Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology Unit 2 > (9-23) Antimicrobial Medications > Flashcards

(9-23) Antimicrobial Medications Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What did Paul Ehrlich discover in 1910?

A

He discovered that an arsenic-containing compound was effective against Treponema pallidum (the causative agent in Syphilis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What did Gerhard Domagk discover in 1932?

A

He discovered that Prontosil was effective against Streptococcus. [The breakdown product, sulfanilamide, was active.]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What was the first sulfa drug?

A

Prontosil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the definition of an antimicrobial drug?

A

A chemical that inhibits the growth of, or kills, microorganisms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is an antibiotic?

A

An antimicrobial drug naturally produced by mold or bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What did Andrew Fleming discover in 1928?

A

He discovered that mold Penicillium produced a substance (termed “penicillin”) that killed bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mass production of which drug saved many soldiers’ lives during WWII?

A

Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is one example of a semisynthetic antibiotic?

A

Penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does selective toxicity mean?

A

Antibiotics cause greater harm to microorganisms than to human host.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does selective toxicity cause greater harm to microorganisms than to the human host?

A

By interfering with biological structures or biochemical processes common to bacteria, but not to humans.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is the toxicity of a drug expressed?

A

As a therapeutic index

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is the therapeutic index of a drug calculated?

A

The lowest dose toxic to a patient divided by dose typically used for treatment (high therapeutic index = less toxic to patient).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is an antimicrobial’s spectrum of activity?

A

Antimicrobials vary with respect to the range of organisms controlled.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Explain and give examples of 2 spectrums of antibiotics.

A
  1. Narrow spectrum: works on a narrow range of organisms
    ~ ex. G+ or G- bacteria ONLY
  2. Broad spectrum: work on a broad range of organisms
    ~ ex. G+ and G- bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the disadvantage of broad spectrum antibiotics?

A

Disruption of normal flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is antimicrobial action?

A

Drugs may kill or inhibit bacterial growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When a drug’s action is to inhibit bacterial growth, it is termed what?

A

Bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When a drug’s action is to kill bacteria, it is termed what?

A

Bacteriocidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 6 mechanisms of action of antibacterial drugs?

A
  1. Selective toxicity
  2. Inhibition of cell wall synthesis
  3. Inhibition of protein synthesis
  4. Inhibition of metabolic pathways
  5. Inhibition of nucleic acid synthesis
  6. Interference with cell membrane integrity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why can antibiotics inhibit cell wall synthesis?

A

Eukaryotes lack cell walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why can antibiotics inhibit protein synthesis?

A

Ribosomal differences
~ Prokaryotic = 70s ribosome
~ Eukaryotic = 80s ribosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why can antibiotics inhibit metabolic pathways?

A

It utilizes those that are different or lacking in eukaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why can antibiotics inhibit nucleic acid synthesis?

A

Prokaryotic enzymes are different than eukaryotic enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why can antibiotics interfere with cell membrane integrity?

A

They can bind to the membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What level of therapeutic index do Cell Wall Synthesis inhibiting drugs have?

A

Very high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which organisms do Cell Wall Synthesis inhibiting drugs affect and what are they effective against?

A
  1. Only affect prokaryotes

2. Only effective in actively growing bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What type of drug are β-Lactams?

A

Cell Wall Synthesis inhibiting

28
Q

What are 2 classes of β-Lactam drugs?

A
  1. Penicillins

2. Cephalosporins

29
Q

Are β-Lactam drugs more effective against Gram postive or negative bacteria?

A

Gram positive

30
Q

How do β-Lactam Drugs inhibit Cell Wall Synthesis?

A

They inhibit enzyme that forms peptide side chains between NAG-NAM chains of peptiodglycan.

31
Q

How can Semisynthetic versions of β-Lactam Drugs better fight bacteria? List 2 ways, with
an exmple of each.

A
  1. Semisynthetic versions can be broad spectrum
    ~ ex Ampicillin
  2. Semisynthetic versions “resist” β-lactamase
    ~ ex. Methicillin)
32
Q

What enzyme contributes to bacterial resistance of β-Lactam Drugs?

A

Resistance is commonly by β-lactamase enzyme

33
Q

Which bacterial anatomical feature does Vancomycin affect, and what is its mode of operation?

A

Vancomycin binds NAM, inhibiting synthesis of chains, thereby inhibiting cell wall synthesis.

34
Q

Which bacterial anatomical feature does Bacitracin affect, and what is its mode of operation?

A

interferes with transport of cell wall precursors

35
Q

Aminoglycosides are in which class of drugs? What is an example of an Aminoglycoside?

A

They are the Protein Synthesis Inhibition drugs

~ ex, streptomycin

36
Q

What are Aminoglycosides not effective against, and why?

A

Anaerobes

~ Aminoglycosides are actively transported into cell by process that requires respiratory metabolism

37
Q

What do Aminoglycosides do, once they are actively transported into the cell?

A

They irreversibly binds to 30S ribosomal subunit, blocking initiation of translation

38
Q

Which type of drug are Aminoglycosides often often used in combination with?

A

β-lactam drugs

39
Q

How does a bacterium gain resistance against a Protein Synthesis Inhibition drug?

A

Resistance is via a single point mutation in the gene that codes for the protein portion of 30S ribosome

40
Q

Which type of drug is most useful in inhibiting Metabolic Pathways, and what do they do?

A

Folate Inhibitors

~inhibit the production of folic acid

41
Q

Sulfonamides and Trimethoprim belong to which class of antimicrobial?

A

Metabolic Pathway Inhibition drugs

42
Q

How do Sulfonamides (sulfa drugs) work?

A

They competitively inhibit the enzyme that aids in production of folic acid

[Human cells lack enzyme –> selective toxicity]

43
Q

How does Trimethoprim work?

A

It inhibits the enzyme that humans have, but enzymes are different enough so toxicity is low

44
Q

Which drugs Inhibit Nucleic Acid Synthesis? Give one example.

A

Rifamycins

~ ex, Rifampin

45
Q

Which type of drug is effective against Mycobacterium?

A

Rifamycins

46
Q

How do Rifamycins work?

A

They block prokaryotic RNA polymerase, stopping initiation of transcription

47
Q

Where does resistance against Nucleic Acid Synthesis drugs come from?

A

Mutation in gene coding for RNA polymerase

48
Q

What are 3 factors that contribute to the limited range of antimicrobials used in treatment of infections caused by M. tuberculosis?

A
  1. chronic nature of disease
  2. slow growth
  3. waxy lipid in cell wall
49
Q

Why is the cell wall of M. tuberculosis waxy, and in which way does that enhance the bacterium’s ability to resist antibiotics?

A

Waxy cell wall due to mycolic acid is impervious to many drugs

50
Q

Which 2 drugs are effective against M. tuberculosis? How do they operate?

A
  1. Rifampin
    ~ blocks RNA polymerase, stopping initiation of transcription
  2. Isoniazid
    ~ inhibits synthesis of mycolic acid
51
Q

Which antiviral medications eliminate latent virus?

A

NONE of them.

52
Q

What are 3 possible targets of antiviral medications?

A
  1. Polymerase inhibitors
  2. Viral uncoating
  3. Neuraminidase inhibitors
53
Q

How do the Viral uncoating Antiviral Medications, Amantadine and Rimantadine work, and against which virus?

A

They block uncoating of influenza virus after it enters cell

54
Q

How do the Neuraminidase inhibitor Antiviral Medications, zanamivir and oseltamivir, work, and against which virus?

A

They block enzyme essential for release of influenza virus (neuraminidase)

55
Q

Which 4 antiviral medications are used against Influenza?

A
  1. amantadine
  2. rimantadine
  3. zanamivir
  4. oseltamivir
56
Q

What are the 2 broad mechanisms of drug resistance?

A
  1. Drug inactivating enzymes

2. Alteration of target molecule

57
Q

How do Drug inactivating enzymes work?

A

Some organisms produce enzymes that chemically modify drug

~ ex. β-lactamase enzyme breaks β-lactam ring of penicillin antibiotics

58
Q

How do alterations of target molecule lead to drug resistance?

A

Minor structural changes in antibiotic target can prevent binding
~ ex. Changes in ribosomal protein prevents aminoglycosides from binding

59
Q

How can drug resistance be “shared” (transferred)?

A

vertically or horizontally

60
Q

How do Quinolines work?

A

They inhibit heme polymerization

61
Q

List 3 examples of Quinolines.

A

1 Quinine

  1. Chloroquine
  2. Mefloquine
62
Q

Why does Plasmodium polymerize the Heme group of hemoglobin?

A

The Heme group is toxic to the parasite.

63
Q

What do Plasmodium digest for energy, and where does it get it?

A

Plasmodium in RBC digest hemoglobin for energy

64
Q

What part of the hemoglobin does Plasmodium metaboliz, and how does it handlethe rest of the molecule?

A
  1. Able to digest globin part of hemoglobin (protein) but not able to digest the ring-like heme group
  2. cross-links all the heme to form the non-toxic polymer hemozoin
65
Q

Which product of Plasmodium erythrocyte invasion is pigmented, and can easily be seen under the microscope?

A

Hemozoin

Microbiology Unit 2 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions