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Antibiotics - pharmacology 2

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  1. 1What is chemotherapy?Treatment of infectious with specific chemical agents
  2. 2What is an antibiotic (old definition)?Substances produced by microorganism which suppresses growth of other organisms (fleming definition)
  3. 3What is an antibiotic (new definition)?Synthetic compounds which are not produced by bacteria which antibacterial activity
  4. 4An ideal chemotherapeutic agent has selective toxicity/ meaning?inhibits/ destroys pathogen without harming the host
  5. 5How can a chemotherapeutic agent be selectivity toxicThey target something unique to the microbe, like cell walls
  6. 6What is the difference between bactericidal and bacteriostatic?Bacteriocidal means to kill the pathogen
    Bacteriostatic means to inhibit growth
  7. 7Which is preferable bacteriocidal vs bacteriostaticbacteriocidal
  8. 8Why are bacteriocidal preferred with a patient with compromised immune systems?bacteriostatic relies on host defense mechanism for final eradication
  9. 9Which antibiotics uses its ability to punch holes in the plasma membrane to kill pathogens? why is used topically vs parenteral?Polymyxin; it harms host cells
  10. 10What should be limited in chemotherapeutic agents?resistance
  11. 11What is the ideal spectrum of chemotherapeutic agentsbroad spectrum
  12. 12What is a narrow spectrum? example?Gm+, Gm - or just specific group
    Isoniazid against Mycobacterium
    Nafcillin against Gm+ staph
  13. 13What is extended spectrum? Example?Gm+ and same Gm- like ampicillin
  14. 14Describe broad spectrum. ExamplesGm+ and Gm-, Tetracycline, chloramphenicol, imipenem
  15. 15What is wrong with overuse of broad spectrum? Which drug is reversed to reduce this effect?More resistance; Imipenem
  16. 16What type of effects do we avoid in chemotherapeutic agents?allergenic/ adverse/ toxic affects
  17. 17What should an ideal chemotherapeutic agent be able to do?Penetrate sites of infection, be stable and active in the presence of plasma, body fluids or exudates
  18. 18What practical things should an ideal chemotherapeutic agent be?Available and cost-effective
  19. 19What makes a drug more expensivename brand vs generic
    frequency of administration
    multiple drugs
    IV vs IM/ oral (least expensive)
  20. 20What are often the cause of hospital-acquired infections (nosocomial) like UTIs and PNA?Gm - pathogens
  21. 21What is the first mechanism of action for an antibacterial? examplesinhibit synthesis of cell wall (penicillin, cephalosporin, Vancomycin, and bacitracin)
  22. 22What is the second mechanism of action for an antibacterial? ExamplesAfter cell permeability --> leakage of intracellular components (polymyxin)
  23. 23What is the third mechanism of action for an antibacterial?inhibition of bacterial protein synthesis by affecting the function of 30S and 50S ribosome
  24. 24Which antibiotics effect 50S subunitChloramphenicol, macrolides, clindamycin, quinupristine, linezolid
  25. 25Which antibacterial affect 30 S ribosomal?aminoglycosides, tetracycline
  26. 26What is the fourth mechanism of actions for an antibacterial?Inhibit nucleic acid synthesis
  27. 27Which antibiotics inhibit nucleic acid synthesis by targeting DNA gyrase (topoisomerase)?Fluoroquinolenes (ciprofloxacin & levofloxacin)
  28. 28What is another way antibiotics can inhibit nucleic acid synthesis?Inhibiting DNA dependent RNA polymerase
  29. 29What is the fifth (last) mechanism of action for an antibiotic?Mechanism analogs that block metabolic steps
  30. 30What do trimethoprim & sulfonamides block?Enzymes involved in folic acid synthesis
  31. 31What does Isoniazid block in mycobacterial cell walls?synthesis of mycolic acids
  32. 32What type of therapy is used when the identity of the microbe is unknown?Empirical
  33. 33What would you use empirical therapy initially?infection is life threatening
  34. 34What does a patient normally receive with empirical therapy?Broad spectrum abx or a combo of antibiotics
  35. 35What are clues that can be used for the "best guess therapy" empirical?-Gram stain results
    -the site of infection (certain microorganisms tend to cause infection at specific sites)
    -clinical experience
    - antibiogram susceptibility reports (history of what has worked in the past)
  36. 36Once susceptibility tests are performed and the causative organism has been identified empirical therapy should?be changed to rational (narrow spectrum) therapy
  37. 37What is rational therapy based off of?Susceptibility of patients bacterial isolate to various abx is preformed
  38. 38In rational therapy, what is the Kirby bauer disc diffusion test?Antibiotic paper discs placed on agar plate with isolates bacteria to test growth inhibition to measure susceptibility
  39. 39What are the three types of results? What does sensitivity to antibiotic look like>susceptibility, intermediate suspectibility& resistance; large zone of inhibition
  40. 40What are upsides and downsides to abx?simple and inexpensive; indiscrepancies between labs and concentration of Abc may be lower in vivo (failure due to lack of access)
  41. 41What is the minimum inhibitory concentration?The minimal concentration needed to prevent visible growth (bacteriostatic)
  42. 42Describe the test looks like and what does the first "clear vial" meanPlacing the microbe in vials with increased concentrations of antibiotics; the first clear vial determines the smallest dose that causes inhibition
  43. 43What is minimum bactericidal concentration?The minimum concentration of Abx needed to kill the bacteria
  44. 44Describe process of MBC, what is the first clear space determineTake an aliquot of clear MICs and plate it out on agar plate to see which grows, the first clear spot indicates the lowest concentration needed for a killing effect
  45. 45When is MBC most important?For patient with immunosuppression
  46. 46Describe the epsilometer (E) test. What does it determine?A plastic trip containing a gradient of known antibiotics concentrations is placed on top of agar plate with microbe; determines MIC
  47. 47What do serum inhibitory and bactericidal titers determine?Antimicrobial activity in vivo, the greatest dilution of the patient's serum that determines patient serum
  48. 48What is the recommended dosage of drug concentration at the infected site?At least MIC but more advisable for ~ 2-4 times the MIC
  49. 49Why must abscesses be drained prior to treatment?Abx have a hard time penetrating the abscess bc of limited blood supply
  50. 50The blood-brain barrier is difficult to penetrate and may prevent penetration of the drug into the cerebral spinal fluid, what happens during infection?BBB is diminished bc tight junctions of capillaries open up causing increased penetration of drug
  51. 51What does the antibiotic do that prevents it from entering the site of infectionIt binds to plasma proteins which decreases its levels of free drug
  52. 52Does need to adjusted for patients with renal therapeutic failure includingnewborns
  53. 53What threatens future use of antibiotics? What can prevent it?Drug resistance; controlling overuse of antibiotics
  54. 54Giving an antibiotics to treat a viral infection is called? What does it encourage?Indiscriminate (misuse) of abx; resistance
  55. 55Why does a delay in optimal therapy encourage resistance?Slow growing bacteria may not be as susceptible to abx
  56. 56What kind of dose encourage encourages resistance?Suboptimal dose
  57. 57What time of growth cycle is a bad time to dose with abx?Dormant stage
  58. 58If antibiotics cannot reach the site of infectionit encourages resistance
  59. 59What can cause incomplete clearance of the pathogendysfunctional immune system
  60. 60What outside the medical community causes abx resistance?Abx in livestock animals
  61. 61Antibiotics can serve as a selective agent for?random mutations that can be passed onto daughter cells and provide resistance to drug
  62. 62What are three examples of horizontal genetic exchangetransformation, transduction and conjugation
  63. 63What is transductionBacteriophage (virus) to bacteria by carrying DNA on its protein coat
  64. 64What is transformation?Free DNA taken up by bacteria into genome
  65. 65What is conjugation?Gene pass from cell to cell by direct contact of sex pilus
  66. 66What two sets of genes are commonly transferred by plasmids in conjugation? What are they together?DNA for drug resistance (R-determinant)
    + bacterial conjugation gene (resistance transfer factor) = R factor
  67. 67R factor can contain resistance to multiple antibiotics which groups are more common to have thisGm-, hospital derived and intestinal bacteria
  68. 68What are transposonsDNA sequences that can jump from place to place plasmid or chromosome
  69. 69What are the three basic mechanisms to drug resistance?- drug does not reach target
    - drug is not active
    - drug target is altered
  70. 70If an organism changes its membrane permeability it can?Cause resistance because small hydrophilic drugs cannot cross to affect it, so drug cannot reach target
  71. 71Which enzyme available in Gm+ and Gm- can inactivate antibiotics? How?B-lactamases open up the B-lactam ring on Abx and inactive abx
  72. 72Gm- drugs that can acetylate, phosphorylate, adenylate the drug have resistance toAminoglycoside abx
  73. 73What are examples of alterations to drug sites?- mutations in DNA gyrase
    - penicillin-binding protein with affinity for the drug
  74. 74What can healthcare professionals do to prevent the development of resistance?- wash hands between patient visits
    - don't exceed pt's demand for abx
    - when possible prescribe narrow spectrum
    -isolate pt's with multidrug resistant infections
    - be familiar with resistance data
  75. 75What can patients do to prevent the development of resistant microorganisms?- do not demand abx
    - complete Rx and do not save for for future use
    - wash fruit and veggies, avoid raw eggs and meats
    - use soap products with antibacterial chemical more sparingly
  76. 76What is the goal of combined antibiotics therapyto provide coverage of all organism most likely to be involved
  77. 77Synergism decreases what?MIC and MBC
  78. 78What are the three types of antibiotics synergism?Blocking sequential steps in a metabolism pathway
    inhibiting the enzymatic inactivation of abx
    enhancing abx uptake by bacteria
  79. 79What two drugs antagonize each otherBacteriostatic agent will antagonize the bactericidal agent bc bactericidal needs actively growing organisms
  80. 80If you pair a drug that induces beta-lactamases but is resistant to break down with drug that is sensitive to beta lactamases youinactivate it

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Der Nutzer hat seine Fachbereichs-Information gelöscht. Karteikarten am Antibiotics - pharmacology 2 , erstellt von Gelöschter Nutzer am 22/10/2017.
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  • Erstellt von Jen Orellana · 22 Okt 2017
  • Kopiert von Jen Orellana · 22 Okt 2017
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