Chapter 14 *Important* Flashcards

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1
Q

Read 14.1 in textbook

A
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2
Q

What should be considered when choosing a drug?

A
  • Interaction with bacteria and host: Bacteriostatic or bactericidal?
  • Spectrum of activity
  • Dosage
  • Route of administration
  • Drug interactions
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3
Q

Bacteriostatic versus bactericidal?

A
  • Antimicrobial drugs can be bacteriostatic or bactericidal
  • The decision depends on the type of infection and the immune status of the patient
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4
Q

Ex. A person has sepsis due to a blood infection, do you use bacteriostatic or bactericidal?

A

Bactericidal because we want to kill the bacteria and we are in critical condition with not a lot of time to preform tests.

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5
Q

What do narrow-spectrum antimicrobial drugs do?

A

Avoid superinfection and the development of antimicrobial resistance.

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6
Q

When are broad-spectrum antimicrobial drugs issued?

A

Warranted for serious systemic infections for the treatment or prevention of infections with multiple types of microbes.

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7
Q

What do broad-spectrum antimicrobial drugs do?

A

Target a wide variety of bacterial pathogens, including both gram-positive and gram-negative, and is frequently used as empiric therapy.

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8
Q

What is empiric therapy?

A

A medical treatment or therapy based on experience.

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9
Q

What is the problem with broad-spectrum antibiotics?

A

It can kill the good bacteria that is keeping the pathogens under control allowing the pathogens to proliferate and cause a superinfection.

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10
Q

What does half-life mean?

A

The rate at which 50% of a drug is eliminated from the plasma.

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11
Q

What are synergistic combinations?

A

The drugs have a better effect together than the efficacy of either drug alone.

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12
Q

KNOW COMMON ANTIBACTERIAL DRUGS BY MODE OF ACTION CHART

A

Oct. 20th Slide 12

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13
Q

What do antibacterial compounds exhibit?

A

Selective toxicity due to differences between prokaryotic and eukaryotic cell structure.

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14
Q

What are the cell wall synthesis inhibitors?

A

B-lactams, glycopeptides, and bacitracin.

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15
Q

What do cell wall synthesis inhibitors do?

A

Interfere with peptoglycan synthesis, making bacterial cells more prone to osmotic lysis.

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16
Q

What are the drug classes?

A

Penicillins, cephalosporins, monobactams, carbapenems, glycopeptides, bacitracin

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17
Q

What is the mechanism of action of penicillins, cephalosporins, monobactams, and carbapenems?

A

Interact directly with PBPs and inhibit transepeptidase activity.

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18
Q

What is the mechanism of action of glycopeptides?

A

Large molecules that bind to the peptidoglycan subunits, blocking transglycosylation and transpeptidation.

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19
Q

What is the mechanism of action of bacitracin?

A

Block transport of peptidoglycan subunits across cytoplasmic membrane.

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20
Q

CHART SLIDES 14 & 15

A
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21
Q

What are the three major classes of protein synthesis-inhibiting antibacterials?

A
  • Chloramphenicol, macrolides, and lincosamides
  • Aminoglycosides
  • Tetracyclines
22
Q

What do chloramphenicol, macrolides, and lincosamides do?

A
  • Bind to the 50S ribosomal subunit
  • Prevent peptide bond formation
  • Stop protein synthesis
23
Q

What do aminoglycosides do?

A
  • Bind to the 30S ribosomal subunit
  • Impair proofreading, resulting in production of faulty proteins
24
Q

What do tetracyclines do?

A
  • Bind to the 30S ribosomal subunit
  • Block the binding of tRNAs, thereby inhibiting protein synthesis
25
Q

CHART ABOUT SUBUNITS SLIDE 17

A
26
Q

What have aminoglycosides been found to be?

A

Nephrotoxic (damaging to kidney), neurotoxic (damaging to the nervous system), and ototoxic (damaging to the ear).

27
Q

What are some characteristics of membrane function inhibitors?

A
  • Lipophilic
  • Interact with lipopolysaccharide component of outer membrane of gram-negative bacteria
  • Disrupts membranes and kills bacterial cells
28
Q

MEMBRANE CHART SLIDE 19

A
29
Q

NUCLECIC ACID CHART SLIDE 20

A
30
Q

What are antimetabolites?

A

Act as competitive inhibitors for bacterial metabolic enzymes.

31
Q

METABOLIC CHART SLIDE 21

A
32
Q

Why is it difficult to target fungi, protozoans, and helminths?

A

They are eukaryotic organisms like humans so it is difficult to specifically target then with drugs

33
Q

Why is it hard to target viruses?

A

Human viruses replicate inside human cells.

34
Q

What do antifungal drugs do?

A

Interfere with ergosterol synthesis, bind to ergosterol to disrupt fungal cell membrane integrity, or target cell wall specific components or other cellular proteins.

35
Q

ANTIFUNGAL CHART SLIDE 24

A
36
Q

What do antiprotozoan drugs do?

A

Increase cellular levels of reactive oxygen species, interfere with protozoal DNA replication (nuclear versus kDNA, respectively), and disrupt heme detoxification.

37
Q

ANTIPROTOZOAN CHART SLIDE 25

A
38
Q

What do antihelminthic drugs do?

A

Disrupt helminthic and protozoan microtubule formation; block neuronal transmissions; inhibit anaerobic ATP formation and/or oxidative phosphorylation; induce a calcium influx in tapeworms, leading to spasms and paralysis; and interfere with RNA synthesis in schistosomes.

39
Q

ANTIHELMINTHIC CHART SLIDE 26

A
40
Q

What do antiviral drugs do?

A

Inhibit viral uncoating, inhibit nucleic acid biosynthesis, prevent viral escape from endosomes in host cells, and prevent viral release from infected cells.

41
Q

ANTIVIRAL CHART SLIDE 27

A
42
Q

What is antimicrobial resistance the result of?

A
  • Selection of drug-resistant strains in clinical environments
  • The overuse and misuse of antibacterials
  • The use of subtherapeutic doses of antibacterial drugs
  • Poor patient compliance with antibacterial drug therapies
43
Q

How are drug resistance genes passed?

A

Often carried on plasmids or in transposons that can undergo vertical transfer easily and between microbes through horizontal gene transfer.

44
Q

What are common modes of antimicrobial drug resistance?

A
  • Drug modification or inactivation
  • Prevention of cellular uptake or efflux
  • Target modification
  • Target overproduction or enzymatic bypass
  • Target mimicry
45
Q

What problematic microbial strains are emerging?

A
  • Ones that are showing extensive antimicrobial resistance
    Many of these strains can reside as members of the normal microbiota in individuals but also can cause opportunistic infection.
46
Q

Where does the transmission of these highly resistant microbial strains occur?

A

In clinical settings

47
Q

What does the Kirby-Bauer disk diffusion help determine?

A

The susceptibility of a microorganism to various antimicrobial drugs.

48
Q

What information does and doesn’t the Kirby-Bauer disk diffusion test demonstrate?

A

Determine susceptibility and resistance, compared to know standards.
Cannot provide info on bactericidal versus bacteriostatic activity or allow for direct comparison.

49
Q

What are antibiograms useful for?

A

Monitoring local trends in antimicrobial resistance/susceptibility and for directing appropriate selection of empiric antibacterial therapy.

50
Q

What are antibacterial dilution tests used to determine?

A

A particular drug’s minimal inhibitory concentration (MIC) (the lowest concentration of drug that inhibits visible bacterial growth) and minimal bactericidal concentration (MBC) (the lowest drug concentration that kills 99.9% of the starting inoculum).