DNA Function Inhibitors Flashcards
(22 cards)
Fluoroquinolones: examples
- ciprofloxacin
- levofloxacin
- gemifloxacin
- moxifloxacin
Fluoroquinolones: mechanism of action
- DNA transcription inhibitor
- targets bacterial DNA gyrase and topoisomerase IV
- rapidly bactericidal
Fluoroquinolones: pharmacokinetics
- good oral, parenteral also available
- good penetration into most tissues
- primarily kidney excretion
Fluoroquinolones: spectrum/clinical uses
- gram+ cocci (strep. pneumoniae, MSSA)
- gram- cocci (moraxella catarrhalis)
- gram+ bacilli (bacillus anthracis)<–cipro
- gram- bacilli (pseudomonas aeruginosa, E. coli)
- anaerobes
- atypical organisms (chlamydia, mycoplasma pneuemoniae, richettsia)
Fluoroquinolones: adverse reactions
- well tolerated
- increased risk of tendon rupture
- GI disturbances
- drug-drug: reduced absorption w/anacids
Fluoroquinolones: “1st generation” + spectrum
Naldixic acid: gram- anaerobes (++)
Fluoroquinolones: “2nd generation” + spectrum
Cipro & Levo: gram- anaerobes (++), pseudomonas (+), gram+ (+/++)
Fluoroquinolones: “3rd generation” + spectrum
Gemi & Moxi: gram- anaerobes (+), pseudomonas (+/-), gram+ (++), atypical (+), anaerobes (++)
Nitrofurantoin: mechanism of action
- DNA damage-inducer
- concentration-dependent bacteriostatic/bactericidal effect
Nitrofurantoin: pharmacokinetics
- good oral
- short half-life –> urine (renal excretion)
Nitrofurantoin: spectrum/clinical uses
- 2nd line urinary tract antiseptic (cannot safely reach plasma levels, but concentrated in renal tubules)
- E. coli & enterocci
Nitrofurantoin: adverse reactions
- GI disturbances
- possible link to birth defects
Metronidazole: mechanism of action
- DNA damage inducer
- prodrug–>reactive nitro radical anion
- radical anion damages DNA
- bactericidal
Metronidazole: pharmacokinetics
- good oral
- good distribution (including bone/CSF)
- liver metabolism
- excreted in breast milk
Metronidazole: spectrum/clinical uses
- anaerobes (C. difficile, Bacteriodes fragilis)
- protozoa
Metronidazole: adverse reactions
- some GI disturbance
- headaches, dry mouth
- candidal superinfection
Sulfonamides: mechanism of action
- DNA synthesis inhibitor
- inhibits folic acid synthesis (PABA analog) which is required for DNA synthesis
- bacteriostatic
Sulfonamides: pharmacokinetics
- good oral (best on empty stomach)
- widely distributed
- some protein binding
- n-acetylation metabolism (can be toxic)
- excreted by kidney
Sulfonamides: spectrum/clinical uses
- broad spectrum; most common use in TMP/SMX form
- gram+ cocci (MRSA)
- gram- cocci (Moraxella catarrhalis)
- gram- bacilli (enetrobacter, shigella, pseudomonas aeruginosa)
- atypical (chlamydia)
Sulfonamides: adverse reactions
- generally safe
- sensitization reactions
- drug-drug: displace from proteins –> bilirubin, anticoagulants
Sulfonamides: bacterial resistance
- widespread in vivo
- acquired: increase PABA production or DHPS altered to decrease binding to sulfonamides
- escape: obtain end products of metabolic pathway from pus (why we must drain some purulent infections)
- natural: organisms w/no folic acid requirement
Sulfonamides: common drug combination
- synergy w/trimethoprim (TMP)
- sulfamethoxazole + TMP (aka TMP/SMX or “Bactrim”= bactericidal
