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MD4001 Week 7 > 4. Pain > Flashcards

4. Pain Flashcards

1
Q

Pain definition?

A

Pain is an unpleasant sensory and emotional experience associated with either actual or potential tissue damage.

It is actually subjective and not a substantive construct of the real World

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2
Q

Functions to protect the _____
The sense of Pain only occurs in your _____, prior to that its just a code
Pain is therefore highly ______ and contextual

A

Functions to protect the body
The sense of Pain only occurs in your brain, prior to that its just a code
Pain is therefore highly subjective and contextual

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3
Q

Signal perception is modulated by…

A

Situation, Emotion, Genetic susceptibility, previous experience

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4
Q

Peripheral aspect on pain detection al nocireceptors?

A

1.Nociceptive receptors 2.Nociceptive activation 3.Sensitization of receptors 4.Nociceptive fibres

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5
Q

Nociceptive nerves have free ……….. with……….

A

Nociceptive nerves have free unspecialised nerve endings with ‘pain’ channels inserted in the membrane

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6
Q

Most common nocireceptor?

A

The most common is the Transient Receptor Potential family of channels (TRP)

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7
Q

Sensitivity of the TRP channels

A 
Sensitive to (amongst others) O2, pH osmolarity and valinoids (capsicum) and heat (NB potentially involved in infra red vision in reptiles)
Can be sensitised by substance P, bradykinins, serotonin, pH, ATP, NO etc
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8
Q

Structure of TRP channel?

A

Composed of a 6 unit trans-membrane portion and a ‘basket’ of regulatory complex in the cytoplasm.
Allows Ca2+ into the cell

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9
Q

Temperature, mechanical and chemical activation of nociceptors?

A

Temperature:
Extreme heat and extreme cold open ‘Transient receptor potential vanilloid’ (TRPV) channels inserted in the membrane.
Allows Na2+ and Ca2+entry and so depolarises the cell to give an action potential

Mechanical :
Actual mechanism still unknown. Presumed to be a form of insensitive mechanoreceptor which allows Na entry when activated.

Chemical:
Apart from TRPV receptors, it’s largely unknown but chemical transmission can cause sensitisation of pain receptors

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10
Q

Describe the sensitisation process of pain receptors?

A

All these processes increase the sensitivity to pain and non pain stimuli.

  1. Bradykinin activates pain fibres directly and causes increase in prostaglandins
  2. Tissue damage produces H ions which give muscle ache (e.g. weight lifting)
  3. Prostaglandin E2 is made by cyclooxygenase. Aspirin and other NSAIDs act to inhibit this enzyme
  4. Calcitonin gene related peptide (CGRP )and SP both recruit silent receptors which increase summation in the dorsal horn.
  5. Histamine causes hyperalgesia through its effects on blood vessels.
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11
Q

Purpose of pain sensitisation

A

To prevent future damage to area via memory

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12
Q

features of a-delta fibres?

A

Myelinated
Sharp 1st pain
Mechanical pinching
Extreme hot or cold

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13
Q

Features of c fibres?

A

Unmyelinated
Secondary slow pain (diffuse)
Mechanical pinching, Thermal and Chemical stimuli (polymodal)

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14
Q

Mode of nocirecptive singal transmission?

A

Via a-delta and c fibres

USE neurotransmitters:
On stimulation they release…
1. Glutamate
2. Substance P
3. Calcitonin gene-related peptide (CGRP)
@ both central synapses and peripheral synapses.

Peripheral release (recall histamine practical) give the red flare and tenderness associated with pain.

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15
Q

Substance P & CGRP release is responsible for the 3 local physiological signs of pain

A
  1. Calor (heat)
  2. Rubor (redness)
  3. Tumor (swelling)

1 & 2 caused by local hyperaemia and the third by plasma extravasation

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16
Q

What are the anteolateral tracts for ascending pain?

A

Spinothalamic tracts:

  1. Paleo (dull, old pain via the DM intralaminar of Thalamus to the limbic system association cortices)
  2. The neo (fast, sharp via VPL of thalamus to the primary somatosensory cortex)
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17
Q

Nociceptive fibres synapse in the dorsal horn (quick to cross) with 2 types of ascending axons. Name the axons?

A
  1. Nociceptive specific (NS) – C and Aδ only and
  2. Wide dynamic range neurons (WDR)- any sensory input including pain, can fire in a graded fashion based on C fibre frequency of input (higher the pain higher the input)

The NS and WDR neurons are points of descending pain modulation from PAG in the brainstem

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18
Q

What is the role of central sensitisation? i.e. dorsal horn wind up

A

Wind up is a long term sensitisation of post synaptic neurons in the dorsal horn
It id mediated by WDR neurons which, when firing at high frequency, open NMDA channels.
The inrush of Calcium causes nuclear expression resulting in increased Na channels and a blockade of K channels. The net result is a resting potential closer to threshold and a more sensitive cell. This effectively amplifies the pain signal like turning up the amp on a microphone
SUMMARY
A system by which the intensity of signal from the C fibres is translated through the WDR neurons into variation in sensitivity.
The stronger the C fibre (pain) signal the more the dorsal horn post synaptic fibres become sensitive to input.
The mechanism is quite complex and is based on the special characteristics of the NMDA receptor and Ca++ ion flow. And induces changes in nuclear expression and membrane channel activity/expression

19
Q

Wind up can occur in seconds and last for hours, this conveys

A
  1. Priority salience in the cortex (you notice it more than normal)
  2. Protection from further injury
  3. Memory – increased duration of stimulation increases the
    chance of consolidation
20
Q

3 processes for pain modulation

A
  1. Gate theory
  2. Sensitisation (wind up – covered)
  3. Descending analgesia & Endogenous opioids
21
Q

Mechanism of gate theory for pain modulation?

A

Rubbing the area around a source of pain activates inhibitory input to the anterolateral system. Similar theory behind transcutaneous nerve stimulation TENS and capsaicin treatment
It is the balance between these two systems which determines the pain that gets through to the brain

(Tracts:
C fibers: Bad/ pain signal
A-beta fibre: Turns pain signal off
Balance of 2)

22
Q

Mechanism of descending analgesia in pain modulation?

A

Descending analgesia system in the spinal cord, showing (1) inhibition of incoming pain signals at the cord level and (2) presence of encephalin-secreting neurons that suppress pain signals in the cord.
Note that this system is exploited by a number of CNS centers to increase salience of selected signals as well as decrease certain prolonged unimportant signals

23
Q

Endogenous opioids are a group of neurotransmitters called…

A

Endorphinins
Encephalins
Dynorphins

24
Q

Endogenous opioids :
Sensitive to?
Where present?
Efficacy?

A

Sensitive to opiates
Present at all levels of the pain pathways, therefore doses of opiates can act simultaneously at all levels of the pain pathway, hence their HIGH efficacy

25
Q

Features of the cortical pain matrix?

A
  1. Somatosensory topographic discrimination
  2. Limbic system including the cingulate gyrus (activated when we see others in pain as well as ourselves) and insula. Function is emotional, motivational and modulatory
  3. Saliency- the relative potentiation of a specific nociceptive input
26
Q

Structures that make up the cortical pain matrix?

General arrangement?

A 
Brainstem structures
Hypothalamus
Limbic system amygdala
Cortex
Opioid PAG system
Dorsal horn

Generally arrangement reciprocally around the brainstem structures. Brainstem structures up or down regulate nociception to provide saliency (gate system). This action is based on info from other brain centres.

27
Q

Electrical stimulation of the PAG induces strong ______ (blocked by Nalaxone).
Placebo effect of parental ____

A

Electrical stimulation of the PAG induces strong analgesia (blocked by Nalaxone).
Placebo effect of parental kiss

28
Q

Name 8 types of pain?

A
  1. Chronic/Acute 2. Nociceptive/Neuropathic/Phantom limb
  2. Maladaptive
  3. Visceral (hollow structures)
  4. Referred
  5. Sharp/Ache
  6. Headache
  7. Complex regional pain syndrome
29
Q

Nociceptive pain:
Source?
Stops when?
Responds well to?

A

Results from conditions such as sprains, bone fractures, burns, bumps bruises, inflammation (from infection or arthritic disorder

Normally pain stops when the problem is healed

Normally responds well to painkillers such as opioids

30
Q

Types of chronic pain?

A
  1. Nociceptive pain 2.Neuropathic pain

3. Central maladaption

31
Q

Name 5 examples of persistent neuropathic pain?

A
  • Causalgia (peripheral nerve trauma)
  • Phantom limb pain
  • Entrapment neuropathy (carpel tunnel syndrome)
  • Peripheral neuropathy (widespread nerve damage
  • Nociceptive pathway damage
32
Q

What does hyperalgesia mean?

A

Strong reaction of low intensity noxious stimuli

33
Q

What does Allodynia mean?

A

Painful reaction to a non-noxious stimuli like a light touch on sunburn

34
Q

What does summation mean?

A

Repeated low innocuous stimuli causing increasing intensity of response

35
Q

What does paresthesias mean?

A

Tingling without stimulation

36
Q

What does dysesthesias? mean?

A

Burning/shooting pain without stimulation

37
Q

In persistent neuropathetic pain, the pain persists beyond the healing process of damaged tissues. These includes abnormal pain sensations such as?

A
  1. Hyperalgesia (strong reaction to low intensity noxious stimuli)
  2. Allodynia (painful reaction to a non noxious stimuli like a light touch on sunburn)
  3. Summation (repeated low innocuous stimuli causing increasing intensity of response
  4. Paresthesias (tingling without stim) or Dysesthesias (burning or shooting pain without stim) which can sometimes be associated with a thalamic syndrome (thalamic infarct)
38
Q

Cause of persistent neuropathic pain?

A

Maladaptation of the dorsal horn wind up and sensitisation systems.

39
Q

What is central maladaption?

A

A type of sensitisation
This type of sensitisation can lead to long term changes in the structure of the synapses in the dorsal horn or the spinal cord
Increases in ionotropic glutamate receptors (NMDA) cause a sensitivity in second order neurons which then more readily send pain signals to the thalamus
A second component is where descending modulation of the inhibitory interneurons becomes maladapted. This can lead to a reduction in the inhibition of WDR neurons and so a disinhibition of the second order neurons

40
Q

Cause of headaches?

A

The majority of headaches are due to irritation or destruction of the sensitive areas around the venous sinuses, the dura at the base of the skull or the meninges and the associated blood capillaries

41
Q 
How does the following cause a headache:
Meningitis
Hangovers
Low CSF
Migraine
A

Meningitis
Causes inflammation of all these and results in the worst headaches

Hangovers:
Caused by excessive drinking, in extreme cases due to alcohol irritating
the meninges, most cases due to dehydration. Cure , drink less

Low CSF:
Causes the brain to settle onto the base of the skull causing deformation of
the dura at the base of the skull and the meninges and so this causes headaches

Migraine:
Nobody knows. Possible due to vasoconstriction followed by massive vasodilation, but unproven.

42
Q

Mechanism of referred pain?

A

Signals of noxious stimuli and normal cutaneous stimuli enter the spinal cord at the same point
Cross talk in the dorsal horn between modalities is common
Signals from viscera get picked up by ascending nerve fibres that are mapped cortically to dermis

43
Q

Pain can never be re-experienced from memory, it is only an ______________ of the experience
But the _____ of pain is very real and therefore important
to your future patients

A

Pain can never be re-experienced from memory, it is only an intellectualisation of the experience
But the fear of pain is very real and therefore important
to your future patients

44
Q 
Pelvic pain: conceptual framework
Background factors?
Mediators?
Neurophysiology?
Current pathology?
Previous sensitising episodes?
A

Background factors:

  • Sociocultural context
  • Family dynamics
  • Economic status
  • Abuse history

Mediators:

  • Vigilance
  • Motivation
  • Catastrophising

Neurophysiology:

  • Uterine contractions
  • Visceral nociception
  • Pelvic floor muscle tone
  • Control sensitisation

Current pathology:

  • Adenomyosis
  • Endometriosis
  • Interstitial cystitis
  • Cervical stenosis

Previous sensitising episodes:

  • Urinary tract infection
  • Chlamydia
  • Endometriosis
  • Childbirth

MD4001 Week 7 (8 decks)

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