antimicrobials Flashcards

1
Q

Why would a bacteriostatic agent be used?

A

if you can stop growth, immune system can take over

-not a good option in immunosuppressed patients

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2
Q

post antibiotic effect

A

inhibition does cont fairly long time after a drug is d/c’d

  • persistent suppression of microbial growth after antimicrobial agent has been cleared
  • Long PAE with intracellular bacteriostatic agents, short or no PAE with beta-lactams
  • might make length of dosing interval versus the the drug half life less of a concern
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3
Q

MBC vs MIC

A
MBC = minimal bactericidal concentration
MIC = minimal inhibitory concentration

antibiotic in the blood should exceed the MIC by 2-8x to offset tissue barriers to infection site (pus, CNS, tissue)

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4
Q

Which mechanisms of action are bacteriostatic

A

folic acid metabolism inhibition, PRO synthesis inhibition

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5
Q

concentration dependent antibiotics

A

antibiotic effectiveness is dependent on achieving peak concentration periodically in multiple dosing regiment Peak/MIC or AUC/MIC
-common for bactericidal agents to show concentration dependent technology

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6
Q

time dependent antibiotics

A

effectiveness dependent on time (%) that concentration remains above MIC (time > MIC)

  • common for drugs like cell wall synthesis inhibitors, slow killing req maintained concentrations
  • ex: PCN
  • requires minimization of dosing interval relative to drug t1/2 or IV infusion
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7
Q

narrow spectrum antibiotics

A
  • effectively mainly against either Gm+ or Gm-
  • optimal against specific organisms
  • lower risk of superinfections
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8
Q

extended spectrum antibiotics

A

-affects a variety of Gm+ and Gm-

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9
Q

broad spectrum

A

affects both Gm+ and Gm - bacterial, plus other micororg as well (rickettsia

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10
Q

clinical effectiveness of antibiotics

A

dependent on drug’s maximal efficacy (limit of the dose-response relation), not its potency

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11
Q

what contributes to antimicrobial drug resistance

A
  • misdiagnosis
  • inherent microbial resistance (certain strains)
  • acquired drug resistance
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12
Q

Forms of acquired microbial resistance

A
  • drug fails to reach target (transporters)
  • drug is inactivated (enzymes, pumped out of cells by efflux pump)
  • drug target is altered (rapid multiplication leads to rapid mutation)

-occurs as a result of antibiotic use

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13
Q

how is drug resistance acquired genetically?

A
  • chromosomal resistance (mutant genes and PRO, drug target is altered)
  • sex, plasmid, and transposon mediated resistance
  • conjugation (imp for gram neg)
  • transduction (imp)
  • transformation (not imp)
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14
Q

non-genetic drug resistance

A
  • growth latency, anaerobic conditions

- protoplasts (no cell wall)

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15
Q

definitive antimicrobial therapy

A
  • identificaiton of specific pathogen prior to rx
  • presumptive dx of infection, severity/need for immediate rx, and probable pathogens
  • formulate a microbial dx
  • direct examination, gram stain, etc.; growht & sensitivity tests
  • select most appropriate antibiotic therapy
  • evaulate effectiveness (72h) and reassess
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16
Q

empiric antimicrobial rx

A

-rx without formal id of specific pathogen
-used in critical conditions or when dx is likely to be unneccessary or cost prohibitive
-presumptive dx of infection, severity/need for rx, and probable pathogens
-rx with antimicrobial agents likely to be effective
(consider local bacterial resistance patterns, generally involves broader spetrum agents, isolation of cultures prior to antimicrobial rx, eval effectiveness and reassess)

17
Q

adverse effects of antimicrobial therapy

A
  • allergy
  • superinfection (appearance of a secondary infection during antimicrobial rx of a primary infection)
  • organ tox
  • selection of resistant microbes
18
Q

valid indications for combination antimicrobial therapy

A
  • empirical therapy of severe infection of unknown cause
  • rx of polymicrobial infections
  • enhancement of antibacterial activity in the treatment of specific infections
  • preventing the emergence of resistant microbes
19
Q

disadvantages of combination antimicrobial therapy

A
  • synergistic toxicity (one agent enhances toxicity of the other)
  • cost
  • antagonism
  • selection for drug resistant bugs
20
Q

prophylaxis of antimicrobial therapy

A
  • pre-surgery patients with indwelling medical devices
  • prevent wound infection following surgery (oral, GU, bowel)
  • sexual contacts of patients with STDs
  • dental procedures in patients with indwelling medical devices, heart defects (recommendations have changed)