Analgesia 2 Flashcards
Where do NSAIDS work?
At the site of injury - they decrease inflammation
Morphine
Strong opioid
Hydromorphone
Strong opioid
Fentanyl
Strong opioid
Heroin
Strong opioid
Codeine
Weak opioid
Tramadol
Weak opioid
Dextropropoxyphene
Weak opioid
Indomethacin
NSAID
Diclofenac
NSAID
Naproxen
NSAID
What are enkephalins?
Endogenous opioids
IMPORTANT: WHICH DRUGS MIMIC THE ACTIVITY OF ENKEPHALINERGIC INTERNEURONES?
OPIOIDS
Give an example of inhibitory interneurons
Enkephalinergic and GABAergic - they suppress transmission by both pre- and post- synaptic mechanisms
μ opioid receptors
Responsible for most of the analgesic action of opioids but have some major adverse effects:
- respiratory depression
- constipation
- euphoria
- sedation
- dependence
δ opioid receptors
Contribute to analgesia but activation can be proconvulsant
κ opioid receptors
Contribute to analgesia at the spinal and peripheral level and activation associated with sedation, dysphoria and hallucinations
(PROCONVULSANT)
ORL1 opioid receptors
Activation of these receptors produces an anti-opioid effect
COX1 and COX2, one of these is constitutively active and the other is induced by inflammation, which is which?
- COX1 always active
- COX2 induced by inflammation
Benefit of NSAIDS is because they stop COX2
Most cells generate ____ in response to mechanical, thermal or chemical injury?
PGE2
(PGE2 sensitises nociceptive neurones and causes hyperalgesia)
i.e. sensitises pain sensing neurones and causes an increased sensitivity to pain
Why do NSAIDS have a limited analgesic efficacy?
There are tonnes of pain pathways, not just the ones that involve arachidonic acid etc
COX-1 produces ____ which helps protect against the gastric environment?
PGE2
Why can COX-2 inhibitors be pretty bad?
They are prothrombotic
Rofecoxib
Selective COX-2 inhibitor
