DA4 - Lecture 8 - sulfonamides

  1. Sulfonamides are structural analogs of _____
    PABA (para-amino benzoic acid)
  2. Sulfonamides compete with _____ for binding the active site of _________ synthase
    Considered ________ antagonists.
    • PABA
    • dihydropteroate synthase
    • folate
  3. How are folate levels compensated for with use of sulfonamides?
    Cells use pre-formed folate from the environment (diet)
  4. Sulfonamides are bacteri______ and are reversible
  5. Antibacterial spectrum for sulfonamides
    gram positive and gram negative
  6. Commonly sulfonamide resistant bacteria (3)
    • Neisseria meningitidis
    • Shigella
    • Eschericia coli
  7. Resistance of sulfonamides may be due to
    -_____ binding to dihydropteroate
    -_____ entry or ____ efflux of drug
    -acquisition of alternative metabolic pathway to produce ________ _______
    -_____ production of PABA to compete with drug
    • decreased
    • decreased, increased
    • dihydrofolic acid
    • increased
  8. Sulfonamides may be used alone or in combination against _______ or _______ infections.
    Used in combination with pyrimethamine against _______
    Used in prophylaxis, especially for those with ______ allergy
    • UTI or Nocardiosis
    • toxoplasmosis
    • penicillin
  9. Class __ sulfonamides are long-acting, t1/2 100-230 hours, includes sulfadoxine
  10. Class __ sulfonamides are absorbed and excreted rapidly
    ________ is used in combination with trimethoprim
    • 1
    • sulfamethoxazole
  11. Sulfasalzine is a class ___, poorly absorbed, and active in the _____ lumen
    • 2
    • bowel
  12. Class 3 sulfacetamide and silver sulfadiazine are used _________
  13. sulfonamides can potentiate effects of (3)
    • warfarin
    • sulfonylurea
    • hydantoin anticonvulsants
  14. Sulfonamide ADEs:
    ______ especially in dehydrated patients
    Hypersensitivty, ____ common than penicillin
    Rash, _____ necrosis, anorexia, nausea, vomiting
    • crystalluria
    • less
    • liver
  15. Trimethoprim is also a folate antagonist
    It inhibits _______ enzyme
    ______ selective in prokaryote than mammalian
    • DHFR (dihydrofolate reductase)
    • More
  16. T/F: Trimethoprim and Sulfamethoxazole
    combination have additive effects.
    What are the parts of each used?
    • False: synergistic
    • 5 parts sulfamethoxazole to 1 part trimethoprim
  17. T/F: Trimethoprim and Sulfamethoxazole
    Combination is effective against both gram positive and gram negative
  18. Some therapeutic uses of Trimethoprim and Sulfamethoxazole
    UTI, AOM, respiratory tract infections, GI infections, pneumocystis carinii infection, prophylaxis
  19. Most ADEs of Trimethoprim and Sulfamethoxazole
    Combination involve____ _________
    Also, nausea, vomiting, _____(swelling of tongue) and ________ (inflammation of the mucous lining of the mouth)
    • skin conditions
    • glossitis
    • stomatitis
  20. If a fluoride is present in the ____ positition than a quinolone is called a fluoroquinolone
  21. Quinolone names you should know (MC LONG)
    • moxifloxacin
    • ciprofloxacin
    • levofloxacin
    • ofloxacin
    • norfloxacin
    • gemifloxacin
  22. Which quinolones out of MC-LONG are fluoroquinolones?
    all of them
  23. quinolones are bacteri_____
  24. MOA of quinolone found mostly in gram negative bacteria
    inhibit DNA gyrase
  25. MOA of quinolone found mostly in gram positive bacteria
    Topoisomerase IV inhibition
  26. DNA gyrase 's MOA is to _____ bond to phosphate on replicating DNA and break _____ bonds in one strand of the DNA
    DNA gyrase relieves the _____ DNA
    • covalently
    • phosphodiester
    • overwound
  27. what molecule is used to free two circular dsDNA that are interlocked?
    topoisomerase IV
  28. T/F: Quinolones target a broad range of bacteria and resistance has been relatively slow to develop
  29. quinolone resistance has been documented for all the following EXCEPT:
    -c. jejuni
    -neisseria gonorrhea
    -e. coli
    -strep pneumoniae
    e. coli
  30. quinolones are _____ absorbed orally and have ______ distribution in tissues
    • well
    • wide
  31. quinolones and trimethoprim-sulfamethoxazole are not recommended for E. coli 0157:H7 because..
    increased shiga toxin release, causing diarrhea
  32. _______ can be used for anthrax treatment and prophylaxis
  33. T/F: quinolones can be used against prostate infections and some STDs
  34. quinolones are _______ during pregnancy
    generally well tolerated, however may be associated with _____ rupture
    • contraindicated
    • tendon
  35. Other UTI treatments (3)
    • methenamine
    • nitrofurantoin
    • phenazopyridine
  36. T/F: phenazopyridine is an antibiotic and also an analgesic, it may also color urine blue
    False: not an antibiotic! orange/red urine!
  37. decomposition of methenamine at low pH in urine produces __________
    effective against nearly all UTI bacteria except those that _________________
    • formaldehyde
    • raise urine pH
  38. Nitrofurantoin is reduced into active form by ______ ______
    Higher activity in _____ acidity
    • bacterial enzymes
    • high (low pH)
Card Set
DA4 - Lecture 8 - sulfonamides
sulfonamides, trimethoprim, quinolone, uti