Antibiotics in practice Flashcards

1
Q

How are we increasing resistance?

A

*Doctors and vets - over prescribe antibiotics
*Patient does not comply to advice on administration
*Poor hygiene/lack of infection prevention and control
*People/animals travelling around the world, spreading resistant bacteria

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2
Q

How do bacteria become resistant?

A

*turn on certain internal resistance processes
*change to protect themselves from an antibiotic
*receive resistant genes from other bacteria.

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3
Q

Describe AMR?

A

Antimicrobial resistance threatens the effective prevention and tx of an ever-increasing range of infections caused by: bact, parasites, viruses & fungi

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4
Q

Describe AR -> Antibiotic Resistance

A

Compromise the success of major surgery, cancer chemotherapy, organ transplants & diabetes management become very high risk

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5
Q

Describe antimicrobial/ biotic stewardship?

A
  • Measures that can help mitigatea a public health crisis and preserve the effecitveness of available AM agents
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6
Q

What is the 3 R framework of continuous improvement ?

A

Reducing, Replacing, refining (use of AM agents)

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7
Q

What are some potential ‘solutions’ for AMR ressitance?

A
  • Research - improved detection and diagnosis of infections.
  • Refined dosing regimens- simultaneously effective while not selecting resistance.
  • Finding alternatives to antimicrobial agents.
  • Development of improved vaccines to enhance immunity and reduce disease
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8
Q

What si the 7 pt plan from BVa?

A
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9
Q

Detail the ‘protect me’ acronym?

A
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10
Q

Describe Empirical Therapy?

A

*organism unknown - cover likely pathogens
*site of infection and assume most likely organism and susceptibility
e.g. skin infections-Staphylococcus spp., most UTIs- Escherichia Coli

……Consider need / feasibility of culture & sensitivity follow up. Gram stain if possible

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11
Q

Describe Definitive Am Therapy

A

*Infective organism is known (culture & sensitivity tested)
*Narrow-spectrum antibiotics preferred over broad-spectrum
……The more at risk a patient is for AMR to be present, the more important C&S becomes

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12
Q

Describe Prophylactic AM therapy?

A

*Used in healthy individuals to prevent infection
e.g. surgery taking >90 minutes or where an implant has been inserted.
………No need in sterile routine surgery- being brave!!!….trusting your skills!!!!

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13
Q

how should we consider Location & severity of infeciton in AM chocie?

A
  • Bacteria at the infection site - concentration of AB at site
  • Perfusion limitations
  • Permeability limitations - drug distribution to the CNS, eye, epithelum EXCEPTION - meningitis
  • Location of the bact/ microrg -> intracellular pathogens less susceptible
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14
Q

Give some examples of intracellular pathogens?

A

Salmonella, Brucella, Toxoplasma, Listeria, Mycobacterium

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15
Q

What host factors to consider?

A
  • Immunocompetent patient -> bacteriostatic ABs may be sufficient!
  • Immunocompromised -> bactericidl for cure
  • Paediatric/ geriatric -> body size/ organ dev/ dysfunction
  • Recent AB therapy without a cute -> current infection under selective pressure of another AM agent and can eb resistant
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16
Q

What LOCAL factors?

A
  • The larger the bacterial inoculum at the infection site, the greater the concentration of AB needd
  • Surface biofilms - Form in FBs or natural surfaces and dec the effectiveness of ABs
  • AB efficacy signifcantly reduced in pus, necrotic or oesdematous tissue
17
Q

Client factors?

A

❑ Dosing schedule - correct antibiotic concentrations in infected tissue
❑ Completing therapy duration - Premature cessation- lead to relapse/
contribute to AMR
❑ Cost factors – both medicine cost and sensitivity testing - willingness
to pay for optimal treatment? – better client education ?
❑ Inappropriate storage of medicine may affect pharmaceutical quality.
❑ Inappropriate route – client unable to tablet their cat

18
Q

What to consider with Efficacy & pharmacokinetics?

A

❑ MIC – minimum inhibitory concentration / kill organism
❑ Remain below the level toxic to the patient –‘sensitive’ vs ‘resistant’
❑ Insufficient dose - AMR - aim for IC80-IC90 at infection site
❑ Concentration-dependent; fluoroquinolones, aminoglycosides
❑ Time-dependent; beta-lactams
❑ Synergistic effects - appropriate combinations - resistant infection
render susceptible

19
Q

What safety considerations?

A

❑ Antibiotic targets - specific to prokaryotic cells, tend to be safe.
❑ Host toxicity – different mechanism to antimicrobial mechanisms
–e.g. aminoglycoside toxicity due to accumulation in renal tubules
❑ Paediatric/ geriatric patients - susceptible to drug toxicity
❑ Impaired renal or hepatic function- increased risk
❑ Pregnancy- increase sensitivity to antibiotics (mother, foetus)
❑ Lactating females- transfer antibiotics to nursing neonates
❑ Hypersensitivity reactions- less in veterinary patients than humans.

20
Q

How to dose accurately?

A

take weight
-> Inc dose for:
- serious or chronic infections
- tissues difficult to penetrate
- infections ass with detrimental changes at - site of infection

21
Q

Conc vs Time dependent?

A
  • Concentration-dependent antibiotics- high dose once a day
  • Time-dependent antibiotics- frequently administered to maintain drug concentration at
    the site of infection above the MIC (e.g. beta-lactams)
22
Q

What duration considerations?

A
  • Longer not always better
  • Shorter / stopping prematurely can have lower cost & less toxicity BUT potential AMR, reoccuring infection, spread to others & inc need to hospitalise
23
Q

How should we choose durations then?

A
  • Uncomplicated acute infections 5-7 days (or less);
  • Response seen in 2-3 days if treatment.
  • Revaluate diagnosis/treatment if response is inadequate
  • Best to continue 2 to 3 days beyond resolution of clinical signs.
  • Chronic infections - 4–6 weeks or more with susceptibility testing and re evaluation