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BMS 212 > Chapter 13: Antimicrobial Drugs Slides > Flashcards

Chapter 13: Antimicrobial Drugs Slides Flashcards

1
Q

What are drugs?

A

Chemicals that affect physiology in any manner.

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2
Q

What are chemotherapeutic agents?

A

Drugs that act against diseases.

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2
Q

What are chemotherapeutic agents?

A

Drugs that act against diseases.

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3
Q

What are antimicrobial agents (antimicrobial)?

A

Drugs that treat infections.

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4
Q

What are natural antibiotics?

A

Drug naturally occurring in nature (bacteria and fungus).

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5
Q

What are semisynthetic antimicrobials?

A

Modified version of natural antibiotic that have a better shelf life and work better against bacteria.

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6
Q

What are synthetic antimicrobials?

A

Developed from a drug not found in nature (made in a lab).

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7
Q

What happens when you take a bacteriostaic drug away?

A

When a bacteriostatic drug is taken away, the bacteria can start growing again.

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8
Q

What happens when you take a bacteriocidal drug away?

A

The bacteria cannot grow even after the antibiotic is gone.

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9
Q

What does chemotherapy do for selective toxicity?

A

Targets enzyme/pathway critical for bacterial survival
Targets enzyme/pathway not present/very divergent in humans

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10
Q

What drugs are limited due to selective toxicity?

A

Drugs to treat eukaryotic infections and antiviral drugs.

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11
Q

What is the most common way drugs cause inhibition of the synthesis of bacterial walls?

A

Most common agents prevent cross-linkage of NAM subunits (peptidoglycan).

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12
Q

What is the most prominent group when it comes to drugs that inhibit the synthesis of cell walls?

A

Beta-lactams.

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13
Q

What is transpeptidase?

A

Part of a class of enzyme that crosslinks the peptidoglycan layer and reshaping the cell wall during growth a division.

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14
Q

What enzyme do Beta-lactams attach?

A

Transpeptidase.

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15
Q

What is attacking the cell wall a good way of killing the cell?

A

We don’t have cell walls
When bacteria’s cell walls are weak, they eventually lyse.

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16
Q

Why are the semisynthetic derivatives of beta-lactams better?

A

More stable in acidic environments (stomach)
More readily absorbed (in places like the bloodstream)
Less susceptible to deactivation (by bacteria)
More active against more types of bacteria

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17
Q

How does vancomycin hurt cell walls?

A

They prevent the enzyme from finishing the NAM cross-bridge in Gram-positive bacteria.

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18
Q

How have bacteria become resistant to vancomycin?

A

They have changed their amino acids for making peptidogylcan, some vancomycin is not cannot bind and block the enzyme.

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19
Q

How does cycloserine affect bacterial cell walls?

A

They interfere with particular bridges that link NAM subunits in many Gram-positive bacteria.

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20
Q

How does bacitracin affect bacterial cell walls?

A

Blocks the transport of NAG and NAM from cytoplasm so they have nothing the rebuild their peptidoglycan walls.

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21
Q

How does isoniazid and ethambutol affect bacterial cell walls?

A

They disrupt mycolic acid formation in mycobacterial species (specialized for diseases like TB).

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22
Q

Why is inhibiting protein synthesis a good way of selective toxicity?

A

Prokaryotic ribosomes are 70S (30S and 50S)
Eukaryotic ribosomes are 80S (40S and 60S)
Drugs can selectively target translation.

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23
Q

What is the danger of inhibiting protein synthesis?

A

Mitochondria of animals and humans also contain 70S ribosomes.

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24
Q

How do aminoglycosides inhibit protein synthesis?

A

They cause a change in 30S shape, so mRNA is misread. The bacteria can still build proteins, but they are not useful/functional.

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25
Q

How do tetracyclines inhibit protein synthesis?

A

They block docking sites of tRNA, specifically the A site. Protein synthesis stops.

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26
Q

How do tetracyclines inhibit protein synthesis?

A

They block docking sites of tRNA, specifically the A site. Protein synthesis stops.

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27
Q

How does chloramphenicol inhibit protein synthesis?

A

It blocks the peptide bond formation. No protein synthesis can occur.

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28
Q

How do lincosamides inhibit protein synthesis?

A

They bind to the 50S subunit, blocking proper mRNA movement through ribosomes. This slows the whole process down like an anchor. Protein synthesis stops.

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29
Q

What does linezolid do to inhibit protein synthesis?

A

It prevents the subunits from sandwiching the DNA between them by affecting the large subunit. Protein cannot be made.

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30
Q

What is polymyxin?

A

An antibiotic that disrupts the cytoplasmic membranes of Gram-negative bacteria.

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31
Q

Why are antibiotics that disruption cytoplasmic membranes a little dangerous?

A

They can be toxic to organs like the kidneys if taken orally. Therefore, most are applied topically.

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32
Q

When are antimetabolic agents effective?

A

When pathogen and host metabolic processes differ (metabolic antagonists).

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33
Q

What is an example of what antimetabolic agents affect?

A

Some strike the folic acid production pathway because we do not produce our own folic acid.

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34
Q

What do most antivirals block?

A

DNA/RNA synthesis.

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35
Q

Why do drugs that block DNA replication or RNA transcription have selective toxicity issues?

A

DNA and RNA are similar in pathogens and hosts so it’s hard to have selective toxicity.

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36
Q

How do quinilones and fluoroquinolones inhibit the synthesis of nucleic acids?

A

They act against prokaryotic DNA gyrase by either “locking” topoisomerase/gyrase in places with DNA or preventing the enzyme from “resealing” double-stranded breaks.

37
Q

What happens when topoisomerase/gyrase is “locked” into place?

A

The DNA cannot rezip and replication halts leading to a slow death in bacteria.

38
Q

What happens when the double-stranded breaks into DNA cannot be “resealed”?

A

There is an accumulation of oxygen species, leading to the SOS response, leading to a rapid death.

39
Q

Can both “locking” and the prevention of “resealing” happen?

A

No. Either one or the other can happen.

40
Q

What are narrow-spectrum antibiotics?

A

They are effective against few organism.

41
Q

What is an advantage of narrow-spectrum antibiotics?

A

They reduce side effects.

42
Q

What are broad-spectrum antibiotics?

A

They are effective against many organisms.

43
Q

What is a downside to broad-spectrum antibiotics?

A

They many allow for secondary or superinfections to develop (usually through GI tract).

44
Q

What are some safety and side effect issues of antibiotics?

A

Cause of many adverse reactions poorly understood
Drugs may be toxic to kidneys, liver, or nerves.
Consideration needed when prescribing drugs to pregnant women
Could kill your flora.

45
Q

What is the best way to adminster antibiotics quickly?

A

Intravenous.

46
Q

What is the most convenient way to take antibiotics?

A

Orally.

47
Q

What is a minimal inhibitory concentration test?

A

Uses agar or broth dilution methods to measure, under defined test conditions, the lowest effective concentration of an antimicrobial agent the inhibits visible growth of a bacterium of interest.

48
Q

What is a minimum bacteriocidal concentration test?

A

Determines the lowest concentration at which an antimicrobial agent will kill a particular microorganism.

49
Q

What changes if we lose effective antibiotics?

A

Our ability to treat infections.
Transplants and chemotherapy
Immunocompromised people
HIV
Surgeries

50
Q

How is resistance to antibiotics acquired by bacteria?

A

New mutations of chromosomal genes.
Acquisition of R plasmids via transformation, transduction, and conjugation.

51
Q

True or False: Some pathogens are naturally resistant to antibiotics.

A

True

52
Q

What are the six mechanisms of microbial resistance?

A

Production of enzyme that destroys or deactivates drugs.
Efflux pumps remove antibiotics before they affect bacteria.
Changes in cell membrane/wall reduce antibiotic uptake.
Changes in structure of target.
Changes metabolic pathways.
Bacteria in biofilms can resist antimicrobials.

53
Q

How does beta-lactamase deactivate beta-lactams?

A

The break the beta-ring.

54
Q

What organisms have beta-lactamase?

A

Gram positives (staphs).

55
Q

What do efflux pumps do?

A

They have the ability to get things out of cells quickly.

56
Q

Why are efflux pumps effective?

A

The antibiotic cannot get a high enough concentration in the cell.

57
Q

Why is changing the cell membrane an effective way of stopping antibiotics?

A

The antibiotics can not longer penetrate the cell membrane.

58
Q

What are the different things bacteria can modify to reduce antibiotic uptake?

A

They can modify their membranes, cell walls, and metabolism of ETC.

59
Q

Why is changing the structure of the target an effective way of stopping antibiotics?

A

The antibiotic can no longer bind to the correct thing in the cell.

60
Q

What class of drugs changes their metabolic pathways to stop antibiotics?

A

Sulfa drugs.

61
Q

Why is changing the metabolic pathways a bacteria uses an effective way of stopping antibiotics?

A

The drugs cannot do anything because their target is no longer there/useful to the bacteria.

62
Q

Why do bacteria in biofilms have higher resistance to antibiotics?

A

They biofilms provide lots of protect, so the outside cells may die, but the inside cells will survive.

63
Q

What is a common way pathogens can acquire resistance to more than one drug?

A

When R plasmids are exchanged.

64
Q

Where is a common place bacteria can develop resistance and why?

A

They can develop in hospitals and nursing homes.
The constant use of drugs eliminates sensitive cells.

65
Q

What are multiple-drug-resistant pathogens?

A

Pathogens that are resistant to at least three antimicrobial agents.

66
Q

What is cross-resistance?

A

Resistance to other drugs within an antibiotic class or to unrelated drugs.

67
Q

What are some ways we can prevent drug resistance?

A

Only use antibiotics when appropriate.
Complete full round of antibiotics.
Using multiple antibiotics going after different targets.
Reduce use of antibiotics within the food supply.

68
Q

Why are antibiotics used in the food supply?

A

It helps prevent disease between animals and they make the animals fat.

69
Q

What are the five stages of the viral replication cycle?

A

Attachment
Entry
Synthesis
Assembly
Release/Budding

70
Q

What do most antiviral drugs block?

A

Synthesis (genome replication).

71
Q

What do antivirals target?

A

They block necessary pathways that are often unique to viral pathogens.

72
Q

True or False: Every step of the replication cycle has an antiviral drug that targets that step for every virus.

A

False.
For every step, but not for every virus.

73
Q

Why do most antivirals block genome replication?

A

Viral polymerases are error-prone because they do genetic replication faster.

74
Q

How do antivirals disrupt virus penetration and uncoating?

A

They block the removal of capsid proteins.
They block the release of genetic material.

75
Q

How do antivirals block the removal of capsid proteins?

A

They prevent the making of an environment where viruses can uncoat.

76
Q

What does pleconaril do to stop viruses?

A

Binds to the cleft of picornavirus preventing uncoating.

77
Q

What do amantadine and rimantadine do to stop viruses?

A

They inhibit the acidification of endosomes this blocking viral uncoating.

78
Q

What is amantadine and rimantadine used to treat?

A

Parkinson’s.

79
Q

What is the disadvantage to using amantadine and rimantadine?

A

They resistance is high (influenza).

80
Q

How do genome-blocking antivirals work?

A

They incorporate a DNA analog that creates mispairing or that is unable to bind to an additional nucleotide causing elongation termination.

81
Q

What does Acyclovir (AVC) do?

A

It is a viral-derived kinase phosphorylates drug that allows only infected cells to be targeted.

82
Q

How does AVC get activated?

A

Host kinases add two additional phosphate groups rendering the drug active.

83
Q

What does AVC cause?

A

Elongation termination because it lacks the 3’ hydroxyl group.

84
Q

How do viruses resist AVC?

A

Resistance occurs through mutation of the viral kinase or through mutation of viral polymerase.

85
Q

True or False: In healthy cells, AVC is inactivated. In viral cells, AVC is activated.

A

True

86
Q

Is blocking protein synthesis a good target for antivirals?

A

Most viruses use host ribosomes so targeting protein synthesis is generally a poor strategy.

87
Q

What is saquinavir?

A

Competes for active site of HIV protease which inhibits virion formation and can cause abnormal fat distribution in patients-lipodystrophic syndrome.

88
Q

True or False: proteases that cleave polypeptides can be viral or host in nature.

A

True.

89
Q

How do viruses synthesize proteins?

A

Many viruses produce long mRNA that is translated into a single polypeptide; polypeptides are then processed/cleaved to generate active units.

90
Q

How do neuraminidase inhibitors like zanamivir (relenza) and oseltamivir (Tamiflu) work?

A

They stop virons from being released from the cell through budding, so the viron gets stuck on the cell.

91
Q

Why does mutation is neuraminidase cause resistance?

A

Neuraminidase is the target, so the antiviral is no longer effective.

BMS 212 (24 decks)

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