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Pharmacology > SPR L6 Antimicrobials 2 > Flashcards

SPR L6 Antimicrobials 2 Flashcards

1
Q

What is covered in this lecture

A
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2
Q

Protein Synthesis Inhibitors

Give examples

A
  • Aminoglycosides
  • Tetracyclines
  • Macrolides
  • Oxazolidinones
  • Fusidic acid
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3
Q

Protein Synthesis Inhibitors - Aminoglycosides

Give examples

A
  • Gentamicin
  • Tobramycin
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4
Q

Protein Synthesis Inhibitors - Aminoglycosides

  1. What are these?
  2. How do they act?
  3. What do these require?
    1. What does this mean they are ineffective against?
A
  1. Bactericidal antibiotics
  2. Inhibit bacterial protein synthesis
  3. oxygen-dependent transport mechanism to enter the bacteria
    1. therefore ineffective against anaerobes but work synergistically with cell-wall-active antibiotics like β-lactams and vancomycin
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5
Q

Protein Synthesis Inhibitors - Aminoglycosides

Outline their mechanism of action

A

Bind to the 30S-subunit ribosomal proteins

Protein synthesis inhibited in 3 ways:

  1. Interfere with the initiation complex of peptide formation
  2. Induce mis-reading of mRNA
  3. Break up polysomes (ribosome clusters)
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6
Q

Protein Synthesis Inhibitors - Aminoglycosides

Outline their mechanism of action

A

Bind to the 30S-subunit ribosomal proteins

Protein synthesis inhibited in 3 ways:

  1. Interfere with the initiation complex of peptide formation
  2. Induce mis-reading of mRNA
  3. Break up polysomes (ribosome clusters)
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7
Q

Protein Synthesis Inhibitors - Aminoglycosides

Uses

  1. What are these effective against?
  2. What are they particularly used in?
  3. What is a use for Tobramycin?
A
  1. aerobic Gm-ve and some Gm+ve organisms
  2. Especially in Gm-ve sepsis - (Gent) in combination with a penicillin (synergy)
  3. Pseudomonas infections often in combination with another anti-pseudomonal antibiotic
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8
Q

Protein Synthesis Inhibitors - Aminoglycosides

Pharmacokinetics

  1. Describe the molecules?
  2. So how must these be administered?
  3. Describe the penetration into body fluids.
  4. How is this eliminated? What is the half-life?
  5. What must be done in renal impairment?
A
  1. Highly polar molecules
  2. therefore IV admin
  3. Variable
  4. Eliminated by kidney T1/2 2-3 hours - elimination mirrors eGFR
  5. MUST reduce dose and frequency to prevent dose dependent side effects
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9
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A
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10
Q

Protein Synthesis Inhibitors - Aminoglycosides

What are the two main adverse effects?

A

Ototoxicity and Nephrotoxicity

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11
Q

Protein Synthesis Inhibitors - Aminoglycosides

Adverse Effects - Ototoxicity

  1. Describe the course of this effect
  2. What does it involve?
  3. What are the signs/symptoms?
  4. When is this side effect more common?
A
  1. Progressive, usually irreversible
  2. damage of sensory cells in the vestibulo-cochlear apparatus
  3. Deafness and/or vertigo/ataxia
  4. Especially if on aminoglycoside for >2/52 or if used in combination with other ototoxic drugs like a loop diuretic
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12
Q

Protein Synthesis Inhibitors - Aminoglycosides

Adverse Effects - Nephrotoxicity

  1. What pathological changes take place?
  2. When is this more likely to happen?
  3. What vicious cycle does this result in?
A
  1. Damage to the tubules, usually reversible when drug stopped
  2. Especially if previous renal impairment Especially if concomitant use of other nephrotoxic drugs (cephalosporins /NSAIDs / Anti-fungals)
  3. See picture. Neprotoxicity, Reduced clearance, Neprotoxitiy, Renal Failure. LOOP
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13
Q
A
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14
Q

Protein Synthesis Inhibitors - Aminoglycosides

Monitoring

  1. What needs to be monitored every 8 hourly?
  2. What about other conditions?
  3. What should be measured after 1st dose?
  4. What should the peaks and troughs be?
  5. What else should be monitored?
A
  1. Endocarditis
  2. daily
  3. serum trough levels after 1st dose (i.e. just before 2nd dose)
  4. Peak 5-10 mg/L (3-5 mg/L if tds), Trough < 1-2mg/L
  5. Obviously should also monitor U+E
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15
Q

Protein Synthesis Inhibitors - Aminoglycosides

What are the trust guidelines for ICU

In particular, for septic shock?

A

Vancomycin (cell wall active - glycopeptide)

1g 12hourly IV per levels

See picture

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16
Q

Septic Shock

Defintions of sepsis and septic shock require all three of the following criteria to met

A
  • Strong clinical impression of severe infection
  • 2 of the following
    • Temp >38oC or <36oC
    • HR >90 bpm
    • RR >20 or PaCO2 <4.3kPa
    • White cell count >12 or <4
  • Signs and symptoms of new organ failure or shock (systolic BP <90mmHg or fall of 40mmHg from baseline)
17
Q

Protein Synthesis Inhibitors - Tetracyclines

  1. Give examples
  2. How do they act?
  3. What are they used for?
  4. What are they usually given for?
    1. Outline this management
  5. Who are they NEVER given to?
A
  1. Tetracycline

Doxycycline

  1. Inhibit protein synthesis
  2. Broad spectrum bacteriostatic antibiotics
  3. orally as an alternative for community acquired pneumonia or cellulitis
    1. See picture
  4. NEVER to mothers / children - Chelate Calcium
18
Q

Cell Wall Active Agents - Carbapenems

Give examples

A
  • Meropenem
  • Imipenem
19
Q

Cell Wall Active Agents - Carbapenems

  1. What is their mechanism of action?
  2. What do they have activity against?
  3. What are they reserved for?
  4. What are the main adverse effects?
  5. What can they be used for in ICU?
A
  1. same as other β-lactams i.e. interfere with the synthesis of the bacterial cell wall peptidoglycan (cross-sensitivity)
  2. Broad spectrum activity against aerobic and anaerobic Gm +ve and –ve bacteria.
  3. Tend to be reserved for severe resistant infection under ID guidance
  4. GI upset similar to other β-lactams
  5. Septic shock - Meropenem 2g 8hourly IV
20
Q

Cell Wall Active Agents - Monobactams

Give an example

A

Aztreonam

21
Q

Cell Wall Active Agents - Monobactams

Aztreonam

  1. What is a benefit of this drug?
  2. What is it’s ROA?
  3. What is it effective only against?
  4. What are the adverse effects?
A
  1. Resistant to most β-lactamases
  2. Only given IV
  3. only against Gm-negative aerobic rods (e.g. pseudomonas) – targeted Rx
  4. GI upset similar to other β-lactams but rarely cross-sensitivity
22
Q

Cell Wall Active Agents - Monobactams

Vancomycin

  1. What is this drug?
  2. How does it act?
  3. What can’t it cross?
  4. What is it used for orally?
  5. What is it used for IV?
  6. What are the adverse effects?
A
  1. Glycopeptide bactericidal antibiotic
  2. Inhibits cell wall sythesis
  3. Cannot cross the gut wall
  4. Orally used for severe c. difficle colitis
  5. Intravenously used to treat MRSA (Methicilin Resistant Staph Aureus)
  6. Rash / ototoxicity / nephrotoxicity
23
Q

Which patients are at high risk of MRSA infection?

A
  • Previous MRSA infection or colonisation
  • Multiple previous hospitalisations
  • Long duration of present hospitalisation episode
  • normally resident in nursing home
24
Q

Agents Acting on Nucleic Acid Synthesis - Metronidazole

  1. What is this?
  2. What process needs to take place?
  3. What is it used against 1st line?
  4. What else is it used against?
  5. What are some adverse effects?
A
  1. Anti-protozoal agent that also has good anaerobic cover and activity against clostridia
  2. Nitro group reduced to reactive products
  3. Used as 1st line against c. difficle colitis
  4. Used for anaerobic cover in intra-abdominal sepsis
  5. Metallic taste

Minor GI disturbance

Dizziness / headache

** reaction when taken with alcohol**

25
Q

Action on nucleoside precursors - Trimethoprim

  1. What is this?
  2. What is it commonly used for?
  3. What is it sometimes combined with?
    1. What is the product then used to treat?
A
  1. Bacterial dihydrofolate reductase inhibitor, Bacteriostatic
  2. simple UTI
  3. sulfamethoxazole to make co-trimoxazole
    1. P Carinii, Toxoplasmosis, nocardiasis
26
Q

Which antibiotics should be avoided in pregnancy?

A
  • Aztreonam
  • Cotrimoxazole (action on nucleoside precursors)
  • Trimethoprim (action on nucleoside precursors)
  • Chloramphenicol
  • Doxycycline
  • Levofloxacin
27
Q

Agents acting on nucleic acid syntesis - Nitrofurans

Nitrofurantoin

  1. What is it’s class?
  2. What is it’s mode of action?
  3. What are it’s uses?
  4. When should it NOT be used?
  5. What are the common adverse effects?
    1. Important adverse effects?
  6. When should it be used with caution?
A
  1. Nitrofuran antibiotic
  2. Poorly understood - It is thought to inhibit a number of bacterial enzymes including those involved in protein synthesis and is DNA toxic
  3. UTIs (not if pseudomonal or proteus)
  4. DO NOT USE if septicaemia (poor serum levels) DO NOT USE if renal impairment (less effective and potentially increased risk of peripheral neuropathy)
  5. GI disturbance (nausea, vomiting, diarrhoea)
    1. Peripheral neuropathy

Pulmonary fibrosis

Hypersensitivity reactions involving skin and bone marrow

Haemolytic anaemia

  1. Anaemia

Diabetes mellitus

Vitamin B12 and folate deficiency

Pulmonary disease

Hepatic and renal impairment

Any condition associated with peripheral neuropathy (severe and irreversible neuronal damage may result)

28
Q

Summary

A
  • Antibiotic choice is based on
    • Severity of illness
    • Most likely organisms
    • Antibiotic that can act at the infected site
  • This part of the thought process has been done for you by the guideline setters
  • You must stay up to date with local guidelines for the common conditions
29
Q

What the next lecture covers

A

Pharmacology (26 decks)

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