Antimicrobial Drugs Flashcards

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1
Q

Chemotherapy

A

The use of drugs to treat a disease.

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2
Q

Antimicrobial drugs

A

Interfere with growth of microbes within a host

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3
Q

Antibiotic

A

A substance produced by a microbe that, in small amounts, inhibits another microbe

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4
Q

Selective toxicity

A

Killing harmful microbes without damaging the host.

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5
Q

Who discovered Penicillin, produced by Penicillium?

A

Fleming (1928)

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6
Q

What is Prontosil red dye used for?

A

Streptococcal infections- a sulfanilamide: sulfur based

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7
Q

When were the first clinical trial of penicillin?

A

1940

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8
Q

Today there’s a growth problem of:

A

Antibiotic resistance

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9
Q

In 1940, who performed the first clinical trials of penicillin?

A

Howard Florey and Ernst Chain

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10
Q

Narrow spectrum of microbial activity:

A

Drugs that affect a narrow range of microbial types

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11
Q

Broad-spectrum antibiotics

A

Affects a broad range of gram + or gram - bacteria.

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12
Q

Bacteriocidal

A

Kills microbe directly (a drug used to kill bacteria)

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13
Q

Bacteriostatic

A

Prevents microbes from growing

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14
Q

Superinfection

A

overgrowth of normal microbiota that is resistant to antibiotics

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15
Q

5 major action modes of antimicrobial drugs
1st action

A
  1. inhibition of cell wall synthesis: penicillins, cephalosporins, bacitracin, vancomycin
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16
Q

5 major action modes of antimicrobial drugs
2nd action:

A

Inhibition of protein synthesis: erythryomycin, tetracyclines, streptomycin, chloramphenicol.

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17
Q

5 major action modes of antimicrobial drugs
3rd action

A
  1. Inhibition of nucleic acid replication and transcription: quinolone, rifampin. (Drugs that are usually specific t viruses)
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18
Q

5 major action modes of antimicrobial drugs
4th action

A
  1. Injury to plasma membrane: polymyxin B
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19
Q

5 major action modes of antimicrobial drugs
5th action:

A

Inhibition of essential metabolite synthesis: sulfanimide, trimethoprim

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20
Q

Inhibitors of cell wall synthesis (inhibit new cell wall formation)

A

-penicillin
-natural penicillins
-semisynthetic penicillins
-extended-spectrum penicillins

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21
Q

Penicillin contains:

A

β-lactam ring: active ingredient that prevents cross-linking
The types are differentiated by the chemical side chains attached to the ring

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22
Q

Penicillin prevents

A

The cross-linking of peptidoglycans, interfering with cell wall construction (especially gram positives)

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23
Q

Natural penicillins extracted from:

A

Penicillium cultures: penicillin G (injected) and penicillin V (oral)

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24
Q

Natural penicillins are susceptible to:

A

penicillinases (β-lactamases)
- narrow spectrum of activity

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25
Q

Semisynthetic penicillins

A

• Contain chemically added side chains, making them resistant to penicillinases

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26
Q

Oxacillin:

A

Narrow spectrum, only gram-positives, but resistant to penicillinase

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27
Q

Ampicillin:

A

Extended spectrum, many gram-negatives

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28
Q

Penicillinase-resistant penicillins

A

Methicillin and oxacillin

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29
Q

Extended-spectrum penicillins

A

Effective against gram-negatives as well as gram-positives
• Aminopenicillins: ampicillin, amoxicillin

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30
Q

Penicillins plus β-lactamase inhibitors

A

Contain clavulanic acid, a noncompetitive inhibitor of penicillinase

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31
Q

Carbapenems

A

Substitute a C for an S and add a double bond to the penicillin nucleus
• Broad spectrum
• Primaxin, doripenem

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32
Q

• Monobactam

A

Synthetic; single ring instead of the β-lactam double ring
• Low toxicity; works against only certain gram-negatives
• Aztreonam

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33
Q

Cephalosporins

A

Work similar to penicillins
• β-lactam ring differs from penicillin
• Grouped according to their generation of development

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34
Q

Polypeptide antibiotics

A

Bacitracin (wounds; first aid ointment
• Topical application; works against gram-positives
• Vancomycin
• Glycopeptide
• Last line against antibiotic-resistant MRSA

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35
Q

Antimycobacterial Antibiotics:

Isoniazid (INH)

A

• Inhibits the mycolic acid synthesis in mycobacteria

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36
Q

Antimycobacterial Antibiotics

Ethambutol

A

• Inhibits incorporation of mycolic acid into the cell wall

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37
Q

Inhibition of Cell Wall Synthesis

A

Prevent bacteria from increasing amount of peptidoglycan
• Have no effect on fully formed bacteria
• Effective only for growing, young populations

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38
Q

Inhibition of Cell Wall Synthesis= No effect on plant or animal cells; Why?

A

Cross bridges are already in place
None of these cell walls have peptidoglycan

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39
Q

Inhibiting Protein Synthesis

A

Target bacterial 70S ribosomes
• Large or small subunit
• Chloramphenicol, erythromycin, streptomycin, tetracyclines

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40
Q

Chloramphenicol inhibits

A

Peptide bond formation

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41
Q

Chloramphenicol binds to:

A

50S subunit of the 70S ribosome

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42
Q

Chloramphenicol can suppress ______ and affect ________

A

Bone marrow
Blood cell formation
Can be synthesized chemically; broad spectrum

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43
Q

Aminoglycosides are

A

• Amino sugars linked by glycoside bonds

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44
Q

Aminoglycosides change

A

the shape of the 30S subunit of the 70S ribosome

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45
Q

Aminoglycosides can cause

A

auditory damage (not recommended for pregnant) • Streptomycin, neomycin, gentamicin
• Teratogenic – harmful to a pregnancy

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46
Q

Some antibiotics are known to be teratogenic and should be avoided entirely during pregnancy. These
include ____________ and _____________ (which may cause hearing loss) and tetracycline (which can lead to weakening, hypoplasia, and discoloration of long bones and teeth).

A

Streptomycin and kanamycin

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47
Q

Tetracyclines are produced by

A

Streptomyces spp.

48
Q

Tetracyclines interfere with

A

the tRNA attachment to the ribosome

49
Q

Tetracyclines can suppress:

A

Normal intestinal microbiota
Broad spectrum; penetrates tissues, making them valuable against rickettsias and chlamydias

50
Q

Inhibitors of Protein Synthesis

Glycylcyclines:

A

Broad spectrum; bacteriostatic

51
Q

Inhibitors of Protein Synthesis

Glycylcyclines bind to

A

30S ribosomal subunit

52
Q

Inhibitors of Protein Synthesis

Glycylcyclines inhibits

A

rapid efflux; administered intravenously

53
Q

Inhibitors of Protein Synthesis

Glycylcyclines useful against

A

MRSA

54
Q

Inhibitors of Protein Synthesis
Macrolides contain:

A

Macrocyclic lactone ring

55
Q

Inhibitors of Protein Synthesis
Macrolides:

A

• Narrow spectrum against gram-positives
• Erythromycin

56
Q

Inhibitors of Protein Synthesis

Streptogramins attach to

A

the 50S subunit

57
Q

Inhibitors of Protein Synthesis

Streptogramins work against

A

gram-positives that are resistant to other antibiotics

58
Q

Inhibitors of Protein Synthesis

Oxazolidinones bind to the

A

50S/30S subunit interface

59
Q

Inhibitors of Protein Synthesis

Oxazolidinones:

A

Synthetic; combat MRSA (linezolid)

60
Q

Inhibitors of Protein Synthesis
Pleuromutilins

A

Retapamulin: topical and effective against gram- positives

61
Q

Injury to the Plasma Membrane
Lipopeptides:

A

Structural changes in the membrane, followed by arrest of the synthesis of DNA, RNA, and protein
MRSA

62
Q

Injury to the Plasma Membrane
Polymyxin B

A

Topical
Combined with bacitracin and neomycin in over-the-counter preparation

63
Q

Injury to the Plasma Membrane

Amphotericin B (polyene):

A

attaches to ergosterol found in fungal membranes
• Humans somewhat susceptible because cholesterol similar to ergosterol
• Bacteria lack sterols; not susceptible

64
Q

Inhibition of nucleic acid synthesis

A

Interfere with DNA replication and transcription • Nucleoside analogs (used against viruses)

65
Q

• Inhibition of synthesis of essential metabolites

A

• Anti-metabolites compete with normal substrates for an enzyme
• Sulfanilamide competes with para-aminobenzoic acid (PABA), stopping the synthesis of folic acid

66
Q

Nucleic Acid Synthesis Inhibitors

Rifamycin inhibits

A

mRNA synthesis

67
Q

Nucleic Acid Synthesis Inhibitors

Rifamycin penetrates

A

tissues; antitubercular activity

68
Q

Nucleic Acid Synthesis Inhibitors

Quinolone and fluoroquinolones

A
  • Nalidixic acid
    • Synthetic; inhibits DNA gyrase
    • Norfloxacin and ciprofloxacin
    • Broad spectrum; relatively nontoxic
69
Q

Sulfonamides: folic acid synthesis

Sulfonamides inhibit

A

the folic acid synthesis needed for nucleic acid and protein synthesis

70
Q

Sulfonamides competitively bind

A

to the enzyme for PABA production, a folic acid precursor

71
Q

Sulfonamides are a Combination of

A

trimethoprim and sulfamethoxazole (TMP-SMZ) is an example of drug synergism

72
Q

Inhibition of a metabolic function: Competitive Inhibitors

• Sulfonamides (sulfa drugs)

A

Inhibit folic acid synthesis
• Broad spectrum

73
Q

Antifungal Drugs: Inhibition of Ergosterol Synthesis

Polyenes:

A

§ Amphotericin B

74
Q

Antifungal Drugs: Inhibition of Ergosterol Synthesis

Azoles: topical ointment

A
  • Miconazole
    • Triazole
75
Q

Antifungal Drugs: Inhibition of Ergosterol Synthesis

Allylamines

A

• For azole-resistant infections

76
Q

Antifungal Drugs

Agents affecting fungal cell walls

A

Echinocandins
• Inhibit the synthesis of β-glucan

77
Q

Antifungal Drugs

Agents inhibiting nucleic acids

A

Flucytosine
• Cytosine analog interferes with RNA synthesis

78
Q

Antifungal Drugs
• Griseofulvin

A

• Produced by Penicillium
• Inhibits microtubule formation
• Active against superficial dermatophytes

79
Q

Antifungal Drugs

• Tolnaftate

A

Athletes foot

80
Q

Antifungal Drugs

Pentamidine

A

• Anti-Pneumocystis; may bind to DNA

81
Q

Antiviral Drugs

A

Entry and fusion inhibitors
• Block the receptors on the host cell that bind to the virus • Block fusion of the virus and cell
• Uncoating, genome integration, and nucleic acid synthesis inhibitors
• Prevent viral uncoating
• Inhibit viral DNA integration into the host genome • Nucleoside analogs inhibit RNA or DNA synthesis

82
Q

A nucleoside analog:

A

The structure and function of the antiviral drug acyclovir.

83
Q

Antiviral Drugs

A

Interference with assembly and release of viral particles
• Protease inhibitors
• Block the cleavage of protein precursors
• Exit inhibitors
• Inhibit neuraminidase, an enzyme required for some viruses to bud from the host cell

84
Q

Interferons (for RNA viruses)

A

• Produced by viral-infected cells to inhibit further spread of the infection
• Imiquimod
• Promotes interferon production

85
Q

Antivirals for Treating HIV/AIDS

A

• Antiretroviral
• Nucleoside analog (zidovudine)
• Nucleotide analog (tenofovir)
• Non-nucleoside inhibitors (nevirapine) • Protease inhibitors (atazanavir)
• Integrase inhibitors (raltegravir)
• Entry inhibitors (miraviroc)
• Fusion inhibitors (enfuvirtide)

86
Q

• Antiprotozoan drugs

A

• Quinine and chloroquine
• Treat malaria

87
Q

Artemisinin

A

• Kills Plasmodium that causes malaria

88
Q

Metronidazole (Flagyl): parasitic/c diff

A

Also interferes with anaerobic bacteria
• Treats Trichomonas, giardiasis, and amebic dysentery

89
Q

Antihelminthic drugs

A

Niclosamide
• Prevents ATP production
• Treats tapeworms

90
Q

Praziquantel

A

Alters membrane permeability • Treatstapewormsandflukes

91
Q

Mebendazole and albendazole

A

Interfere with nutrient absorption • Treat intestinal helminths

92
Q

Ivermectin (ppl thought it could decrease covid?)

A

Paralysis of helminths
• Treats roundworms and mites

93
Q

Antibiotic Resistance

A

• A variety of mutations can lead to antibiotic resistance
• Resistance genes are often on plasmids or transposons that can be transferred between bacteria

94
Q

Mechanisms of resistance (method of blocking or denaturing a drug)

A
  1. Blocking entry/: tougher cell wall
  2. Inactivation by enzymes
  3. Alteration of target molecule
  4. Efflux of antibiotic
95
Q

Mechanisms of Resistance

A

Enzymatic destruction or inactivation of the drug
• Prevention of penetration to the target site within the microbe • Alteration of the drug’s target site
• Rapid efflux (ejection) of the antibiotic
• Variations of mechanisms of resistance

96
Q

Resistance to antimicrobial drugs-
Persisted cells are:

A

microbes with genetic characteristics allowing for their survival when exposed to an antibiotic (this is why you must finish complete dose of antibiotic)

97
Q

Resistance to antimicrobial drugs-
Superbugs:

A

bacteria that are resistant to large numbers of antibiotics

98
Q

Resistance genes are

A

often spread horizontally among bacteria on plasmids or transposons via conjugation or transduction

99
Q

Antibiotic resistance

A

Misuse of antibiotics selected for resistance mutants

100
Q

Antibiotic resistance misuse includes:

A

• Using outdated or weakened antibiotics
• Using antibiotics for the common cold and other inappropriate conditions
• Using antibiotics in animal feed (slaughtered as a healthy animal for consumption)
• Failing to complete the prescribed regimen
• Using someone else’s leftover prescription (leaving the body susceptible to mutants)

101
Q

Antibiotic Safety

A

• Therapeutic index: risk versus benefit
• Reactions of antibiotics with other drugs
• Damage to organs
• Risk to the fetus

102
Q

Effects of combination drugs: SYNERGISM AND ANTAGONISM

A

SYNERGISM AND ANTAGONISM

103
Q

Synergism

A

The effect of two drugs together is GREATER than the effect of either alone

104
Q

Antagonism

A

the effect of two drugs together is LESS than the effect of either alone

105
Q

Area of synergistic inhibition looks:

A

CLEAR

106
Q

Area of growth=

A

CLOUDY

107
Q

Methods of analyzing EFFICACY(safety+how much is needed to work)
DIFFUSION METHODS:

A

Disk-diffusion method (also called Kirby-Bauer test)

108
Q

Disk-diffusion method (also called Kirby-Bauer test) tests the effectiveness of:

A

Chemotherapeutic agents

109
Q

Disk-diffusion method (Kirby-Bauer test) are:

A

Paper disks with a chemotherapeutic agent are placed on agar containing the test organism

110
Q

Disk-diffusion method (Kirby-Bauer test)
Zone of inhibition around the disk

A

determines the sensitivity of the organism to the antibiotic

111
Q

The disk-diffusion method for determining the activity of antimicrobials:

A

Measure the diameter of zones in mm (no zone=no clear circle surrounding it)
> 22mm = susceptible
< 22mm = resistant

112
Q

What is the E test in diffusion methods?

A

Determines the minimal inhibitory concentration (MIC)
(Always start with minimum)

113
Q

E tests are lowest in ?

A

Lowest antibiotic concentration preventing bacterial growth

114
Q

Broth dilution tests are used to determine:

A

The MIC and minimal bactericidal concentration (MBC) of an antimicrobial drug

115
Q

Broth dilution tests are used to test:

A

An organism placed into the wells of a tray containing dilutions of a drug; growth is determined.

116
Q

What are Antibiograms in broth dilution tests?

A

Reports that record the susceptibility of organisms encountered clinically

117
Q

Future of chemotherapeutic agents

A

-target virulence factors
-sequester iron, which feeds pathogens
Antimicrobial peptides produced by various organisms
Phage therapy: bacterial virus
Bacteriocins: antimicrobial peptides produced by bacteria