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Pharmacology Exam 3 > Ch.30: Principles of Antibiotic Therapy (Vickroy) > Flashcards

Ch.30: Principles of Antibiotic Therapy (Vickroy) Flashcards

1
Q

Principle of Selective Toxicity

A

agents can have selective actions on microbes vs. the host animal because they target a process that is unique to the microorganism that the host doesn’t have

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2
Q

Can agents be bacteristatic AND bactericidal?

A

Y

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3
Q

antibiotic

A

a substance produce by bacteria or fungi that, at low concentrations, inhibits or kills other microorganisms

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4
Q

antimicrobial

A

any substance of natural, semi-synthetic, or synthetic origin that kills or inhibits the growth of a microorganism, but CAUSES LITTLE OR NO HOST DAMAGE

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5
Q

chemotherapeutic triangle

A

Points in triangle: Drug, Patient, Microbe

1) Drug elicits antimicrobial actions on microbe, microbe elicits drug resistance on drug
2) Drug elicits side effects on patient, patient elicits drug elimination (PK) on drug
3) Patient elicits host defense responses on microbe, microbe elicits infection on patient

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6
Q

broad-spectrum agent

A

agent that is highly effective against an array of BOTH gram + and gram - organisms

  • does NOT include all members of an abx class
  • shouldn’t be universal first choice!
  • higher risk of disruptimg normal flora**
  • greater risk of resistance
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7
Q

Narrow-spectrum agent

A
  • effective against specific families of bacteria

- provide targeted approach to tx

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8
Q

broader the spectrum of drug, the more/less likely side effects will be

A

more

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9
Q

bacteriostatic drug

A

agent that attenuates or stops replication but does NOT kill sensitive microbes

  • have slower onset of clinical action
  • very reliant on host immune response (don’t use in immunocompromised patients!)
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10
Q

bactericidal drug

A

agent that causes IRREPARABLE damage an DEATH of sensitive microbes

  • exert faster clinical effect
  • less reliant on host immune system
  • bacterioSTATIC at low doses**
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11
Q

classifications of cidal or static depend on 3 things:

A

1) drug conc.
2) exposure time to drug
3) target organism

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12
Q

most commonly used abx that target DNA replication

A

fluoroquinolones

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13
Q

how do cell-wall targeting abx work?

A

inhibit cross-linking –> cell wall weakness –> cell wall bursting under osmotic pressure

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14
Q

which abx/classes of abx target ribosomes?

A

tetracyclines (tetracycline, doxy)
aminoglycosides (gentamicin, amakacin)
macrolides (erythromycin, azithromycin)
phenicols (chloramphenicol, florfenicol)

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15
Q

how do ribosome-targeting abx work?

A

inhibit protein synthesis in ribosomes

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16
Q

Name REVERSIBLE ribosome-targeting abx***

A

phenicols
tetracyclines
macrolides

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17
Q

Name IRREVERSIBLE ribosome-targeting abx***

A

aminoglycosides

macrolides

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18
Q

sulfonamides site of action

A

anti-metabolites (DNA)

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19
Q

penicillins MOA

A

cell wall inhibitors

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20
Q

which abx are bacteriostatic***

A

phenicols
tetracyclines
macrolides
sulfonamides

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21
Q

which abx are bacteriocidal***

A 
penicillins
aminoglycosides
macrolides
fluoroquinolones
cephalosporins
carbapenems
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22
Q

what happens when you combine static + static agent?

A

additive action

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23
Q

what happens when you combine cidal + cidal agent?***

A

synergistic action

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24
Q

what happens when you combine static + cidal agent?

A

antagonistic action

25
Q

Will be exam question on which combo of antimicrobial agents best to give? (pick 2 cidal agents)***

A

:)

26
Q

2 basic patterns for bacterial killing

A

1) conc.-dependent killing (dose-dependent)
2) time-dependent killing
“hybrid agents” exhibit both 1 and 2

27
Q

conc-dependent killing

A

kill rate relates to aggregate drug exposure (AUC/MIC) or peak plasma drug conc

28
Q

time-dependent killing

A

kill rate determined by net time above MIC

29
Q

MIC =

A

minimum inhibitory concentration

30
Q

AUC =

A

area under curve

31
Q

Why is kill pattern important?**

A

influences clinical dosing regimen in frequency and drug dose

32
Q

If you are treating an infection by an organism that is less sensitive to an abx and the agent exhibits dose-dependent killing, the best way to enhance clinical efficacy would be to administer:***

A

higher doses at usual or less frequent intervals

33
Q

If you want to maximize the efficacy of a time-dependent abx, you should administer:***

A

higher doses at the usual intervals, or same doses at more frequent intervals

34
Q

kill rate for conc.-dependent drugs is related to the ___ of a drug

A

intensity

35
Q

preferred dosing regimen for a conc-dependent drug

A

high and less frequent doses. Goal = maximize Cpmax relative to MIC

  • TIME PDC remains above MIC less important
  • if conc. well below target, it promotes resistance!
36
Q

kill rate for time-dependent agents is dependent on:

A

TIME that drug conc. remains at or above MIC
Goal = maximize time for PDC > MIC during tx (should be at least 25% of the time)
*if conc. below MIC, can promote resistance!

37
Q

preferred dosing regimen for a time-dependent drug

A

lower and more frequent doses

38
Q

why is time-dependent killing difficult with penicillins?

A

have short half-life, so have to re-dose often

39
Q

What things cause antimicrobial resistance?

A
  • misuse/overuse
  • prior exposure
  • zoonotic pathogens: using abx in food animal feed?
  • veterinary abx use, esp. in food animals
40
Q

Reasons NOT to eliminate abx use in food-prod. animals?

A
  • impacts on animal health/well-being
  • impacts on productivity
  • impact on feed use, food prices, etc.
  • “Danish Experience”: even though “non-therapeutic” use of abx in food animals were eliminated, net abx use still increasing increasing for “production” use
41
Q

Which classes of abx are considered by WHO to be Class II: “Highly important”?

A

aminoglycosides
cephalosporins
phenicols
*all others that you have to know are Class I: “Critically Important”

42
Q

How to avoid antimicrobial resistance

A
  • appropriate drug choice
  • treat to clear the infection completely
  • know the “likely” pathogens using a body system approach
43
Q

resistance mechs. for aminoglycosides

A

inactivation
extrusion
reduced target affinity

44
Q

resistance mechs. for cephalosporins

A

inactivation
extrusion
reduced target affinity

45
Q

resistance mechs. for fluoroquinolones

A

altered target binding

46
Q

resistance mechs. for macrolides

A

membrane impermeability

47
Q

resistance mechs. for penicillins

A

inactivation
exclusion
reduced target affinity

48
Q

resistance mechs. for sulfonamides

A

substrate competition
alternate pathways
reduced target affinity

49
Q

resistance mechs. for tetracyclines

A

membrane impermeability

50
Q

Post-antibiotic effect (PAE)

A

persistent suppression of bacterial growth after drug is “gone”

51
Q

PAE in vitro

A

time for innoculum to increase 10 fold following drug removal

52
Q

PAE in vivo

A

time for colony forming units to increase 10-fold after PDC drops below MIC

53
Q

PAE is proportional to:

A

Cpmax

54
Q

PAE is longer in what type of microbes?

A

Gram +

55
Q

PAE is longer with use of which agents?

A

conc-dependent agents

56
Q

Steps for proper clinical use of antibiotics

A

1) select appropriate antimicrobial agent
2) choose suitable dosing regimen
3) provide supportive therapy (anti-inflamm/diarrhea, bronchodilators, fluids, etc. but beware of drug interactions!!)

57
Q

considerations for choosing an antimicrobial

A 
patient status
host toxicity
drug interactions
sampling and sensitivity testing
location/identity of pathogen(s)
drug lvls needed
govt. regulations
58
Q

Acronym for choosing an abx

A 
"SPACED":
Species
Pharm. considerations
Adverse rxns
Compatibility/Compliance
Economics
Duration of Therapy/Dose Regimen
59
Q

what is microbiological (true) resistance?

A

condition wherein high conc. of antimicrobials are required to kill (arrest growth) of a microorganism

  • MIC increased to a lvl that can’t be safely achieved
  • can impact multiple classes of drug simultaneously

Pharmacology Exam 3 (11 decks)

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