoisomerase IV
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MOA of Sulfonamides
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Bacteriostatic inhibitors of folic acid synthesis. As antimetabolites of PABA, they are competitive inhibitors of dihydropteroate synthase- (think SS)
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MOA of trimethoprim
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Selective inhibitor of bacterial dihydrofolate reductase that prevents formation of the active tetrahydro form of folic acid
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Mechanism of resistance to sulfonamides
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Dec intracellular accumulation of the drug, inc production of PABA, or a dec in the sensitivity of dihydropteroate synthase
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Mechanism of resistance to trimethoprim
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production of dihydrofolate reductase that has a reduced affinity for the drug
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Clinical use of Sulfonamides
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gram + and gram - organisms, Chlamydiae, and Nocardia
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Sulfonamide used for simple UTI
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Oral reg, triple sulfa, sulfisoxazole
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Sulfonamide used for ocular infections
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Topical (eg. sulfacetamide)
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Sulfonamide used for burn infections
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Topical (eg. mafenide, silver sulfadiazine)
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Sulfonamide used for UC, RA
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Oral (eg Sulfasalazine)
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Sulfonamide used for Toxoplasmosis
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Oral sulfadiazine plus pyrimethamine (a dihydrofolate reductase inhibitor) plus folinic acid
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DOC for prevention and tx of pneumocystis pneumonia
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TMP-SMX
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DOC in nocardiosis
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TMP-SMX
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Drug combo effective orally in tx of UTIs and in respiratory, ear, and sinus infections caused by Haemophilus influenzae and Moraxella catarrhalis
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TMP-SMX
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Hypersensitivity rxns caused by sulfonamides
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skin rashes and fever are common; exfoliative dermatitis, polyareritis nodosa, and Stevens-Johnson syndrome
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GI toxicity of sulfonamides
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Nausea, vomiting and diarrhea are common
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Hematotoxicity caused by sulfonamides
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Granulocytopenia, thrombocytopenia, and aplastic anemia; Acute hemolysis may occur in persons w/ G6PD deficiency
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Nephrotoxicity of sulfonamides
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May precipitate in the urine at acidic pH, causing crystalluria and hematuria
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Antibiotics that can displace bilirubin from plasma proteins, w/ the risk of kernicterus in the neonate if used in the 3rd trimester
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Sulfonamides
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Toxicity of trimethoprim
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predictable adverse effects of an antifolate drug, including megaloblastic anemia, leukopenia, and granulocytopenia
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1st generation fluoroquinolone derived from nalidixic acid, has activity against the common pathogens that cause UTIs
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Norfloxacin
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2nd gen fluoroquinolones that have greater activity against gram negative bacteria and are also active against the gonococcus, many gram + cocci, mycobacteria, and agents of atypical pneumonia
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Ciprofloxacin and ofloxacin
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3rd gen fluoroquniolones that are slightly less active than cipro and ofloxacin against gram-negative bacteria but have greater activity against gram + cocci, including S. pneumoniae and some strains of enterococci and MRSA
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Levofloxacin, gatifoxacin
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Broadest spectrum fluoroqunilones w/ enhanced activity against anaerobes
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gemifloxacin, moxifloxacin
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Fluoroquinolone that does not achieve adequate plasma levels for use in most systemic infections
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Norfloxacin
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Drug that can block elimination of fluoroquinolones by preventing active tubular secretion
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Probenecid
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MOA of fluoroquinolones
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interfere w/ bacterial DNA synthesis by inhibiting topoisomerase II (DNA gyrase), especially in gram - and topoisomerase IV, especially in gram +. Block the relaxation of supercoiled DNA that is catalyzed by DNA gyrase, a step required for normal transcription and duplication. Inhibition of topoisomerase IV by fluoroquinolones interferes w/ the separation of replicated chromosomal DNA during cell division
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Mechanism of resistance to fluroquinolones seen in M tuberculosis, S aureus, and S pneumoniae
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Efflux pumps
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Mechanism of resistance to fluoroquinolones seen in gonococci
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Mutations in the quinolone resistance-determining region of the gyrA gene that encodes DNA gyrase
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General use of fluoroquinolones
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UG and GI infections
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Fluoroquinolone that will eradicate accompanying organisms such as Chlamydia trachomatis, but a 7 day course is required
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Ofloxacin
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Fluoroquinolone w/ activity against most organisms assoc w/ CAP, including chlamydiae, mycoplasma, and legionella
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Levofloxacin
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Most common SE of fluoroquinolones
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GI distress
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Effects of fluoroquinolones on theophylline and other methylxanthines
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increases the plasma levels and increases toxicity
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Effect of newer fluoroquinolones (gemifloxacin, levofloxacin, moxifloxacin) on ECG
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prolonged QTc interval
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Reason Grepafloxacin was withdrawn
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Serious cardiotoxicity
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