Pain 2 (analgesia) Flashcards Preview

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Flashcards in Pain 2 (analgesia) Deck (21)
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1
Q

What is stress analgesia?

A

The body’s own pain relieving pathway that occurs under extreme stress

2
Q

Describe the stress analgesia pathway?

A

1) Neurones in periventricular nuclei of hypothalamus activated
2) signals then relayed > periqueductal gray of the mesencephalon and upper pons > raphe magnus nucleus of pons > inhibitory interneurones ( in dorsal horn of spinal cord)
3) In response inhibitory interneurones release GABA and enkephalin neurotransmitters

3
Q

What is the function of GABA in analgesia?

A
  • prevent signals being carried along 2nd order projection neurones by:
  • opening Cl- channels on postsynaptic DHN cells, causing hyperpolarisation (reduces firing of APs in DHN)
4
Q

What is the function of enkephalins in analgesia?

A
  • prevent signals being carried along 2nd order projection neurones by:
  • activating opioid receptors in A(d) and C fibres and dorsal horn neurones (DHN)
  • will open K+ channels on DHN (presynaptic) and inhibit Ca2+ channels on C or A(d) (postsynaptic) which stops depolarisation of DHN
5
Q

What signalling molecule mediates neurotransmission between inhibitory neurones

A

serotonin

6
Q

How can you activate natural analgesia neurotransmitters?

A
  • TENS (transcutaneous electrical nerve stimulation), peripheral inhibitory pathways by releasing enkephalins
  • applying pressure (rubbing wound will reduce pain as inhibitory interneurones activated by A(beta) fibres (mechanical)
7
Q

When can hot or cold treatments be useful in analgesia?

A

Hot - stiff joints or lower back pain

Cold - reduce inflammation and nociceptor activation

8
Q

How do medical analgesics generally work?

A

1) reduced nociceptor activation
2) reduced activation of ascending DHNs
3) Activating descending inhibitory pathways

9
Q

Describe MoA of opioids?

A
  • inhibit transmission of pain signals in spinal cord
  • to do this they activate opioid receptors
  • and stimulate RMN which will then activate inhibitory interneurones to reduce DHN activation
10
Q

Describe MoA of NSAIDs?

A
  • inhibit prostaglandin production by COX inhibitors

- reduces the hyperalgesia associated with inflammation

11
Q

What are the negative side effects of opioids?

A
  • constipation
  • nausea
  • vomiting
  • respiratory depression
12
Q

What are the positive side effects of opioids?

A
  • Euphoria/sense of well being

- sedative

13
Q

What are the symptoms of opioid withdrawal?

A
  • reduced capacity to experience pleasure
  • increased anxiety
  • nausea
  • muscle ache
  • diarrhoea
  • low mood
14
Q

What do prostaglandins do?

A
  • ## Cause peripheral sensitisation by increasing nociceptor sensitivity
15
Q

What do prostaglandins do?

A
  • Cause peripheral sensitisation by increasing nociceptor sensitivity
  • cause vasodilation, anti-coagulation and hyperalgesia
16
Q

What are the side effects of NSAIDS?

A

GI bleeding, sodium and water retention, stroke, MI

17
Q

Give examples of NSAIDS?

A

Non-selective COX inhibitors: Diclofenac, Ibuprofen and Naproxen
Selective COX-2 inhibitors: Celecoxib
COX-3 selective: Paracetemol

18
Q

Give examples of NSAIDS?

A

Non-selective COX inhibitors: Diclofenac, Ibuprofen and Naproxen
Selective COX-2 inhibitors: Celecoxib
COX-3 selective: Paracetemol (acts centrally)

19
Q

What is the MoA of local anaesthetics (LA)?

A
  • block initiation and propagation of AP by pain fibres
  • un-ionized LA enters cell through membrane
  • ionized in the cell due to acidity
  • LA closes inactivation gate of Na+ channels this prevents transmission of pain signals
  • If extracellular environment becomes more acidic LA can be ionized outside cell and can only enter cell through pore (slower)
20
Q

What are the side effects of local anaesthetic?

A
Common
- Nausea 
- dizziness 
- bruising 
- redness 
- itching  
- swelling on injection site 
Less common
- drowsiness
- mental mood swings 
- vision changes
- tremor
21
Q

How do antidepressants produce analgesia?

A
  • serotonin re-uptake inhibitors increase serotonin levels at inhibitory interneuron synapse and descending analgesic pathways
  • increased activation of inhibitory neurones means less C and A(d) mediated pain signals are transmitted up ascending pathways