Antibiotics Flashcards

1
Q

What was the first AB discovered and how?

A

Penicillin was the first AB discovered when Alexander Fleming had his S.Aureus culture contaminated with Penicillium Notatum. Penicillin in the agar caused lysis of S.Aureus.

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2
Q

Why may immunosuppressed not respond to ABs? Give examples of people considered immunosuppressed

A

Antibiotic + Immunity → Bacterial Clearance

  • Due to this immunosuppressed individuals may not respond to AB treatment
  • This includes Babies, Elderly, HIV+, Cancer Treatment, Transplant Recipient and Diabetics
  • Also neutropenia, asplenia, renal disease, diabetes, alcoholism
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3
Q

What are ABs made of?

A

Natural products of fungi and bacteria - natural antagonism and selective advantage, kills or inhibits growth of other microbes.
Most are semi synthetic as they are derived from the products but chemically modified to increase their pharm properties and effect.
Some are completely synthetic e.g. sulphonamides.

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4
Q

When do we use ABs?

A

Treatment of bac infections. Prophylaxis for close contacts of transmissible disease e.g. in peri operative cover for gut surgery, also given to those with increased susceptibility for infection

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5
Q

List the factors that make a good antibiotic

A

Selective toxicity, good killing activity, slow emergence of resistance, narrow spec of activity, non toxic to host (TI), long plasma half life, multiple dosing forms (IV, IM, PO, topical), no interaction with other drugs

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6
Q

What determines the dosage for a patient? What must we consider?

A

This will depend on patient factors: Weight, Renal Function, Age and Liver Function, Severity of Infection

As kidney or liver will get rid of the AB
Also depends on the Susceptibility of the Organism causing infection
It also depends on the pharmacodynamic properties of the antibiotic i.e. which determine if we can give a concentration higher that the MIC

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7
Q

What are the two pharmacodynamic properties of ABs?

A

The pharmacodynamic properties of ABs that describe killing activity are:

  1. Time-Dependence which is the time spent over the MIC ? idk
  2. Concentration-Dependence which is the Area Under Concentration (AUC) that is above the MIC?
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8
Q

What is stage 1 of AB therapy?

A

Stage 1 - Day 0 -2: patient is unstable due to infection, we are unaware of site and pathogen so prescribe empirically with parenteral broad spectrum drugs

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9
Q

What is stage 2 of therapy?

A

Day 2 - 7: patient now stabilising, now know the pathogen and site so now change therapy so more efficient so parenteral monotherapy or oral narrow spec drugs depending on stability improvement of pt

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10
Q

What is stage 3 of therapy?

A

Day 7 - 10: patient stable, now start oral ABs

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11
Q

Factors that affect drug-host-microbe

A
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12
Q

Who decides which AB to give, and how decide?

A

This is decided by Specialists, Medical Microbiologists and Local Policies.
Depends on drug characteristics.
Depends on how drug distributes in body - must be similar to bacteria distribution: - Some drugs aren’t absorbed from gut (but useful for treat gut infection), dont cross the BB barrier, don’t penetrate abscess, some drugs accumulate inside cells.
Also depends on drug characteristics

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13
Q

What factors must we consider when deciding which AB to give a patient?

A

Spectrum of activity - Cidal vs Static, Toxicity, Excretion, Patient Age - Renal Capacity, Route of Administration - Oral / i.v / i.m / Topical, Clinical Condition, Type of Bacteria, Sensitivity of Bacteria - Resistance? / Which MOA, Cost

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14
Q

When do we give combinations of ABs?

A

Before an organism is identified in life-threatening conditions

To give less toxic doses to an individual as possible

Polymicrobial Infections such as in GI Perforations where there may be both Aerobes and Anaerobes which require different treatments
Some ABs work in Synergy with one another such as:
Penicillin and Gentamycin

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15
Q

Why may AB therapy not work/failure?

A

Issue with drugs, host, bacteria and/or lab

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16
Q

What issues with the drug may cause failure of AB therapy?

A
  • Inappropriate Drug
  • Improper Route of Administration
  • Poor Tissue Penetration
  • Increased Excretion
  • Inadequate Dose ∴ Not the MIC
17
Q

What issues with the host may cause failure of AB therapy?

A
  • Immunocompromised Host
  • Retained Foreign Body such as a Catheter
  • Poor Circulation / Damaged Tissue such as Scar tissue
  • Unusual Site for Pathogen
18
Q

What issues with the bacteria or issues with lab may cause failure of AB therapy?

A
  • Natural or Acquired Resistance
  • Dormant ∴ Non Growing
  • Dual Infections are Not usually Expected
  • Biofilms such as in Endocarditis
  • Errors in Identifying the pathogen
  • Equivocal / Inconclusive Tests
19
Q

Describe selective toxicity of AB

A

This occurs due to Differences in Structure, Metabolism and Biology between the host and pathogen

  • These should harm microbes and not the host
  • It should only target the microbe if possible
20
Q

What is therapeutic index? Name two drugs which have a narrow one and their toxic effects

A

Ratio comparing the conc of active dose and conc of toxic dose.
There is no ‘Safe’ Drug as it depends on the dose

The margin for toxic drugs is very narrow such as Aminoglycosides and Vancomycin which are both Ototoxic and Nephrotoxic.

21
Q

What is microbial antagonism? How may AB affect this?

A

Normal bacterial flora of the body provides some defense by limiting the Growth of Competitors and Pathogens via competition but not causing damage.

As a result, a loss of flora results in Bacterial/Pathogen Overgrowth which is a possible effect of AB misuse which may eliminate normal bacteria too

22
Q

What is pseudomembranous colitis? What effects does it cause?

A

AB associated colitis is known as pseudomembranous colitis. Caused by growth of Clos diff which in normal flora of 3% of people. Lead to ulceration, severe diarrhoea and Serious hospital cross-infection risks.

23
Q

Difference between narrow spec and broad spec ABs? Example of each

A

Broad Spectrum - Effective against many types such as Cefotaxime

Narrow Spectrum - Effective against very few types such as Penicillin G

24
Q

What are the 5 mechanisms of action/target sites by ABs?

A

Cell wall synthesis, protein synthesis, nucleic acid synthesis, metabolic pathways, cell membrane function

25
Q

What do beta lactams target and name the two

A

Cell wall synthesis - beta lactam is a structural mimic of natural substrate. It binds PBP so peptidoglycan wall cannot be cross linked -> cell lysis.
There are two types: pencillins and cephalosporins

26
Q

Name penicillins

A

Basic (pen G, not acid stable so im or iv, SOME + and - /pen V acid stable so oral, less - and same +), anti staph (narrow spec, BLame resisant, less potent, NOT for MRSA, flucloxacillin), broader spec (More -ve and enterococci than basics, ampicillin), anti pseudomonal (extended spec incl +, -, anaerobes, piperacillin)

27
Q

Name cephalosporins

A

Cefalexin (1st, oral, UTI) cefuroxime (2nd, parenteral, - and +), cefotaxime (3rd, parenteral, more - activity), ceftazidime (3rd, parenteral, extended spec to incl pseudomonas aeruginosa)

28
Q

Name a combo of beta lactam and BLase inhibitor

A

Co-amoxiclav, spec of amoxicillin but includes more -ve and staph aureus.

29
Q
A