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  1. What is it called when antimicrobials target specific structures, pathways and processes?
    Selective toxicity
  2. Chemicals that affect physiology in any manner
  3. Drugs that act against diseases
    chemotherapeutic agent
  4. Magic bullets
    • Paul Ehrlich
    • antimicrobial agents that would bind to receptors on germs to kills them, but ignore host cells that didn't have that receptor
  5. antimicrobial agents that are produced naturally by an organism
    • antibiotics
    • Penicillin
  6. antimicrobials produced by altering the chemical structure of antibiotics
    semi synthetics

    • more effective
    • longer lasting
    • easier to administer
  7. antimicrobials that are completely synthesized in the laboratory
  8. 6 ways antimicrobial drugs affect growth of pathogens
    inhibit cell wall synthesis

    • inhibit protein synthesis
    • disrupt components of cytoplasmic membrane

    inhibit metabolic pathways not used by humans

    inhibit nucleic acid synthesis

    block pathogen's recognition of attachment to host
  9. what is the limitation of an antimicrobial that inhibits cell wall synthesis?
    • only effective on growing/reproducing cells
    • need to prolong treatment so it kills all cells as they go through their reproduction cycle
  10. What process is inhibited when antimicrobials target protein synthesis?  What cell structure?
    • translation
    • targets differences between prokaryotic and eukaryotic ribosomes
  11. which antimicrobial mechanism is best for fungal infections?  how does it work?
    • disrupting components of cytoplasmic membrane
    • attaches to ergosterol in fungal membranes (cholesterol is similar but it doesn't bind as well)
  12. how do antimicrobials disrupt translation?
    • block tRNA docking site
    • change shape of subunit
  13. how do antisense nucleic acids play a part in antimicrobials?
    single-stranded DNA that is designed to be complementary to specific RNA molecules of pathogen, block ribosomal subunits
  14. what method is sometimes used to slow cancer growth or viruses?
    • inhibiting nucleic acid synthesis
    • blocks reverse transcriptase
  15. why aren't antibiotics effective against viruses?
    antibiotics target structures/processes characteristic to bacteria.  the structure of a virus is too different and is not effected.
  16. 6 characteristics of ideal antimicrobial agent?
    • readily available
    • inexpensive
    • chemically stable
    • easily administered
    • nontoxic and nonallergenic
    • selectively toxic against wide range of pathogens
  17. what characteristics do doctors look for in antimicrobials (since ideal doesn't exist)?
    • spectrum of action (range of pathogens it can fight)
    • efficacy
    • routes of administration
    • overall safety
    • side effects
  18. antimicrobial agents that fight few organisms
    • narrow-spectrum drugs
    • penicillin
  19. drug that's effective against many organisms
    • broad-spectrum
    • tetracycline
  20. what is a drawback to broad spectrum drugs?
    • may also kill normal flora in the body, reducing microbial antagonism
    • won't be able to fight off bad stuff
  21. Define microbial antagonism
    • competition between normal microbes and pathogens for nutrients/space 
    • reinforces body' defenses because it limits pathogens and growth of normal flora
  22. what is the difference between a secondary infection and super infection?
    • secondary: a second infection takes advantage of weakened immune system
    • Super infection: an infection following a previous infection, especially when caused by microorganisms that have become resistant to the antibiotics used earlier
    •    -normal bacteria grows unchecked because regulatory microbes are affected by the drug
  23. what is the diffusion susceptibility test?
    • kirby-bauer test
    • make bacterial lawn
    • different concentrations of antibiotics form "zones of inhibition"
  24. once you have determined the zones of inhibition in the kirby-bauer test, what test do you need to do next?
    • minimal bactericidial concentration
    • find lower possible does of drug to give that is still effective
    • must find does that allows no growth to occur
  25. bactericidal v. bacteriostatic
    kills bacteria v. inhibits
  26. advantage of topical/local administration
    • good for external infections
    • doesn't treat internally
  27. advantages of oral administration 
    • pros: easy, no needles, self administered
    • cons: low concentration levels
    • patient may not follow provider's directions
  28. advantages and disadvantages of intramuscular administration
    • Pro: allows drug to diffuse slowly
    • con: not as high drug concentration as IV
  29. advantages and disadvantages of intravenous administration
    • pro: very high concentration levels, drug goes directly to bloodstream
    • con: amount of drug can drop rapidly as it is removed by liver/kidneys
    • -requires constant readministration
  30. three main categories of side effects of antimicrobial therapy
    • toxicity
    • allergies
    • disruption of normal microbes
  31. how is resistance acquired?
    • new mutations of genes
    • acquisition of resistant genes through transformation, transduction and conjugation
  32. how do populations of resistant microbes arise?
    bacterial cells may have resistance due to gene mutation, but are in the minority and don't reproduce as efficiently as normal cells.  when antibiotics kill off the normal cells, the resistant ones survive to reproduce and pass on their resistance and are now in the majority.  Doesn't produce resistance, just amplifies what was already there.
  33. why do resistant strains of bacteria more often develop in hospitals and nursing homes?
    because there are so many antimicrobial drugs being used that resistant cells are more likely to survive and reproduce
  34. 6 ways microorganisms may be resistant to antimicrobial drugs
    • 1.  slow or prevent entry into cell
    • 2.  alter receptor of drug so it can't bind
    • 3. alter metabolic chemistry (i.e. abandon that part of its metabolic pathway)
    • 4. produce enzyme that destroys/deactivates drug
    • 5.  pump drug out before it can act
    • 6. mutate own DNA so it can't bind
  35. what is it called when a bacterial cell pumps out the antibiotic before it can work, preventing a concentration from building up?
  36. 3 ways genes for drug resistance are spread between bacteria
    • 1.  Transformation
    • 2. Transduction
    • 3. Conjugation
  37. free floating DNA is picked up by another cell
  38. virus infects bacteria, incorporates resistant DNA into its own genome and passes it along when it infects the next bacteria
  39. resistant DNA is passed through pili
  40. cross resistance
    • resistance to one antimicrobial drug confers resistance to other similar drugs
    • occurs when drugs are similar in structure
  41. multiple resistance
    microorganism is resistant to three or more types of antimicrobial agents
  42. 4 ways to slow development of resistance
    • finish entire prescription
    • -make sure all sensitive cells are killed, resistant ones delayed long enough for immune system to attack

    combination therapy

    limit use of antimicrobials to only necessary cases

    develop new variations of existing drugs
  43. two kinds of combination therapy
    • Synergism: one drug enhances effect of other
    • Antagonism: one drug interferes with the other
Card Set:
2013-05-21 00:28:40
Microbiology antimicrobials

Chapter 10
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