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Antimicrobial Medications Flashcards

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1
Q

Resistance that develops due to genetic changes, including mutation and horizontal gene transfer.

A

Acquired Resistance

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2
Q

A compound naturally produced by molds or bacteria that inhibits the growth of or kills other microorganisms.

A

Antibiotic

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3
Q

An antibiotic or other chemical that kills microbes or inhibits their growth.

A

Antibiotic; also called an antimicrobial drug.

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4
Q

A chemical that is used to treat a viral infection and acts by interfering with the infection cycle of the virus.

A

Antiviral Medication; also called an antiviral drug.

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5
Q

Describes a chemical or other agent that kills bacteria.

A

Bactericidal

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6
Q

Describes a chemical or other agent that stops the growth of bacteria without killing them.

A

Bacteriostatic

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7
Q

An antibiotic that is effective against a wide range of bacteria, generally including both Gram-positive and Gram-negative bacteria.

A

Broad-Spectrum Antibiotic

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8
Q

A chemical used to treat disease.

A

Chemotherapeutic Agent

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9
Q

Resistance due to inherent characteristics of an organism.

A

Intrinsic (Innate) Resistance

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10
Q

An antibiotic that is effective against a limited range of bacteria.

A

Narrow-Spectrum Antibiotic

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11
Q

A plasmid that encodes resistance to one or more antimicrobial Medications.

A

R Plasmid

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12
Q

Who discovered that some chemicals could selectively kill microbes?

A

Paul Ehrlich (1854-1915)

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13
Q

What is the general formula for therapeutic index?

A

Lowest dose toxic / necessary thereby dose

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14
Q

Define therapeutic window.

A

The range between the dose used therapeutically and the toxic dose.

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15
Q

Which would be safer to use: an antimicrobial that has a low therapeutic index or one that has a high therapeutic index? Why?

A

A high therapeutic index because:
toxic dose / therapeutic dose

The higher the toxic dose and the lower the therapeutic dose, the larger the index.

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16
Q

In what clinical situation is it most appropriate to use a broad-spectrum antimicrobial?

A

Typically when specific species or group of bacteria is unknown, or when infection with multiple groups of bacteria is suspected.

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17
Q

Why would antimicrobials that have toxic effects be used at all?

A

Only when the alternative is worse. If there are no other options, it is sometimes worth risking serious injury instead of guaranteed death.

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18
Q

What does penicillins, Cephalosporins, carbapenems, and monobactams have in common?

A

A β-lactam ring structure

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19
Q

Target of β-lactam antimicrobial medications; their role in bacteria is peptidoglycan synthesis.

A

penicillin-binding proteins (PBPs)

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20
Q

How do some bacteria resist β-lactam drugs?

A

β-lactamse synthesis that breaks down the β-lactam ring, inactivating the medication.

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21
Q

How do glycopeptide antibiotics work?

A

By binding to the amino side chain of NAM molecules that connect peptidoglycan, blocking cross-linking between adjacent glycan chains.

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22
Q

When are glycopeptide antibiotics used?

A

They are typically reserved for serious infections by Gram-positive bacteria.

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23
Q

What kind of antibiotic is vancomycin?

A

Glyopeptide Antibiotic

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24
Q

How is vancomycin administered?

A

intravenously except when used to treat intestinal infections. It is poorly absorbed.

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25
Q

Name 2 glycopeptide antibiotics other can vancomycin. (There are many)

A
  • telavancin
  • dalbavancin
  • oritavancin
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26
Q

How does bacitracin work?

A

By interfering with the transport of petidoglycan precursors across the cytoplasmic membrane.

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27
Q

How is bacitracin typically used?

A

Due to its toxicity, it is usually used in topical applications.

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28
Q

Why don’t antibacterial protein synthesis inhibitors affect human cells?

A

Bacterial 70S ribosomes are composed of a 50S and 30S subunit which is different enough from the 80S ribosome of human cells to not be affected.

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29
Q

What typically causes protein synthesis inhibitors to be toxic?

A

Mitochondrial ribosomes of eukaryotes are similar to bacteria, which contributes to the toxicity of some of these drugs.

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30
Q

Name 2 macrolide antibiotics. (there are many)

A
  • erythromycin
  • clarithromycin
  • azithromycin
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31
Q

What are macrolides effective against?

A

Gram-positive bacteria

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32
Q

Why are macrolides used instead of penicillins?

A

When patients are allergic to penicillins.

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33
Q

Why is chloramphenical use generally limited even in very low doses?

A

In extremely rare cases, they can cause aplastic anemia–the inability for the body to form white and red blood cells.

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34
Q

What are lincosamides effective against?

A

A variety of gram-positive bacteria and some gram-negative anaerobes.

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35
Q

What are the risks of lincosamides?

A

C. diff infection risk is greater for people taking lincosamides.

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36
Q

What kind of antibiotic is clindamycin?

A

Lincosamide

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37
Q

What makes lincosamides useful?

A

They are useful for treating infections from intestinal perforations because they inhibit Bacteroides fragilis, a member of the normal instestinal microbiota.

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38
Q

How do aminoglycosides work?

A

They irreversibly bind to the 30S ribosomal subunit, blocking translation and causing mRNA misreads.

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39
Q

What are the drawbacks of aminoglycosides?

A

They can cause severe side effects, including hearing loss and vertigo as a result of damage to sensory components of the inner ear.
They can also cause kidney damage.

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40
Q

When are aminoglycosides used?

A

Only when less toxic alternatives are not available or not an option for some other reason.

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41
Q

What are aminoglycosides generally not effective against? Why?

A

Against anaerobes, enterococci, and streptococci because they enter bacterial cells by a process that requires respiratory metabolism.

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42
Q

Name 2 aminoglycosides

A
  • streptomycin
  • gentamicin
  • tobramycin
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43
Q

How to tetracyclines work?

A

They reversibly bind to the 30S ribosomal subunit, blocking the attachment of tRNA and preventing translation from continuing.

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44
Q

What antibiotics can cause discoloration in teeth when used by young children?

A

Tetracyclines and glycylcyclines.

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45
Q

Original penicillins produced by the mold Penicillium chrysogenum.

A

Natural penicillins

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46
Q

Scientists developed these in response to the problem of penicillinase-producing Staphylococcus aureus strains.
Methicillin and dicloxacillin.

A

Penicillinase-resistant penicillins

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47
Q

Active against not only penicillin-sensitive Gram-positive bacteria, but also many Gram-negative bacteria.
amipicillin
amoxicillin

A

Broad-spectrum penicillin

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48
Q

Name penicillinase-resistant penicillins

A
  1. methicillin
  2. dicloxacillin
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49
Q

Name 2 broad-spectrum penicillins

A
  1. amoxicillin
  2. ampicillin
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50
Q

These have greater activity against most of the Enterobacteriaceae as well as Pseudomonas aeruginosa.
Gram-negative bacteria are common causes of healthcare-associated infections and are often resistant to many other antimicrobial Medications.
ticaricillin
piperacillin

A

Extended-spectrum penicillins.

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51
Q

Name 2 extended-spectrum penicillins

A

ticarcillin
piperacillin

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52
Q

This is a combination of agents that protects penicillin against enzymatic destruction.
amoxicillin and clavulanic acid, for example.

A

Penicillins + B-lactamase inhibitor

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53
Q

Name 2 penicillinase-resistant penicillins

A

methicillin
dicloxacillin

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54
Q

Could penicillin be used to treat MRSA infections? Explain (critical thinking)

A

No, methicillin-resistant Staphylococcus aureus will not respond to a penicillinase-resistant penicillin like dicloxacillin or methiscillin.
Typically glycopeptide antibiotics are recommended for MRSA, like vancomycin.

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55
Q

What makes cephalosporins unique?

A

The chemical structure of cephalosporins protects them from destruction by certain B-lactamases.

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56
Q

What makes carbapenems unique?

A
  1. Carbapenems are effective against a wide range of Gram-negative and Gram-positive bacteria.
  2. They are not inactivated by extended-spectrum B-lactamases (ESBLs)
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57
Q

What type of bacteria produce extended-spectrum B-lactamases (ESBLs)?

A

certain Gram-negative bacteria

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58
Q

Name 2 carbapenems

A

imipenem
ertrapenem
meropenem
doripenem

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59
Q

What makes monobactams unique?

A

Monobactams are antibiotics each containing a B-lactam ring but lacking another ring fused to it.

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60
Q

What are monobactams used for?

A

Specifically for members of the family Enterbacteriacaea

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61
Q

_______ are synthetic compounds that inhibit one or more of a group on enzymes called topoisomerases, which maintain the supercooling of DNA within the bacterial cells.

A

Flouroquinolones

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62
Q

Flouroquinolnes used to be used widely in the past, why aren’t they anymore?

A

Severe side effects

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63
Q

name 2 flouroquinolones

A

ciprofloxacin
levofloxacin
moxifloxacin
ofloxacin

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64
Q

_______ are antibiotics that block bacterial RNA polymerase from initiating transcription.

A

Rifamycins

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65
Q

______ is a relatively new bactericidal antibiotic that interferes with transcription by binding to RNA polymerase. It passes through the intestinal tract without being absorbed and is particularly useful for treating C. diff.

A

Fidaxomicin

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66
Q

A synthetic compound that interferes with DNS synthesis and function, but only in anaerobic microorganisms.

A

Metronidazole (Flagyl)

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67
Q

Of the metabolic pathway antibacterials, which are most used as folate synthesis inhibitors?

A

solfonamides and trimethoprim

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68
Q

Explain how sulfa drugs (sulfanomides) work.

A

They are similar to para-aminobenzioc acid (PABA) which is found in folate synthesis pathways. Human cells lack this enzyme, making it selectively toxic to PABA binding proteins.

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69
Q

Name antibiotics that interfere with cell membrane integrity

A

Daptomycin
Polymyxins
Glycopeptides

70
Q

What is the bacterial name for TB?

A

Mycobacterium tuberculosis

71
Q

Why are B-lactam antibiotics bactericidal only to growing bacteria? (MicroAssessment 20.3)

A

Because B-lactam interferes with the formation of peptidoglyan on the NAM binder which occurs during cellular growth.

72
Q

What is the target of macrolides? (MicroAssessment 20.3)

A

Macrolides are 50S ribosomal subunit inhibitors.

73
Q

Considering that all B-lactam antibiotics have the same target, why do they vary in their spectrums of activity? (Critical Thinking MicroAssessment 20.3)

A
  1. Cell wall structure of gram-positive bacteria varies greatly while gram-negative bacteria variations sometimes prevent B-lactams from reaching the peptidoglycan layers at all.
  2. Variety in penicillin binding proteins (PBPs). Some bind worse or better to others.
74
Q

What is the purpose of a Kirby-Bauer test?

A

To determine the susceptibility of a given bacterial strain to a variety of antimicrobial Medications.

75
Q

What is a zone of inhibition in a Kirby-Bauer experiment? What does it mean?

A

A zone of inhibition is an area around a medication that shows no visible growth. The size of the area indicates the sensitivity of the bacteria to that antibiotic.

76
Q

When developing a new antimicrobial medication, how is the zone of inhibition chart determined?

A

A broth dilution test is conducted to determine the minimum inhibitory concentration (MIC). It is determined by growing the test strain in broth cultures containing different concentrations of the antimicrobial.

77
Q

The lowest concentration of a specific antimicrobial medication needed to prevent the visible growth of a given microbial strain in vitro.

A

Minimum inhibitory concentration (MIC)

78
Q

The lowest concentration of a specific antimicrobial medication that kills 99.9% of cells of a given strain in vitro.

A

Minimum bactericidal concentration (MBC)

79
Q

List two factors other than a strain’s susceptibility that influences the size of the zone of inhibition around an antimicrobial disc. (MicroAssessment 20.4)

A

chemical Molecular weight
chemical stability
chemical concentration

80
Q

Explain the difference between the MIC and the MBC. (MicroAssessment 20.4)

A

Minimum inhibitory concentration (MIC) is the lowest concentration of a specific antimicrobial needed to prevent visible growth.
Minimum bactericidal concentration (MBC) is the lowest concentration of a specific antimicrobial medication that kills 99.9% of cells of a given strain.

81
Q

Why would it be important for the Kirby-Bauer test to use a standard concentration of the bacterial strain being tests? (Critical Thinking MicroAssessment 20.4)

A
82
Q

What are the mechanisms of acquired antimicrobial resistance?

A
  1. Medication-inactivating enzymes
  2. Alteration in the target molecule
  3. Decreased uptake of the medication
  4. I created elimination of the medication
83
Q

Explain how using a combination of two antimicrobial medications helps prevent the development of spontaneously resistant mutants. (MicroAssessment 20.5)

A

The likeliness of spontaneous resistant mutants to two treatments at once is much less likely than for only one.

84
Q

Explain the significance of a member of the normal microbiota that harbors an R Plasmid. (MicroAssessment 20.5)

A

While the normal microbiota will not harm you when in balance, normal microbiota species that harbor R plasmid resistances to treatments can pass these on to pathogens through horizontal gene transfer.

85
Q

A student argued that “spontaneous mutation” meant that an antimicrobial could cause mutations. Is the student correct? Why or why not? (Critical Thinking MicroAssessment 20.5)

A

No, the student is not correct directly, but he/she is correct anecdotally. Spontaneous mutations are just that, spontaneous. They are not caused by antimicrobials. However, antimicrobials do create an environment of survival of the fittest, allowing the mutants to survive without competition while non mutants die off.

86
Q

What antibiotic class targets protein synthesis?

A

Tetracyclines

87
Q

What antibiotics targets nucleic acid synthesis?

A

Rifamycin

88
Q

Aztreonam is a monobactam antibiotic that Blank______.

A

inhibits cell wall synthesis

89
Q

What are the 4 methods of attachment and entry inhibition for antiviral medications?

A
  1. attachment inhibitor
  2. post-attachment inhibitor
  3. CCR5 antagonist
  4. fusion inhibitor
90
Q

Fostemsavir is what type of antiviral inhibitor

A

attachment inhibitor

91
Q

Ibalizumab, a monoclonal antibody (mAb) that binds to CD4, is what kind of inhibitor for antivirals?

A

Post-attachment inhibitor

92
Q

What is the mechanism of post-attachment inhibition in antivirals?

A

prevents virus that binds the receptor from then binding to a co-receptor.

93
Q

What is the mechanism of attachment inhibitor antivirals?

A

Occupation of the surface protein so that viruses cannot bind.

94
Q

Maraviroc (MCV) is what kind of antiviral inhibitor?

A

CCR5 antagonist

95
Q

What is the mechanism of antiviral CCR5 antagonists?

A

By binding the specific CCR5 molecule used by HIV strains.

96
Q

Enfuvirtide (ENF) is what kind of antiviral inhibitor?

A

fusion inhibitor

97
Q

What is the mechanism of antiviral fusion inhibitors?

A

Binds to an HIV protein that otherwise promotes fusion of the viral envelope with the cell membrane.

98
Q

What are the 2 groups of antiviral medications that target the uncoating process?

A

Amantadine
Rimantadine

99
Q

What virus do the medications amantadine and rimantadine act on?

A

Influenza A, but most strains are widespread resistant

100
Q

What type of inhibitor is the antiviral lenacapavir (LEN).

A

capsid inhibitor

101
Q

What does capsid inhibitors do to viruses?

A

Binds to the protein subunits of the viral capsid, interfering with capsid assembly and disassembly.

102
Q

What is a nucleoside/nucleotide analog antiviral?

A

Chemical structurally similar to the building blocks of DNA/RNA that interfere with nucleic acid synthesis.

103
Q

What is an antiviral nucleotide analog, specifically?

A

A chain terminator during nucleic acid synthesis.

104
Q

Name 2 nucleoside analogs used to speed the healing of the lesions associated with shingles, chickenpox, cold sores, and genital herpes?

A
  1. Acyclovir
  2. famciclovir
  3. valacyclovir
105
Q

What antiviral is very effective in combination therapy against HCV?

A

Sofosbuvir

106
Q

HIV and HBV are both examples of what kind of virus?

A

reverse-transcribing viruses

107
Q

What is a broad term for all nucleoside and nucleotide analogs that interfere with the activity of reverse transcriptase?

A

NRTIs

108
Q

abacavir, emtricitabine, lamivudine, tenofovir disoproxil fumarate, and azidothymidine are all examples of what type of antiviral?

A

nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs)

109
Q

What NRTIs are used to treat chronic Hep B (HBV)?

A
  1. tenofovir
  2. adefovir
  3. lamivudine
110
Q

What nucleoside analogs have severe side effects and are only used for severe infections (life or sight threatening cytomegalovirus) in immunocompromised patients?

A

Ganciclovir

111
Q

Name the 2 nucleoside analogs that are now being used to treat COVID-19 patients.

A

remdesivir
molnupiravir

112
Q

Compounds that inhibit the activity of viral polymerases by binding to a site other than the nucleotide-binding site.

A

Non-nucleoside polymerase inhibitors

113
Q

Inhibit the activity of reverse transcriptase by binding to a site other than the nucleotide-binding site of the enzyme.

A

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

114
Q

Name 2 NNRTIs

A

doravirine
efavirenz
etravirine
nevirapine
rilpivirine

115
Q

Name 2 NS5A inhibitors

A

elbasvir
ombitasvir
velpatasvir

116
Q

What is cap snatching done by some viruses?

A

they “steal” the 5’ cap from host cell mRNA so that functional viral mRNA can be produced.

117
Q

Name the antiviral medication that target cap snatching in influenza viruses by interfering with the function of the viral endonuclease that catalyzes the process–polymerase acidic (PA) protein.

A

baloxavir marboxil (baloxavir)

118
Q

What does INSTI stand for?

A

Integrate strand transfer inhibitors (often shortened to integrase inhibitors)

119
Q

What is the actions of INSTIs?

A

they interfere with the action of the HIV-encoded enzyme integrase, preventing the virus from inserting the DNA copy of its genome into the host cell genome.

120
Q

Name 2 INSTIs antivirals

A

dolutegravir (DTG)
elvitegravir (EVG)
raltegravir (RAL)
bictegravir (BIC)

120
Q

What does PI stand for in antiviral actions?

A

Protease inhibitors

121
Q

What do proteases do?

A

Break up polyproteins into functional groups. Viral-proteases are virus specific and are encoded to cleave viral polyproteins to release individual proteins.

122
Q

What does the suffix -navir mean in antivirals that treat HIV?

A

It is is a protease inhibitor (PI)

123
Q

name 2 PI antivirals for HIV

A

atazanavir (ATV)
darunavir (DRV)
ritonavir (RTV)

124
Q

what does the suffix -previr mean?

A

protease inhibitors (PIs) used to treat HCV infections

125
Q

Name 2 PIs used to treat HCV

A

grazoprevir
paritaprevir
simeprevir

126
Q

an influenza virus-encoded enzyme required for the release of viral particles from infected cells

A

Neuraminidase

127
Q

Name 2 neuraminidase inhibitors

A

oseltamivir (oral)
zanamivir (inhaled)
peramivir (IM)

128
Q

Explain why acyclovir has fewer side effects than do other nucleoside analogs. (MicroAssessment 20.6)

A
128
Q
A
129
Q

How do proteases inhibitors interfere with the production of infectious viral particles? (MicroAssessment 20.6)

A

PIs block virally-encoded proteases from cleaving polyproteins, thereby preventing functional proteins from forming.

130
Q

Why are nucleoside analogs active only against replicating viruses?

A

Because they mimic DNA/RNA during the polyprotein translation process. Translation only occurs during viral replication.

131
Q

What is the target of most antifungal medications?

A

ergosterol

132
Q

Class of synthetic compounds that function by inhibiting ergosterol synthesis, resulting in defective fungal membranes that leak cytoplasmic contents.

A

Azoles

133
Q

What are the three families of antifungal Azoles?

A

Imidazoles
Triazoles
tetrazoles

134
Q

Commonly used in non-perscription creams, ointments, and suppositories Topically treat vulvovaginal candidiasis.
Topically to treat dermatophyte infections.

A

Imidazoles

135
Q

Miconazole and clotrimazole family.

A

Imidazoles

136
Q

Family of antifungals for
fluconazole
voriconazole
posaconazole
isavuconazole

A

Triazoles

137
Q

Name 2 triazole antifungals

A

fluconazole
voriconazole
posaconazole
isavuconazole

138
Q

Family of antifungals that are extremely important for treating systemic fungal infections.

A

Triazoles

139
Q

Used to treat a wide variety of localized fungal infections like thrush and vulvovaginal candidiasis IN ADDITION to being used in systemic fungal infections.

A

fluconazole

140
Q

use for topically treating nail infections in addition to systemic fungal infections.

A

eficonazole

141
Q

Has higher specificity for ergosterol, resulting in fewer side effects. A new family of azoles.

A

Tetrazoles

142
Q

This drug has been approved for the oral treatment of complicated vulvovaginal candidiasis.

A

Oteseconazole

143
Q

A group of antibiotics produced by certain species of Streptomyces, bind to ergosterol. Quite toxic to humans

A

Polyenes

144
Q

A formulation of polyenes that is too toxic to be used systemically but can be used because it is not absorbed in skin creams, lozenges, and oral suspensions to treat Candida albican infections.

A

nystatin

145
Q

What group of antifungals is Nystatin?

A

Polyenes

146
Q

How do allylamines, tolnaftate, and butenafine work?

A

antifungals that inhibit an enzyme in the pathway of ergosterol synthesis.

147
Q

What are in fungal cell walls that are not produced by animal cells that are targeted by echinocandins and triterpenoids?

A

Beta-1,3 glucan

148
Q

Two families of antifungals that interfere with beta-1,3 glucan synthesis, causing the cells to burst

A

echinocandins
triterpenoids

149
Q

Name 2 echinocandins

A

caspofungin
micafungin
anidulafungin

150
Q

Beta1,3 glucan antifungal family that is particularly useful for treating systemic Candida infections.

A

Echinocandins

151
Q

How are caspofungin, micafungin, and anidulafungin (echinocandins) administered?

A

intravenously

152
Q

A echinocandins that can also be used for treating invasive aspergillosis that does not respond to other medications.

A

caspofungin

153
Q

A fungal strain that is resistant to echinocandins that is of particular concern.

A

C. auris

154
Q

A new antifungal class of beta-1,3 glucans that are represented by ibrexafungerp. (also called the fungerps)

A

triterpenoids

155
Q

The only medication in the triterpenoids family, currently. A beta-1,3 glucan

A

ibrexafungerp

156
Q

Antifungal drug that targets cell division.

A

griseofulvin

157
Q

interferes with the action of tubulin, the protein that polymerizes to form microtubules in fungi.

A

griseofulvin

158
Q

Active only against fungi that invade keratinized cells and is used to treat skin and nail infections

A

griseofulvin

159
Q

A synthetic derivative of the nucleobase cytosine that interferes with nucleic acid synthesis in yeast cells.

A

flucytosine

160
Q

Because resistant mutants are common, this drug is used mostly in combination with amphotericin B or an alternative. However, side effects can be significant, so it is used only for serious yeast infections.

A

flucytosine

161
Q

An antifungal medication that inhibits protein synthesis by interfering with an enzyme that “charges” a tRNA molecule by attaching the correct amino acid.

Used topically to treat nail infections.

A

tavaborole

162
Q

Why is amphotericin B used only for treating life-threatening infections? (MicroAssessment 20.7)

A

The side effects are so severe.

163
Q

Why is flucytosine generally used only in combination with other drugs? (MicroAssessment 20.7)

A

Because resistant mutants are common in yeast cells

164
Q

Why is it reasonable to assume that the therapeutic index of fluconazole is higher than that of nystatin? (Critical Thinking MicroAssessment 20.7)

A

Because the toxicity of nystatin is too high for systemic use; however, fluconazole can be used systemically.

165
Q

What is the likely method of action for most parasites and worm medications?

A

Probably interfere with biosynthetic pathways protozoans and neuromuscular function of worms.

166
Q

Why are there relative little R&D into antiparasitic medications?

A

Because most parasitic diseases are neglected tropical diseases (NTDs); NTDs are in resource-limited areas of the world

167
Q

What antibacterial drugs can be used for treating diseases caused by apicomplexan protozoa, including Plasmodium spp. and Toxoplasma gondii?

A

doxycycline
tetracycline
clindamycin

168
Q

What do doxycycline, tetracyclines, and Clindamycin appear to target in parasites?

A

structures called apicoplasts, which appear to be of bacterial origin and thought to be a product of secondary endosymbiosis

169
Q
A

Microbiology (4 decks)

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