Pharmacology - Macrolides 3

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kyleannkelsey
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259169
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Pharmacology - Macrolides 3
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2014-01-29 20:52:59
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Pharmacology Macrolides
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Pharmacology - Macrolides 3
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Pharmacology - Macrolides 3
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  1. Can clindamycin treat MRSA?
    Yes, some
  2. Clindamycin has a similar spectrum to what two antibiotics?
    Vancomycin and metronidazole, though less efficacious compared to both for the most part, except in its activity against anaerobes, whereas it is a better choice
  3. Clindamycin binds to the same binding site as what other drugs?
    Macrolides and chloramphenicol
  4. Should you use chloramphenicol or macrolides with Clindamycin?
    No, they all have the same MOA/binding site
  5. How do bacteria develop resistance to Clindamycin?
    Altered ribosomal RNA, decreased membrane permeability, metabolize drug
  6. Does clindamycin have a narrow or broad spectrum?
    Narrow
  7. What bacteria are included in the Clindamycin spectrum?
    Strep. pneumoniae and viridians, B-hemolytic streptococci, Staph aureus, anaerobic bacilli and cocci, Bacteriodes fragilis
  8. What is the main issue that is caused by Strep. viridians?
    Endocarditis, particularly in those with rheumatic fever
  9. Does Clindamycin enter the bones well?
    Yes
  10. Would you use Clindamycin to treat anaerobic bacterial infections of the oral cavity?
    Yes
  11. What is the half life of Clindamycin?
    2-3 hours
  12. Is Clindamycin absorbed orally?
    Yes, well
  13. How can Clindamycin be administered?
    IV, IM, orally or topically (includes vaginally)
  14. What is clindamycin palmatate used for?
    Oral administration to pediatrics, easier on their GI tracts
  15. How is Clindamycin excreted?
    As metabolites in the urine and bile
  16. Does Clindamycin cross the placenta?
    Yes
  17. Does Clindamycin cross the BBB?
    No
  18. Is Clindamycin highly metabolized?
    Yes, by the liver
  19. Does Clindamycin bind to plasma proteins?
    Yes, highly bound
  20. What PAE does clindamycin have?
    Affects bacteria in the gut for up to two weeks after the last dose
  21. Why does Clindamycin tend to cause superinfections like C. diff?
    Because of its two week PAE on the gut bacteria
  22. Would you use Clindamycin to treat an abscess, why or why not?
    Yes, because it penetrates well
  23. What are the adverse effects of Clindamycin?
    Diarrhea (toxicity), pseudomomembranous colitis (often due to C. diff), rash, stevens Johnson syndrome, neuromuscular blockade, bloody dyscrasias, Thrombophlebitis (IV)
  24. What are the symptoms of pseudomomembranous colitis?
    Diarrhea, pain, fever, bloody stools
  25. What is the normal therapy for pseudomomembranous colitis?
    Withdraw antibiotic and administer Metronidazole, Fidaxomicin or Vancomycin
  26. Why should you notify your anaesthesiologist if you have been using Clindamycin?
    Can cause neuromuscular blockade and effect anesthetic use
  27. What is Blood dyscrasias?
    Blood imbalance that effects the bone marrow, which can lead to gluconemia and hemophilia
  28. What are the indications for Clindamycin?
    Anaerobic infection, lung abscess, aspiration pneumonia, osteitis, osteomyelitis, vaginal infections, oral infections, acne, pneumocystis jiroveci
  29. If you were trying to treat Pneumocystis jiroveci with Clindamycin, what other drug would you use in combination?
    Primaquine
  30. Pneumocystis jiroveci is mainly a disease of what patient population?
    AIDS patients
  31. Can Clindamycin be used to treat Malaria?
    Yes, but only in combo and only in certain situations
  32. Are tetracyclines broad or narrow spectrum?
    Extremely broad
  33. What does Tetracycline bind to, causing absorption issues?
    Metal ions(cations/antacids)
  34. What types of bacteria do tetracyclines treat?
    Aerobic, Anaerobic, G-, G+, etc. (very broad)
  35. What specific bacteria are tetracyclines regularly use to treat?
    H. pylori, rickettsiae, mycoplasma, Chlamydia, borrelia
  36. What is the MOA of tetracyclines?
    Bind to the 30S ribosome (low affinity) and prevent tRNA binding to mRNA, prevents elongation
  37. How do Tetracyclines enter bacteria?
    Transported into the cell and diffuse through G- outer membrane porins
  38. Is resistance to tetracyclines common or rare?
    Common, widespread
  39. How does resistance to tetracyclines develop?
    Increased transport of drug out of cell, alteration of outer membrane, change in ribosome
  40. What bacteria are commonly resistant to tetracyclines?
    Stepto/Staphylococci, N. gonorrhoeae, E. coli, Shigella and Pseudomonas aeruginosa
  41. What are the routes of administration available for tetracyclines?
    IV and oral
  42. What is the half life of most tetracyclines?
    6-20 hours
  43. Where are tetracyclines not distributed to?
    CNS
  44. Where do tetracyclines concentrate within the body?
    The skin
  45. Can tetracyclines distribute in the bones?
    Yes, can be incorporated into forming bone and teeth
  46. How are tetracyclines excreted?
    Renally (Main route) and hepatically (enterohepatic loop)
  47. Other than tetracyclines, what other antibiotics have we seen that chelate with metal ions?
    Flouroquinolones
  48. The more lipophilic a tetracycline is, the shorter or longer the half life will be?
    Longer
  49. What side effect is caused by tetracyclines concentrating in the skin?
    Photosensitivity

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