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2011-02-16 20:57:37


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  1. True or false, first generation quinolones are only used to treat systemic infections.
    False, the second generation quinolones are used only for systemic infections
  2. Nalidixic acid and Cinoxacin are ________ generation quinolones.
  3. Ciprofloxacin, Enoxacin, Lemofloxacin, and Norfloxacin are ________ generation quinolones.
  4. Bactericidal
    Broad Spectrum
    Widely distributed in the body
    Not recommended for pregnant women and children <16
    Fluroquinolones (second generation quinolones)
  5. True or false, fluroquinolones have a higher affinity for DNA Gyrase than Bacterial Topoisomerase IV.
  6. What is the MOA for quinolones in gram negative bacteria?
    Inhibit DNA synthesis by inhibiting DNA Gyrase
  7. What is the MOA for quinolones in gram positive bacteria?
    Inhibit DNA synthesis by inhibiting Bacterial Topoisomerase IV
  8. True or false, quinolones can inhibit mammalian type II DNA topoisomerase at the clinical dose.
    False, at the clinical dose it will NOT inhibit this enzyme but at very high concentrations it will inhibit that enzyme
  9. What are the 2 mechanisms for microbial resistance to the quinolones?
    • 1- Expression of an altered DNA gyrase or topoisomerase IV (target modification)
    • 2- active efflux
  10. Which quinolone causes serious liver injuries and has been resitricted by the FDA for use in only life-threatening infections?
  11. Quinolones are _______ of cyt P450 and will ________ levels of theophylline, digoxin, caffeine, wafarin, and cyclosporine.

  12. What 4 toxicities can be caused by quinolones?
    • 1- Chelation
    • 2- Cartilage malformations (arthropathy)
    • 3- Tendonitis or tendon rupture
    • 4- Phototoxicity
  13. Which 2 quinolones are the most phototoxic?
    • 1- Sparfloxacin
    • 2- Lomefloxacin
  14. What 2 drugs can reduce the bioavailabilty of quinolones?
    • 1- sulcralfate (aluminum ions)
    • 2- didanosine (magnesium and aluminum)
  15. What polypeptide antibiotics disrupt cell membrane permeability?
    • 1- polymixins
    • 2- gramicidin
  16. True or false, polypeptide antibiotics are neutral and gramicidins are basic.
    False, polypeptides are basic and gramicidins are neutral
  17. Large molecules
    Nephrotoxic and neurotoxic
    NOT absorbed in the GI-tract
  18. What are the 2 polymixins on the market?
    • 1- polymixin B
    • 2- polymixin E (colistin)
  19. True of false, polymixins are not active against Gram positive bacteria
  20. True or false, the polymixins penetrate the CSF, synovial fluid, aqueous humor or the eye, or across the placenta.
    False, polymixins DO NOT penetrate these areas
  21. Polymixins have a ____ affinity for bacterial and mammalian cell membranes and there is _______ systemic absorption folowing topical administration

  22. True or false, polymixin can be administered parenterally or orally.
    False, it can only be administered parenterally
  23. Why are polymixins rarely used systemically?
    Due to their toxicity
  24. What is the MOA for polymixins?
    They bind ionically to phospholipids and penetrate into the structure of the cell membrane disrupting the cell membrane permeability
  25. Which antibiotics are amphipathic, surface active agents and act like cationic detergents?
  26. Activity of the polymixins is _______ by the presence of divalent cations like ____ which interfere with binding.

  27. What is the cyclic lipopeptide antibiotic?
  28. Bactericidal
    Treats gram positive bacteria
    Admisitered via IV
    Cyclid Lipopeptides (Daptomycin)
  29. What is the MOA (2 total) of Daptomycin?
    Inhibits the biosynthesis of lipoteichoic acid in gram-positive bacteria

    Depolarizes the membrane potential
  30. What are the toxicities (2) associated with daptomycin?
    • 1- superinfection
    • 2- peripheral/cranial neuropathy
  31. Sulfonamides belong the the _________ class.
  32. What are 4 ways to minimize the risk of crystalluria in sulfonamides?
    • 1- Use sulfanilamides with lower pKa values
    • 2- increase the pH of urine
    • 3- increase urine flow
    • 4- avoid any decrease in the pH of urine
  33. How can you increase the pH of your urine?
    Taking sodium bicarbonate
  34. What pKa do the sulfonamides have?
    between 5-8
  35. Sulfonamides are structural analogs AND _______ antagonists of ________

    PABA (p-aminobenzoic acid)
  36. True or false, sulfonamides do affect mammalian cells.
    False, they DO NOT affect mammalian cells
  37. What is the MOA for sulfonamides?
    It is a competive inhibitor with PABA to inhibit dihydropteroate synthesis
  38. What happens if PABA has a higher concentration than the sulfonamides?
    Dihydropteroate synthase will not be inhibited
  39. True or false, human cells do not use PABA therefore sulfonamides do not inhibit human cells.
  40. What are the 4 mechanisms of resistance to sulfonamides?
    • 1- expression of an altered dihydropteroate synthase (target modification)
    • 2- decreased bacterial permeablilty/active efflux
    • 3-developing an alternative metabolic pathway for the synthesis of THF
    • 4- Increased production of PABA
  41. Cross resistance among the sulfonamides is _____%
  42. True or false, sulfonamides are rarely used as single agents.
  43. What are the toxicities associated with sulfonamides? (5)
    • 1- hypersensitiviy
    • 2- hemolytic anemia
    • 3- aplastic anemia
    • 4- agranulocytosis
    • 5- crystalluria
  44. True or false, sulfonamides are not well distributed in the body.
    False, they are well distributed and are absorbed in the GI-tract and CSF, they also cross the placenta
  45. The sulfamethoxazole-trimethoprim is _______ at the clinical dose and is ________.

  46. What is the trimethoprim MOA?
    It is a competive inhibitor of dihyrofolate reductase which prevents the conversion of dihydrofolic acid ototetrahydrofolic acid
  47. What is the benefit of using Bactrim?
    The drugs are synergistic and will block sequential steps in the pathway inhibiting DNA synthesis
  48. Does trimethoprim have a higher affinity for binding to the bacterial dihydrofolate reductase of the mammalian one?
    The bacterial DHFR
  49. What is the most synergistic concentration of sulfamethoxazole/trimethoprim?
    20:1 ratio
  50. What is the most common resistance mechanism for Bactrim?
    A plasmid that cosed for an altered DHFR (target modification)
  51. What are the toxicities associated with bactrim?
    • 1- leukopenia
    • 2- megaloblastosis
    • 3- thrombocytopenia

    in patients with folate deficiency due to inhibition of DHFR
  52. What are the first line antituberculosis agents? (6)
    • 1- Isoniazid
    • 2- Rifampin
    • 3- Rifabutin
    • 4- Ethambutol
    • 5- Pyrazinamide
    • 6- Streptomycin
  53. What are the second line antituberculosis agents? (8)
    • 1- p-aminosalicylic acid
    • 2- ethionamide
    • 3- cycloserine
    • 4- capreomycin
    • 5- kanamycin
    • 6- amikacin
    • 7- moxifloxacin
    • 8- linezolid
  54. Which 2 anti-TB drugs are bactericidal?
    • 1- isoniazid
    • 2- pyrazinamide
  55. What is the MOA for p-Aminosalicylic acid?
    Inhibits folic acid synthesis
  56. What is the MOA for Isoniazid?
    inhibits the synthesis of mycolic acids in the cell wall of mycobacteria
  57. What is the MOA for Ethambutol?
    Inhibits the synthesis of mycolic acids
  58. What is the MOA for Ethionamide?
    Inhibits bacterial protein synthesis
  59. Which 2 anti-TB drugs have an unknown MOA?
    • 1- Pyrazinamide
    • 2- Capreomycin