Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BACTERIOLOGY > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

Antibiotics that are generally bacteriostatic

A

Chloramphenicol, Erythromycin/Macrolide, Clindamycin, Sulfonamide, Trimethoprim, Tetracycline, Tigecycline, Linezolid, Quinupristin/Dalfopristin

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

Antibiotics that are generally bactericidal

A

Vancomycin, Daptomycin, Fosfomycin, Aminoglycosides, Beta-lactams, Tedizolid, Levofloxacin, Rifampin, Metronidazole, Colistin

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

Mechanism of action for Penicillin, Cephalosporin, Carbapenem, Monobactam, Bacitracin

A

Inhibits enzymes for peptidoglycan synthesis (Cell wall synthesis inhibitors)

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

Mechanism of action for Vancomycin

A

Binds to peptidoglycan (Cell wall synthesis inhibitor) - Active against GP, MRSA

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

Mechanism of action for Daptomycin

A

Binds and disrupts cell membrane (Cell membrane synthesis inhibitor) - Active against GP

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

Mechanism of action for Colistin and Polymyxin

A

Binds and disrupts cell membrane (Cell membrane synthesis inhibitor) - Active against GN

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

Mechanism of action for Aminoglycosides and Tigecycline

A

Inhibits 30s ribosomal subunit (Protein synthesis inhibitors) - Active against GP and GN

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

Mechanism of action for Chloramphenicol, Macrolides, and Clindamycin

A

Inhibits 50s ribosomal subunit (Protein synthesis inhibitors) - Active against GP and GN

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

Mechanism of action for Linezolid, Tedizolid, and Streptogramins

A

Inhibits 50s ribosomal subunit (Protein synthesis inhibitors) - Active against GP

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

Mechanism of action for Fluoroquinolones and Nalidixic acid

A

Inhibits DNA synthesis (Nucleic acid synthesis inhibitors) - Active against GP and GN

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

Mechanism of action for Nitrofurantoin

A

Damages DNA directly (Nucleic acid synthesis inhibitor) - Active against GP and GN (UTI only)

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

Mechanism of action for Sulfonamides and Trimethoprim

A

Interferes with folic acid pathway - Active against GP and many GN bacteria

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

Mechanism of action for Rifampin

A

Inhibits RNA synthesis - Active against GP and Neisseria meningitidis

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

Antibiotics effective only against GP bacteria

A

Vancomycin (except VRE, Lactobacillus, Leuconostoc, Pediococcus), Daptomycin, Linezolid, Tedizolid, Streptogramins

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

Antibiotics effective only against GN bacteria

A

Colistin, Polymyxin

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

Antibiotics effective against both GP and GN bacteria

A

Penicillin, Cephalosporin, Carbapenem, Monobactam, Bacitracin, Aminoglycosides, Tigecycline, Chloramphenicol, Macrolides, Clindamycin, Tetracycline, Fluoroquinolones, Sulfonamide, Trimethoprim

17
Q

Vancomycin resistance in GN bacteria

A

All GN bacteria are resistant except Chryseobacterium, Moraxella, and Acinetobacter

18
Q

Colistin and Polymyxin resistance in GP bacteria

A

Most GP are resistant, while most GN are susceptible

19
Q

Reduced susceptibility of an organism to a particular antimicrobial.

A

Biologic resistance

20
Q

Occurs when an antimicrobial can no longer be used clinically against a certain bacteria.

A

Clinical resistance

21
Q

Resistance due to the microorganism’s normal genetic, structural, or physiological state.

A

Intrinsic resistance

22
Q

Resistance resulting from altered cellular physiology and structure caused by genetic changes.

A

Acquired resistance

23
Q

Intrinsic resistance: GP bacteria

24
Q

Intrinsic resistance: GN bacteria, Lactobacilli, Leuconostoc

A

Vancomycin

25
Q

Intrinsic resistance: Pseudomonas aeruginosa

A

SXT, tetracycline, chloramphenicol

26
Q

Intrinsic resistance: Stenotrophomonas maltophilia

27
Q

Intrinsic resistance: Klebsiella

A

Ampicillin

28
Q

Intrinsic resistance: Enterococci

A

Aminoglycoside, Cephalosporin

29
Q

Intrinsic resistance: Anaerobic bacteria

A

Aminoglycoside

30
Q

Intrinsic resistance: Aerobic bacteria

A

Metronidazole

31
Q

Mechanism of resistance: Enzymatic destruction

A

Beta-lactamase destroys the β-lactam ring of antibiotics; e.g., Staphylococcus resistance to penicillin; Enterobacterales and P. aeruginosa resistance to β-lactam drugs.

32
Q

Mechanism of resistance: Enzymatic modification

A

Modifying enzymes alter antibiotic binding sites, causing GP and GN resistance to aminoglycosides.

33
Q

Mechanism of resistance: Altered target in bacteria

A

Mutation in original PBP to PBP2a; e.g., MRSA (PBP -> PBP2a), VRE, VRSA.

34
Q

Mechanism of resistance: Cell wall alteration

A

Structural changes lead to resistance; e.g., S. pneumoniae and Viridans resistance to β-lactam drugs.

35
Q

Mechanism of resistance: Decreased antibiotic uptake

A

Porin channel reduction blocks antibiotic entry; e.g., P. aeruginosa resistance to imipenem, GN resistance to aminoglycosides.

36
Q

Mechanism of resistance: Efflux of antibiotic

A

Bacteria pump the drug out before it binds to the target; e.g., Staphylococcus and Streptococcus resistance to macrolides.

BACTERIOLOGY (49 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions