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Health.2 > Pain And Analgesia > Flashcards

Pain And Analgesia Flashcards

1
Q

LECTURE: PAIN
‘
What is pain?

A
  • an unpleasant sensory and emotional experience associated with actual or potential tissue damage
  • combination of sensory (discriminative) and affective (emotional) components
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2
Q

What is noiception?

A

· sensory nervous system’s process of encoding noxious stimuli. This may include sensing pain

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3
Q

What are the functions of nociceptors?

A
  • Recognise pain sensitive afferent fibres, or neurons (whole neuron can be a nociceptor)
  • Only respond to potentially damaging (noxious) stimuli
    pick up signal
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4
Q

Why are free nerve endings termed “free”?

A
  • they are devoid of connective tissue capsule or Schwann cell covering
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5
Q

What is nociceptive transmission?

A
  • Conduction of the electrical impulses to the CNS which corresponds to the pain that is felt
  • Transfers information about intensity, duration and location
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6
Q

Where are noxious stimuli picked up by free nerve endings?

A

skin, muscle and viscera

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7
Q

What are examples of noxious stimuli?

A

o Injury

o Heat extreme

o Cold

o Inflammation

o pH

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8
Q

What determines whether a stimulus can be picked up by a nerve ending?

A

What determines whether a stimulus can be picked up by a nerve ending?

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9
Q

What happens after reception of the noxious stimuli?

A
  • receptor generates AP

- intensity of pain is encoded via firing rate of the action potential

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10
Q

Where are the nerve endings located in relation to the axon fibre?

A

at the end of the axon

pillock

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11
Q

What are primary sensory neurons?

A

Neurons that conduct impulses along efferent pathways -> CNS for interpretation

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12
Q

Where are primary sensory neurons located?

A

cell body is located in the dorsal root ganglion

NT release

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13
Q

How many axons come from 1 cell body (in dorsal root ganglion)?

A

2 separate axons - peripheral (down) and central end (up)

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14
Q

What is the mechanism that occurs when a stimulus is received by nociceptors?

A
  • reception of stimulus => AP fired at the nerve
  • AP travels up axon -> SC, where there is NT release at central nerve ending
  • axons are afferent (take info TO brain) and primary ( first of a multi-synaptic pathway)
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15
Q

What are the 2 types of nociceptor?

A

· Mechanical – A-delta fibres (hammer blow)

· Polymodal – C fibres (majority of signals picked up)

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16
Q

What is the mechanism once the primary afferent neurones reach the CNS?

A
  • Primary afferent axons -> SC and synapse to a second order neuron
  • Synapse formed in dorsal horn of SC (substantia gelitanosa)
  • Axon can split. 1 branch -> straight to brain (in touch not pain)
  • In pain the axon -> SC
  • In a motor reflex, sensory info -> ventral horn where motor neurons are, and exit SC via the ventral root
    … withdraw hand from fire- unconscious
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17
Q

What is the gate theory of pain?

A
  • SC contains a neurological “gate” that blocks pain signals OR allows them to continue to brain.
  • Pain signal must overcome inhibition (gate) to be sent to brain (by network of dorsal horn neurons)
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18
Q

How does analgesic effect relate to the gate theory of pain?

A

close gate
- prevent overcoming of the inhibition = analgesic effect as we are not allowing pain signals to be passed to the brain (wont feel pain)

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19
Q

What is TENS and how does it work?

A

Transcutaneous electrical nerve stimulation (TENS)

  • non-invasive peripheral stimulation technique used to relieve pain.
  • ⬆ activity of non-noxious axons and amount of non-noxious info -> SC for analgesic effect…closing the spinal gate

given to women during childbirth/ to dec back pain too

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20
Q

What is the ascending spinothalamic pathway?

A

the pathway in which the signal travels up to the brain once it leaves the dorsal horn

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21
Q

What happens to the sensory information once it reaches the brain? (Spinothalmic pathway)

A
  • axon reaches thalamus and synapses to the tertiary neurons which sends signal -> cortex
  • synapse -> tertiary neuron is located at the subcortical level – this is where the perception of pain occurs
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22
Q

Where is pain localised within the brain?

A

cortical level:

cortex

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23
Q

What is the limbic system?

A
  • subcortical level of the brain

- this is an affective component - involved in our behavioural and emotional responses

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24
Q

What are the descending pathways?

A
  • They are pathways that are carrying info down SC from the brain
  • this can increase/decrease the amount of pain we can feel
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25
Q

What is the function of the cortex in the descending pathway?

A

can send signals down to the brain stem nuclei and then the dorsal horn of the spinal cord, and can modulate the circuitry here

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26
Q

What does the brainstem nuclei contain?

A
  • rich in endogenous opioids (pleasure peptides)
  • responsible for release of serotonin (5-HT), NAd, and enkephalin – these close the spinal gate and cause analgesia (this is the Intrinsic Analgesia system)
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27
Q

What is persistent pain in relation to normal pain?

A
  • Increased sensitivity of pain

- happens through mechanisms of peripheral + central sensitization via modification of neurotransmission

28
Q

how is sensation of pain felt?

A

primary afferent input (duration and intensity)

29
Q

What is allodynia?

A
  • Type of pain.
  • People with allodynia are extremely sensitive to touch.
  • Activities that aren’t usually painful (like combing one’s hair) can cause severe pain
30
Q

What is Hyperalgesia?

A
  • Increased sensitivity to feeling pain and an extreme response to pain.
  • may occur when there is damage to the nerves or chemical changes to nerve pathways involved in sensing pain
31
Q

How can sensitisation of peripheral nociceptors occur?

A
  • stimulus damages tissue, triggers inflamm mechanisms (redness, welling, vasodilation, immune cell migration)
  • immune cells produce inflamm soup: Prostaglandins, H+, Bradykinin, NGF, Cytokines
  • immune cell products signal back -> nerve ending = sensitization of polymodal nociceptor (⬇ stimulus threshold for AP to occur)
  • this is primary hyperalgesia - increased sensitivity in damaged tissue alone
32
Q

How does increased peripheral sensitisation affect central sensitisation?

A
  • increases central sensitisation
  • more APs being fired which will enter the spinal cord

· more APs = increased response of the dorsal horn second order neuron

33
Q

What are the major neurotransmitters present in the synapse of the dorsal horn?

A
  • Glutamate - bind to AMPA and NMDA receptors (post-synaptic)
  • Substance P - bind to NK-1 receptor (post-synaptic)
34
Q

Which neurotransmitter is released into the synaptic cleft following action potential of a primary afferent neuron (normal signalling)?

A
  • Glutamate alone

- binds to AMPA receptor alone to signal the pain and active the second order neuron

35
Q

What is the relationship between pain received by second order neuron and pain signal released to the brain (in normal signalling)?

A
  • they are EQUAL

- this is Fidelity signalling

36
Q

Which neurotransmitter is released into the synaptic cleft following action potential of a primary afferent neuron (Sensitised pain signalling)?

A
  • Glutamate and Substance P
  • Substance P release depends on rate of primary afferent firing
  • NMDA is now bound by glutamate (was blocked before)

p654

37
Q

How is blockage of NMDA removed on the post synaptic neuron?

A
  • via the activation of the other receptors (causing a high level of membrane depolarization)
38
Q

Why is the involvement of NMDA key to responsiveness of the post synaptic neuron?

A
  • unblocking allows for the influx of calcium ions

- Calcium influx triggers secondary messenger cascades and prostaglandin production.. amplification of signal

39
Q

What are the results of increased responsiveness of the post synaptic receptors?

A

-> increased frequency of signals sent to brain from second order neuron

– this is facilitated signalling

40
Q

What is the relationship between pain received by second order neuron and pain signal released to the brain (in sensitised pain signalling)?

A

Presynaptic signalling < post synaptic signalling

41
Q

2 mechanisms underlying heightened pain sensation?

A

peripheral sensitisation

central sens…

42
Q

L ANALGESIC DRUGS

How do NSAIDs work?

A
  • inhibition of COX enzymes (cyclooxygenase)
  • COX enzymes produce prostoglandins
  • NSAIDS blocks the ability for prostaglandins to cause pain
43
Q

How do COX enzymes produce prostaglandins?

2 modes. 1= unwated SEs, 1= clinical effects

A

COX1 constitutive - make PGs
protection of gastric mucosa
haemostasis
:(

COX2 inducible - make PGs
mediate pain, inflamm, fever
:)

44
Q

What is the importance of COX-1?

A
  • made in the body and is required for life

- Helps with homeostasis and protection of the gastric mucosa

45
Q

What is COX-2 used for?

A
  • mediate pain and inflammation
46
Q

What are the consequences of inhibiting COX-1?

A
  • may get unwanted side effects
47
Q

In which 2 locations can the productions of prostaglandins be stopped?

A
  • site of pain

- Dorsal horn

48
Q

At the the site of pain how are prostoglandins produced and what is the effect of the lack of prostoglandins?

A
  • produced by inflammatory cells

- ⬇ PG production -> ⬇ nociceptor sensitization – analgesic effect

49
Q

How is analgesic effect caused by prostoglandins in the dorsal horn?

A

⬇ prostaglandin will ⬇ the central sensitization

50
Q

What are the Different types of NSAIDs?2

A
  • Non selective INhibitors (aspirin/ ibuprofen)- weakly COX 1 selective
  • COX-2 selectives (Coxibs)
51
Q

What are the side effects of non-selective COX inhibitors? e.g. aspirin, ibuprofen

A

· GI disturbance

· discomfort

· dyspepsia

· diarrhoea

· nausea and vomiting

· gastric bleeding and ulceration

· skin reactions (idiosyncratic)

kidney damage (o.d. chronic use)

52
Q

What are the Different classes of Coxibs (COX-2 selective)

A
  • Weakly selective (Diclofenac/ Celecoxib)
  • Very selective (Etoricoxib/ Etoricoxib/ Parecoxib)
  • Highly selective (Rofecoxib)
53
Q

Is paracetamol an NSAID?

A
  • No, It is a centrally acting analgesic
  • has no anti-inflammatory activity
  • There is some suggestion that there is inhibition of A 3rd COX enzyme in the brain
54
Q

Paracetamol OD-> what

A

potentially fatal liver damage

55
Q

What are the mechanisms of Opioids? morphine, codeine

A
  • stimulate the µ-opioid receptors

- > mimics effects of endogenous opioids which produce and analgesic effects

56
Q

Where do opioids act within the body?

A

lot of places as their receptors are present in a lot of places
brain…

57
Q

How do opioids work in the periphery?

A
  • inhibit AP firing from the primary afferent neuron

- inhibit release of inflammatory mediators from immune cells once a stimulus is received

58
Q

How do opioids work in the CNS?

A
  • Inhibition of NT release in brain + SC
  • have excitatory effect on brain (⬆ descending pathways)
  • used to close the spinal gate and produce analgesic effect
59
Q

What are some weak opioids? 4

A

· Codeine

· Dihydrocodeine

· Dextropropoxyphene

· Tramadol

60
Q

What are some strong opioids?

A

· Morphine

· Methadone

· Fentanyl

· Hydromorphone

· Diamorphine (heroin)

· Pethidine (meperidine)

· Oxycodone

· Buprenorphine

· Levorphanol

· Dextromoramide

61
Q

What are some problems of Opioids?

A

· Nausea and vomiting

· Decreased GI tract motility – leading to chronic constipation

· Depression of respiratory center (overdose risk)

· Increased Tolerance (more drug required to have same effect)

· Dependence – there are euphoric effects (leading to addiction)

62
Q

What are common combination drugs for Opioids?

A
  • Co-proxamol = Paracetamol + dextropropoxyphene
  • Co-codamol = Paracetamol + Codeine
  • Nurofen Plus = Ibuprofen + Codeine
63
Q

What can adjuvant analgesics be used for?

A

Commonly used ‘off-label’ for difficult to treat pain caused by injury to the nervous system (‘neuropathic’ pain)

64
Q

What are some examples of adjuvant analgesics?

A

· Anticonvulsants: gabapentin (Neurontin®), pregabalin - (Lyrica®); carbamazepine

· Antidepressants: amitriptyline

good at low doses

65
Q

what drugs used for difficult to treat neuropathic pain?

A

off label use of anticonvulsants + antidepressants (adj analgesics)

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