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BMS 212 > Chapter 13: Antimicrobial Drugs Slides > Flashcards

Chapter 13: Antimicrobial Drugs Slides Flashcards

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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
How do aminoglycosides inhibit protein synthesis?
They cause a change in 30S shape, so mRNA is misread. The bacteria can still build proteins, but they are not useful/functional.
25
How do tetracyclines inhibit protein synthesis?
They block docking sites of tRNA, specifically the A site. Protein synthesis stops.
26
How do tetracyclines inhibit protein synthesis?
They block docking sites of tRNA, specifically the A site. Protein synthesis stops.
27
How does chloramphenicol inhibit protein synthesis?
It blocks the peptide bond formation. No protein synthesis can occur.
28
How do lincosamides inhibit protein synthesis?
They bind to the 50S subunit, blocking proper mRNA movement through ribosomes. This slows the whole process down like an anchor. Protein synthesis stops.
29
What does linezolid do to inhibit protein synthesis?
It prevents the subunits from sandwiching the DNA between them by affecting the large subunit. Protein cannot be made.
30
What is polymyxin?
An antibiotic that disrupts the cytoplasmic membranes of Gram-negative bacteria.
31
Why are antibiotics that disruption cytoplasmic membranes a little dangerous?
They can be toxic to organs like the kidneys if taken orally. Therefore, most are applied topically.
32
When are antimetabolic agents effective?
When pathogen and host metabolic processes differ (metabolic antagonists).
33
What is an example of what antimetabolic agents affect?
Some strike the folic acid production pathway because we do not produce our own folic acid.
34
What do most antivirals block?
DNA/RNA synthesis.
35
Why do drugs that block DNA replication or RNA transcription have selective toxicity issues?
DNA and RNA are similar in pathogens and hosts so it's hard to have selective toxicity.
36
How do quinilones and fluoroquinolones inhibit the synthesis of nucleic acids?
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
What happens when topoisomerase/gyrase is "locked" into place?
The DNA cannot rezip and replication halts leading to a slow death in bacteria.
38
What happens when the double-stranded breaks into DNA cannot be "resealed"?
There is an accumulation of oxygen species, leading to the SOS response, leading to a rapid death.
39
Can both "locking" and the prevention of "resealing" happen?
No. Either one or the other can happen.
40
What are narrow-spectrum antibiotics?
They are effective against few organism.
41
What is an advantage of narrow-spectrum antibiotics?
They reduce side effects.
42
What are broad-spectrum antibiotics?
They are effective against many organisms.
43
What is a downside to broad-spectrum antibiotics?
They many allow for secondary or superinfections to develop (usually through GI tract).
44
What are some safety and side effect issues of antibiotics?
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
What is the best way to adminster antibiotics quickly?
Intravenous.
46
What is the most convenient way to take antibiotics?
Orally.
47
What is a minimal inhibitory concentration test?
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
What is a minimum bacteriocidal concentration test?
Determines the lowest concentration at which an antimicrobial agent will kill a particular microorganism.
49
What changes if we lose effective antibiotics?
Our ability to treat infections. Transplants and chemotherapy Immunocompromised people HIV Surgeries
50
How is resistance to antibiotics acquired by bacteria?
New mutations of chromosomal genes. Acquisition of R plasmids via transformation, transduction, and conjugation.
51
True or False: Some pathogens are naturally resistant to antibiotics.
True
52
What are the six mechanisms of microbial resistance?
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
How does beta-lactamase deactivate beta-lactams?
The break the beta-ring.
54
What organisms have beta-lactamase?
Gram positives (staphs).
55
What do efflux pumps do?
They have the ability to get things out of cells quickly.
56
Why are efflux pumps effective?
The antibiotic cannot get a high enough concentration in the cell.
57
Why is changing the cell membrane an effective way of stopping antibiotics?
The antibiotics can not longer penetrate the cell membrane.
58
What are the different things bacteria can modify to reduce antibiotic uptake?
They can modify their membranes, cell walls, and metabolism of ETC.
59
Why is changing the structure of the target an effective way of stopping antibiotics?
The antibiotic can no longer bind to the correct thing in the cell.
60
What class of drugs changes their metabolic pathways to stop antibiotics?
Sulfa drugs.
61
Why is changing the metabolic pathways a bacteria uses an effective way of stopping antibiotics?
The drugs cannot do anything because their target is no longer there/useful to the bacteria.
62
Why do bacteria in biofilms have higher resistance to antibiotics?
They biofilms provide lots of protect, so the outside cells may die, but the inside cells will survive.
63
What is a common way pathogens can acquire resistance to more than one drug?
When R plasmids are exchanged.
64
Where is a common place bacteria can develop resistance and why?
They can develop in hospitals and nursing homes. The constant use of drugs eliminates sensitive cells.
65
What are multiple-drug-resistant pathogens?
Pathogens that are resistant to at least three antimicrobial agents.
66
What is cross-resistance?
Resistance to other drugs within an antibiotic class or to unrelated drugs.
67
What are some ways we can prevent drug resistance?
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
Why are antibiotics used in the food supply?
It helps prevent disease between animals and they make the animals fat.
69
What are the five stages of the viral replication cycle?
Attachment Entry Synthesis Assembly Release/Budding
70
What do most antiviral drugs block?
Synthesis (genome replication).
71
What do antivirals target?
They block necessary pathways that are often unique to viral pathogens.
72
True or False: Every step of the replication cycle has an antiviral drug that targets that step for every virus.
False. For every step, but not for every virus.
73
Why do most antivirals block genome replication?
Viral polymerases are error-prone because they do genetic replication faster.
74
How do antivirals disrupt virus penetration and uncoating?
They block the removal of capsid proteins. They block the release of genetic material.
75
How do antivirals block the removal of capsid proteins?
They prevent the making of an environment where viruses can uncoat.
76
What does pleconaril do to stop viruses?
Binds to the cleft of picornavirus preventing uncoating.
77
What do amantadine and rimantadine do to stop viruses?
They inhibit the acidification of endosomes this blocking viral uncoating.
78
What is amantadine and rimantadine used to treat?
Parkinson's.
79
What is the disadvantage to using amantadine and rimantadine?
They resistance is high (influenza).
80
How do genome-blocking antivirals work?
They incorporate a DNA analog that creates mispairing or that is unable to bind to an additional nucleotide causing elongation termination.
81
What does Acyclovir (AVC) do?
It is a viral-derived kinase phosphorylates drug that allows only infected cells to be targeted.
82
How does AVC get activated?
Host kinases add two additional phosphate groups rendering the drug active.
83
What does AVC cause?
Elongation termination because it lacks the 3' hydroxyl group.
84
How do viruses resist AVC?
Resistance occurs through mutation of the viral kinase or through mutation of viral polymerase.
85
True or False: In healthy cells, AVC is inactivated. In viral cells, AVC is activated.
True
86
Is blocking protein synthesis a good target for antivirals?
Most viruses use host ribosomes so targeting protein synthesis is generally a poor strategy.
87
What is saquinavir?
Competes for active site of HIV protease which inhibits virion formation and can cause abnormal fat distribution in patients-lipodystrophic syndrome.
88
True or False: proteases that cleave polypeptides can be viral or host in nature.
True.
89
How do viruses synthesize proteins?
Many viruses produce long mRNA that is translated into a single polypeptide; polypeptides are then processed/cleaved to generate active units.
90
How do neuraminidase inhibitors like zanamivir (relenza) and oseltamivir (Tamiflu) work?
They stop virons from being released from the cell through budding, so the viron gets stuck on the cell.
91
Why does mutation is neuraminidase cause resistance?
Neuraminidase is the target, so the antiviral is no longer effective.

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