Opioid Analgesics, NSAIDs and pain processing. Flashcards
How does morphine work?
Bind to the opioid receptors. Alters ion channels through G-protein coupling to channels. Opens K+ and close Ca2+. This causes hyperpolarisation. and a decrease in neurotransmitter release.
Where do opioid receptors in the spinal cord cluster?
Where the C-fibres terminate.
What are some clinical issues of opioid receptors.
Choice of opioid, tolerance build up, pain sensitivity and route of administration (speed of onset and duration of effect)
What does nalaxone do?
Counter’s the effect of opioid, especially in overdose. reverses the depression of CNS, respiratory system and hypotension.
Opioids cause plasticity in chronic pain. Give examples.
Tissue damage - chronic pain mediated by C-fibres, cause hyperalgesia.
Nerve damage - affects C fibres and A-fibres, continuous opioid use can cause hyperalgesia and allodynia.
What are other morphine like analgesics?
Codeine and Diamorphine. Synthetic opioids such as fentanyl, an anaesthetic and pethidine, used in labour.
PGs are generated how? and why?
Generated de novo from phospholipids, normally in response tissue damage.
What is the main source of PGs?
Arachidonic acid.
What is arachidonic acid metabolised by?
COX-1 AND COX-2.
Cox-2 produces mediators of inflammation. What are these?
PGI2, PGE2, PGD2, TXA2.
Out of the mediators of inflammation, Which:
- Are hyperalgesics?
- Are vasodilators?
- Is a vasocontrictor?
- Is a thrombotic?
- Decrease platelet aggregation?
- Released by mast cells?
- Are the main 2?
- Released by monocytes and macrophages in chronic inflammation?
- PGI2, PGE2.
- PGI2, PGE2, PGD2.
- TXA2.
- TXA2.
- PGI2, PGD2.
- PGD2
- PGI2, PGE2.
- PGE2, TXA2.
PGs potentiate the actions of what on bloodvessels?
Bradykinin and Histamine.
Bradykinin is synthesised how?
De novo, during tissue injury.
Does bradykinin increase or decrease PG production?
Increase.
What are the characteristics of NSAIDs?
Anti-inflammatory, Analgesic, Antipyretic - lower temperature by resetting the hypothalamic thermostat. Mainly due to inhibition of PG production in hypothalamus. Inhibit Cox enzyme and reduce generation of PGs.