Analgesia outcomes

Question 1

Segmental nociception

Answer 1

Gate control theory (stops pain input travelling to CNS)

Question 2

Supraspinal nociception

Answer 2

Descending pathways from the brainstem

Important brain regions:
Locus coruleus
PAG
Nucleus raphe magnus

Question 3

What does the locus coruleus produce?

Answer 3

NA

Question 4

What does the NRM produce?

Answer 4

Serotonin

Enkephalins

Question 5

What stimulates the PAG?

Answer 5

Opioids

Electrical stimulation

Question 6

How do opioids work?

Answer 6

Inhibit calcium channels opening (pre-synaptic inhibition)

AND they open K+ channels (post synaptic inhibition)

Question 7

μ

Answer 7

responsible for most of the analgesic action of opioids – but also some major adverse effects (e.g. respiratory depression, constipation, euphoria, sedation, dependence)

Question 8

Side effects of μ

Answer 8

Respiratory depression
Constipation
Euphoria
Sedation
Dependence

Question 9

δ

Answer 9

contributes to analgesia but activation can be proconvulsant

Question 10

Side effects of δ

Answer 10

May be proconvulsant

Question 11

κ

Answer 11

contribute to analgesia at the spinal and peripheral level and activation associated with sedation, dysphoria and hallucinations

Question 12

Side effects of κ

Answer 12

Sedation
Dysphoria
Hallucinations

Question 13

ORL1

Answer 13

Anti-opioid effect

Question 14

Difference between COX-1 and COX-2?

Answer 14

COX1 is constitutively active, COX-2 is induced by inflammation, benefit derives from inhibition of COX-2

Question 15

Which PG do most cells produce in response to mechanical/thermal/chemical injury?

Answer 15

PGE2

PGE2 sensitises nociceptive neurones and causes hyperalgesia

Question 16

Name 2 selective COX-2 inhibitors and their risks?

Answer 16

Rofecoxib
Celecoxib

-PRO-THROMBOTIC