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.Pharmacology > Part 1: Antimicrobial Agents > Flashcards

Part 1: Antimicrobial Agents Flashcards

1
Q

what is the overall goal of antimicrobial therapies?

A

to kill infectious organisms while sparing beneficial or symbiotic micro-organisms and host tissues

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2
Q

most infectious microorganisms are ____ (prokaryotic or eukaryotes)

A

prokaryotic

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3
Q

what is the benefit of most microorganisms having different cellular features and processes than our own cells?

A

makes it easier to target just the infection when taking an antimicrobial

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4
Q

why can cell wall inhibitors like penicillin be given at such high doses?

A

our host cells do not have cell walls

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5
Q

give an example of a metabolic pathway that drugs can target more effectively in microorganisms than in our host cells

A

folic acid pathway

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6
Q

t/f at high doses, antimicrobials that target folate metabolism may also interfere with host cell metabolism, but the dose needs to be very high

A

true

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7
Q

which microorganisms are the toughest to target?

A

viruses

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8
Q

why are viruses so challenging to target?

A

they enter host cells and use the host cell components to replicate

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9
Q

briefly describe the process of a virus entering a host cell, replicating and releasing

A
  1. virus attaches and enters host cell in endosome
  2. genetic material released into cytoplasm where it is replicated
  3. components of new viral particles are packed and released into circulation to infect new host cells
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10
Q

t/f some viruses do enough damage to a host cell during their infection/replication process that the host cell dies

A

t

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11
Q

aside from the virus, what else can cause a lot of tissue damage during viral infection?

A

host immune system response

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12
Q

what activates the immune system in a viral infection?

A

host cells displaying the viral antigen

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13
Q

the few antiviral drugs that exist often target what processes?

A

entry into host, uncoating, viral genome replication and release of new viral particles

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14
Q

instead of cholesterol (our cells), what is found in the cell membrane of fungal cells?

A

ergosterol

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15
Q

what are the primary targets of anti fungal drugs?

A

fungal membrane integrity and ergosterol synthesis (cause fungal cells to rupture)

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16
Q

what are unique fungal specific transporter and enzyme used in the making of fungal proteins?

A

transporter: cytosine permease
enzyme: cytosine deaminase

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17
Q

what is the benefit of the cytosine permease transporter being found at high levels in fungal cells?

A

allows for drug accumulation in the fungal cell

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18
Q

the cytosine deaminase enzyme activates pro-drug into a ___ agents

A

cytotoxic

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19
Q

the most common antimicrobial therapies are against ____ type infections

A

bacteria

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20
Q

a major target for bacterial drug targeting is the ___ cell wall

A

peptidoglycan

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21
Q

cells with an outer membrane around their cell wall are classed as Gram ___

A

negative

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22
Q

gram negative have a ____ (thinner/thicker) peptidoglycan cell wall?

A

thinner

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23
Q

what colour is gram + stain?

A

purple

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24
Q

what colour is gram - stain?

A

red/pink

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25
Q

t/f the outer membrane of gram - cells makes drug permeation difficult

A

true

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26
Q

bacteria have __ and ___ ribosomal subunits and our cells have __ and ___ subunits

A

30s & 50s; 40s & 60s

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27
Q

several antibiotics bind specifically to different sites on bacterial ribosomes to disrupt ___

A

bacterial protein synthesis

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28
Q

what is the shape of bacterial DNA?

A

single circular strand

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29
Q

t/f bacterial DNA replication requires transcription machinery that is different from host

A

true

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30
Q

explain bacteriostatic and bactericidal drug treatment

A
  1. bacteriostatic: stalls bacterial growth and gives immune system a chance to catch up to clear the infection
  2. bactericidal: drug kills the bacteria and there is less reliance on the host immune system
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31
Q

antibacterial drugs are also called ___

A

antibiotics

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32
Q

when are bactericidal antibiotics preferred?

A

when the host immune system is impaired

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33
Q

give 4 examples of why an antimicrobial treatment may fail

A
  1. poor patient adherence
  2. poor pharmacokinetics
  3. dose too low
  4. microbe is not sensitive to the drug given
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34
Q

how might poor patient adherence lead to antimicrobial treatment failure?

A

if not taken as directed, the infection may not be adequately controlled and worsening or resurgence of infection is likely

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35
Q

how might poor pharmacokinetics impact treatment failure?

A

may not get to the site of action adequately enough

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36
Q

the minimum concentration required to inhibit or kill bacteria is called the ____

A

MIC

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37
Q

t/f in most cases, doses of antimicrobials are given to ensure the concentration at the site of infection exceeds the MIC

A

t

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38
Q

if increasing the concentration of drug increases the rate of antibiotic effect, the drug is said to be ___

A

concentration dependent antibiotic

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39
Q

t/f if the antibiotic is concentration dependent, in some cases, it may be beneficial to give larger doses to clear the infection more quickly

A

t

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40
Q

explain time-dependent antibiotics

A

work for a set period of time and increasing the concentration past about 3x will not increase the antibiotic effect

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41
Q

for which type of antibiotic is it especially important to take at the time indicated by the prescriber?

A

time-dependent

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42
Q

give an example of an antibiotic class that has post-antibiotic effects

A

ahminoglycosides

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43
Q

how do ahminoglycosides exhibit their post-antibiotic effects?

A

large doses are given to kill many bacteria quickly, but after the drug enters the bacteria it persists, so those bacteria that aren’t immediately killed aren’t able to keep replicating

44
Q

t/f even after the systemic levels or amino glycoside dry, there is still an antibacterial effect remaining for some time

A

true

45
Q

the post-antibiotic effect of ahminoglycosides is advantageous to the ___ of dosing. why is this beneficial?

A

frequency; they have significant ADRs, so less frequent dosing is advantageous

46
Q

t/f sometimes more than one antimicrobial agent may be needed

A

t

47
Q

when administering 2 antimicrobial agents, it is important to consider of they are ___ or ____ wrt to each other

A

antagonistic or synergistic

48
Q

what is mutual antagonism?

A

both drugs X and Y results in worse outcome than having either drug on their own

49
Q

what is indifference?

A

the two drugs don’t intereact and they exhibit their antibiotic effects independently of each other

50
Q

if there is question surrounding whether an infectious organism will be sensitive to a particular drug, what testing should be performed in advance?

A

sensitivity testing to determine the best therapeutic choice

51
Q

how can microbes be inherently resistant to a drug?

A

if the drug is targeting something the microbe doesn’t have (ex: trying to use antibiotic to cure the rhinovirus)

52
Q

genes for antimicrobial resistance can be genetically passed by ___ or ____

A

gene transfer; or bacterial replication

53
Q

t/f most health authorities and general hospitals keep publications of local resistance patterns to help guide treatment decisions when sensitivity testing is not possible or practical

A

t

54
Q

what are the 6 most common pathways of microbial resistance to drugs?

A
  1. alteration of target sites
  2. enzymatic inactivation
  3. overproduction of target sites
  4. decrease in cell permeability
  5. efflux pumps
  6. alternate growth patterns
55
Q

what are the 3 main features of microbial drug resistance?

A
  1. drug doesn’t bond to target anymore
  2. drug doesn’t accumulate in the cell to a high enough concentration (inactivated, cant get in, or is pumped out)
  3. microbe alters its biochemical pathways
56
Q

vancomycin is subject to what type of microbial resistance?

A

alteration of target sites

57
Q

beta-lactams are subject to what type of microbial resistance?

A

enzymatic inactivation

58
Q

sulfanomides are subject to what type of microbial resistance?

A

overproduction of target sites

59
Q

fluoroquinolones are subject to what type of microbial resistance?

A

decrease in cell permeability

60
Q

tetracylines are subject to what type of microbial resistance patterns?

A

efflux pumps

61
Q

should prophylaxis with antibiotics be the norm for healthy patients?

A

no! microbial resistance risk! only for those with a compromised immune system

62
Q

most antimicrobial prescribing for mild cases is based off of clinical presentation of symptoms and an educated guess called ____ therapy

A

empiric

63
Q

what antibiotics are typically the first choice for infection (provided no allergy)?

A

penicillins

64
Q

penicillins have good activity against Gram ___

A

+

65
Q

what is a situation where sensitivity testing would be needed?

A

serious infection with suspected resistance

66
Q

which has a lower chance of treatment failure, targeted or empiric antibiotic treatment?

A

targeted

67
Q

why may sensitivity testing be inconvenient?

A

takes time, infection can worsen in that time

68
Q

If a patient presents with a serious infection, what is the general course of action for antibiotics?

A

start empiric until test results show what to target

69
Q

most empiric therapy antibiotics have what spectrum of activity?

A

broad

70
Q

what are extended spectrum antibiotics?

A

in between narrow and broad, effective against some G+ and some G-

71
Q

t/f antibiotics are the most commonly used Rx drugs, s their effects are more commoly reported

A

t

72
Q

ADRs of antimicrobials is typically not caused by the antimicrobial MOA of the drug, but rather caused by ___

A

off target effects of the drug or secondary effects of disrupting the balance of microorganisms in the body

73
Q

what are some of the more common ADRs of antimicrobials?

A

effects on normal flora (diarrhea, opportunistic infections)
contraceptive failure

74
Q

what are some of the more rare ADRs of antimicrobial therapy?

A
  1. antibiotic teratology
  2. antibiotic induced mania
  3. long QT interval syndrome
  4. antibiotic induced agranulocytosis
75
Q

what are two opportunistic infections that can happen if too much good bacteria are killed by antibiotic?

A
  1. c. diff (colon, toxins, cell death in intestine, diarrhea)
  2. candidiasis (oral thrush, vaginal yeast infection)
76
Q

t/f sometimes the secondary infections after antimicrobial treatment can resolve on their own, but sometimes they also need to be treated

A

t

77
Q

what types of antibiotic are most common for secondary opportunistic infections?

A

broad spectrum (amoxicillin, 3rd gen cephalosporins, clindamycin)

78
Q

t/f there is a lot of debate over if antimicrobials can cause contraceptive failure leading to pregnancy

A

true

79
Q

by what mechanism might antimicrobials reduce efficacy of birth control?

A

can induce CYP, causing low levels of circulating hormones, which can result in failure and pregnancy

80
Q

the hormones in birth control pills are metabolized by what enzymes?

A

CYP

81
Q

how may Rifampin lead to contraceptive failure?

A

induce CYP

82
Q

t/f other than Rifampin, no other antibiotics have been shown to induce CYP, but the old-wives tale about antibiotics and contraceptive failure still persists

A

t

83
Q

what are 3 proposed mechanisms of antibiotics leading to contraceptive failure?

A
  1. CYP induction
  2. reduced GI absorption of BC due to diarrhea
  3. reduction in enterohepatic circulation by causing reduced oral F of BC
84
Q

what is enterohepatic circulation?

A

process by which bacteria in the GI tract increase the F of drugs

85
Q

MO in the GI tract use ___ as a nutrient source

A

hormone metabolites

86
Q

explain the process of enterohepatic circulation with estrogen in BC pills as an example substrate

A
  1. estrogen orally = subject to 1st pass metabolism in the liver
  2. sulfate metabolite is produced from liver metabolism
  3. metabolite goes into GI tract where bacteria take the sulfate and spit the estrogen back into the GI tract
  4. recycled estrogen can be reabsorbed and some to systemic and some remetabolized
87
Q

t/f there is no concrete evidence that antibiotics except rifampin cause contraceptive failure, but it is best practice to warn patients

A

true

88
Q

what is the formula for how long extra protection against pregnancy should be used after taking an antibiotic?

A

t 1/2 of the antibiotic x 5

89
Q

True / False

Limit the duration of prophylaxis to be as short as the time in which maximum contamination is expected

A

True

90
Q

True / False

Consider narrow-spectrum antibiotics targeted at the most important infectious organisms

A

True

91
Q

True / False

The prophylactic dose is generally lower than when the same drug is used for acute treatment

A

True

92
Q

True / False

In routine prophylaxis, there is a need to preserve the native biome as much as possible

A

True

93
Q

Patient A and B took the same antiTB drugs rifampicin and isoniazid as maintenance treatment for 6 monts with good compliance.

Upon completion, A still showed TB lesions, while B has clear results. This is an example of

**
a. between-patient variability
b. development of resistance
c. interoccasion variabilit
d. within patient variability**

A

Between patient variability

94
Q

The most valualbe and time-tested method for immediate identification of bacteria is examination of the infected secretion of body fluid using

**
a. all of the choices
b. complete blood count
c. culture and sensitivity
d. gram staining
e. c-reactive protein (CRP)**

A

Gram staining

95
Q

True about definitive therapy

a. pathogen has been identified and susceptibility results are already known
b. combination therapy is preferred
c. important in preventing resistance to monotherapy
d. all of the choices

A

Definitive therapy: pathogen has been identified and susceptibility results are already known

96
Q

The most common recommended prophylactic antimicrobial for surgery

A

Cefazolin

97
Q

Which if the following statements is correct?

  • to minimize resistance, drugs should be discontinued
  • an ineffective drug may be given in combination to enhance effect
  • combination therapy should have similar mechanism of action
  • drugs with similar toxicity should be avoided
A
98
Q

Which of the following contributes to drug resistance?

  • increase activation of prodrugs
  • retains target enzyme
  • decrease DNA repair
  • decrease drug accumulation
A
99
Q

True / False

Hydrophilic antibiotics are primarily cleared by the liver

A

False

100
Q

True / False

Levofloxacin is a good antibiotic for urinary tract infections

A

True

101
Q

Drugs that posses concentration dependent killing with good or prolonged post antibiotic effect

A

aminoglycosides

102
Q

True / False

For eye infections, standard therapy is via oral route

A

False

standard therapy is direct instillation of antibiotics into the ocular cavity

103
Q

Not true about drugs with timed-dependent killing

  • with prolonged post antibiotic effect
  • drugs are given several times a day
  • drug concentration persists above MIC for longer duration
  • example is ampicillin
A

with prolonged post antibiotic effect

104
Q

**

What type of drug resistance is present in enterococcus which after developing vancomycin resistance, develops vancomycin-requiring strains

A

Incorporation of the drug

105
Q

The infection is controlled but not completely eradicated by the initial round of antimicrobial treatment. Therapy is continued at a lower dose

A

Suppressive therapy

.Pharmacology (55 decks)

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