Opioid Analgesics, NSAIDs and pain processing. Flashcards

1
Q

How does morphine work?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where do opioid receptors in the spinal cord cluster?

A

Where the C-fibres terminate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some clinical issues of opioid receptors.

A

Choice of opioid, tolerance build up, pain sensitivity and route of administration (speed of onset and duration of effect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does nalaxone do?

A

Counter’s the effect of opioid, especially in overdose. reverses the depression of CNS, respiratory system and hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Opioids cause plasticity in chronic pain. Give examples.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are other morphine like analgesics?

A

Codeine and Diamorphine. Synthetic opioids such as fentanyl, an anaesthetic and pethidine, used in labour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

PGs are generated how? and why?

A

Generated de novo from phospholipids, normally in response tissue damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the main source of PGs?

A

Arachidonic acid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is arachidonic acid metabolised by?

A

COX-1 AND COX-2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cox-2 produces mediators of inflammation. What are these?

A

PGI2, PGE2, PGD2, TXA2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Out of the mediators of inflammation, Which:

  1. Are hyperalgesics?
  2. Are vasodilators?
  3. Is a vasocontrictor?
  4. Is a thrombotic?
  5. Decrease platelet aggregation?
  6. Released by mast cells?
  7. Are the main 2?
  8. Released by monocytes and macrophages in chronic inflammation?
A
  1. PGI2, PGE2.
  2. PGI2, PGE2, PGD2.
  3. TXA2.
  4. TXA2.
  5. PGI2, PGD2.
  6. PGD2
  7. PGI2, PGE2.
  8. PGE2, TXA2.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PGs potentiate the actions of what on bloodvessels?

A

Bradykinin and Histamine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bradykinin is synthesised how?

A

De novo, during tissue injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Does bradykinin increase or decrease PG production?

A

Increase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the characteristics of NSAIDs?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly