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8.3. Physiology of pain sensation. Flashcards

1
Q

I. Pain
1. What are the pain receptors? Their features?

A
  • Pain receptors are called nociceptors, because they detect ‘’noxious’’ stimuli that may indicate damage taking place (ex: tissue damage).
  • All nociceptors are free nerve endings of Aδ- or C-fibers.
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2
Q

I. Pain
2A. What are the 4 types of nociceptors?

A
  1. Mechanical nociceptors (Aδ + (C) – fibers)
  2. Thermal nociceptors (Aδ + (C) – fibers)
  3. Thermal nociceptors (Aδ + (C) – fibers)
  4. Silent nociceptors (C-fibers)
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3
Q

I. Pain
2B. What are the features of Mechanical nociceptors?

A

Mechanical nociceptors (Aδ + (C) – fibers)
- respond to mechanical stimuli, like being hit by a hammer

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4
Q

I. Pain
2C. What are the features of Thermal nociceptors?

A

Thermal nociceptors (Aδ + (C) – fibers)
- activated by noxious heat (>45 degrees)
- activated by noxious cold (<5-10 degrees)

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5
Q

I. Pain
2D. What are the features of Polymodal nociceptors?

A

Polymodal receptors (C-fibers)
- respond to many different stimuli (mechanical, thermal, extreme acidity -> tissue damaging)

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6
Q

I. Pain
2E. What are the features of Silent nociceptors (C-fibers)?

A
  • do not respond to mechanical, thermal or extreme acidic conditions, but do mediate
    pain sensation
    -> if they are sensitized -> sensitization can occur, e.g. in inflammation
  • if an inflammation occurs, then the silent nociceptors will get activated and mediate
    pain sensation
  • present in skin and viscera (internal organs)
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7
Q

I. Pain
3. What happen if there is itching?

A

Itching belongs to these groups, but it is different from pain sensation.
- Specific free nerve endings are responsible for mediating itching.
- The nerve endings have histamine receptors - will activate these fibers when histamine is present.

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8
Q

I. Pain
4. What is pain sensation?

A

Pain sensation is an independent sensory modality, and not an ‘’over-activation’’ of mechanoreceptors.

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9
Q

I. Pain - Propagation of pain sensation in sensory nerves:
5A. What type of nerve fibers responsible for pain sensation in sensory nerves?

A

Aδ- and C-fibers are responsible for pain sensation

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10
Q

I. Pain - Propagation of pain sensation in sensory nerves
6. Describe Propagation of pain sensation in sensory nerves

A
  • Aδ- and C-fibers are responsible for pain sensation
  • Pain is felt in 2 different stages, because it is carried by slow and fast fibers
  • First pain:
    +) Sharp, well-localized pain sensation
    +) Mediated by the faster Aδ-fibers (arrives first to the cortex)
  • Second pain:
    +) Diffuse, dull, aching/burning pain sensation
    +) Mediated by the slower C-fibers
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11
Q

I. Pain - Nerve endings – ion channels
7. What types of fibers are heat and pain sensing fibers?

A

Heat and pain sensing fibers are free nerve endings

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12
Q

I. Pain - Nerve endings – ion channels
8. What makes the free nerve endings specific to a certain sensation?

A

ion channels

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13
Q

I. Pain - Nerve endings – ion channels
9A. What are the features of Capsaicin (chili) receptor (TRP-V1?

A

1/ TRP = transient receptor potential, V1 = vanilloid type 1
2/ TRP channels are cation channels -> opened by acidic pH + hot temperatures

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14
Q

I. Pain - Nerve endings – ion channels
10B. Receptor: TRP–V1
- Heat sensitivity: ???
- Activating agent: ???
- Sensation: ???

A
  • Heat sensitivity: ≥ 43°C
  • Activating agent: Capsaicin
  • Sensation: (noxious) Heat sensation
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15
Q

I. Pain - Nerve endings – ion channels
9C. Receptor: TRP–V2
- Heat sensitivity: ???
- Activating agent: ???
- Sensation: ???

A
  • Heat sensitivity: ≥ 52°C
  • Activating agent: -
  • Sensation: (noxious) Heat sensation
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16
Q

I. Pain - Nerve endings – ion channels
9D. Receptor: TRP–V3
- Heat sensitivity: ???
- Activating agent: ???
- Sensation: ??

A
  • Heat sensitivity: ≥ 34°C
  • Activating agent: Camphor (creams/lotions)
  • Sensation: (non-noxious) Warm sensation
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17
Q

I. Pain - Nerve endings – ion channels
9E. Receptor: TRP–V4
- Heat sensitivity: ???
- Activating agent: ???
- Sensation: ???

A
  • Heat sensitivity: ≥ 27°C
  • Activating agent: -
  • Sensation: (non-noxious) Warm sensation
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18
Q

I. Pain - Nerve endings – ion channels
9F. Receptor: TRP–M8
- Heat sensitivity: ???
- Activating agent: ???
- Sensation: ???

A
  • Heat sensitivity: ≤ 28°C
  • Activating agent: Menthol
  • Sensation: Cold sensation (act. of cold sensing fibers)
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19
Q

I. Pain - Nerve endings – ion channels
9G. Receptor: TRP–A1
- Heat sensitivity: ???
- Activating agent: ???
- Sensation: ???

A
  • Heat sensitivity: < 17°C
  • Activating agent: Mustard oil
  • Sensation: Noxious cold sensation
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20
Q

I. Pain - Nerve endings – ion channels
10. Why do we need presence of these receptors?

A

The presence of these receptors make the free nerve endings specific for different sensory modalities

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21
Q

I. Pain - Pain sensation
10. Pain sensation
- Formal definition: ‘’unpleasant sensory and emotional experience associated with actual or potential tissue damage’’
-> How can sensory experience be separated?

A
  • The sensory experience can be separated from the emotional experience:
  • Sensory experience: pain is a feeling
  • Emotional experience: pain is unpleasant
  • Pain is also a sensation of tissue damage -> nociception = sensation of noxious
    stimuli
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22
Q

I. Pain - Basic terms
11. What are the features of Congenital insensitivity to pain?

A
  • Cannot feel pain or feel less pain than normal due to genetic causes
  • Often correlates with shorter life expectancy, due to inability to perceive dangerous
    situations -> pain is basically a warning of tissue damage
  • Example: joint problem -> person will force movement which ↑ the damage
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23
Q

I. Pain - Basic terms
12. What are the features of Acquired pain sensitivity?

A
  • As in the case of syringomyelia, which is the degradation of tissue (white + gray matter) around the central canal of spinal cord
  • Causes loss of pain sensation in certain body areas
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24
Q

I. Pain - Basic terms
13. What are the features of Acute, persistent and chronic pain?

A
  • Acute pain: noxious stimulus -> pain sensation
  • Persistent and chronic pain: pain is constantly present and patient cannot remove the stimulus or ‘’run away’’ -> suffering (e.g. tumors/cancers: cause tissue damage + strong pain sensation)
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25
Q

I. Pain - Basic terms
14. What are the features of Analgesia?

A

Reduction/removal of pain.
=> 2 kind of analgesics:
- Minor: for acute pain – interfere with synthesis of prostaglandins
- Major: for chronic pain – morphine and its derivatives

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26
Q

II. Types of pain
1. What are the 3 types of pains?

A
  1. Nociceptive pain
  2. Neuropathic pain
  3. Central pain
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27
Q

II. Types of pain
2. What is Nociceptive pain?

A

pain related to tissue damage (noxious stimuli)

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28
Q

II. Types of pain
3A. What is Neuropathic pain?

A

pain caused by a problem with the free pathway, such as damage to the sensory nerve fibers

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29
Q

II. Types of pain
3B. What are the 2 examples of Neuropathic pain?

A
  • Deafferentation pain: sensory nerve damaged/cut -> degeneration -> pain
  • Phantom pain: occurs after surgical removal of extremities -> patient can localize pain in amputated hand/leg
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30
Q

II. Types of pain
4A. What is central pain?

A

It is the central pathway of the pain sensory mechanism is affected

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31
Q

II. Types of pain
4B. What is an example of central pain?

A

Thalamic pain syndrome: damages to the thalamus

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32
Q

III. Nociceptive pathways in the dorsal horn of the spinal cord
1. Describe Nociceptive pathways in the dorsal horn of the spinal cord

A

The central axon of the pseudounipolar neuron and the projection neurons get connected in the dorsal horn of the spinal cord  projection will go to the thalamus
- The Aδ-fibers give connections with projection neurons in lamina 1 + 5
- C-fibers go to interneurons and connect with projection neurons in lamina 2
- The Aβ-fibers, which are not nociceptors but mechanoreceptors (=touch), also give collaterals to projection neurons in the dorsal horn

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33
Q

III. Nociceptive pathways in the dorsal horn of the spinal cord
2. What is the role of the Aδ-fibers?

A

The Aδ-fibers give connections with projection neurons in lamina 1 + 5

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34
Q

III. Nociceptive pathways in the dorsal horn of the spinal cord
3. What is the role of C-fibers?

A

C-fibers go to interneurons and connect with projection neurons in lamina 2

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35
Q

III. Nociceptive pathways in the dorsal horn of the spinal cord
4. What is the role of Aβ-fibers?

A

The Aβ-fibers, which are not nociceptors but mechanoreceptors (=touch), also give collaterals to projection neurons in the dorsal horn

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36
Q

III. Nociceptive pathways
1. What are the main Nociceptive pathways?

A
  1. Spinothalamic tract: Anterior and Lateral spinothalamic tracts
  2. Spinoreticular PW
  3. Spinomesencephalic PW
37
Q

III. Nociceptive pathways
2. What are the features of Spinothalamic tract

A

The PW has 2 parallel components (VPL + VPM):
- Lateral spinothalamic tract: carries pain information – going to thalamus (VPL/VPM), and then projecting to the somatosensory cortex
- anterior ventral spinothalamic tract: contains fibers going to the intralaminar nuclei of the thalamus and is responsible for emotional component of pain. This PW project to cortical areas (like cingulate gyrus, prefrontal lobe, insula

38
Q

III. Nociceptive pathways
3. What are the features of Spinoreticular PW?

A

Spinoreticular PW: from spinal cord to reticular formation (medulla + pons)
- Responsible for arousal reaction caused by pain sensation (e.g. wake up due to pain)

39
Q

III. Nociceptive pathways
4. What are the features of Spinomesencephalic PW?

A

goes to the midbrain
-> periaqueductal grey matter
-> stimulate descending PW and regulate pain

40
Q

IV. Changes in pain sensitivity
1. What are the features of Hyperalgesia?

A
  • It is heightened sensitivity to pain.
  • Pain normally has a relatively high threshold, but once we start increasing the pain, the increase is exponential.
  • Hyperalgesia involves a lower threshold.
41
Q

IV. Changes in pain sensitivity
2. What are the 3 types of hyperalgesia?

A
  1. Primary hyperalgesia
  2. Secondary hyperalgesia
  3. Central hyperalgesia: (wind-up phenomenon)
42
Q

IV. Changes in pain sensitivity
3A. What are the features of Primary hyperalgesia?

A

Damaged cells release mediators that cause increased sensitivity to pain

43
Q

IV. Changes in pain sensitivity
3B. What are the molecular events when Primary hyperalgesia?

A
  • K+-ions: K+ leaks out of cell when damaged, causing local hyperkalemia. This ↑[K+]EC causes depolarization/increased excitability of nociceptive nerve endings
  • Protons: area becomes more acidic  sensory nerve endings respond with ↑ sensitivity (TRP channels)
  • Bradykinin + serotonin + PGl: initiate 2nd messenger mechanism -> TRP sensitivity↑
  • Prostaglandins: derivatives of arachidonic acid which is converted into endoperoxides by cyclooxygenase (COX) enzymes. Aspirin inhibits COX enzymes (= aspirin reduces pain)
44
Q

IV. Changes in pain sensitivity
3C. How do K+ ions participate in Primary hyperalgesia?

A

K+ leaks out of cell when damaged, causing local hyperkalemia.
=> This ↑[K+]EC causes depolarization/increased excitability of nociceptive nerve endings

45
Q

IV. Changes in pain sensitivity
3D. How do Protons participate in Primary hyperalgesia?

A

Area becomes more acidic
=> sensory nerve endings respond with ↑ sensitivity (TRP channels)

46
Q

IV. Changes in pain sensitivity
3E. How do Bradykinin + serotonin + PGl participate in Primary hyperalgesia?

A

Initiate 2nd messenger mechanism
=> TRP sensitivity↑

47
Q

IV. Changes in pain sensitivity
3F. How do Prostaglandins participate in Primary hyperalgesia?

A

Derivatives of arachidonic acid which is converted into endoperoxides by cyclooxygenase (COX) enzymes.
- Aspirin inhibits COX enzymes (= aspirin reduces pain)

48
Q

IV. Changes in pain sensitivity
4A. What are the features of secondary hyperalgesia?

A

Near to the damaged cells there is hyperalgesia, although this region itself is not damaged (axon reflex – free nerve endings give collaterals to surround free nerve endings
=> SP + CGRP are releasedactivation of more free nerve endings)

49
Q

IV. Changes in pain sensitivity
4A. What are the features of secondary hyperalgesia?

A

Near to the damaged cells there is hyperalgesia, although this region itself is not damaged (axon reflex – free nerve endings give collaterals to surround free nerve endings
=> SP + CGRP are releasedactivation of more free nerve endings)

50
Q

IV. Changes in pain sensitivity
4B. What are the 4 prominent substances in secondary hyperalgesia?

A
  • Substance P: vasodilation
  • CGRP (calcitonin gene related peptide): vasodilation
  • Bradykinin: vasodilation (+ produces a Ca2+ signal ->causing hyperalgesia)
  • Histamine: released by mast cellsvasodilation
51
Q

IV. Changes in pain sensitivity
4C. What is the effect of substance P in secondary hyperalgesia?

A

vasodilation

52
Q

IV. Changes in pain sensitivity
4C. What is the effect of CGRP in secondary hyperalgesia?

A

CGRP (calcitonin gene related peptide): vasodilation

53
Q

IV. Changes in pain sensitivity
4D. What is the effect of Bradykinin in secondary hyperalgesia?

A

vasodilation (+ produces a Ca2+ signal -> causing hyperalgesia)

54
Q

IV. Changes in pain sensitivity
4E. What is the effect of Histamine in secondary hyperalgesia?

A

Histamin is released by mast cells
=> vasodilation

55
Q

IV. Changes in pain sensitivity
5A. What are the characteristics of Central hyperalgesia?

A

Pain sensation stimulates local network area in substantia gelatinosa, causing an increase in excitability of neurons connected to the area near the injury.
=> This causes a partial activation of non-injured nerve endings

56
Q

IV. Changes in pain sensitivity
5B. What is Allodynia? (Central hyperalgesia)

A

Allodynia: term for when there is a pain sensation after a normal, non-nociceptive stimulus, as in light touch to the skin.
-> This occurs, for example, if you lightly touch sunburned tissue. The touch is not damaging, but it still hurts.

57
Q

V. Referred pain
1. What is referred pain?

A

Pain sensation in areas that are not the same as where the nociceptive stimulus is

58
Q

V. Referred pain
2. Give an example of referred pain

A

Example is the classic myocardial infarction pain that is left in the left arm.
- The segmental organization of the system overlaps so that the heart viscera and left arm skin occupy the same origin of the dorsal horn, and the excitability of the neurons spreads to other that are nearby.

59
Q

VI. Peripheral and central regulation of pain sensation
1. What are characteristics of central regulation?

A

A soldier may not feel pain during battle due to excessive cortical stimuli/stress, but feels it after withdrawing from the battle

60
Q

VI. Peripheral and central regulation of pain sensation - peripheral regulation
2A. What are characteristics of peripheral regulation?

A

Excessive painful stimuli causes person to touch pain area, and this non-nociceptive stimulus causes an analgesic effect

61
Q

VI. Peripheral and central regulation of pain sensation - peripheral regulation
2B. Explain gate control theory of nociception

A

1.Gate control theory of nociception: (can explain why rubbing the skin reduces pain)
- the central axon of the pseudounipolar cell (C-fiber: nociceptive) brings the nociceptive information to the dorsal horn and connects to a projection neuron = stimulatory (+) connection
- the projection will ascend in the spinothalamic tract and go towards the cortex
- there will also be some inhibitory interneurons which connect to the projection neuron, but will be inhibited by the C-fibersstronger activation = stronger pain signal (inhibition of inhibitory interneuron)
- there are also some Aβ-fibers (myelinated non-nociceptive) which will give stimulatory impulses to the inhibitory interneuronreduce the pain sensation

62
Q

VI. Peripheral and central regulation of pain sensation - peripheral regulation
2C. Explain iffuse noxious inhibitory control (DNIC)

A
  • noxious stimuli (e.g.: puncturing skin with needle) can cause diffuse inhibition of pain sensing pathways -> nociceptive stimulus will stimulate analgesia
  • physiological basis of acupuncture
63
Q

VII. Descending analgesic pathways (CENTRAL REGULATION)
1. What are the characteristics of Descending analgesic pathways?

A
  • the stimulation of the periaqueductal grey matter will initiate the activation of the
    descending analgesic PWs
  • the PW will go to the dorsal horn of the spinal cord and inhibit pain transmission
  • descending PW uses NE + serotonin as transmitters (monoamines)
64
Q

VII. Descending analgesic pathways (CENTRAL REGULATION)
2A. What is the mechanism of pain sensation?

A
  • the dorsal horn is the point when the incoming nociceptive afferent will switch to the projection neuron of the spinothalamic tract, which will ascend and cause pain sensation
  • when we have stimulation coming from the periphery, AP will depolarize the presynaptic axon terminal and open VD-Ca2+-ch. -> Ca2+-influx -> Ca2+ will cause the release of the vesicles which are stored in the nerve ending and glutamate + substance P will be released
  • the presynaptic terminal is connected to the projection neuron, which has Glu + SP receptors -> will cause EPSPs, and if it reaches the threshold, an AP will be formed on the axon of the projection neuron -> the nociceptive information will be propagated to the cortex via spinothalamic tract
65
Q

VII. Descending analgesic pathways (CENTRAL REGULATION) - the mechanism of pain sensation
2B. What is the role of dorsal horn in pain sensation mechanism?

A

The dorsal horn is the point when the incoming nociceptive afferent will switch to
the projection neuron of the spinothalamic tract, which will ascend and cause pain
sensation

66
Q

VII. Descending analgesic pathways (CENTRAL REGULATION) - the mechanism of pain sensation
2C. In pain sensation mechanism, what happen when we have stimulation coming from the periphery?

A

When we have stimulation coming from the periphery, AP will depolarize the
presynaptic axon terminal and open VD-Ca2+-ch.
-> Ca2+-influx
-> Ca2+ will cause the release of the vesicles which are stored in the nerve ending and glutamate + substance P will be released

67
Q

VII. Descending analgesic pathways (CENTRAL REGULATION) - Mechanism of descending analgesic PW
3A. What are the features of Mechanism of descending analgesic PW

A
  • in the dorsal horn, there is an inhibitor interneuron which will connect to the pre- + postsynaptic terminal
  • the interneuron is enkephalinergic, because the released transmitter is enkephalin, which is an endogenous opiate, and it will act on opiate receptors (GPCRs)
  • the opiate receptors activate Gi/o G-proteins
68
Q

VII. Descending analgesic pathways (CENTRAL REGULATION) - Mechanism of descending analgesic PW
3B. The opiate receptors activate Gi/o G-proteins
-> What are the consequences?

A

The opiate receptors activate Gi/o G-proteins. They have several effects
- presynaptic: inhibition of Ca2+-channels -> ↓Ca2+-influx -> less transmitter releasedinhibitory effect on pain sensation
- postsynaptic: open K+-channels -> hyperpolarization -> reduce the depolarizing effect
of Glu + SP -> postsynaptic inhibitory effect
=> descending PWs reduce pain sensation, because these PWs will lead to stimulation of inhibitory interneurons which inhibit the pain transmission in the dorsal horn
=> opiates exert an inhibitory effect on inhibitory neurons (lift the inhibition of the descending analgesic PWs)
=> opiates stimulate the descending analgesic signal (opiates = analgesic)

69
Q

VIII. Opiates
1. What are the features of opiates?

A
  • opiates imitate the action of morphine, which is the active component of a drug called opium
  • morphine also has an analgesic effect -> major analgesics = morphine and its derivatives
  • act on opiate receptors
  • mostly used in e.g. terminal cancer
70
Q

VIII. Opiates - Family of endogenous
2A. What are the characteristics of endogenous opioids ?

A
  • endogenous opioids are peptides
  • cleavage of pro-peptides will give the release of endogenous opioids
  • the endogenous opioids act on opioid receptors
71
Q

VIII. Opiates - Family of endogenous
2B. What are the 4 major opioids pro-peptide?

A
  1. POMC
  2. Proenkephalin
  3. Prodynorphin
  4. Pro-nociceptin (pro-orphanin FQ)
72
Q

VIII. Opiates - Family of endogenous
2C. What does the cleavage of POMC result in? What are the receptors for these products?

A
73
Q

VIII. Opiates - Family of endogenous
2D. What does the cleavage of Proenkephalin result in? What are the receptors for these products?

A
74
Q

VIII. Opiates - Family of endogenous
2E. What does the cleavage of Prodynorphin result in? What are the receptors for these products?

A
75
Q

VIII. Opiates - Family of endogenous
2F. What does the cleavage of Pro-nociceptin (pro-orphanin FQ) result in? What are the receptors for these products?

A
76
Q

VIII. Opiates - Family of endogenous
3. What are the mechanisms for opiate receptors?

A

All opiate receptors share the same mechanism:
-> GPCRs
-> Gi/o
-> cAMP↓,Ca2+-channel↓,K+-channel↓

77
Q

VIII. Opiates - Family of endogenous
4A. What are the 4 main effects/problems of major analgesics?

A
  1. Tolerance
  2. Withdrawal symptoms
  3. Dependence
  4. Addiction
78
Q

VIII. Opiates - Family of endogenous
4B1. What are the features of tolerance in major analgesics?

A

repeated treatment with morphine
-> administered dose has to be increased to have the same biological effect

79
Q

VIII. Opiates - Family of endogenous
4B2. Tolerance: repeated treatment with morphine -> administered dose has to be increased to have the same biological effect
=> What are the 4 biological effects?

A
  1. Increased metabolism (metabolic tolerance)
  2. Receptor desensitization
  3. Receptor downregulation
  4. Compensatory mechanism (counteract)
80
Q

VIII. Opiates - Family of endogenous
4B3. What does Increased metabolism (metabolic tolerance) mean?

A

metabolism of degradation increased = more dose needed

81
Q

VIII. Opiates - Family of endogenous
4B4. What does Receptor desensitization mean?

A

opiate (GPCR) receptors get desensitized
-> the activated GPCR will become a substrate of phosphorylating enzymes
-> get phosphorylated and β-arrestin proteins will bind to the receptor
-> uncouple the receptor from the G-protein

82
Q

VIII. Opiates - Family of endogenous
4B5. What does Receptor downregulation mean?

A

number of receptors decreases, because repeated stimulation with morphine will initate PWs which inhibit the synthesis and stimulate degradation of the receptors

83
Q

VIII. Opiates - Family of endogenous
4B6. What does Compensatory mechanism (counteract) mean?

A
  • ,orphine reduces cAMP (Gi), but the counteract increases cAMP.
  • If we keep administrating morphine, more morphine is required because of the compensatory mechanism which counteracts
84
Q

VIII. Opiates - Family of endogenous
4C. What are the features of Withdrawal symptoms in major analgesics?

A
  • Develop due to the compensatory mechanisms.
  • The compensatory mechanisms will still be there, even if no morphine is administeredcan cause symptoms
85
Q

VIII. Opiates - Family of endogenous
4D. What are the features of Dependence in major analgesics?

A

Develops because of the withdrawal symptoms. 2 levels: (1) psychological: compensatory mechanism
-> craving will develop (2) physical: BP changes, GI-tract function, measurable parameters

86
Q

VIII. Opiates - Family of endogenous
4E. What are the features of Addiction in major analgesics?

A
  • If both the physical and psychological dependence are present -> addiction.
  • Most serious stage of morphine dependence
87
Q

IX. Endocannabinoids
1. What are the characteristics of Endocannabinoids?

A
  • Cannabinoid system is also an endogenous system
  • Endocannabinoids are present in human body
  • Cannabinoid receptors: CB1 (dominant in CNS) + CB2
  • Endocannabinoids are lipids -> also activate Gi/o -> analgesic effects (less
    pronounced than morphine)
  • Exogenous stimulant: marijuana
88
Q

IX. Endocannabinoids
2. What are the RECEPTORS of Endocannabinoids?

A

Cannabinoid receptors: CB1 (dominant in CNS) + CB2

89
Q

IX. Endocannabinoids
3. What is the Exogenous stimulant of Endocannabinoids?

A

marijuana

A Physiology (88 decks)

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