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I & I Part III > Antibiotics: Inhibitors of Protein Synthesis > Flashcards

Antibiotics: Inhibitors of Protein Synthesis Flashcards

1
Q

Fluoroquinolones

A

• Synthetic fluorinated analogs of the quinolone nalidixic acid

  • Ciprofloxacin
  • Levofloxacin
  • Moxifloxacin
  • Newer class of antibiotics but widely used - broad spectrum of activity
  • Resistance emerging
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2
Q

Fluoroquinolones MOA

A
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3
Q

Fluoroquinolones - Pharmacokinetics

A
  • Oral bioavailability is excellent but is reduced by divalent cations (e.g. antacids)
  • Good distribution to tissues; little experience in treating meningitis
  • Most eliminated through the kidney
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4
Q

Fluoroquinolones – Spectrum and Clinical Use

A
  • Gram-neg bacilli
  • Traveler’s diarrhea
  • Salmonella
  • UTI (E. coli)
  • Pseudomonas

– Ciprofloxacin > others

– Only PO drugs that cover Pseudomonas

• S. pneumoniae, Haemophilus

– “respiratory”

– Cipro ineffective

  • Atypicals (e.g. Mycoplasma)
  • Second-line as part of TB regimen
  • Prophylaxis for N. meningitidis (not for treatment)
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5
Q

Fluoroquinolones FDA Black Box Warning

A
  • Risks outweigh benefits for:
  • Bacterial sinusitis
  • Acute-on-chronic bronchitis
  • Uncomplicated UTI
  • Benefits outweigh risks for:
  • Bacterial pneumonia
  • Anthrax
  • Plague
  • Others
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6
Q

Fluoroquinolones - Adverse Reactions

A
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7
Q

Metronidazole MOA

A

• Activated in bacterial cell by reduction via endogenous nitroreductase

  • Only anaerobic bacteria produce nitroreductase
  • Aerobic bacteria lack nitroreductase

• Intermediate free radical metabolites disrupt DNA and inhibit DNA synthesis

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8
Q

Metronidazole Pharmacokinetics and Pharmacodynamics

A
  • Well absorbed from the GI tract
  • Large volume of distribution, including brain / CSF
  • Metabolized in liver; excreted in urine
  • Nausea and vomiting
  • Disulfiram-like effect
  • Peripheral neuropathy (rare)
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9
Q

Metronidazole – Clinical Use

A

• Anaerobic infections

  • Broadest anaerobic drug
  • Intra-abdominal abscesses
  • CNS polymicrobial infections

• Clostridial infections

  • C. difficile
  • C. tetani

• Protozoal infections

  • Entamoeba histolytica
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10
Q

Rifampin

A
  • Oral and IV formulations
  • Inhibits bacterial DNA-dependent RNA polymerase
  • Penetrates all tissues, including CNS
  • Hepatic metabolism, biliary excretion
  • Significant drug interactions (azoles, warfarin, immunosupressives, etc)
  • Adverse effects:
  • Turns urine and tears orange, stains contact lenses • Hepatitis
  • Cholestasis (elevated direct bilirubin)

• Clinic use:

  • Adjunctive therapy for S. aureus – never given alone for MSSA/MRSA due to rapid development of resistance
  • Latent tuberculosis (monotherapy)
  • Active tuberculosis (as part of a combination)
  • Non-TB mycobacteria (as part of a combination) Classification by Mech
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11
Q

Antifolates

A
  • Mammalian cells use exogenous preformed folate
  • Bacteria must synthesize folate from PABA
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12
Q

Sulfonamides

A

• Sensitive organisms

  • those that must synthesize own folate

• Acquired resistance

– Altered DHPS

– Increased PABA producti

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13
Q

Sulfonamides Adverse Reactions

A
  • Highly allergenic
  • Hypersensitivity reactions, especially patients with HIV
  • Stevens-Johnson Syndrome
  • Toxic epidermal necrolysis
  • Life-threatening
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14
Q

Trimethoprim

A
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15
Q

Trimethoprim / Sulfamethoxazole

A
  • 20-100 X greater activity than sulfa alone
  • Both excreted unchanged by kidney
  • “Co-trimoxazole” (Bactrim, Septra)
  • Spectrum of activity
  • MSSA/MRSA are susceptible
  • GAS are resistant
  • Listeria (2nd-line)
  • GNRs – E. coli, Salmonella, etc
  • Stenotrophomonas maltophilia
  • Nocardia
  • Pneumocystis jiroveci
  • Toxoplasma gondii
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16
Q

Trimethoprim / Sulfamethoxazole Clinical Use

A
  • MSSA/MRSA are susceptible–> skin/soft tissue infection (with another drug) because GAS are resistant
  • Listeria (2nd-line)
  • GNRs – E. coli, Salmonella, etc -> infectious diarrhea, UTI
  • Stenotrophomonas maltophilia -> highly resistant nosocomial pathogen
  • Nocardia
  • Pneumocystis jiroveci -> drug of choice for PJP therapy and prophylaxis
  • Toxoplasma prophylaxis
17
Q

Dapsone

A

• Prevents synthesis of folic acid

– Competitive inhibitor of PABA

• Adverse effects

– Hemolysis in G6PD deficiency

– Methemoglobinemia

• Clinical use

– Leprosy

– Prophylaxis for Pneumocystis jirovecii

18
Q

Nitrofurantoin

A
  • Mechanism unknown; bacteriostatic
  • No cross-resistance with other antibiotics
  • Blood concentrations very low - only effective in urine
  • Enterobacteriaceae, enterococci, but not Proteus
  • Adverse effects

– Acute febrile reaction

– Hemolytic anemia in patients with G6PD deficiency

– Prolonged use

  • peripheral neuropathy, pulmonary fibrosis

• Clinical use: uncomplicated urinary tract infection and prophylaxis

I & I Part III (26 decks)

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