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Pharmacology Block 3 > Antibacterials > Flashcards

Antibacterials Flashcards

1
Q

B-lactams MOA:

A

Inhibit PBPs, which catalyze cell wall crosslinks. Competitive and irreversible.

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2
Q

B-lactams MOR:

A
  1. B-lactamase (most prevalent).

2. Altered PBP (MRSA).

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3
Q

B-lactams SEs:

A

Allergic reactions: Anaphylaxis, rash.
Diarrhea, enterocolitis.
Seizures (rare).

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4
Q

Penicillin G and V:

A
  • GM+ anaerobes (B-lactamase negative Strep).
  • Syphilis
  • Neisseria meningitidis (behind Ceftriaxone).
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5
Q

Oxacillin:

A
  • B-lactamase-producing staphylococci.

- MSSA

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6
Q

Amoxicillin:

A
  • B-lactamase-negative GM+ (Streptococcus, listeria).
  • GM- (Haemophilus)
  • First-line treatment for otitis media.
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7
Q

Ampicillin:

A

-Same as amoxicillin, plus treats meningitis (Neisseria, Listeria), GI infections.

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8
Q

Ticarcillin:

A
  • Broad GM- effectiveness, including pseudomonas aeruginosa.
  • Often used with a B-lactamase inhibitor to hit anaerobes.
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9
Q

Piperacillin:

A
  • Broad GM- effectiveness, including pseudomonas and klebsiella (ticarcillin-resistant)
  • Often used with a B-lactamase inhibitor.
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10
Q

2 B-lactamase inhibitors:

A
  1. Clavulanic acid.

2. Tazobactam

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11
Q

Cephalosporins spectrum of activity:

A

1st generation: best for GM+
2nd generation: more GM- activity.
3rd generation: best for GM -

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12
Q

Cefazolin:

A
  • 1G
  • GM+
  • Surgical prophylaxis against skin flora.
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13
Q

Cephalexin:

A
  • 1G

- Oral form of Cefazolin.

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14
Q

Cefuroxime:

A
  • Only 2nd gen to penetrate CSF.

- Best of 2nd gen against Haemophilus.

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15
Q

Cefoxitin:

A
  • 2G

- Cefuroxime plus added benefits against anaerobes such as Bacteroides.

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16
Q

Ceftriaxone:

A
  • 3G

- 1st line against gonorrhea, meningitis (Neisseria).

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17
Q

Ceftazidime:

A
  • 3G

- Active against Pseudomonas.

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18
Q

Cefepime:

A
  • 4G
  • Similar spectrum to Ceftazidime, except more resistant to type I B-lactamases.
  • Empirical treatment of serious inpatient infections.
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19
Q

Imipenem use and side effects:

A

-Broad-spectrum.
-Resistant to many B-lactamases, including ESBLs.
-Not effective against MRSA.
-Give with cilastatin, a renal peptidase inhibitor.
-Use if mixed or ill-defined infection, those not responsive to other drugs.
Side effects: Hypersensitivity, seizures, dizziness, confusion, GI effects.

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20
Q

Aztreonam:

A

-Used against GM- aerobic rods.
-Resistant to many B-lactamases.
-Can be used in those with known hypersensitivities to penicillins.
Side effects: seizures, GI effects, anaphylaxis, transient EKG changes.

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21
Q

Vancomycin MOA:

A

MOA: Inhibits cell-wall synthesis: by interfering with cross-linking and elongation of the peptidoglycan chains.

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22
Q

Vancomycin uses:

A

GM+ ONLY.

  • First line against HA-MRSA.
  • Severe C diff infections (behind metronidazole).
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23
Q

Vancomycin SEs:

A
  • “Red neck” syndrome.
  • Nephrotoxicity.
  • Phlebitis.
  • Ototoxicity.
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24
Q

Fosfomycin MOA:

A

Inactivates enolpyruvyl transferase, an early stage cell wall synthesis enzyme.

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25
Q

Fosfomycin uses:

A

-Uncomplicated UTIs caused by E. coli, enterococcus.

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26
Q

Bacitracin MOA:

A

Interferes with lipid carrier that exports early cell wall components through the cell membrane.

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27
Q

Bacitracin uses:

A

Topical agent against GM+

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28
Q

Polymyxins MOA:

A

Cationic detergents that bind LPS in the outer membrane of GM-

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29
Q

Polymyxin B:

A

Topical agent against GM-, pseudomonas.

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30
Q

Daptomycin MOA:

A

Binds to bacterial cytoplasmic membrane, causing rapid membrane depolarization.

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31
Q

Daptomycin uses:

A

-Complicated skin infections (Staph. Aureus, streptococcus, enterococcus).

32
Q

Quinolones MOA & MOR:

A

MOA: Inhibits bacterial DNA gyrase, thus interfering with replication and repair.

MOR: 1. Altered DNA gyrase.

  1. Decreased permeability.
  2. Combo of the two.
33
Q

Quinolones misc:

A

AUC killers.

34
Q

Quinolones SEs and contraindications:

A
  • Contraindicated in those with seizure disorders, pregnancy, children.
  • EKG irregularities.
  • Athropathy, tendon rupture.
35
Q

Name the quinolones:

A
  1. Norfloxacin
  2. Ciprofloxacin
  3. Moxifloxacin
36
Q

Norfloxacin:

A

UTIs (achieve therapeutic concentrations only in the UG region).

37
Q

Ciprofloxacin:

A

UTIs, infectious diarrhea, skin infections, bone and joint infections, chlamydia.

38
Q

Moxifloxacin:

A
  • Better GM+ spectrum than most quinolones.
  • Respiratory infections (NOT strep throat).
  • CA pneumonia, bacterial bronchitis.
39
Q

Nitrofurantoin MOA, use, SEs:

A

MOA: Nitroreductase enzyme converts drug to reactive compounds which can damage DNA.

Use: Lower UTIs.

SEs: -Peripheral neuropathy.

  • Pulmonary fibrosis in elderly.
  • GI upset.
40
Q

Rifampin MOA:

A

Inhibitor of RNAP, thereby inhibiting RNA synthesis.

41
Q

Rifampin uses:

A
  • Primarily for treatment of pulmonary TB.
  • Prophylaxis of meningococcal meningitis, haemophilus influenza.
  • Part of combination therapy for leprosy.
42
Q

Rifampin SEs:

A
  • Orange urine, tears, sweat.

- Strongly induces CYP3A.

43
Q

Fidaxomicin uses:

A
  • 3rd line for C diff (behind metronidazole, vancomycin).
  • Only hits clostridium, so useful for allowing patient to restore normal gut flora.
  • Less recurrence of C diff than vanco and metronidazole.
44
Q

Fidaxomicin MOA:

A

Inhibitor of RNAP, thereby inhibiting RNA synthesis.

45
Q

Metronidazole uses:

A
  • C diff enterocolitis.
  • Combination therapy for H. pylori.
  • Gardnerella vaginalis.
46
Q

Metronidazole MOA:

A

Anaerobes reduce the nitro group, resulting product disrupts DNA.

47
Q

Metronidazole SEs:

A
  • Long-term treatment: leukopenia, neutropenia.

- Bacterial and fungal superinfections (Candida).

48
Q

Aminoglycosides MOA:

A

Transported into bacteria by an energy-requiring aerobic process. Binds to several ribosomal sites, stopping initiation, causes premature release of ribosome from mRNA, and mRNA misreading.

49
Q

Aminoglycosides uses:

A
  • More effective against GM- than GM+, but when using against GM+, use with quinolone or cell wall inhibitor.
  • Use only against serious infections because of toxicity.
50
Q

Aminoglycosides misc:

A
  • Concentration-dependent killing.
  • -Post-antibiotic effect: sustained activity for several hours after aminoglycoside concentration has dropped below effective levels. Allows for less frequent dosing.
  • -Do not mix B-lactams with aminoglycosides in vitro – will inactivate the drug.
51
Q

Name the aminoglycosides:

A
  1. Gentamicin
  2. Tobramicin
  3. Amikacin (most broad spec)
52
Q

Name the tetracyclines:

A
  1. Minocycline

2. Doxycycline

53
Q

Tetracyclines MOA:

A

Blocks protein synthesis by binding to the 30S ribosomal subunit, preventing attachment of aminoacyl-tRNA to the acceptor site.

54
Q

Tetracyclines MOR:

A
  1. Efflux pumps.

Cross-resistance.

55
Q

Tetracyclines uses:

A
  • Preferred agents for rickettsia, chlamydia, Mycoplasma, Ureaplasma, Borrelia.
  • Ca++ inhibits absorption.
56
Q

Tigecycline MOA:

A

Same as the tetracyclines, but binds additional sites on ribosomes.

57
Q

Tigecycline uses:

A
  • Used against many GM+, including MRSA.

- A few GM-, but NOT pseudomonas.

58
Q

Chloramphenicol MOA:

A

Blocks protein synthesis: Inteferes with binding of aminoacyl-tRNA to 50S subunit, and inhibits peptide bond formation.

59
Q

Chloramphenicol uses:

A

Broad spec – only use in serious cases.

-Alternative agent for meningitis, brain abscesses.

60
Q

Chloramphenicol SEs:

A
  • Bone marrow depression, can progress to a fatal aplastic anemia.
  • Grey baby syndrome.
  • Optic neuritis.
61
Q

Macrolides MOA:

A

Block protein synthesis by binding to the 50S ribosomal subunit, blocking the translocation step.

62
Q

Macrolides SEs:

A

-Increases risk of arrhythmias and cardiac arrest (QT prolongation).

63
Q

Erythromycin uses:

A
  • Enhances GI motility.
  • Primarily against GM+ (Staph and Strep)
  • Also against Chlamydia, mycoplasma, bordetella, campylobacter.
  • Interferes with CYP3A metabolism of other drugs.
64
Q

Clarithromycin:

A
  • Better kinetics than erythromycin (less frequent dosing).
  • Less GI motility.
  • Somewhat wider spectrum.
  • Uses are same as erythromycin
  • Also part of combination therapy for H pylori.
  • Also used for MAC treatment, prophylaxis.
65
Q

Azithromycin:

A
  • Respiratory infections.

- Gonorrhea (ceftriaxone + azithromycin or doxycycline).

66
Q

Clindamycin MOA:

A

Same as macrolides, but not a macrolide.

67
Q

Clindamycin uses:

A
  • Inhibits most GM+ cocci, and many anaerobes, incl. Bacteroides fragilis.
  • Suppresses bacterial toxin production (Strep and Staph).
68
Q

Linezolid MOA:

A

Blocks protein synthesis by binding to the 50S ribosomal subunit, interfering with the formation of 70S initiation complex.

69
Q

Linezolid uses:

A
  • 1st line against CA-MRSA.
  • VRE
  • Staph
  • Strep
70
Q

Linezolid SEs:

A
  • Bone marrow depression.

- Non-selective inhibitor of MAO (avoid foods with tyramine).

71
Q

Sulfonamides MOA:

A

Inhibit folate synthesis in bacteria by competitive inhibition of dihydropteroate synthase.

72
Q

Sulfonamides SEs:

A
  • Renal damage from crystalluria.

- Inhibit CYP2C9 – potentiates action of other drugs (Warfarin).

73
Q

TMP/SMX:

A

UTIs, bacillary dysentery, typhoid fever.

74
Q

Silver sulfadiazine:

A

Use on burn wounds.

75
Q

Trimethoprim uses:

A

Given in conjunction with sulfamethoxazole – combined effects are bactericidal.
Used for UTIs, URIs and otitis media.
-Also for Pneumocystis jiroveci.

76
Q

Trimethoprim MOA:

A

Inhibit folate synthesis in bacteria by competitively inhibiting dihydrofolate reductase.

77
Q

Trimethoprim SEs:

A

Bone marrow suppression.

Pharmacology Block 3 (11 decks)

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