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NMS sem2 > W4: Control Of Pain > Flashcards

W4: Control Of Pain Flashcards

1
Q

What is pain?

A

Subjective element produced by the stimulation of nociceptic neurones in the periphery.

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2
Q

What is neuropathic pain?

A

Damage to neurones in nociceptive pathways.

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3
Q

What are analgesics?

A

Drugs that relieve pain, e.g., opioids, NSAIDS

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4
Q

Where do opioids act?

A

On opioid receptors

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5
Q

Examples of endogenous opioids

A

Enkephalins

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6
Q

What are opioids used for?

A

Treating moderate to severe pain, e.g., post-operation

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7
Q

How are different opioids given?

A

Strong agonists are usually given parenterally (by injection):

  • morphine can be given orally for chronic pain but usually by injection
  • pethidine by injection for acute pain like after childbirth
  • fentanyl given in patches for chronic pain states
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8
Q

Agonists of morphine (therapeutic opioids)

A

Heroin (strong), codeine (weak)

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9
Q

Antagonists of morphine (therapeutic opioids)

A

Naloxone

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10
Q

Synthetic opioid agonists

A

Pethidine, fentanyl, methadone

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11
Q

Synthetic opioid partial agonists

A

Buprenorphine

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12
Q

What can be given to treat headaches?

A

Mild pain so weak agonists like codeine given orally

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13
Q

What can be given to treat inflammatory pain?

A

Combine codeine with NSAIDS

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14
Q

Where can opioids act?

A

At receptors at different sites: spinal cord, brainstem, periphery

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15
Q

Describe the site of action of opioids at the spinal cord

A

Dorsal horn: opioids inhibit (decrease) synaptic transmission at the synapse between the spinach sensory afferent (nociceptive neurone) and the second order neurone that will travel up the spinothalamic tract to the thalamus, by binding to receptors presynaptically and postsynaptically

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16
Q

Describe the site of action of opioids in the brainstem

A
  • acts in the Periacqueductal Grey (PAG) and then Rostro-ventral medulla (RVM) (in brainstem)
  • opioids increase activity of inhibitory pathways (down the spinal cord) onto the dorsal horn, enhancing the inhibition of nociceptic transmission
  • they act via the PAG, increasing activity of RVM, which sends inhibitory signals to the dorsal horn, reducing the nociceptive signals of pain.
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17
Q

Describe the site of action of opioids in the periphery

A
  • opioids reduce excitability of nociceptive neurones in the periphery
  • stimulation of opioid receptors in the terminals of nociceptive neurones means they are less likely to generate APs, due to inhibition brought about by opioid drugs.
18
Q

How do opioids affect mood?

A

Psychogenic element of pain is due to the activity of the limbic system, impacting nociceptive pathways. Opioids affect limbic system. Can cause addiction.

19
Q

What opioid receptors are there?

A

mew, delta, k

20
Q

What type of receptors are opioid receptors?

A

G protein coupled receptors

21
Q

Describe the mechanism of action at opioid receptors upon agonist binding

A

G protein activation leads to modulation of ion channels (direct)
- increased opening of K+ channels leading to hyperpolarisation of neurones, making them less excitable and thus inhibited
- decreased opening of Ca2+ channels leading to decreased release of transmitter at the synapse
Inhibition of adenylyl cyclase leading to a decrease in cAMP

22
Q

Functional effects of opioids at mew receptors

A

Analgesia (all sites), euphoria (in the eye to cause pupil constriction), miosis, respiratory depression, physical dependence

23
Q

Functional effects of opioids at delta receptors

A

Analgesia (spinal)

24
Q

Functional effects of opioids at k receptors

A

Analgesia (peripheral), miosis, sedation, dysphasia (altered mood and anxiety)

25
Q

What are functional effects of opioids at all receptors?

A

Constrict smooth muscle (GIT, bronchi), nausea/vomiting, constipation

26
Q

What are the problems with opioid use?

A

Hyperalgesia with prolonged use
Tolerance
Dependence

27
Q

Describe the issue of hyperalgesia with opioid use

A

Pain sensitisation due to the pain pathways expressing more receptors to allow transmission

28
Q

Describe tolerance due to opioid use

A

Increased dose needed to maintain the effect due to desensitisation of receptors.
Little tolerance to GIT and pupil effects, so patients will get more and more constipated with constricted pupils.

29
Q

Describe dependence due to opioid use

A

Due to increased expression of adenylyl cyclase - causing over-activity of signalling when drug is removed.
Physically causes nausea, diarrhoea, restlessness, fever, piloerection - withdrawal symptoms
Psychologically causes craving

30
Q

What is the action of NSAIDs?

A

Action via inhibition of production of prostaglandins (which are released in high amounts during inflammation)

31
Q

How do NSAIDs have analgesic effects?

A
  • PGs sensitive nociceptive nerve terminals to inflammatory mediators (e.g., bradykinin which binds to nerve terminals and sets up APs)
  • inflammatory pain: toothache, dysmenorrhoea, bone metastases
  • PGs cause cerebral vasodilation = headache
32
Q

How do NSAIDs have anti-inflammatory effects?

A

Since PGs cause vasodilation.

NB NSAIDs don’t prevent tissue damage (caused in chronic inflammation)

33
Q

How do NSAIDS have antipyretic effects?

A

Antipyretic = to reduce fever

- inflammation leads to increased PGs, affecting the hypothalamus, leading to increased temperature set-point = fever

34
Q

What are the main classes of NSAIDS

A 
Salicylates (aspirin)
Proprionic acids (ibuprofen)
35
Q

What is the mechanism of action of NSAIDs?

A

Suppresses PG production

Inhibits cyclo-oxygenase (COX)

36
Q

What does COX do?

A

COX catalysed arachidonic acid (rate limiting step in the production of PGs)

37
Q

What is the difference between COX-1 and COX-2?

A

COX-1: constitutive (homeostasis) - able to regulate blood vessel diameter, controlling blood flow
COX-2: induced by inflammation

38
Q

What are the differential actions on COX?

A

Aspirin has irreversible effects on COX-1 and 2
Ibuprofen has a competitive effect on COX-1 and 2
Celecoxib has selective effects on COX-2

39
Q

Describe paracetamol

A

May affect another subtype of COX but is not an NSAID. Little anti-inflammatory action but is good for pain relief (action in CNS)

40
Q

How do NSAIDS cause gastric mucosal damage?

A
  • PGs (via COX-1) stimulate mucous release, protecting the mucosa and stomach lining
  • so NSAIDS are direct irritants
  • NSAIDS allow exposure of the mucosal lining and damage due to the drug and HCl in stomach
  • causes inflammation, bleeding, ulceration
41
Q

What conditions can cause neuropathic pain?

A

Trigeminal neuralgia, diabetic neuropathy, postherpetic neuralgia

NMS sem2 (14 decks)

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