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Lecture notes Neuropharmacology (LSC-20061)

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Learning objectives - Physiology and pathology of pain - Pharmacological treatments to provide analgesia - types, local anaesthetic mechanisms + duration + types of administration - general anaesthesia results, premedication, anaesthesia agents, stages, inhalation anaesthetics, metabolism and ...

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  • June 10, 2022
  • 8
  • 2021/2022
  • Lecture notes
  • Ella maysami
  • All classes

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Analgesia 3

Learning objectives
- Physiology and pathology of pain
- Pharmacological treatments to provide analgesia

Part 3 - NSAIDs

Non-steroidal anti-inflammatory drugs (NSAIDs)
- Weak organic acids with anti-inflammatory, analgesic, antipyretic properties
- Most inhibit activity of cyclooxygenase-1 & 2 (COX-1&2) -> inhibits synthesis of prosta
- COX 1 : gastric protection, vascular homeostasis, platelet aggregation, kidney function
- COX 2 : induced during inflammation and tissue damage. Inhibition of COX-2 -> anti-in

Cyclooxygenase (COX)

Arachidonic acid -> (COX) -> prostaglandins and throm

Prostaglandins
- Sensitise nerve terminals to other agents by:
- Inhibiting K channels
- Facilitating 2nd messenger-mediated phosphor


Prostaglandin (PG) functions
- Bind GPCR, function as local signalling molecules
1. Pain
- PGE2 increases sensitivity of nociceptive fibres
2. Temperature
- Pyrogen -> increases PGE2 synthesis (leukocyte) -> elevates temp set point in hypotha
3. Inflammation
4. Gastrointestinal protection (COX1)
- PGI2 (prostacyclin) inhibits gastric acid secretion
- PGE2 and PGF2 stimulate protective mucous secretion
5. Platelet aggregation
6. Kidney
- PGE2 and PGI2 maintain renal perfusion, synthesised in response to reduced perfusion
7. Vasodilation

Aspirin
- Analgesic, antipyretic, anti-inflammatory, anti-platelet

,aglandins and thromboxanes
n. Inhibiting COX-1 in large doses (e.g. aspirin) -> gastrointestinal bleeding and ulcers
nflammatory, analgesic and antipyretic effects



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