Antimicrobials Flashcards

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1
Q

What are the 5 main methods on how anti-microbials work?

A
  • inhibiting cell wall synthesis (B-lactams, vancomycin)
  • inhibiting nucleic acid synthesis (fluoroquinolones, rifamycins)
  • stopping metabolite production folate (trimethoprim, sulfonamides)
  • inhibiting cell membrane synthesis (daptomycin)
  • inhibiting protein synthesis (linezoid, tetracyclines, macrolides, aminoglycosides)
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2
Q

What is the difference between bactericidal and bacteriostatic agents?

A

Bactericidal

  • means destroying, or killing bacteria
  • works optimally when bacteria divides at USUAL rate so sometimes combining both will not work in patient’s favour

Bacteriostatic

  • stopping divisions and replication of bacteria
  • slowing the growth
  • bacteria are still alive and rely on body’s usual mechanisms
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3
Q

Give some examples of penicillins, their mechanism and whether static or cidal

A
  • amoxicillin and flucloxicillin
  • mechanism: acts on cell wall
  • bactericidal
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4
Q

Give some examples of ceflasporins, mechanism and whether static or cidal

A
  • ceftriaxone, cephalexin
  • acts on cell wall
  • cidal
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5
Q

Give examples of quinolones, mechanism of action, whether static or cidal

A
  • ciprofloxacin, levofloxacin
  • DNA/RNA synthesis
  • both static and cidal
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6
Q

Give examples of macrolides, mechanism of action, whether static or cidal

A
  • erythromycin, clarithromycin
  • inhibits protein synthesis
  • static
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7
Q

Give examples of tetracycline, mechanism of action, static or cidal

A
  • doxycycline
  • inhibits protein synthesis
  • static
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8
Q

Give examples of aminoglycosides, MOA, whether static or cidal

A
  • gentamicin
  • inhibits protein synthesis
  • both
  • requires monitoring
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9
Q

Give examples of glycopeptides, MOA, static or cidal

A
  • vancomycin (needs monitoring)’
  • acts on cell wall
  • cidal
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10
Q

Give examples of carbopenams, MOA, static or cidal

A
  • meropenem
  • acts on cell wall
  • cidal
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11
Q

How does antibiotic resistance develop?

A
  • presence of beta lactam enzymes
  • efflux pumps
  • plasmid DNA can be passed from cell to cell
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12
Q

Why do we need to do drug monitoring?

A
  • narrow therapeutic window
  • maximize effect of antibiotic
  • there is risk of toxicity
  • examples: vancomycin and gentamicin
  • need to do blood tests at a specified time
  • for vancomycin, a level must be taken at every 4th dose as a minimum and must be taken an hour before next dose is due
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13
Q

What is the difference between time dependent and concentration dependent killing of bacteria?

A
  • MIC (minimum inhibitory concentration) needed to kill bacteria
  • time dependent: long half lives are beneficial, they spend longer at the binding sites (needs frequent dosing to be kept over MIC)
  • concentration dependent: levels important, need a certain concentration at the binding sites
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14
Q

Why do we use antibiotics?

A
  • short term management of bacterial infections
  • prophylaxis in acute setting such as high risk procedures, but dont give unnecessary antibiotics
  • long term prophylaxis: only give if suitable, local UHL guidelines, associated risks
  • sometimes if giving antibiotics, you’ll kill all but the resistant ones, so they survive and produce an infection that’s even worse
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15
Q

What are combination antibiotics used for? Explain co-amoxiclav

A
  • provide a synergistic effect
  • examples: tazocin, co-trimoxazole
  • co-amoxiclave: combo of clavulanic acid and amoxicillin
  • clavulanic acid: inhibits effects of some B lactamase enzymes so amoxicillin can work better
  • amoxicillin: acts on cell walls of bacteria in usual standard MOA
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16
Q

How do you know when acyclovir can be used in the treatment of herpes simplex virus?

A
  • aciclovir is an anti-viral medication
  • can be used in other viral conditions such as chicken pox and shingles aka varicella-zoster
  • dose depends on what you are treating (first presentation vs relapse, immunocompromised)
  • topical aciclovir used for cold sores (type 1)
  • oral aciclovir used for genital ulcers (type 2)
17
Q

What are the factors governing antibiotic choice accounting for likely infectious agent and patient group to be used in?

A
  • many factors
  • what is the likely source of infection?
  • sources lend themselves to common groups of bacteria
  • is patient in a “high risk group?” (Then use second line treatment)
  • trends, previous results, including resistance patterns (ex: MRSA colonized patient, wouldn’t use penicillin as first-line antibiotic)
  • special groups: hepatic/renal impairment, pregnancy
  • allergies and reactions
  • be careful with overuse
  • start with broad treatment, and then narrow down
  • I-five and A to F