PT Infectious Disease: Exam 1

  1. Sulfonamides are considered __________________ drugs.
  2. Why are sulfonamides considered synthetic antibacterial drugs?
    They are bacteriostatic- only prevent bacteria from proliferating
  3. What is the MOA of sulfonamides?
    • - Compete with PABA (competively)
    • - Inhibits dihydropteroate synthase
    • - Prevent the synthesis of Dihydrofolic acid
    • - Prevents DNA synthesis
  4. How are sulfonamides metabolized?
    • Partially deactivated by acetylation and glucoronidation
    • they become polarized and cleared quickly
  5. Why do sulfonamides cause crystaluria?
    • Sulfonamides with HIGH pKa's are basic and would form a sodium salt (amines were unprotected)
    • It would become supersaturated in the bladder
    • And form crystals
  6. What were the ways (chemically and therapeutically) to prevent crystaluria with sulfonamides?
    • Add heterocyclic rings (to lower pKa)
    • Use more than one type of sulfonamide (amt of each would not reach threshold to form crystals)
    • Drink plenty of water
  7. How many active metabolites does Triemthoprim have?
  8. Why is trimethoprim used with sulfamethoxazole? And whats the ratio?
    • Combo is synergistic in vitro
    • less likely to induce bacterial resistance than either alone
    • SMZ/TMP is 1:5
  9. What is the MOA of Trimethoprim?
    • Blocks dihydrofolate reductase (folate reductase inhibitor)
    • SMZ/TMP block 2 steps in folate pathway- sequential blockade
  10. Why is Folic acid important in bacterial growth?
    • Folates are essntial intermediates for synthesis of DNA bases
    • Bacteria synthesize theor own folic acid
    • Microbes CANNOT use dietary folic acid
  11. What is Dapsone?
    • Considered a sulfone
    • Same MOA as sulfonamides
    • Stops proliferation of Mycobacterium leprae---leprosy
  12. What is the MOA of quinolones/fluoroquinolones?
    • Inhibits DNA gyrase--- inhibits DNA synthesis
    • Bacteriocidal
    • Anti-bacterial
  13. The anti-bacterial activity of ofloxacin resides mostly in the ___-isomer which is named ___________________.
    • L
    • Levofloxacin
  14. At which carbo does Ciprofloxacin have a fluorine?
    C-6 position
  15. Why can't milk, antacids, or multivitamins be taken with Cipro?
    The open COOH has a divalent cation reaction with the Ca, Mg, and Fe causing it to become inactive
  16. What is the MOA of Nitrofurantin?
    May inhibit acetlycoenzyme A--- which interferes with bacterial carbohydrate metabolism (cell wall synthesis)
  17. What is the composition and MOA of methenamine?
    • Low polymer of ammonia and formaldehyde
    • Formaldehyde is the active antimicrobial component
  18. What is the MOA of tetracyclines?
    • bacteriostatic
    • Diffuse inside and bind reversibly to 30S subunit
    • Block addition of AA to peptide chain
  19. What is the importance of Tetracyclines being amphoteric?
    • Have 3 pK values
    • C-4 dimethyl amino moiety
    • Form salts with acids or bases (short half life)
  20. Explain the epimerization of tetracyclines?
    • UV light changes to inactive form
    • shortest expiration date
  21. What are the side effects of tetracyclines?
    • GI irritation
    • Deposits in calcified tissue (teeth fluoresence)
    • Dizzieness (vestibular/CNS toxicity)
    • Antianabolic effect
    • Photosensitivity
  22. What is Tygacil's (tigecycline) class?
    • glycylcycline antibacterial (IV)
    • distributes beyond plasma volume and into tissues
    • not extensively metabolized
    • biliary excretion, glucoronidation
  23. How is Clindamyacin & Lincomycin metabolized?
    Liver: N-demethylation
  24. What is special about the Macrolides ring?
    • decorated with sugar (inc. H2O solubility)
    • Lactone- acid sensitive (any acid will cleave ring and become inactiviated)
  25. Macrolides are ___________ antibiotics.
  26. What is the MOA of macrolides?
    • inhibit protein synthesis
    • bind 50S subunit
  27. What is the drug of choice to treat Legionaires disease?
  28. What is Troleandomycin a prodrug for?
    • oleandomycin
    • (similar spectrum to erythro. but less active and freq cross resistant with)
  29. What is the MOA of penicillins?
    • bacteriocidal
    • inhibition of cell wall synthesis
  30. What are bacterial cell walls made of?
    peptidoglycan (murein)--- makes up most of gram (+) walls
  31. Why are penicillins safe to use in humans?
    There is no molecule similar to peptidoglycan in humans thus selective for bacteria
  32. What is the site of action of Beta-Lactams?
    • Tanspeptidase- muramoylpentapeptide carboxypeptidase
    • Antibiotics have structure similar to that of the substrate of the enzyme (D-ala-D-ala)
    • serine residue
  33. What is the site and action of beta-lactamase?
    • the hydrolysis of the beta-lactam ring
    • antibiotic becomes inactive
  34. Why are amoxicillina dn clavulanic acid used synergistically?
    • the clavulanic acid kills the beta-lactamase
    • so beta-lactam can bind to transpeptidase
  35. What are the 3 beta-lactamase inhibitors?
    • clavulanic acid
    • sulbactam
    • tazobactam
  36. What combinations of penicillin are used synergistically? antagonistically?
    • Streptomycin
    • Tetracycline
  37. Under basic conditions what product is formed when penicillin is degraded?
    peniloic acid
  38. Under acidic conditions what products are formed when penicillin is degraded?
    • penaldic acid
    • penicillamine
  39. What is the best of the beta-lactam antiobiotics and beta-lactamase inhibitors?
    Thienamycin & Imipenem
  40. What makes thienamycin different from the beta-lactams?
    the sulfur atom is not apart of the 5 member ring, but has been replaced by a methylene group
  41. Which enzyme deactivates Imipenem? And which drug inhibits this enzyme?
    • renal dehydropeptidase-1
    • Cilistatin
  42. Which monobactam is a totally synthetic antibiotic whose bacterial spectrum is devoted almost exclusively to gram (-)?
  43. What is aztreonam also capable of inactivating?
  44. What makes cephalosporins & aminoglycosides better than penicillins & carbapenems?
    more stable against beta-lactamase
  45. What is the enzymatic hydrolysis & lactonization of natural cephalosporin c?
    • enzyme cleaves lactone
    • internal cyclation
    • creates natural cephalosporin (inactive)
    • considered a pro-drug
  46. What are the differences between the cephalosporin generations?
    • 1st: resemble amox. but greater beta-lactamase resitance
    • 2nd: more gram(-) species
    • 3rd: most active against e. coli, proteus mirabelis, p. aerogenosa
  47. What is the MOA of cephalosporins?
    • bind to penicillin binding protein
    • cell wall synthesis
  48. How are aminoglycosides excreted?
    • glomerular filtration
    • dosage must be adjusted based on CrCl
  49. What is the major adverse effect of aminoglycosides?
    ototoxicity (reversible)
  50. What type of bacteria are aminoglycosides effective on?
    gram (-)
  51. What is the MOA of aminoglycosides?
    • Bind 30S subunit
    • block foramtion initiation complex
    • cause misreading of code
    • inhibits translocation
  52. What is tobramycin most commonly used for?
    • complicated and recurrent UTIs
    • some cross resistance w/ gentamycin (are interchangable)
  53. What is streptomycin most commonly used for?
    • Mycobacterium tuberculosis
    • has some activity against other gram (-)'s but largely replaced by gentamycin
  54. Whats is the mechanism of spetinomycin?
    • binds 30S subunit (inhibits protein synthesis)
    • aminoglycoside-like anitbiotics
  55. What is the MOA of Vancomycin?
    • direct effect on cytoplasmic membrane
    • inhibition if RNA synthesis
    • inhibition of cell wall mucopeptide synthesis
  56. What is the main target of Vancomycin?
    • D-alanyl-D-alanine terminal dipeptide of peptidoglycan precursor
    • binds with substrate, NOT enzyme
  57. What class of antibiotics is Linezolid apart of?
    oxazolidinones (bacteriostatic)
  58. What is the MOA of Linezolid?
    • inhibtion of protein synthesis (bacteriostatic)
    • binds to 30S near 50S interface
    • prevents initiation of protein synthesis
  59. What anitbiotic is the first streptogramin?
  60. What are the components of Synercid?
    quinupristin & dalfopristin
  61. What is the site of action of quinupristin & dalfopristin?
    the bacterial ribosome
  62. What is the MOA of Synercid?
    • irreversibly binds to 50S subunit
    • quinupristin inhibits peptide chain elongation
    • dalfopristin interferes with petidyl transferase
  63. What class of antibiotics is Daptomycin apart of?
    • cyclic lipopeptide
    • limited to gram (+) pathogens
  64. What is the MOA of Daptomycin?
    • disruption of bacterial plasma membrane
    • peptidoglycan synthesis
    • lipoteichoic acid synthesis
    • bacterial membrane potential
    • dose NOT penetrate cytoplasm
    • Concentration dependent bacteriocidal activity
  65. Normal flora of the mouth?
    • viridans strep
    • prevotella
  66. Normal flora of the lower GI tract?
    • enterobacteriacea
    • gram (-) anaerobes
  67. Normal flora of the respiratory mucosa?
    • streptococci
    • haemophilis
    • staph
  68. Normal flora of the skin?
    • staph
    • strep
    • propionbacterium
    • dptheroids
  69. What are segs?
    neutrophils with a segmaneted nucleus (mature WBC)
  70. What are bands?
    immature neutrophils
  71. What is left shift?
    increase in immature WBCs compared to mature
  72. What is leukocytosis?
    increase in WBC (neutrophils)
  73. What is neutropenia?
    severe decrease in neutrophil count
  74. What is an antibiogram?
    a compilation of organisms isolated in cultures in a specific place/region and the sensitivity profile of these organisms
  75. What is the equation to convert F to C?
    (°F - 32) x 5/9 = °C
  76. What is the equation to convert C to F?
    °C x 9/5 + 32 = °F
Card Set
PT Infectious Disease: Exam 1
Spring 2012 PT Module IV- ID Exam 1