Brainscape's Knowledge GenomeTM

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


See full index

CMOD- Block1 > Pharm: Antibiotic Drug Classes > Flashcards

Pharm: Antibiotic Drug Classes Flashcards

1
Q

Name the four distinct major mechanisms of action of antimicrobial agents.

A

Inhibition of cell wall synthesis
Inhibition of protein synthesis
Inhibition of folic acid biosynthetic pathways
Inhibition of DNA/RNA synthesis

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

Is it applicable to combine drugs with different MOA to achieve a synergistic cell kill effect?

A

YEAHHHHH

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

Penicillins belong to a class of antibiotics known as:

A

B-lactams

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

Name two narrow-spectrum B-lactam abx

A

Oxacillin, Nafcillin

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

Name two aminopenicillin abx

A

Ampicillin, amoxicillin

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

Name a broad-spectrum penicillin

A

Piperacillin

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

True or false: all B-lactams (penicillins, carbapenams, and cephalosporins) act through Binding of penicillin-binding proteins followed by destruction of the bacterial cell wall.

A

True

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

True or false: virtually all bacteria contain penicillin-binding proteins

A

True

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

Do different penicillin-binding proteins all have the same affinities for B-lactams? If not, what impact does this have on their sensitivities to B-lactams?

A

No. Different bacteria will demonstrate different sensitivities to B-lactams

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

What are transpeptidases?

A

Enzymes that cross-link peptidoglycan molecules in bacterial cell walls

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

What does cross-linking peptidoglycan do for the cell wall?

A

Gives strength to the cell wall

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

How do B-lactams work?

A

Inhibit transpeptidases; preventing it from forming cross-links. Results in structurally deficient cell wall, typically leading to bacterial lysis.

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

Are gram neg. or gram pos. organisms more susceptible to B-lactams?

A 
Gram positives (thick peptidoglycan layer)
Gram negatives are less susceptible due to LPS layer which protects the peptidoglycan layer from B-lactam activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name two B-lactamase inhibitors that are added to some B-lactam abx to overcome resistance caused by B-lactamase.

A 
Clavulanic acid (added to amoxicillin)
Tazobactam (added to piperacillin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why are narrow-spectrum penicillins narrow-spectrum?

A

N-S penicillins contain a larger molecule on the penicilin molecule side chain that confers steric hindrance: the ability to twist the molecule into other stereoisomers. This results in these penicillins being resistant to B-lactamase but at the same time restricts their spectrum of activity.

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

How are aminopenicilins different from penicillins?

A

Have an added amino group (NH2) that makes the molecule more hydrophilic and thus able to cross the LPS layer more easily (better against Gram -)

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

Describe broad-spectrum penicillins.

A

They are modifications of aminopenicillins: nitrogen and carbon atoms are added to the molecule. This Increases the range of bacteria that are sensitive to the antibiotic. They are usually admin. with a B-lactamase inhibitor due to their increased B-lactamase sensitivity.

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

What makes the Monobactam Aztreonam unique among cell wall synthesis inhibitors?

A

Unlike the penicillins and cephalosporins, which contain a thiazolidine ring attached to the B-lactam ring, Aztreonam’s (a monobactam) B-lactam ring contains a sulfonic acid group that gives it its activity as a preferential binder of penicillin-binding proteins that are located inside the bacterial cell wall.

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

How do carbapenems differ structurally from penicillins?

A

The 5-membered ring adjacent to the B-lactam ring contains a carbon atom, rather than a sulfur atom.

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

What 3 traits make Imipenem (Carbapenem) an effective abx?

A
  1. More efficient penetration through the bacterial cell wall
  2. Resistance to bacterial enzymes
  3. Affinity for all bacterial P-BPs
    These characteristics give Imipenem a broader spectrum of activity than many other B-lactams
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does Cilastatin improve the efficacy of Carbapenem abx Imipenem?

A

Cilastatin (think “stop cilia”) is a reversible, competitive inhibitor of DHP-1, an enzyme found in the brush border (cilia) of the PCT cells of the kidneys that breaks down Imipenem. Thus, reducing renal metabolism of Imipenem.

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

What distinguishes the cephalosporins from the natural penicillins?

A

The cephalosporins are more acid stable and can be taken with or without food.
Instead of a 5 membered (thiazolidine) ring adjacent to the Lactam ring, they have a 6 membered ring.

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

True or false: with each successive drug generation, gram positive abx activity is gained.

A

False. In general, gram-positive activity is lost with each successive drug generation, whereas activity against gram-negative organisms is gained.

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

Describe the use of 1st generation cephalosporins.

A
  • skin infections (against Strep/Staph)
  • Surgical prophylaxis (Cefazolin)
  • Cephalexin, orally, is the most commonly prescribed cephalosporin for outpt use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the use of 2nd generation cephalosporins.

A

mild gram-negative Bacteroides infection (intraabdominal infections)

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

What is the drug of choice for treating pediatric meningitis?

A

Ceftriaxone (3rd gen. cephalosporin)

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

True or false: 4th gen. cephalosporins are reserved for severe nosocomial (hosp. acquired) infections

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the MOA of vancomycin?

A

Inhibits cell wall synthesis by attaching to the end of the peptidoglycan precursor units (D-ALA-D-ALA) that are required to be laid down into the matrix. Prevents precursor from being released from the carrier, thus stopping peptidoglycan synthesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why is vancomycin not effective against gram negative organisms?

A

Gram neg. orgs. have an LPS layer that blocks vancomycin from reaching the thin peptidoglycan layer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the best way to administer vancomycin for a GI infection?

A

Orally (glycopeptides are poorly absorbed from the GI tract)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the best way to administer vancomycin for an infection that is not in the gut?

A

IV (glycopeptides are poorly absorbed from the GI tract)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the MOA of Fosfomycin. Please. Thank you.

A

Transported into bacterial cell by G-6-P/Glycerol-3-P transport systems, epoxide group irreversibly inactivates enzyme enolpyruvyl transferase by replacing PEP. Inactivation of enzyme blocks condensation of nucleotides, a first step in cell wall synthesis. Inhibition of peptidoglycan synthesis results in accumulation of nucleotide precursors and subsequent death and bacterial cell lysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

List the 6 major groups of Abx that inhibit protein synthesis.

A

SAMLOT:
1. Streptogramins (Quinupristin/dalfopristin)
2. Aminoglycosides (Genta[mycin], neo, strepto, tobra, amikacin)
3. Macrolides (Azithro[mycin], Clarithro, Erythro, Telithro)
4. Lincosamides (Clindamycin)
5. Oxazolidinones (Linezolid)
6. Tetra[cyclines] (Doxy, Tige, Mino, Tetra)
Others: Mupirocin, Chloramphenicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why do aminoglycosides have poor penetration of biological membranes?

A

Polar structure

35
Q

Are aminoglycosides absorbed well in the GI tract?

A

No (polar structure)

36
Q

Are aminoglycosides administered orally?

A

No, poor GI absorption

37
Q

Why are aminoglycosides nephrotoxic?

A

accumulate in the cells of the PCT of the kidney

38
Q

Describe the prokaryotic ribosome.

A
  • 70S ribosome
  • small (30S) & large (50S) subunits
  • 50S subunit = 5S+ 23S+ 34 other proteins
39
Q

Describe the eukaryotic ribosome.

A
  • 80S ribosome

- small (40S) & large (60S) subunit

40
Q

Where does tRNA bind to the ribosome?

A

Aminoacyl (A) site

41
Q

Where is the existing amino acid chain elongated in the ribosome?

A

Peptidyl (P) site

42
Q

Where does the tRNA release from the growing AA chain?

A

Exit/Egress (E) site

43
Q

Please describe how aminoglycosides work.

A

Irreversibly bind the 30S ribosomal subunit. Recent studies show that the initial site of action is the outer cell membrane where the cationic abx creates fissures and pores in the outer membrane, resulting in leakage of intracellular contents and enhanced abx uptake.

44
Q

Are aminoglycosides particularly effective against gram + or gram - bacteria?

A

Gram negative

45
Q

Why are aminoglycosides, in contrast to other protein synthesis inhibitors, considered to be bactericidal in addition to bacteriostatic?

A

Because of their cationic action, creating fissures and pores in the outer membrane.

46
Q

What is the MOA of the macrolide class of abx?

A

Bind the 23S rRNA molecule of the 50S ribosomal subunit. and inhibit peptidyl transferase, blocking the transfer of the new AA onto the growing chain. Inhibits initiation of translation

47
Q

Are macrolides considered bacteriostatic or bactericidal?

A

Bacteriostatic except in high concentrations

48
Q

Please describe the MOA of Lincosamides.

A

Bind the 23S rRNA molecule of the 50S ribosomal subunit and inhibit peptidyl transferase, blocking the transfer of the new AA onto the growing AA chain. Inhibits initiation of translation.

49
Q

Are Lincosamides considered bacteriostatic or bactericidal?

A

Bacteriostatic except in high concentrations

50
Q

What abx within the Lincosamide class is particularly useful against toxin producing pathogens and why?

A

Clindamycin because of its inhibition of protein synthesis which is also necessary for production of toxins (made of proteins).

51
Q

Describe the MOA of Tetracyclines.

A

Bind reversibly to the 16S subunit of the 30S ribosomal subunit and inhibit translation. Prevents addition of AAs to growing peptide.

52
Q

Are Tetracyclines considered bacteriostatic or bactericidal?

A

Bacteriostatic

53
Q

Why are Eukaryotic cells not affected by tetracycline?

A

Eukaryotic cells lack the active transport mechanisms that bacteria use to take up tetracycline.
Also, different ribosome sizes/shapes.

54
Q

Please, pretty please, describe the MOA of Streptogramins.

A

Bind the 50S ribosomal subunit inhibiting protein synthesis. Cooperative and synergistic binding of Dalfopristin and Quinupristin yields bactericidal activity.

55
Q

Describe the MOA of Mupirocin.

A

Inhibits bacterial protein synthesis by reversibly binding and inhibiting isoleucyl transfer-RNA synthetase. No cross-resistance with other classes of Abx.

56
Q

How is Mupirocin administered and what is its effect on specific bacteria?

A

applied topically and is bactericidal against many Gr+ and select G- bacteria. It has good activity against Strep pyogenes, methicillin-susceptible and methicillin-resistant S. aureus (MRSA).

57
Q

Please, for the love of God, describe the MOA of Chloramphenicol.

A

Binds the 50S RSU at the peptidyltransferase site and inhibits the transpeptidation reaction.

58
Q

What classes of Abx can interfere with the action of Chloramphenicol and why?

A

Clindamycin and macrolides. Because they act near the binding site of chloramphenicol and thus they may interfere with each other’s actions if given concurrently.

59
Q

Please describe the MOA of Fluoroquinolones.

A

Bind to and inhibit DNA gyrase (gram -)/topoisomerase IV (gram +) from uncoiling DNA for transcription. Halting cell division.

60
Q

Why, why GOD do Fluoroquinolones not affect eukaryotes?

A

We have different forms of DNA gyrase and topoisomerase IV

61
Q

Describe the MOA of Rifamycins. Please.

A

Rifampin (subgroup) inhibits bacterial RNA synthesis by binding prokaryotic RNA polymerase. Prevents initiation of RNA synthesis.

62
Q

Why Buddha does Rifampin not inhibit human RNA synthesis?

A

Does not bind human RNA polymerase.

63
Q

What class of abx readily enters mycobacterial cell walls and why?

A

Rifampin (rifamycin), because it is highly lipophilic.

64
Q

Since Rifampin is highly lipophilic, what other practical uses does it have?

A

Penetration of biofilms
CNS distribution (Bacterial meningitis)
Entering phagocytic cells and killing intracellular pathogens within.
Organisms within abscesses (poorly vascularized, so it diffuses through tissue)

65
Q

What class of drugs is particularly effective against anaerobic bacteria due to the lack of oxygen and presence of nitroreductase (enzyme)?

A

Nitroimidazole-Metronidazole

66
Q

What is the MOA of Metronidazole (prodrug)

A

Reduction of the prodrug Metronidazole results in the oroduction of toxic products and other free radicals that damage DNA (killing bacteria)

67
Q

Cotrimoxazole is a combination drug composed of:

A

trimethoprim and sulfamethoxazole

68
Q

Describe the MOA of Cotrimoxazole (trimethoprim/sulfamethoxazole).

A

The combination of the two components acts on two steps of the enzymatic synthesis of tetrahydrofolic acid (inhibition of folic acid synthesis).

69
Q

Given that both eukaryotes and prokaryotes need dihydrofolate reductase to survive, how is it that cotrimoxazole does not affect humans.

A

Much greater concentration needed to inhibit human dihydrofolate reductase.

70
Q

Cotrimoxazole is useful for treating:

A

uncomplicated UTI, and for acute exacerbations of chronic bronchitis. Also effective against Pneumocystis jiroveci

71
Q

Describe the MOA of Daptopeptides.

A

Interfere with integrity of cell wall structure by depolarizing membrane potential (do not penetrate cell membrane). This loss of membrane potential leads to inhibition of protein, DNA adn RNA synthesis&raquo_space;> cell death.

72
Q

What reduces the efficacy of Daptomycin in treating pneumonias and why?

A

Surfactant. Sequesters the abx rendering it useless because it cannot reach the bacteria.

73
Q

Please describe the MOA of Fidaxomicin.

A

Inhibits RNA synthesis by inhibiting sigma-dependent transcription of bacterial RNA polymerases. No cross-resistance with Rifamycins.

74
Q

Fidaxomicin is highly specialized for treatment of:

A

pseudomembranous colitis or C. diff associated diarrhea.

75
Q

Ciprofloxacin’s MOA inhibits synthesis of what?

A

DNA/RNA

76
Q

Why would you treat an infection with multiple anti-microbials?

A
  1. to treat a polymicrobial infection
  2. to decrease emergence of resistance
  3. to decrease dose-related toxicity
  4. to enhance cell kill
77
Q

How does combination antimicrobial therapy enhance cell kill?

A

An example would be one anti-microbial destroys the cell wall, and a weaker cell wall lets in the second anti-microbial; now it’s more effective than it would be without the first

78
Q

What is antagonism (in the context of mechanistically different drugs working together)?

A

one anti-microbial interferes with the other anti-microbial’s action; example would be a bacteriostatic anti-microbial, which requires cell growth/division in order to be effective, alongside a bactericidal anti-microbial; another example is one that increases activity of beta-lactams

79
Q

Give 2 conceptual examples of synergistic combinatorial functions of anti-microbials.

A
  1. sequential blockade of steps in a longitudinal process
  2. enzyme inhibitors that prevent antagonistic effects of drug, such as beta-lactamase inhibitors
  3. increased drug uptake, ex by making the cell wall more permeable
80
Q

T/F: Cephalosporins are B-lactam abx.

A

True

81
Q

What is the MOA of cephalosporins?

A

Mimic D-Ala-D-Ala pentapeptides and inhibit transpeptidase from cross-linking peptidoglycan.

82
Q

Do methicillin or cephalosporins require B-lactamase inhibitors to work?

A

No

83
Q

Do B-lactamases play a more important role in Gram - or Gram + resistance to B-lactam Abx?

A

Gram - because secreted into periplasmic space and are effective at lower concentrations compared to Gram +s secreted into extracellular environment that require greater concentration (more bacteria secreting) for equal effect.

CMOD- Block1 (36 decks)

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