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Host and Defense > Intro to Antimicrobial drugs > Flashcards

Intro to Antimicrobial drugs Flashcards

1
Q

facts about the human microbiome

A

1 in 10 cells in the body are human
1-3 pounds of your total body weight is microbes
more than 3.3 million genes are bacterial only 22,000 are human

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2
Q

antibiotic

A

a low molecular substance produced by a microorganism that inhibits or kills other microorganisms while causing little or no damage to itself

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3
Q

antimicrobial

A

is any substance of natural, semisynthetic,, or synthetic origin that kills or inhibits the growth of microorgansims while causing little or no damage tot he host

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4
Q

T/F all antibiotics are antimicrobials, not all antimicrobials are antibiotics

A

true

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5
Q

T/F a drugs spectrum of action is not the same as its useful therapeutic range

A

true

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6
Q

is there a antimicrobial that is effective against all microbes?

A

nope

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7
Q

disc diffusion test

A

estimates the minimal inhibitory concentration of antimicrobials (MIC)

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8
Q

what is the MIC

A

it is the minimum concentration of an antibiotic that will inhibit the growth of a bacterial strain

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9
Q

broth dilution test

A
  • determines both MIC and MBC (minimum bactericidal concentration).
  • look at broth tubes for lack of turbidity=MIC
  • then plate out the dilutions until there are no colonies=MBC
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10
Q

bactericidal antibiotics usually have very similar or different MIC and MBC values?

A

similar, narrow range between the two values

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11
Q

bacteriostatic antibiotics have much lower or higher MBC than MIC values?

A

much wider or high range of values

may not have a MBC value

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12
Q

prophylaxis treatment

A

treatment when there is no infection

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13
Q

pre-emtive treatment

A

treatment of an infection

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14
Q

empiric treatment

A

treatment of symptoms

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15
Q

definitive treatment

A

treatment of an isolated pathogen

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16
Q

suppressive treatment

A

treatment to complete resolution

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17
Q

what is the difference between a prophylactic and a definitive treatment?

A

definitive treatment is when successful identification of the infection pathogen has happened

18
Q

pharmacokinetics

A

the relationship of the time course of drug absorption, distribution, metabolism and excretion.
*Body working on the drug
ADME

19
Q

pharmacodynamics

A

the relationship of the drug concentration at the site of action and the resulting effects, including time course and intensity of therapeutic and adverse effects
*drug effect on the body

20
Q

what is important to keep in mind about MIC levels in the body?

A

the MIC is compared to plasma concentrations, but these may or may not reflection the concentration at the site of infection

21
Q

what should doses provide overkill without causing toxicity in the host?

A
  • need to achieve a bactericidal concentration at the site

- need to discourage emergency of resistant bacteria

22
Q

what phase of bacterial growth is most sensitive to antimicrobial intervention?

A

the log or exponential phase

23
Q

bactericidal antibiotics

A

kill bacteria

24
Q

bacteriostatic antibiotics

A

stop bacteria from growing or reporducing

25
Q

Type I pattern of activity of antimirobials

A

concentration dependent killing and prolonged persistent effects
*maximize concentrations is the goal

26
Q

Type II pattern of activity of antimicrobials

A

time dependent killing and minimal persistent effects

**maximize duration of exposure

27
Q

type III pattern of activity of anitmicrobials

A

time-dependent killing and moderate to prolonged persistent effects
**maximize amount of drug
persistent post-antibiotic effect (PAE)

28
Q

Persistent Post-Antibiotic Effect

A

provide suppression of bacterial growth following exposure.

29
Q

in type II antibiotic why is there a reduced risk of adverse effects?

A

because you are taking multiple doses at a lower concentration, yet providing more time above the MIC than with a type I antibiotic which gives a large dose at a high concentration.

30
Q

what are the 5 key rules for treating serious infections?

A
  1. begin treatment ASAP
  2. Use the safest effective drug
  3. Use the largest reasonable dose
  4. Monitor plasma concentrations of antibiotic if it is needed to guide dose or to avoid toxicity
  5. must continue treatment at least 2 days past apparent cure
31
Q

the ideal AMT is defined by what?

A

specificity of action in host vs bacteria

*high selectivity=reduced adverse effects

32
Q

All adverse effects are dose-dependent T/F?

A

false, many are but some are not

33
Q

what is the therapeutic index

A

the ratio of dose toxic to the host to the effective therapeutic dose (TD/ED)
-higher or wider the therapeutic index the better (safer) the antibiotic .

34
Q

analogous adverse effects

A

an effect on human cells resulting from the same mechanism as the antimicrobial effect

35
Q

independent adverse effects

A

irritation

allergy

36
Q

Mechanisms of AMT

A

cell wall synthesis/function/permeability
protein synthesis (50s and 30s)
inhibition of metabolic pathways (folic acid)
nucleic acid synthesis disruption

37
Q

why use combination therapy?

A 
broaden spectrum of infection
improve efficacy (synergism)
lower drug concentrations
delay emergence of resistance
empiric therapy of uncharacterized serious infection
38
Q

what is a superinfection

A

the overgrowth of pathogens resulting from use of antimicrobial drugs
*the larger the disruption of the microbiome, the greater the opportunity for pathogens to overgrow

39
Q

what are some was a superinfection can happen?

A
  • use of a broad-spectrum antimicrobial agent

- use of a higher than normal concentration of even a narrower-spectrum antimicrobial drug

40
Q

no new classes of antibiotics have been introduced since when?

A

1987

41
Q

what is the GAIN act?

A

it is an act to incentivize discovery and development of new antimicrobials

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