Antibiotics, Anti-microbials, and Resistance (complete) Flashcards

1
Q

What is a chemotherapeutic agent

A

a drug that fights against diseases

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

What is an antimicrobial agent

A

a drug that treats infections

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

What is an Antibiotic

A

Antimicrobial agents produced by microorganisms that kill or inhibit the growth of other organisms

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

What is a semisynthetic agent

A

an agent whose parent compound was made by a microbe, but was then chemically modified.

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

which types of antibiotics work to inhibit cell wall synthesis

A

cephalosporins
penecillins
vancomycin
penems

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

Which types of antibiotics work to inhibit protein synthesis

A
Eyrthromycin
clindamycin
chloramphenicol
tetracycline
aminoglycosides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

which types of antibiotics inhibit Nucleic Acid Synthesis

A
Quinolones (ciproflaxin)
rifampin
sulfa drugs
metronidazole
nucleoside analogs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which types of antibiotics inhibit metabolic pathways

A

sulfa drugs
trimethoprim
amantadine

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

Which types of antibiotics alter cell membrane permeability

A

nystatin
amphotericin B
Polymixins

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

how do the Beta-Lactam rings inhibit cell wall synthesis

A

They bind to the enzymes that are responsible for cross linking NAM subunits of the bacterial cell wall. So when those enzymes are bound, the cell wall can’t be properly synthesized, they will be weak, and the bacteria will lyse

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

What are some important beta-lactam drugs

A
penicillin
methicillin
cephalosporins
monobactams
carbapenems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does augmentin (beta-lactamase inhibitor) help the beta-lactam drugs to be more effective

A

it deactivates the bacterial beta-lactamase enzymes, so that the bacteria can’t fight back against the beta-lactams drugs. normally bacteria with beta-lactamase activity can resist beta-lactam drugs

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

What can be the problem with broad spectrum antimicrobials

A

they can kill off some of the normal flora, which can lead to the development of superinfections or secondary infections.

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

Which antimicrobial drugs interfere with particular alanine-alanine bridges that link NAM subunits in many gram positives

A

Vancomycin and Cycloserine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which antimicrobial is topical only and blocks the secretion of NAG and NAM from the cytoplasm

A

bacitracin

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

which drugs disrupt formation of arabinogalactan-mycolic acid complexes in mycobacterial species

A

Isoniazid and ethambutol

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

what is the affect of cell wall inhibiting drugs on growing cells, mature cells, animal cells, and plant cells

A

They destroy growing cells, (don’t let peptidoglycan form properly)
They have no effect on mature cells (because they only prevent the peptidoglycan from forming, they don’t have any affect on the existing peptidoglycan)
They have no effect on plant or animal cells since those don’t have peptidoglycan.

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

Why can drugs that inhibit protein synthesis be harmful in large doses

A

because animals have mitochondrial ribosomes that are similar to the bacterial ribosomes that are the target of these drugs that inhibit protein synthesis

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

For what type of infection is amphotericin B used

A

fungal infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the mechanism of action of amphotercin B against fungi

A

it attaches to ergosterol that is found in fungal membranes. This negatively affects the integrity of the fungal membrane by creating pores in the membrane

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

Why can humans be susceptible to Amphotericin B?

A

because the ergosterol of fungi is similar to the choleterol in humans

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

What is the target of the antibacterial Polymixin

A

it binds to LPS and disrupts both of the gram negative membranes

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

why are polymixins usually used as a last resort

A

because they are relatively neurotoxic and nephrotoxic

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

How do the drugs that inhibit metabolic pathways of bacteria work

A

the drugs are structural analogs that bind to necessary metabolic enzymes and block them from performing their normal function

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

can antimetabolic drugs have an impact on viruses and parasitic worms

A

yes, they can paralyze the worms, and they can block viral activation

26
Q

Why are sulfa drugs (sulfonamides) and trimethoprim used together (they are combined in bactrim and septra)

A

they both inhibit bacterial metabolic pathways, but they do it by inactivating different enzymes. so it is more effective when blocking both enzymes

27
Q

What are the drugs that inhibit the metabolism of viruses

A

amantadine and rimantadine

28
Q

what is the main problem with drugs that are used to inhibit nucleic acid synthesis

A

there are only a few slight differences between prokaryotic and eukaryotic

29
Q

What are the mechanisms by which drugs that inhibit nucleic acid synthesis work

A
  1. they are nucleoside analogs, so they are inserted into nucleic acids instead of the actual nucleosides
  2. or they inhibit necessary enzymes in nucleic acid synthesis
30
Q

What are drugs that inhibit nucleic acid synthesis usually used against

A

viruses and rapidly dividing cancer cells

31
Q

What are the three most common nucleoside analogs

A

ribvarin
acyclovir
azidothymine

32
Q

how do quinolones and fluoroquinolones work to inhibit nucleic acid synthesis

A

they act against prokaryotic DNA gyrase

33
Q

how does rifampin work to inhibit nucleic acid synthesis

A

it binds to and inhibits RNA polymerase during transcription

34
Q

can prevention of viral attachment be a plausible target of antiviral drugs

A

yes, there are drugs that do just that

35
Q

name the common antifungal drug groups

A

polyenes (nystatin, amphotercin)
Azoles (miconazole, ketoconazole, fluconazole)
DNA analogues (Flucytosine)

36
Q

What do the antifungal Azoles do to fight fungi

A

they inhibit the synthesis of ergosterol

37
Q

What do the antifungal polyenes do to fight fungi

A

bind to the sterols in the cell membrane, causing leakage and death

38
Q

What are the 6 characteristics of an ideal antimicrobial agent

A
  1. Readily available
  2. inexpensive
  3. chemically stable
  4. easily administered
  5. non-toxic, non-allergenic
  6. selectively toxic against many pathogens
39
Q

What are the three ways to test the efficacy of antimicrobials

A

Diffusion susceptibility tests
minimum inhibitory concentration tests
minimum bactericidal concentration tests

40
Q

how is a diffusion susceptibility test performed

A

you have a plate with growing colonies of your selected microbial, then you put little dabs of different antimicrobials on the plate, and observe which anti-microbials kill the microbial, and how drastically they do so

41
Q

What does the minimum inhibitory concentration test show

A

it shows the lowest concentration at which an antimicrobial drug will leave no visible bacterial colonies after a night of incubation

42
Q

what does the minimum bactericidal concentration test show

A

it shows the lowest concentration at which no bacterial colonies grow

43
Q

What is topical administration

A

external application, applied directly to the infected area

44
Q

What are the four maint types of drug administration

A

Topical
Oral
Intramuscular
Intravenous

45
Q

What is the difference in relative concentration of the drug over time when given orally, intramuscular, and intravenously

A

Orally, slow increase, and decrease of a small amount of Drug
Intramuscular. a failry quick increase, of a moderate amount of Drug, followed by a fairly quick decline
Intravenous, Very quick rise or a high concentration of Drug

46
Q

What are the three main side effects of anti-microbials

A

toxicity
allergies
disruption of normal microbiota

47
Q

Are Drugs fine to take after they expire, why or why not

A

no, because some can become toxic after expiration

48
Q

how common are allergies caused by anti-microbials

A

they are rare

49
Q

what are the problems associated with anti-microbials that disrupt the normal microbiota?

A
  1. they can create secondary infections (too much open space for bacteria)
  2. they can lead to an overgrowth of normal flora (superinfection)
50
Q

What are the two ways in which bacteria acquire drug resistance

A
  1. New mutations of chromosomal genes

2. Acquisition of R-plasmids from other bacteria

51
Q

What are the four main ways in which microbes resist antibiotics

A
  1. inactivation of the drug
  2. altered uptake of the drug
  3. modification of the structural target of the drug
  4. altered metabolic pathway
52
Q

What are mechanisms by which a microbe can inactivate a drug

A

cleavage of the drug

phosphorylation, adenylation, methylation

53
Q

What ways does a bacteria alter its uptake up a antibiotic

A

alters its permeability

uses efflux pumps (after the drug gets in, the bacteria pumps it out)

54
Q

Are resistances to antibiotics passed from one bacteria to another through plasmids

A

yes

55
Q

How do populations of resistant organisms develop

A

you start with a population of organisms with only a few resistant organisms. then there is exposure to a drug which kills most of the non-resistant organisms. the few remaining organisms reproduce, leaving a population of mostly drug resistant organisms

56
Q

can a single pathogen be resistant to multiple drugs

A

yes

57
Q

Where do many of the organisms that are resistant to multiple drugs, or have acquired cross-resistance

A

in hospitals

58
Q

What is cross-resistance in bacteria

A

cross-resistance is resistance acquired when a bacteria comes in contact with a substance similar to an antibiotic, and creates a resistance to it, and thus to the antibiotic

59
Q

How do you prevent resistance to antibiotics

A
  1. use high concentrations of a drug, for long periods of time ]
  2. take advantage of synergism
  3. limit antimicrobials to necesssary cases
  4. Develop new drugs
60
Q

what is synergism between antimicrobials

A

when two drugs used together work better than either of them do on their own.

61
Q

What are CRE’s

A

carbapenem-resistant enterobacteriaceae

62
Q

What’s the scary thing about CRE’s

A

these infections are very hard to treat, and have high mortality rates