Pharmacology Penicillins 1

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Pharmacology Penicillins 1
2014-01-22 09:50:51
Pharmacology Penicillins
Pharmacology Penicillins 1
Pharmacology Penicillins 1
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  1. What is an antimicrobial agent?
    Chemotherapy against invading organisms
  2. What is the difference between an antibiotic and an antimicrobial?
    Antibiotics: Natural Antimicrobials: Natural and synthetic
  3. What is the main difference between microbial and mammalian cell walls?
    Presence of cell wall in microbe
  4. What color will a G- cell be?
  5. What color will a G+ cell be?
  6. Is the peptidoglycan layer for G- cells thicker or thinner than a G+?
  7. Which has an outer membrane, G+ or G-?
  8. What are the major MOAs for antibiotics?
    Inhibit cell wall, cell membrane, protein or nucleic acid synthesis, anti-metabolite (anti-growth)
  9. What is the difference between bactericidal and BacterioSTATIC?
    BacterioSTATIC: inhibiting growth Bactericidal: Kills bacteria
  10. If an antibiotic is bacteriostatic against an bacteria, can you assume it will be bacteriostatic against another bacteria?
    No, an antimicrobial can be be -cidal or static based on environmental factors and the organism it is trying to kill
  11. What factors effect whether an organism is bacteriostatic or cidal under a given situation?
    The organism it is working against and the concentration
  12. What group would you not use a bacteriostatic antimicrobial in and why?
    Immunosuppressed, because a bacteriostatic antibiotic inhibits growth, but depends on the immune system to clear the infection
  13. What are common MOA's for Bacteriostatic antimicrobials?
    Protein and folic acid inhibitors (anti-metabolites)
  14. Are aminoglycosides usually bacteriostatic or cidal?
  15. What are the MOAs of most bactericidal drugs?
    Target cell wall, cell membrane and nucleic acid synthesis
  16. What are common reasons for using bacteriostatic drugs?
    Immunocomprimised patient or endovascular infections
  17. Bactericidal classification may be dependent on what factor?
    Concentration of the drug and the bacteria type
  18. What is the post antibiotic effect (PAE)?
    When the drug conc. drops below the effective level, but the antibiotic still has an effect
  19. What two types of drugs have post antibiotic effects?
    Aminoglycosides and quinolones
  20. Are Penicillin G and V broad or narrow spectrum?
  21. Is tetracycline a broad or narrow spectrum antibiotic?
  22. What is a common MOA for broad spectrum antibiotics?
    Protein synthesis inhibitors
  23. In general why would you want to use a narrow spectrum antibiotic?
    To reduce superinfections and to maintain natural flora
  24. How is a superinfection treated?
    1.) Stop antimicrobial therapy 2.) Identify pathogen 3.) Use narrow spectrum antibiotic to treat it
  25. How is an organism identified?
    Sampling, gram stain, culture growth, PCR and antigen testing
  26. Ideally, should you identify the pathogen or start the therapy first?
    Identify the pathogen
  27. After a pathogen is identified, what should be done before selecting and antibiotic?
    Test drug sensitivity, identify host factors
  28. What are important host factors used to evaluate the choice of antibiotic?
    Site of infections, status of host and host's immune system, age, pregnancy, liver, renal, metabolism of drugs, genetic factors and hypersensitivity
  29. When would you use antimicrobials prophylactically?
    Surgery, endocarditis, neutropenia/immunocomprimised, recurrent UTIs and HIV, TB or sexually transmitted diseases
  30. Without a pathogen identified, what can you base your choice of antibiotic on?
    Site of infection, symptoms and immediate lab results (called Empiric therapy)
  31. What is a Definitive therapy?
    One using the knowledge of pathogen identity
  32. What does MIC stand for?
    Minimal inhibitory concentration
  33. (True/False) In some instances the MIC is exceeded by 8 to 10 fold. Why or why not?
    True, in certain tissues this can occur depending on the permeability, etc.
  34. If you have a low MIC, is the pathogen sensitive or resistant?
  35. If you have a high MIC, is the pathogen sensitive or resistant?
  36. What are the indications for a combination therapy of antibiotics?
    Empiric therapy for serious infections, mixed bacterial infection, reduce toxicity of drug, prevent other strains and to enhance drug activity
  37. What does it mean for an antibiotic to have additive effects?
    Treatment with 2 drugs for 2 infecting microbes
  38. What does it mean for an antibiotic to have synergistic (potentiative) effects?
    Combination therapy enhances the effects of the drugs to a greater potential than if used alone
  39. What type of interaction do trimethoprim and sulfamethoxazole have when given in combination?
  40. What type of interaction do penicillin and aminoglycosides have when given in combination?
  41. What does it mean for an antibiotic to have antagonistic effects?
    Combination therapy causes reduced effect of one or both drugs
  42. What type of interaction do bacteriostatic and bactericidal antibiotics have when given in combination?
  43. What type of interaction do imipenem and piperacillin have when given in combination and why?
    Antagonistic, cause induction of enzyme interaction causing the enzyme to degrade the second drug
  44. What part of penicillin is attacked by beta-lactamases?
    The (0=C)-N bond in the beta lactam ring XXXXXXXXX
  45. What does the cell mistake a penicillin for?
    Two Alanines (the two rings) attached together
  46. What is the MOA of B-lactam antibiotics?
    B-lactam ring weakens the cell wall by binding to penicillin-binding protein such as transpeptidases and autolysins
  47. What is the action of transpeptidases?
    Main: Enzymes that form cross-linking or cell wall Other: contribute to cell lysis or change in cell function or morphology and some have no effect
  48. What is the action of Autolysins and how do B-lactams effect them?
    Promote the active destruction of the cell wall and are induced by B-lactams
  49. What are the three major stages of bacterial cell wall synthesis?
    1.) Monomer synthesis 2.) glycan polymerization 3.) Polymer cross-linking by transpeptidase
  50. When cross-linking of the bacterial cell wall occurs, what happens?
    The alanine-alanine is bound to the glycine of another molecule and one alanine is removed
  51. In what ways can inactive PBPs cause resistance to develop?
    The cell can throw out lots of inactive/no-function PBPs to work as decoys and "mop" up all the penicillin
  52. How can penicillin resistance occur?
    Failure to reach PBPs, inability to bind PBPs, B-lactimase excretion
  53. Are penicillins good empiric therapy choices?
  54. What are the most common organism that produce B-lactamases?
    Staph aureus, Neiserria gonorrheae, Pseudomonas auruginosa
  55. What are the classifications of Penicillin?
    Natural penicillins, Penicillinase-resistant, Aminopenicillins, Antipseudomonal penicillins
  56. Which classes of penicillins are broad spectrum?
    Aminopenicillins and Antipseudomonal penicillins
  57. Is MRSA susceptible to Penicillinase-resistant penicillins?
    No, this group contains Methicillin
  58. What are the narrow spectrum classes of penicillins?
    Natural and Penicillinase-resistant penicillins
  59. Which class of Penicillins are antistaphylococcal?
    Only penicillinase-resistant penicillins