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Pharmacology (Fall) > Antibiotics I: Principles of Antibiotic Therapy > Flashcards

Antibiotics I: Principles of Antibiotic Therapy Flashcards

1
Q

Who is Alexander Fleming?

A

▪ 1945 Nobel prize for discovery of penicillin (1st antiobiotic)

▪ Fleming isolate benzylpenicillin from Penicillium notatum (mold)

▪ Accidental discovery while studying staphylococcus aureus

▪ One culture was contaminated with fungus-noted that the staphylococcus around the fungus were destroyed

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2
Q

Why can’t Alexander Fleming’s experiment be repeated?

A

b/c penicillin can’t be used to treat S. aureus (resistant) ?

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3
Q

What is Selective Toxicity?

A

Drug will harm the invading organism without harming the host (human)

Takes advantage of differences between organisms (such as bacteria and fungi) and humans

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4
Q

What are the factors in selecting an antibiotic?

A
  • Bacteria
  • Host
  • Drug

want to have the middle overlap of these
- drug effective against bacteria but also helps the host

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5
Q

How do we know what is the bacteria?

A

▪ Ideally we would know but sometimes it is an educated guess at what the most likely pathogen(s) is/are.
- ex: more resistant bacteria in hospital typ. so need to bring in big gun antibiotics

▪ Samples are sent to the microbiology lab for culture and sensitivity (C&S)

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6
Q

What are the samples we can take to determine what the bacteria is?

A

▪ Samples are sent to the microbiology lab for culture and sensitivity (C&S)
▪ Blood (2 sites) - b/c 1 might contaminated as it goes through skin
▪ Urine
▪ Wound swabs
▪ CSF (through a tap)
▪ Tissue (ex: neucrotic bone infraction)
▪ sputum

help us choice which antiobiotic to use

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7
Q

What are the factors in selecting bacteria?

A
  • Gram +
  • Gram -
  • Anaerobic
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8
Q

Gram + features

A
  • Outer peptidoglycan cell wall surrounding the cell membrane (phospholipid bilayer)

aerobic

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9
Q

Gram - features

A
  • In addition to cell membrane and peptidoglycan layer there is an outer cell membrane. Outer layer contains Lipid A (bacterial endotoxin)

aerobic

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10
Q

Anaerobic features

A
  • Gram positive or gram negative
  • obligate anaerobes are harmed by the presence of oxygen
  • Facultative anaerobes can survive in both aerobic and anaerobic environments
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11
Q

Which Anaerobes are harder to kill?

A

Facultative anaerobes b/c can survive in both aerobic & anaerobic environments

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12
Q

Pathogenic:

A

▪ Bacteria that can cause disease

▪ Some bacteria only cause disease in certain hosts

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13
Q

Colonizer:

A

▪ Most bacteria are HARMLESS to humans

▪ Colonizers are present but do not cause disease

▪ Sometime due to host factors bacteria that are normally just colonizers can be pathogenic

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14
Q

Can a Colonizer become pathogenic? If so, when?

A

yes!

in immunocompromised people (ex: RA patient)

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15
Q

What are the host factors in selecting an antibiotic?

A
  • Immune system – immunocompromised?
  • colonizers may be pathogenic
  • & also their body can’t do some of the work to clear it
  • Renal function–clearance, drug interactions,
    toxicity
  • Hepatic function–metabolism, drug interactions
  • Perfusion – can we get the drug to the site of action
  • some people have poor perfusion
  • is inf. in a pocket or tucked away area
  • Allergy
  • Age
  • Pregnancy/lactation
  • will it harm unborn fetus
  • or is it in breast milk
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16
Q

What are the drug factors in selecting an antibiotic?

A

▪ Is the drug active against the bacteria?
- sometimes can get there but isn’t active there
ex: diplomycin? - can’t use for pneumonia b/c inactivated by lungs

▪ Will the drug get to the site of action?

▪ Is the drug active at the site of infection?

▪ Bactericidal vs bacteriostatic

▪ Time dependent vs concentration dependent

▪ Safety/Toxicity
- some drugs aren’t as selective

▪ Route of administration
- can it be PO or should we do IV if v. bad inf

▪ Cost

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17
Q

What is the Spectrum of Activity?

A

▪ Helpful to understand basic spectrums of activity (which bugs are covered by which drugs - gram +/- or anerobic) ie. Vancomycin has good gram positive activity but no gram negative or anaerobic activity (narrow spectrum b/c good against gr +)

▪ Narrow vs Broad Spectrum

▪ Learn the exceptions to the rule

*▪ Learn which antibiotics cover which bug.
▪ Which antibiotics cover pseudomonas aeruginosa?
▪ Which antiobiotics cover methicillin resistant staphylococcus aureus (MRSA)

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18
Q

What is the Local Antibiograms?

A

tells about susceptibility of a bacteria to an antibiotic

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19
Q

Bactericidal:

A

▪ Antibiotics that KILL (cidal) the bacteria
- # goes down

20
Q

Bacteriostatic:

A

▪ Antibiotics that INHIBIT bacterial cell GROWTH
- # doesn’t increase/decrease -stays constant

*▪ REQUIRES the HOST IMMUNE SYSTEM to kill the bacteria

21
Q

Which bactericidal or bacteriostatic antibiotic requires the host immune system to kill the bacteria? & who shouldn’t use it?

A

Bacteriostatic

Immunocompromised person shouldn’t use these

22
Q

What is the Minimum Inhibitory Concentration (MIC)?

A

▪ Lowest concentration of antibiotic that inhibits visible bacterial growth
- start to see a clear well

▪ Broth dilution method: MIC determined by serial dilution of antibiotic containing 104 bacteria/mL.

23
Q

What is the E-test?

A
  • diff. gradients as it gets plated
  • will turn red after incubation
  • MIC will be lowest [ ] of bacteria
  • will determine if its sensitive, intermediate or resistant
  • might be sensitive in one part of body & resistant in another b/c can’t get some [ ] in diff. places sometimes
24
Q

What are Breakpoints?

A

a chosen [ ] of an antibiotic that defines whether that species of bacteria is susceptible or resistant to the antibiotic

*If MIC is less than or equal to the breakpoint than that bacterium is SENSITIVE

basically the q is if we need to cross BBB or not

25
Q

What is the Minimum Bactericidal Concentration (MBC)?

A

▪ Lowest concentration of antibiotic that results in bacterial death as determined by the inability to reculture the antibiotic

26
Q

Growth when plated out =

A

MIC

27
Q

No growth when plated out =

A

MBC

28
Q

What is the concentrations of antibiotics? What are the 3 categories?

A

▪ Serum concentrations of antibiotics are used to predict clinical cure

▪ Concentration of antibiotic is plotted over time

▪ 3 categories:
▪ Time dependent antibiotics
▪ Concentration dependent antibiotics
▪ Area Under the Curve (AUC) / MIC

29
Q

What is Time Dependent?

A

▪ Time (how long) above MIC is most important
- give lower doses more freq.

▪ T>MIC

▪ Increasing the peak doesn’t improve effectiveness

30
Q

What are examples of Time Dependent?

A

penicillins, cephalosporins

31
Q

What is Concentration Dependent?

A

▪ Ratio of the PEAK antibiotic concentration to the MIC is most important

▪ Concentration dependent killing-as the concentration increases the killing also increases
- want high peak & let it run out (can go below MIC)

▪ Cmax/MIC

32
Q

What are examples of Concentration Dependent?

A

fluroquinolones, aminoglycosides

33
Q

What is the Post-Antibiotic Effect?

A

▪ Some antibiotics can cause a delay in bacterial growth after the antibiotic is removed

▪ Persistent suppression of bacterial growth after limited exposure to an antibiotic

  • get a high peak & run out, so low [ ] of antibiotic before a redose
34
Q

What is an example of Post-Antibiotic Effect?

A

aminoglycosides cause a 2-6 hour delay in bacterial regrowth after the antibiotic has gone below the MIC

35
Q

What is AUC/MIC?

A

▪ Ratio of the area under the curve to the MIC is most important

▪ AUC/MIC

36
Q

What is an example of AUC/MIC?

A

vancomycin

37
Q

Why the need for a Combination Therapy?

A

▪ Empiric coverage potential pathogens that monotherapy may not cover (i.e. not sure what it is)

▪ Coverage of polymicrobial infections

▪ Double cover potential pathogens that may be resistant

38
Q

What is Synergy?

A

▪ Where the sum of the activity is greater than the sum of activity of either antibiotic alone

39
Q

What is an example of Synergy?

A

Penicillin and aminoglycoside – penicillins “poke” holes in the cell wall that allow aminoglycosides to get in. (in combo - b/c otherwise aminoglycosides normally couldn’t get in)

40
Q

What is Antagonism?

A

▪ Where the combination of drugs results in a diminished effect for one or both drugs.

41
Q

What are examples of Antagonism?

A

combining a drug that is bacteriostatic with a drug that only works when the bacteria is actively growing.

42
Q

What is the route of administration considerations?

A

▪ Absorption – IV vs PO

▪ Can the drug get to the site of action?
▪ Where does it distribute to?
▪ Can do instillations ie intravitreal, intraperitoneal

▪ Can the drug get to the site of action in a high enough concentration?
▪ Ie nitrofurantoin – need kidneys to work well enough to get drug to the bladder. Can’t get high enough concentrations to work for a pyelonephritis (not for this)
- good for regular stenitis or UTI

43
Q

What is the Empiric vs. Targeted Therapy?

A

▪ Typically don’t know the bug prior to starting therapy

▪ We often know the “usual” bacteria that cause certain infections so we target those
first, then narrow once microbiology results are available.

▪ Often the strategy is to *start broad and narrow spectrum once cultures are back

▪ Ideally want to *use broad spectrum for only 48-72 hours then narrow down.

44
Q

Empiric therapy:

A

don’t know what bacteria is but taking educated guess based off what we think is the problem

45
Q

Targeted therapy:

A

once we know what the bacteria is

Pharmacology (Fall) (28 decks)

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