Micro, Ass 3, Renee’s Questions – Flashcards
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| 1. What is a broad spectrum antibiotic? |
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| 1. one the is active against several types of microoorganisms |
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| 2. What is an antibiotic that is active against one or a very few types or microorganisms? |
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| 2. Narrow spectrum |
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| 3. What type of antibiotic inhibits bacterial growth but does not kill? |
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| 3. Bacteriostatic |
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| 4. When bacteriostatic drugs are withdrawn can bacteria continue to grow? |
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| 4. yes |
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| 5. How do most bacteriostatic drugs inhibit growth? |
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| 5. inhibit protein synthesis |
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| 6. What type of antibiotic kills bacteria? |
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| 6. Bactericidal |
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| 7. Why are bactericidal drug actions inhibited by a –static drug? |
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| 7. requires bacterial growth in order to impair |
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| 8. What are some advantages to –cidal drugs? |
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| 8. Reduces the number of bugs, more rapid, irreversible damage to bugs |
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| 9. What is a disadvantages of –cidal drugs? |
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| 9. cytotoxic storm |
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| 10. What do –static drugs prevent that give them an advantage? |
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| 10. inhibition of bacterial toxins and inflammatory mediators |
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| 11. T/F Two static drugs can be used in combination to kill a pathogen. |
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| 11. T – if mechanism is in different part or completely different pathways |
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| 12. T/F The same antibiotic may be cidal or static against different bacteria. |
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| 12. T – Ex. Penicillin – cidal a pneumococci, static a enterococci |
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| 13. What is the lowest concentration of drug that inhibits the growth of the organism called? |
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| 13. Minimal Inhibitory Concentration (MIC) |
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| 14. What are the 2 options for MIC testing? |
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| 14. Turbidity and Viability |
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| 15. How is Turbidity used to determine the MIC? |
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| 15. Determined by growing organism in tubes then adding various concentrations of drugs, lowest concentration tube where broth is clear. |
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| 16. How is Viability used to determine the MIC? |
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| 16. Preinoculate blood agar plate then place antibiotic discs, allow to grow then determine zone of inhibition, diameter is compared to standards to determine sensitivity of the organism to that drug. |
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| 17. What is the Minimal Bactericidal Concentration (MBC)? |
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| 17. Concentration of drug that actually kills the organism rather than the concentration that merely inhibits growth |
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| 18. How is the MBC determined? |
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| 18. transfer clear broth tube to blood agar plate, MBC is the plate without growth |
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| 19. What type of drugs have an MBC equal or very similar to the MIC? |
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| 19. Bacteriocidal |
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| 20. What is the relationship of MBC to MIC in Bacteriostatic drugs? |
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| 20. The MBC is significantly higher than MIC |
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| 21. T/F MIC and MBC concentrations can be used to compare effectiveness of an antibiotic. |
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| 21. F – Effectiveness is based on how much of the drug you can actually administer to the patient |
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| 22. What 5 differences can antibiotics target in bacterial cells? |
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| 22. Cell wall synthesis, Cell membrane, DNA replication + Nucleotide Biosynthesis, Topoisomerases, Protein Synthesis |
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| 23. What type of antibiotics target the crosslinking in bacterial cell walls? |
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| 23. Penicillin, Cephalosporins, Carbapenems, Monobactams |
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| 24. What do Peptide antibiotics target? what are 2 examples? |
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| 24. Cell membrane; Polymyxins, Daptomycin |
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| 25. What drugs target DNA replication and Nucleotide Biosynthesis? |
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| 25. Metronidazole, Sulfonamides, TMP-SMX |
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| 26. What do Quinolones target? |
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| 26. Topoisomerase |
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| 27. What drug targets DNA-directed RNA polymerase? |
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| 27. Rifampin |
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| 28. What causes an overgrowth of drug resistant strains of Clostridium difficile? What is this called? |
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| 28. complication of antibiotics due to suppression of the normal flora of the bowel; Pseudomembranous Colitis |
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| 29. What are the normal cell wall hydrolyzing enzymes? |
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| 29. autolysins |
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| 30. How do autolysins participate in killing the cell when peptidoglycan synthesis is inhibited? |
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| 30. autolysins activity continues without a new unit to insert and cell will eventually lyse in hypotonic environment. |
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| 31. What type of enzyme is Penicillin Binding Proteins? |
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| 31. transpeptidase |
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| 32. What does transpeptidase do? |
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| 32. catalyzes the final crosslinking step in the synthesis of peptidoglycan |
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| 33. What does Penicillin do? |
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| 33. Irreversibly binds at the active site of the transpeptidase enzyme that cross-links the peptidoglycan strands. inhibiting cross-linking |
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| 34. What are 3 ways resistance may develop? |
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| 34. 1. Production of penicillinases or ?-lactamases; 2. Mutated PBP, so penicillin can’t bind 3. develop tolerance – inactivation of autolysin |
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| 35. What are ?-lactam antibiotics structural analogs of? |
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| 35. D-Ala-D-Ala end of peptidoglycan pentapeptide |
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| 36. What are 4 problems with Penicillin G? |
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| 36. 1. Hydrolysis by gastric acid; 2. Penicillinase sensitivity; 3. Allergic response; 4. Ineffective against gram neg. enterics |
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| 37. What is the breakdown product of penicillin that can be used to elicit different drug properties? |
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| 37. 6 aminopenicillanic acid (6-APA) |
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| 38. Which Penicillin has the highest activity against G+ cocci and bacilli? |
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| 38. Narrow spectrum penicillins |
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| 39. What are examples of Narrow spectrum penicillins? |
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| 39. G and V |
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| 40. What are Broader Spectrum Penicillins affective against? |
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| 40. G+ and G- enteric bacilli |
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| 41. What are some examples of Broader Spectrum Penicillins? |
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| 41. Ampicillin, Amoxicillin, Cyclacillin, Carbenicillin, Ticarcillin. |
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| 42. What drugs are considered the Antistaphylocococcal Penicillins? Examples? |
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| 42. Narrow Spectrum/Penicillinase Resistant Drugs; Methacillin, Nafcillin, Oxacillin, closacillin, dicloxacillin |
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| 43. What drug has a similar structure and mechanism of action identical to penicillin? |
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| 43. Cephalosporins |
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| 44. How do cephalosporins differ from penicillins? |
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| 44. acid stability, penicillinase resistance, antigenically dissimilar |
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| 45. What is the progression of 1st to 4th generation cephalosporins? |
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| 45. broadening in G- susceptibility; diminution of activity against G+; increased ?-lactamase resistance; increased capability to enter CSF |
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| 46. What oral cephalosporin is affective against Gram + cocci (staph & strep)? |
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| 46. Cephalexin (Keflex) |
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| 47. What has rendered many 2nd and 3rd generation cephalosporins inaffective? |
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| 47. Extended Spectrum ?-Lactamases |
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| 48. What type of antibiotic crosses the blood brain barrier and is effective against Enteric G- bacteria? |
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| 48. 3rd Generation – Ceftriaxone |
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| 49. What antibiotic is effective against E. Coli? |
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| 49. 4th Generation – Cefepime |
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| 50. What in Carbapenems allows movement through the outer membrane of G- bacteria? |
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| 50. small hydroxyethyl side chain |
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| 51. What is the structure of the Carbapenems? |
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| 51. ?-lactam ring attached to five-membered cyclic ring with carbon |
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| 52. What are Carbapenems highly resistant to? |
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| 52. ?-lactamases |
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| 53. What are 3 examples of Carbapenemases? |
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| 53. KPC, OXA, Metallo-?-lactamases |
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| 54. How do the carbapenems create Resistance? |
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| 54. altered porin channes decreasing permeability |
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| 55. What type of antibiotic can be used in penicillin allergic patients? |
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| 55. Monobactams |
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| 56. What is the drug of choice for MRSA? |
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| 56. Vancomycin |
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| 57. What was the first strain to show resistance to Vancomycin? |
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| 57. Enterococcus faecalis |
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| 58. What is Vancomycin restricted to? |
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| 58. Gram + organisms |
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| 59. What kind of antibiotic is Streptomycin and what kind of action does it have? |
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| 59. aminoglycoside antibiotic, Bactericidal |
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| 60. What is an Aminoglycosides? |
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| 60. aminosugars linked by a glycosidic bond to an aminocyclitol |
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| 61. What kind of damage can Amionoglycosides cause to the human body? |
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| 61. Kidney and/or 8th cranial nerve damage |
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| 62. How do Aminoglycosides produce a –cidal mechanism? |
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| 62. 1. few streptomycin molecules enter the cell through imperfections in the growing membrane; 2. Binds to 30S ribosomal protein, distorts and causes misreading; 3. Misreading causes “bad” proteins to be made, more membrane leakiness, more streptomycin enters; |
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| 63. How does Daptomycin (peptide antibiotic) target bacteria? |
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| 63. Cell membrane |
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| 64. How does it irreversibly bind to the bacterial cell membrane? |
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| 64. calcium-dependent membrane insertion of molecule |
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| 65. What is the mechanism of action of Daptomycin? |
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| 65. Irreversibly binds to bacterial cell membrane, rapidly depolarizes the cell membrane, Efflux of K+, Cell death by multiple failures in biosystems. |
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| 66. What is Daptomycin active against? |
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| 66. G+ infections; MRSA, VRE, S. pyogenes |
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| 67. T/F Resistance to Daptomycin is rare. |
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| 67. T |
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| 68. In the Lungs, what does Daptomycin bind avidly with making it ineffective against pneumonia? |
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| 68. Pulmonary Surfactant |
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| 69. What is an example of an antibiotic that has Nucleotide Biosynthesis activity? |
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| 69. Sulfonamide |
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| 70. What is the mechanism of action of sulfonamide? |
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| 70. Blocks dihydropteroate synthetase; |
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| 71. At what point in the synthesis of folic acid synthesis does trimethoprim inhibit? |
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| 71. dihydrofolate reductase; DHF –Xa THF |
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| 72. How can bacteria become resistant to Trimethoprim? |
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| 72. mutations in DHFR |
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| 73. How does resistance develop to Sulfonamides? |
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| 73. slowly and stepwise |
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| 74. What does the mixture of Trimethoprim-Sulfamethoxazole have activity against? |
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| 74. broad spectrum activity against aerobic bacteria and pheumocystis |
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| 75. What is a way that bacteria can thymidine to get around the inhibition of folic acid? |
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| 75. from DNA released from dead cells in the pus of a cyst or abscess |
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| 76. What Bacterial enzymes are a target for quinolones? |
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| 76. DNA gyrase, Topoisomerase IV |
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| 77. What Quinolone is most active against Gram – aerobic bacteria? |
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| 77. Ciprofloxacin |
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| 78. What spectrum or bacteria are Quinolones active against? |
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| 78. G- aerobic, G- enteric rods or cocci, G+ and anaerobic |
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| 79. How can drugs be used to attenuate protein synthesis in Bacteria while not affecting us? |
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| 79. Bacteria have 70S R with 30S and 50S subunits, while we have 80S R with 40S and 60 S subunits |
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| 80. What drugs are active against 30S? |
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| 80. Aminoglycosides, Tetracyclins |
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| 81. What does Neosporin contain? |
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| 81. Polymyxin B Sulfate (Gram – rods, alters cell membranes), Bacitracin Zinc (Gram+), Neomycin Sulfate (broad spectrum) |
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| 82. What is the Mechanism of Tetracycline? |
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| 82. Inhibition of protein synthesis by binding 30S ribosome, block acceptor site, inhibiting aminoacyl-tRNA binding. |
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| 83. What is Tetracyclin active against? |
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| 83. gram + and gram - |
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| 84. Why should Tetracyclin be avoided during the latter half of pregnancy and in children under 8 years? |
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| 84. can cause permanent discoloration of the teeth and enamel |
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| 85. What is a side effect of Chloramphenicol? |
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| 85. penetrates human mitochondreia and inhibits mitochondrial protein synthesis, causing bone marrow depression |
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| 86. What is a type of Macrolide Antibiotic? |
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| 86. Erythromycin |
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| 87. How do Macrolides terminate the peptide linking? |
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| 87. binds reversibly at 2 sites on the 50S ribosome causing dissociation of the tRNA |
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| 88. Which drug is one of the least toxic drugs? |
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| 88. Erythromycin |
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| 89. What drug was the first ketolide antibiotic and is active against most respiratory tract pathogens? |
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| 89. Telithromycin |
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| 90. What is a serious side effect of clindamycin? |
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| 90. pseudomembranous colitis |
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| 91. What antibiotic is active against Vancomycin-resistant enterococci and MRSA? |
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| 91. Quinupristin/Dalfopristin (Synercid) |
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| 92. What are 5 ways to reduce antimicrobial resistance to antibiotics? |
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| 92. 1. Rapid diagnosis to reduce inappropriate use |
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| 93. What is Innate resistance? |
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| 93. a trait of bacterial species that was present before the introduction of antimicrobial agents |
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| 94. What is Acquired (Emergent) resistance? |
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| 94. antimicrobial agent USE-DRIVEN selection and accumulation of resistant bacterial strains |
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| 95. What are 2 origins of acquired resistance? |
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| 95. New Single Mutation, Acquisition of DNA from other bacteria (Horizontal Gene Transfer) |
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| 96. T/F Once resistant strains of bacteria are present in a population, exposure to antimicrobial drugs favors their survival. |
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| 96. T |
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| 97. What are the 5 principles of Antimicrobial Resistance? |
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| 97. 1. Resistance is likely to emerge |
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| 98. Can integrons contain simultaneous resistance to several classes of antibiotics? |
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| 98. Yes |
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| 99. T/F the use of one antibiotic can activate the expression of a whole gene cassette. |
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| 99. T |
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| 100. How does antibiotic selective pressure create resistance? |
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| 100. Cells that have an integron for resistance of a particular antibiotic will survive. Removal of that antibiotic can cause the integron to be lost because its not necessary. |
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| 101. What is an example of an enzyme used by bacteria for drug inactivation? |
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| 101. ?-lactamases |
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| 102. How do altered porins in G- bacteria create resistance? |
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| 102. decreased access to target |
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| 103. How do altered PBP’s create resistance? |
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| 103. Penicillin cannot bind to the cell’s altered PBP’s allowing cross-linking to occur. |
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| 104. What other proteins can be involved in bacterial resistance to drugs? |
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| 104. Outer membrane Proteins (OMP); Porins; PBP |
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| 105. T/F Virtually all G- express a gene for a ?-lactamase. |
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| 105. T – occurs at least in low levels in the periplasmic space |
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| 106. What is the mechanism that bacteria use for tetracycline resistance? |
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| 106. altered Efflux pumps, protection of ribosomal target sites |
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| 107. T/F Penicillin resistance due to ?-lactamase production occurs in S. pneumonia |
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| 107. F |
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| 108. What do ?-lactamases target? |
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| 108. penicillins and cephalosporins |
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| 109. What will bind to ?-lactamases to inhibit them? |
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| 109. Clauvanic Acid and Sulbactam |
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| 110. What are persisters? What protects them? |
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| 110. small number of dormant survivor bacterial without antibioticresistance mechanism; Biofilms |
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| 111. T/F You intend on being attacked by an Octopus after Assessment 3. |
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| 111. T – Great I’ll help you defend it |
