Antimicrobials Flashcards

1
Q

microbobes in human body

A

100 trillion

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2
Q

weight of microbes in human body

A

1-3 lbs

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3
Q

bacterial genes and # human genes

A

3.3 million and

22,000

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4
Q

Antibiotic

A

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

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5
Q

Antimicrobial

A

any substance of natural (i.e.,
penicillin and alkaloids), semisynthetic (i.e., methicillin and
amoxicillin) or synthetic (i.e., sulfonamides and quinolones)
origin that kills or inhibits the growth of microorganisms while
(ideally) causing little or no damage to the host.

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6
Q

All antibiotics are antimicrobials

A

but not all antimicrobials are antibiotics

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7
Q

microorganisms drugs are active against

A

viruses, bacteria, fungal (antifungal/mycotic), protozoans (antiprotozoal), helminths (antihelmintic)

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8
Q

Classification

A

class and spectrum of microorganisms it effects

the biochemical pathway or target

chemical structure

***pattern of activity (type I,II,III)

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9
Q

Broad specturm

A

drugs are active against wide range * not the same as its useful therapeutic range

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10
Q

Narrow specturm

A

limited activity and primary only useful against particular species

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11
Q

Spectrum of activity

A

no antimicrobial is effective against all microbes, tetracycline have very broad spectrum, isoniazid has narrow specture

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12
Q

Clinical considerations before prescribing antimicrobial therapy (AMT)

A

be very careful, don’t guess! Culture and test, consider drug route and if effective

most effective, least toxic, narrowest spectrum, least expensive, patients immune status

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13
Q

ID the pathogen

A

collect and culture specimens, treatment should be ASAP for serious infections (Handbook of Antimicrobial Therapy HATs)

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14
Q

Disc diffusion test

A

Estimates minimal inhibitory conc (MIC) of antimicrobials

MIC is lowest conc of an antibiotic that will inhibit the growth of a bacterial stain

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15
Q

Broth dilution test

A

determines both MIC (no more turbidity) and MBC (minimum bactericidal conc) no more bacterial growth

Bactericidal antibiotics usually have very similar MIC and MBC values

Bacteristatic antibiotics have much higher (if any) MBC than MIC values.

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16
Q

Prophylactic

A

no infection

17
Q

Definitive

A

pathogen isolated

18
Q

Pharmacokinetics

A

absorption, distribution, metabolism, and excretion of drug

dosing regimen
serum conc

19
Q

Pharmacodynamics

A

he relationship of the drug concentration at the site of action and the resulting effects, including the time course and intensity of therapeutic and adverse effects.

conc in tissues and body fluids
- pharm and toxic effects

conc at infection site
- antimicrobial effect

20
Q

choosing a dose regimen

A

Must keep in mind that although MIC is compared to plasma
concentrations, these concentrations may or may not reflect drug concentration at site of infection.

want OVERKILL without causing toxicity

21
Q

Goals in dose regimen

A

GOAL #1: achieve a bactericidal concentration at the site.

GOAL #2: discourage emergence of resistant bacteria.

22
Q

Growth curve

A

log phase of bacterial growth is the most sensitive to antimicrobial intervention, want to target this

23
Q

Bacteriacidal vs Bacteriostatic drug growth curve

A

bacteriostatic plateaus and will increase if Rx stopped

bactericidal decreases log # of bacteria

Bactericidal antibiotics kill bacteria, while bacteriostatic antibiotics stop bacteria from growing or reproducing.

body still plays a role in removing last bit

24
Q

Antimicrobial Patterns

A

pharmacodynamic properties:
conc-dependence (I)
time-dependence (II)
time-dependence with persistent effects (III)

Rate of effect determined by II and III

25
Persistant Post Antibiotic Effect (PAE)
provide suppression of bacterial growth following antibiotic exposure. (Delayed regrowth of the bacteria after complete removal of an antibiotic allowing less frequent dosing than with agents with no PAE )
26
Drug conc v time graph
use area under cruve
27
Treating Serious infections
``` treat ASAP but still culture use safest drug Give max non-toxic dose monitor plasma conc of drug continue treatment for at least 2 days past apparent cure ``` ex. CNS infections, malaria, TB
28
Selectivity
select for pathogen not host When selectivity is high, the risk of adverse effects are reduced. However, even highly selective antibiotics can have side effects. The “ideal” AMT is defined by its specificity of action in host vs. bacteria.
29
Therapeutic Index (TI)
ratio of dose toxic to the host to the effective therapeutic dose the higher or wider the TI the better and safer
30
Adverse Effects of AMT
Analogous to drug action: same effect on human cells as bacteria Independent to drug action: irritation, allergy
31
Absorbtion
Absorption critically determines the compound's bioavailability. -  Route of administration is an important consideration (i.e., PO, IV, IM, IT)
32
Distribution
lipid, water solubility, cross BBB? Some antibiotics leave the brain by active transport via choroid plexus (e.g., penicillin) inflammation? can increase BBB leaky and things go out and in more easily
33
Metabolism
usual clearance through liver and kidneys immediately begin to metabolize by redox cytochrome p450 enzymes can become more active after broken down to metabolites inactivation by bacterial enzymes give one drug with another to prevent enzymes to break down
34
Excretion
low potency for UTIs because they get more conc as they transport to urine
35
Mechanisms of action of drugs
inhibit microbes cell wall synthesis/permeability/function protein synthesis metabolic pathways nuclei acid synthesis
36
Combination therapy
Okay as long as not antagonistic Too improve efficacy For initial empiric therapy of uncharacterized serious infection. To enable use of lower (i.e., less toxic) drug concentrations. To delay emergence of resistance by avoiding the selection of naturally occurring drug-resistant mutants
37
Superinfections
Antimicrobial use can cause a wide-spread alteration of the microbial ecosystem The current view is that nonpathogenic microbes interact with other bacteria to control growth of pathogens as well as of harmless bacteria in our ecosystem reducing the number of harmless microbes opens niches in the ecosystem reducing the number of harmless microbes opens niches in the ecosystem