Antibiotics in general Flashcards

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1
Q

What affects serum antibiotic levels?

A

Absorption, volume of distribution, metabolism, and excretion all affect serum antibiotic levels.

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2
Q

What is MIC?

A

Mean inhibitory concentration

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3
Q

What is MBC?

A

Minimal bactericidal concentration

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4
Q

How do you maximize success with B-lactam antibiotics?

A

Serum levels should be above the MIC for at least 50% of the time.

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5
Q

How do you maximize success with ahminoglycosides and fluoroquinolone?

A

High peak concentration and high AUC/MIC ratio

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6
Q

How can you prevent antibiotic resistance?

A

High doses to achieve very high AUC/MIC ratios, 50-200, depending on the organism. Also, short courses of antibiotics, ideally 5 days or less, can reduce resistance

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7
Q

What is the 3-day rule?

A

Narrow antibiotics within three days! Within 3-4 days following the administration of antibiotics, sequential cultures of mouth flora reveal that the numbers and types of bacteria begin to change significantly. Normal flora die, and resistant GN rods, GP cocci, and fungi begin to predominate.

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8
Q

How is serum procalcitonin useful in evaluating infection?

A

In response to bacterial infection, this precursor of calcitonin is synthesized and released into the serum by many organs in the body.

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9
Q

How is serum procalcitonin useful in evaluating infection?

A

In response to bacterial infection, this precursor of calcitonin is synthesized and released into the serum by many organs in the body. Production of interferon (IFN) in response to viral infection inhibits this synthesis. Levels can also aid in prognosis.

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10
Q

How can you differentiate between colonization and infection?

A
  1. Growth of resistant organisms is the rule in the patient on antibiotics.
  2. Antibiotics should be switched only on evidence of a new infection.
  3. Evidence for a new superinfection includes
    - new fever or worsening fever pattern
    - increased peripheral leukocyte count with left shift
    - increased inflammatory exudate at the original site of infection
    - increased PMNs on gram stain, and
    - correlation between bacterial morphology on Gram stain and culture
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11
Q

What are the B-lactam antibiotics?

A

Penicillins, cephalosporins, and carbapenems

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12
Q

What is required for B-lactams to work?

A

Active bacterial growth and active cell wall synthesis. Therefore, bacteria in a dormant or static phase will not be killed, but those in an active log phase of growth are quickly lysed.

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13
Q

What are the most common toxicity concerns in B-lactams?

A

Allergic reactions, both delated and immediate hypersensitivity reactions. Penicillin reactions are seen in 1-10%. 1-7% of patients allergic to PCN are also allergic to cephalosporins and carbapenems.

  • Ceftriaxone is excreted in the bile and can crystallize to form biliary sludge
  • Cephalosporins with methylthiotetrazole rings can interfere with vitamin K and increase prothrombin time
  • Nephrotoxicity can occur when cephalosporins are combined with ahminoglycosides.
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14
Q

What are the natural penicillins?

A

PCN G
Procaine PCN G
Benzathine PCN G
PCN V-K

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15
Q

Are the natural PCNs broad or narrow?

A

Narrow

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16
Q

What are the aminopenicillins?

A

Ampicillin
Amoxicillin
Amoxicillin-clavulanate (Augmentin)
Ampicillin-sulbactam (Unasyn)

17
Q

Are the aminopenicillins broad or narrow?

A

Moderate (Ampicillin, amoxicillin) to broad (augmentin, unsyn)

18
Q

What are the penicillinase-resistant PCNs?

A

Oxacillin, nafcillin, cloxicillin/dicloxacillin

19
Q

Are the PCNase-resistant PCNs broad or narrow?

A

Narrow

20
Q

What are the carboxy/ureido-PCNs?

A

Ticarcillin-clavulanate (Timentin)

Piperacillin-tazobactam (Zosyn)

21
Q

Are the carboxy/ureido-PCNs broad or narrow?

A

Very broad

22
Q

About the natural penicillins:

A
  • Excreted renally
  • Narrow spectrum
  • Indicated for strep progenies, S. viridians, mouth flora, Clostridium perfringens, N meningitidis, pasteurella and spirochetes (syphilis and leptospira)
  • Recommended for PCN-sensitive S pneumonia, infections caused by mouth flora; C perfringens or spirochetes
23
Q

About aminopenicillins:

A
  • Parenteral ampicillin: Listeria monocytogenes, sensitive enterococci, proteus mirabilis, and non-B-lactamase-producing H influenza
  • Ampicillin + an amino glycoside is the treatment of choice for enterococci.
  • Amoxicillin is the DOC for otitis media
  • Augmentin has improved coverage of Staph, H influenza, and Moraxella catarrhalis but also causes diarrhea. It is also the DOC for bacterial sinusitis.
24
Q

About PCNase-resistant PCNs:

A
  • Hepatically metabolized
  • Very narrow
  • Poor anaerobic activity
  • Indicated for MSSA and cellulitis
25
Q

About carboxypenicillins and ureidoPCNs:

A
  • More effective resistance to GN B-lactamases
  • Combined with aminoglycosides, these demonstrate synergistic killing of Pseudomonas
  • Excellent broad-spectrum coverage, including MSSA and anaerobes.
  • Useful for intra-abdominal infections, acute prostatitis, in-hospital aspiration pneumonias and mixed soft tissue and bone infections
26
Q

How would you generally describe the action of first generation cephalosporins?

A

Predominantly effective against GP cocci

27
Q

How would you generally describe the action of second generation cephalosporins?

A

Second generation: Increased activity agains aerobic and anaerobic GN bacilli, but with variable GP cocci activity

28
Q

How would you generally describe the action of third generation cephalosporins?

A

Third generation: Even greater activity agains GN bacilli but limited activity against GP cocci

29
Q

How would you describe the action of fourth generation cephalosporins?

A

Broadest spectrum with activity against GP cocci and GN bacilli.

30
Q

How would you describe the action of fifth generation cephalosporin (ceftaroline)?

A

Kills both MRSA and PCN-resistant S pneumonia