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Clinical Pharmacology, Therapeutics & Intro to Prescribing > Lecture 21- Antimicrobials > Flashcards

Lecture 21- Antimicrobials Flashcards

1
Q

antibiotic resistance timeline

A
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2
Q

multi-drug resistant

A

non-susceptibility to at least one agent in three or more antimicrobial categories

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3
Q

extensively drug resistant (XDR)

A

non-susceptibility to at least one agent in all but two or fewer antimicrobial categories

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4
Q

Pan-drug resistant (PDR)

A

non-susceptibility to all agents in all antimicrobial categories

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5
Q

Antimicrobial stewardship summarised to:

A
  • Appropriate use of antimicrobials
  • Optimal clinical outcomes
  • Minimize toxicity and other adverse events
  • Reduce the costs of health care for infections
  • Limit the selection for antimicrobial resistant strains.
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6
Q

Antibiotic choice

A
  • Main thing to focus on is the history/presenting complaint
  • If a patient presents with a respiratory tract illness, you should obviously think of a respiratory pathogen, such as Streptococcus pneumoniae, and choose your antibiotic appropriately following guidelines
  • Follow local guidelines as much as possible, as regional sensitivity/resistance is a thing
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7
Q

before you start Abx you should

A

obtain microbiological samples pertinent to the suspected infection; this will allow laboratory testing for sensitivity and resistance, thus allow you to give more focused treatment

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8
Q

antibiotic guidelines consider

A
  • which pathogen is most likely causative for a given infection type?
  • characteristics of pathogen e.g. Gram , anaerobic vs aerobic
  • does it reach the site of infection
  • is it available in right forumulation
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9
Q

clinician must also consider

A
  • corret formulation?
  • half life/dosing frequency?
  • does it interact with other drugs
  • toxicity concers
  • does antibiotic require therapeutic drug monitoring
  • allergy
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10
Q

Outline CURB and use for this example

A
  • use CURB-65 score to assess pts pneumonia severity
  • her CURB-65= 1
  • commubity acquired pneumonia
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11
Q

What are our main considerations for trying to work out the causative organism in this case?

A
  • Respiratory tract infection
  • Elderly
  • Non-smoker
  • Teetotal
  • No recent travel

Based on the above, we can assume the likely causative organism is Streptococcus pneumoniae (followed by Staphylococcus aureus and Haemophilus influenzae)

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12
Q

treatment for streptococcus pneumoniae causing pneumonia

A
  • Strep pneumoniae = Gram +ve cocci
  • In any case, knowing the most likely organism will lead you to prescribe either a beta-lactam or a tetracycline antibiotic
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13
Q

Different antibiotics have different modes of action, owing to the nature of their structure and degree of affinity to certain target sites within bacterial cells.

A

Inhibitors of cell wall synthesis. …

Inhibitors of cell membrane function. …

Inhibitors of protein synthesis. …

Inhibitors of nucleic acid synthesis.

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14
Q

main cell wall synthesis inhibitors

A

Beta-lactams

  • penicillins
  • cephalosporins
  • cerbapenems
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15
Q
A
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16
Q

beta-lactams

A
  • Bacteria cell wall peptidoglycan
  • Generally bactericidal
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17
Q

Penicillin

A
  • Named for the fungal penicillium from which it is derived
  • Individual sensitivity testing often required, particularly in secondary care
  • think allergy
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18
Q

Co-amoxiclav ​

A

Clavulanic acid + amoxicillin

  • Clavulanic acid= Beta lactamase inhibitor
  • Beta- lactamase is an enzyme used by certain bacteria to break down Beta-lactam antibiotic molecular structure
  • Clavulanic acid is commonly combined with amoxicillin in order to overcome this issue = co-amoxiclav
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19
Q

uses of co-amoxiclav

A
  • Bacterial meningitis
  • Bone and joint infections
  • Skin and soft tissue infections
  • Otits media
  • Pneumonia
  • UTIs
  • STIs
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20
Q

Cephalosporins

A
  • Name from fungal cephalosporium acreminum from which they are derived
    • Individual sensitivity testing often required, particularly in secondary care
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21
Q

cephalosporin uses

A
  • Uses
    • Septicaemia
    • Pneumonia
    • Meningitis
    • Biliary tract infections
    • UTIs (especially in pregnancy or in patients unresponsive to other drugs)
    • Sinusitis
22
Q

carbopenems

A

e.g. meropenem, imipenem

23
Q

antibacterials which target bacterial protein synthesis

A
  • Tetracyclines
  • Aminoglycosides
  • Macrolides
  • nitrofurans
24
Q

Tetracyclines

A
  • Following uptake into susceptible organisms by active transport, tetracyclines act by inhibiting protein synthesis
    • Bind to bacterial ribosomes, preventing binding of tRNA to it, thus preventing the initiation of protein synthesis
    • Bacteriostatic
  • Common examples (oral only):
    • Doxycycline
    • Tetracycline
  • Individual sensitivity testing often required, particularly in secondary care
25
Q

tetracycline uses

A
  • Clinical applications:
    • Respiratory tract infections (particularly atypical organisms)
    • Acne
    • Chlamydia
    • Lyme disease
26
Q

tetracyclin contraindications

A
  • Important to remember: Shouldn’t be given to children <12 years, pregnant and breastfeeding women (causes staining of developing teeth)
27
Q

Macrolides

A
  • Inhibit bacterial protein synthesis by an effect on ribosomal translocation
  • Bactericidal/bacteriostatic
  • Common examples:
    • Clarithromycin
    • Erythromycin
    • Azithromycin
28
Q

macrolide uses

A
  • Uses
    • The antimicrobial spectrum of macrolides is very similar to that of penicillin
    • Also active against atypical respiratory pathogens
29
Q

Nitrofurans

A
  • Most commonly prescribed example is Nitrofurantoin
  • Mechanism of action:
    • Works by being reduced to multiple reactive intermediates by nitrofuran reductase inside the bacterial cell
    • These intermediates then attack ribosomal and DNA proteins within the bacteria, as well as inhibit the Citric acid cycle
30
Q

Pharmacokinetics of nitrofurans

A
  • Up to 50% of an oral dose Nitrofurantoin is excreted in the urine in unchanged form
  • This allows Nitrofurantoin to concentrate within urine, leading to more effective levels within the bladder than in other tissue compartments
  • This makes it one of the first-line agents in treating Urinary Tract Infections
31
Q

antibacterials which target DNA gryase

A

Quinolines e.g. ciprofloxacin

32
Q

Quinolones

A
  • Inhibit topoisomerase II (a bacterial DNA gyrase), the enzyme that produces a negative supercoil in DNA and thus permits transcription or replication
  • Common examples:
    • Ciprofloxacin
    • Levofloxacin
33
Q

quinolones provide great coverage of

A

Gram negative organisms, as well as atypical organisms and Gram positives

34
Q

quinolones uses

A
  • Clinical applications:
    • Complicated UTIs
    • Pseudomonas aeruginosa cover
    • Gonorrhoea
35
Q

side effects of quinolones

A
  • Somewhat unique, and important to remember side-effect profile:
    • Tendinitis +/- rupture
    • Aortic dissection
    • Central nervous system effects (inc. Convulsions)
36
Q

Antibacterial Agents That Interfere With Folate Synthesis or Action

A

Two examples:

  • Sulfonamides
  • Trimethoprim
37
Q

Trimethoprim

A
  • Folate antagonist:
  • Reversible inhibitor of dihydrofolate reductase, which is responsible for the production of Tetrahydrofolic acid necessary for the biosynthesis of bacterial nucleic acids and proteins
  • Binds with a much stronger affinity to bacterial dihydrofolate reductase than human
  • Bacteriostatic/bactericidal
  • Clinical applications:
    • UTIs (careful when prescribing to reproductive age females)
38
Q

name an antiprotazxoal egent

A

metronidazole

39
Q

Metronidazole

A
  • Introduced as an antiprotozoal agent, but good against anaerobic bacteria also active against anaerobic bacteria
  • The exact mechanism of action has not been established
    • it is thought anaerobes and protozoa metabolise Metronidazole, making it active in blocking nucleic acid synthesis
  • Has disulfiram-like action, so patients must avoid using alcohol when on the antibiotic – bad hangover
40
Q

Antivirals

A
  • Many different groups
  • Two most commonly used:
    • Aciclovir (DNA Polymerase Inhibitors)
    • Oseltamivir (Neuraminidase Inhibitors)
41
Q

Aciclovir

A
  • Predominantly activated in infected cells, as the viral enzyme thymidine kinase is more effective at phosphorylating it, thus activating it
  • The fully phosphorylated form then inhibits viral DNA polymerase
  • Clinical applications:
    • Herpes simplex infections (genital herpes, encephalitis)
    • Varicella zoster (chicken pox, shingles)
42
Q

herpes simplex virus

A
  • HSV has two serotypes, which broadly produce two presentations (although some overlap)
    • HSV-1 – predominantly responsible for mouth/lips/eye infections
    • HSV-2 – predominantly responsible for genital infection
  • Aciclovir can be used in either presentation, although there are some notable differences
43
Q

oral herpes (usually HSV-1) treatment

A
  • DO NOT prescribe topical antiviral preparations; these are available OTC, and limited evidence base
  • NICE guidelines DO NOT recommend routine prescribing of oral antivirals for healthy people with herpes labialis
    • Although they do state to use clinical judgement (look at severity, frequency, persistence of lesions
  • More lenient when dealing with immunocompromised patients, but again depends on your own clinical judgement
44
Q

genital herpes (usually HSV-2) treatment

A
  • First episode:
    • Commence oral Aciclovir within 5 days of the start of the episode or while new lesions are forming
    • Topical Aciclovir not recommended, as offers minimal clinical benefit
  • Recurrent episodes:
    • Episodic antiviral treatment – if attacks are infrequent (<6/year)
      • Either 800mg TDS for 2 days or 200mg 5x/day for 5 days
      • Consider self-initiated treatment, to allow for early start
    • Suppressive antiviral treatment – if attacks are more frequent (≥6/year) OR causing psychological distress OR affecting the person’s social life
      • 400mg BD OR 200mg QDS
      • If breakthrough recurrences occur, the dosage should be increased
      • Continue treatment for max. 1 year, after which it should be stopped to assess recurrence
45
Q

CyP450 enzymes

A
  • Present in most tissues of the body, but predominantly the liver
    • Other notable sites are small intestine, lungs, placenta, kidneys
  • Essential for the metabolism of many medications and hormones
  • More than 50 subtypes, but 6 of them jointly responsible for metabolism of 90% of drugs
  • Most significant = CYP3A4 and CYP2D6
46
Q

CYP450 inhibitors

A
  • Inhibitors block the metabolic activity of one or more CYP450 enzymes
    • This means the drugs usually broken down by the inhibited enzyme will be metabolised at a slower rate, essentially leading to an ‘overdose’ (higher conc in plasma)
47
Q

CYP450 inducers

A
  • Inducers increase the enzyme synthesis of one or more CYP450 enzymes
    • This means more enzyme, therefore the drugs broken down by said enzyme break down quicker, leading to below therapeutic levels in the blood
48
Q

example 1 of CYP450 inhibitors and inducers in action

A
49
Q

example 2 of CYP450 inhibitors and inducers in action

A
50
Q

Enterohepatic circulations A.k.a. Enterohepatic recycling (EHR)

A
  • Begins with drug absorption across the intestine into the portal circulation, followed by uptake into the hepatocytes. Next, drug and or conjugated metabolites are secreted into the bile and returned to the intestine, where drug can be reabsorbed into the circulation
  • Think of it as a secondary absorption phase for many different substances which the body secretes via bile: antibiotics, NSAIDs, hormones, opioids, digoxin, warfarin
51
Q

Enterohepatic recycling (EHR) and gut flora

A
  • Gut flora play an important role in EHR, as they produce various enzymes involved in the metabolism of drug conjugates that are secreted in the bile
    • Oral antibiotics can eliminate gut flora, thus lessen/prevent EHR
  • Important interaction noted with oral contraceptives
    • Lower rates of EHR = lower blood concentrations of oestrogen/progesterone = increased risk of becoming pregnant

Clinical Pharmacology, Therapeutics & Intro to Prescribing (39 decks)

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