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Physiology of Pain Flashcards

1
Q

Pain is an unpleasant and emotional experience, but why do we need pain?

A
  • helps us learn to avoid harm/danger
  • prevents further injury/death
  • tells us to rest following injury
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2
Q

Pain can be subdivided into 2 categories. What are they?

A

1 - adaptive
2 - pathological

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3
Q

Pain can be subdivided into 2 categories, adaptive and pathological. What is adaptive pain?

A
  • this is good protective pain
  • we learn and adapt from this type of pain
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4
Q

Pain can be subdivided into 2 categories, adaptive and pathological. What is pathological pain?

A
  • this is bad pain
  • does not serve as a learning/adaptive pain
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5
Q

Pain can be subdivided into 2 categories, adaptive and pathological. Adaptive pain can then be subdivided into nociceptive and inflammatory pain. What is nociceptive pain?

1 - stimulus to sensory afferent neurons eliciting the sensation of pain
2 - stimulus to sensory efferent neurons eliciting the sensation of pain
3 - stimulus to ventral horn of spine eliciting the sensation of pain

A

1 - stimulus to sensory afferent neurons eliciting the sensation of pain
- can be toxic or physical
- nociceptive tell the body about potential danger

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6
Q

Nociceptive pain is pain that is caused by damage to tissue. This pain can be divided into somatic and visceral pain. What is somatic pain?

1 - pain due to activation of nociceptive receptors in peripheral tissues
2 - pain due to activation of nociceptive receptors in central tissues
3 - pain due to activation of nociceptive receptors around internal organs

A

1 - pain due to activation of nociceptive receptors in peripheral tissues
- include the skin, muscles, skeleton, joints, and connective tissues

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7
Q

Nociceptive pain is pain that is caused by damage to tissue. This pain can be divided into somatic and visceral pain. What is visceral pain?

1 - pain due to activation of nociceptive receptors in peripheral tissues
2 - pain due to activation of nociceptive receptors in central tissues
3 - pain due to activation of nociceptive receptors around internal organs

A

3 - pain due to activation of nociceptive receptors around internal organs
- often vague, happens every so often, and feels like a deep ache or pressure

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8
Q

Nociceptive pain is pain that is caused by damage to tissue. This pain can be divided into somatic and visceral pain. Somatic pain can be further subdivided into what 2 categories?

A

1 - deep (tendons, bones, muscles and are poorly localised)
2 - superficial (skin and are well localised)

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9
Q

Pain can be subdivided into 2 categories, adaptive and pathological. Pathological pain can then be subdivided into neuropathic and dysfunctional pain. What is neuropathic pain?

1 - pain affecting nervous system
2 - pain affecting the peripheral tissues
3 - pain affecting central organs
4 - pain affecting the brain

A

1 - pain affecting nervous system
- pain is generally chronic and serves no purpose
- normally due to chronic, progressive nerve disease
- can occur due injury or infection

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10
Q

Pain can be subdivided into 2 categories, adaptive and pathological. Pathological pain can then be subdivided into neuropathic and dysfunctional pain. Neuropathic can be further sub-divided into central and peripheral pain. What is central and peripheral pain?

A
  • central = CNS pain cause by damage to CNS (stroke or Parkinsons disease)
  • peripheral = PNS (burning, shooting, tingling pain)
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11
Q

Pain can be subdivided into 2 categories, adaptive and pathological. Pathological pain can then be subdivided into neuropathic and dysfunctional pain. What is dysfunctional pain?

A
  • pain with no specific cause
  • fibromyalgia and IBS are examples
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12
Q

Nociceptors are a type of neuron that are able to detect noxious stimuli. What type of neurons are these?

1 - 1st order sensory afferent neurons
2 - 2nd order sensory afferent neurons
3 - 1st order sensory efferent neurons
4 - 2nd order sensory efferent neurons

A

1 - 1st order sensory afferent neurons

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13
Q

Nociceptors are a type of neuron that are able to detect noxious stimuli. They are 1st (primary) order sensory afferent neurons. Where are the nerve endings of nociceptors found?

A
  • deep or superficial tissues as this is somatic pain
  • in tissues (skin, muscles, joints, meninges, viscera)
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14
Q

Nociceptors are a type of neuron that are able to detect noxious stimuli. They are 1st (primary) order sensory afferent neurons. The nerve endings can be found in tissues, but where is the cell body generally located?

1 - dorsal root ganglia
2 - ventral root
3 - dorsal root
4 - spinal nerve

A

1 - dorsal root ganglia
- synapses at the dorsal horn with 2nd order neuron

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15
Q

Nociceptors are a type of neuron that are able to detect noxious stimuli. They are primary sensory afferent neurons. Which tract is pain transmitted to the CNS along?

1 - spinothalamic tract (anterior specifically)
2 - spinothalamic tract (lateral specifically)
3 - corticospinal tract
4 - dorsal columns

A

2 - spinothalamic tract (lateral specifically)
- conveys pain and temperature changes

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16
Q

Nociceptors are a type of neuron that are able to detect noxious stimuli. They are 1st (primary) order sensory afferent neurons. Pain is transmitted to the CNS along the lateral spinothalamic tract and is able to convey pain and temperature information. Does pain in the left/right side of the body travel to the left/right side of the brain?

A
  • no as it decussates at the level of the vertebrae where it synapses with 2nd order neuron
  • left sided pain = travels to right side of the brain
  • right sided pain = travels to left side of brain
  • 2nd order neuron decussates at spinal cord
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17
Q

Nociceptors have free nerve endings, which are the most abundant type of nerve endings in the skin. What are free nerve endings?

1 - non-encapsulated dendrites
2 - non-encapsulated ruffini endings
3 - encapsulated dendrites
4 - encapsulated ruffini endings

A

1 - non-encapsulated dendrites

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18
Q

Nociceptors have free nerve endings, which are the most abundant type of nerve endings in the skin. They are essentially non-encapsulated dendrites with no specialised connective tissue. What type of sensory fibre type are these nerve free endings?

1 - a-δ (delta) or C
2 - a-δ (delta) or Aα
3 - a-δ (delta) or Aβ
4 - Aβ (delta) or C

A

1 - a-δ (delta) or C

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19
Q

The nociceptive nerve free end can be a-δ (delta) or C type fibres. What is the relevance of these fibre types?

A
  • determines their size and degree of myelination
  • speed of transmission and signal transmitted
  • a-δ (delta) = thinly myelinated fast transmission - sharp/fast pain
  • c type = unmyelinated slow transmission - slow/dull pain
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20
Q

Do larger or smaller diameter neurons have myelination?

A
  • larger diameter neurons require myelin to effectively transmit action potentials
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21
Q

Afferent nerve fibre types can be subdivided into:

  • C
  • a-δ (delta)
  • Aα
  • Aβ

Which of these nerve fibres are fully myelinated and which has the fastest transmission?

A
  • Aα and Aβ are fully myelinated with large diameters
  • both of these fibres have the fastest transmission at 30-75m/s
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22
Q

Afferent nerve fibre types can be subdivided into:

  • C
  • a-δ (delta)
  • Aα
  • Aβ

Which of these nerve fibres are lightly myelinated with a medium diameter and transmission speed of 5-30m/second?

A
  • a-δ (delta)
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23
Q

Afferent nerve fibre types can be subdivided into:

  • C
  • a-δ (delta)
  • Aα
  • Aβ

Which of these nerve fibres is not myelinated with a small diameter and transmission speed of -0.5-2m/second?

A
  • C fibres
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24
Q

In the image below from a laboratory experiment we can see the response from afferent nerve fibre types A-alpha, B-alpha, A-delta and C fibres. Knowing what we know about the size of these fibres and the degree of myelination, label the Afferent nerve fibre types can be subdivided into A-alpha, B-alpha, A-delta and C fibres on the figure?

A

1 = A-alpha and B-alpha
2 = A-delta
3 = C

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25
Q

In the image below from a laboratory experiment we can see the response from afferent nerve fibre types A-alpha, B-alpha, A-delta and C fibres. Generally what type of sensation would we expect if nociceptive sensory afferent fibres A-delta and C fibres are stimulated?

A
  • A-delta = fast, well localised sharp pain (pin prick)
  • C = slow poorly localised dull pain (burning sensation)
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26
Q

As we know that visceral pain is dull, aching and poorly localised, we can determine which nociceptive sensory afferent fibres mediate visceral pain. Which nerve fibre is this?

1 - C
2 - a-δ (delta)
3 - Aα
4 - Aβ

A
  • C fibres
  • slow transmission and non-specific site of pain
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27
Q

What are the 4 stimuli that can activate nociceptive sensory afferent nerve fibres, which are polymodal (respond to multiple stimuli)?

A

1 - pressure
2 - temperature (hot/cold)
3 - chemical
4 - tissue damage

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28
Q

How do nociceptors that are sensitive to pain, specifically pressure transmit pain to the CNS?

A
  • mechanically activated channels deform under pressure
  • the deformity allows cations to enter the cell
  • depolarisation occurs and transmits signals
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29
Q

Temperature transduction is mediated by which channels?

1 - mechanoreceptors
2 - proprioceptors
3 - transient receptor potential (TRP) cation channels

A

3 - transient receptor potential (TRP) cation channels
- non-selection cation (+ charge) channel

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30
Q

Temperature transduction is mediated by transient receptor potential (TRP) cation channels, non-selection cation (+ charge) channel. How do these channels become stimulated and transmit this information to the CNS?

A
  • channels have permeability that is dependent on temperature
  • permeability allows cations to flow in, generating an action potential
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31
Q

Temperature transduction is mediated by transient receptor potential cation channels (TRPV), non-selection cation (+ charge) channel. These channels have permeability that is dependent on temperature, where changes in temperature increase or decrease permeability, allowing cations to flow in, generating an action potential. Specifically which TRPV channels are sensitive to hot temperature, and what is an agonist of these receptors?

1 - receptor = TRPV1 and agonist = capsaicin
2 - receptor = TRPV1 and agonist = menthol
3 - receptor = TRPM and agonist = capsaicin
4 - receptor = TRPA1 and agonist = capsaicin

A

1 - receptor = TRPV1 and agonist = capsaicin
- capsaicin is an agonist (component of chillis)
- capsaicin (and other molecules) bind with TRPV-1 and tell your body there is something hot

32
Q

Temperature transduction is mediated by transient receptor potential cation channels (TRPV), non-selection cation (+ charge) channel. These channels have permeability that is dependent on temperature, where changes in temperature increase/decrease permeability, allowing cations to flow in, generating an action potential. Specifically which TRPV channels are sensitive to cold temperature, and what is an agonist of these receptors?

1 - receptor = TRPV1 and agonist = capsaicin
2 - receptor = TRPM and agonist = menthol
3 - receptor = TRPM and agonist = capsaicin
4 - receptor = TRPA1 and agonist = capsaicin

A

2 - receptor = TRPM and agonist = menthol

33
Q

Temperature transduction is mediated by transient receptor potential cation channels (TRPV), non-selection cation (+ charge) channel. These channels have permeability that is dependent on temperature, where changes in temperature increase/decrease permeability, allowing cations to flow in, generating an action potential. Specifically which TRPV channels are sensitive to very cold temperature, and what is an agonist of these receptors?

1 - receptor = TRPV1 and agonist = capsaicin
2 - receptor = TRPM and agonist = menthol
3 - receptor = TRPM and agonist = capsaicin
4 - receptor = TRPA1 and agonist = cinnamon

A

4 - receptor = TRPA1 and agonist = cinnamon

34
Q

When we experience pain this is due to tissue injury and/or inflammation. How is this signal of tissue damage transmitted to the CNS?

A
  • chemicals are released at the site of injury
  • chemical released trigger pain response
  • for example: prostaglandins inhibit K+ leaving cells and increase Ca2+ and Na+ entering the cell, causing depolarisation
35
Q

When we experience pain this is due to tissue injury and/or inflammation. The signal for tissue damage is transmitted by chemicals that are released at the site of tissue injury (prostaglandins). What are some of the most common chemicals that are released?

A
  • H+ (protons)
  • bradykinin
  • prostaglandins (converted from arachnoid by COX)
  • nerve growth factor
  • histamine
  • serotonin (5-HT)
  • ATP
36
Q

When we experience pain this is due to tissue injury and/or inflammation. The signal for tissue damage is transmitted by chemicals that are released at the site of tissue injury, such as H+ (protons), bradykinin, prostaglandins (converted from arachnoid by COX), nerve growth factor, histamine, serotonin (5-HT) and ATP. Once these chemicals are release at the site of tissue damage, how do these chemicals transmit this signal to the CNS?

A
  • chemical bind with receptors on peripheral neurons
  • these channels open and cations enter the cell
  • depolarisation follows
37
Q

When we exercise at extreme levels we generate lactic acid. This lactic acid can be recycled for energy in the liver. However, when these levels become too high this can cause pain due to tissue injury. How does the lactic acid build up cause pain?

A
  • lactic acid is essentially an acid
  • acids contain lots of protons (H+)
  • increased acid = increased H+ then stimulates pain receptors
  • channels open and depolarisation occurs
38
Q

Although inflammation is a good thing, as it tells us to rest and heal, it can also cause neurogenic inflammation which can be bad and lead to pathophysiology. When one branch of a nociceptor is activated by inflammation, this can cause chemicals to be released. What are these chemicals and how can they cause neurogenic inflammation?

1 - substance P and calcitonin gene related peptide (CGRP)
2 - substance P and creatine kinase
3 - substance P and lactate dehydrogenase
4 - creatine kinase and calcitonin gene related peptide (CGRP)

A

1 - substance P and calcitonin gene related peptide (CGRP)
- substance P and CGRP move down nerves to surrounding tissues
- non affected branches of nociceptors become inflamed

39
Q

What is hypersensitivity?

A
  • undesirable reactions produced by the normal immune system, including allergies and autoimmunity
  • generally an over-reaction of the immune system and these reactions may be damaging and uncomfortable
40
Q

How can inflammation and pain cause hypersensitivity?

A
  • pain and inflammation occur as a normal response to tissue damage
  • substance P and calcitonin gene related peptide (CGRP) are released and are able to move down nerves
  • they can activate non-affected branches of nociceptors
  • too much of substance P and CGRP and prolonged inflammation causes neurogenic inflammation and hypersensitivity of the nerves
41
Q

Hypersensitivity of the nerves following tissue injury and inflammation can cause pathological neurogenic inflammation. Is this specific to the CNS or the PNS?

A
  • both
42
Q

Hypersensitivity of the nerves following tissue injury and inflammation can cause pathological neurogenic inflammation by activating nociceptors. This can occur in the CNS and the PNS. This can cause hyperalgesia, what is this?

A
  • algesia = pain
  • increased sensitivity to feeling pain and an extreme response to pain
43
Q

Hypersensitivity of the nerves following tissue injury and inflammation can cause pathological neurogenic inflammation by activating nociceptors. This can occur in the CNS and the PNS. This can cause allodynia, what is this?

1 - pain in surrounding tissues
2 - stabbing pain in bilateral point on opposite side of the body
3 - pain from non noxious pain stimuli
4 - pain that is very localised

A

3 - pain from non noxious pain stimuli
- allos = greek for other
- dynia = greek for pain
- could be pain from something like a feather

44
Q

Does pain hypersensitivity of nociceptors always lead to pathological pain?

A
  • no
  • by activating nociceptors close to damaged tissue, this means we protect the area even more
  • continues until repair is complete
45
Q

In the PNS can hyperalgesia (increased sensitisation to pain) and allodynia (pain from non-painful stimulus) both occur?

A
  • no, just hyperalgesia
  • nociceptors are damaged in PNS
  • this is peripheral sensitisation and is protective
46
Q

In the CNS can hyperalgesia (increased sensitisation to pain) and allodynia (pain from non-painful stimulus) both occur?

A
  • yes, called central sensitisation
  • mechanism involved in neuropathic pain when prolonged
  • not an adaptive, but a pathological pain
47
Q

When we become hypersensitive to pain and inflammation, nociceptors in the PNS are affected. What happens to the nociceptors that increases our sensitisation to pain and inflammation in the PNS?

A
  • chemicals (bradykinin) reduce thresholds of heat activated channels, so less heat required to cause pain
  • chemicals (prostaglandins) reduce threshold for Na+ channels
  • more action potentials can therefore be generated
48
Q

Bradykinin triggers the heat sensitive Transient receptor potential-1 (TRPV1) receptors in cells. How can bradykinin cause a change in the threshold of heat and cause peripheral sensitisation?

A
  • bradykinin binds to GPCR
  • protein kinase is activated increasing phosphorylation
  • phosphorylation of TRPV1 channels lowers its threshold for action potential
  • increased action potential firing
49
Q

Which tract does pain and temperature signals transmit along to deliver information to the CNS?

1 - spinothalamic tract (anterior specifically)
2 - spinothalamic tract (lateral specifically)
3 - corticospinal tract
4 - dorsal columns

A

2 - spinothalamic tract (lateral specifically)

50
Q

In the lateral spinothalamic tract, which delivers information relating to pain and temperature the first order neurons synapse with the second order neurons in the dorsal horn of the spinal cord. What is the site where they synapse called?

A
  • substantia gelatinosa
  • collection of cells in the dorsal horn
51
Q

In the lateral spinothalamic tract, which delivers information relating to pain and temperature the first order neurons synapse with the second order neurons in the dorsal horn of the spinal cord. They synapse at the substantia gelatinosa, which is a collection of cells in the dorsal horn. They then go on to form a tract, what is this tract called?

A
  • Lissauer’s tract
  • a pathway formed from the proximal end of small unmyelinated and poorly myelinated fibers in peripheral nerves
52
Q

Once the first order neurons synapse at the substantia gelatinosa and form the tract of Lissauer in the dorsal horn of the spinal cord the second order neurons decussate at the site of the vertebrae and then ascends the lateral spinothalamic tract. What boardmann areas in the brain does this tract eventually synapse with?

1 - areas 1, 2 and 3
2 - area 17
3 - areas 41 and 42
4 - area 4

A

1 - areas 1, 2 and 3
- makes up the somatosensory cortex of the human brain

53
Q

When primary and second order neurons synapse at the dorsal horn, more than one type of neuron can do this. For example, visceral pain, such as that caused by angina in the heart and cutaneous (relates to skin) nociceptors in the skin can synapse at the same time. What phenomenon does this cause?

1 - molecular mimicry
2 - hypersensitivity
3 - deferred pain

A

3 - deferred pain
- brain perceives visceral pain as cutaneous pain
- this is why we feel pain in arms, shoulder and neck when patients have myocardial infarction or angina

54
Q

Second order neurons synapse with third order neurons in the thalamus. Where do these neurons travel through to reach broadmann areas 1, 2 and 3 that make up the primary somatosensory cortex?

1 - corpus collosum
2 - tract of lisseur
3 - lateral sulcus
4 - internal capsule

A

4 - internal capsule

55
Q

In the primary somatosensory cortex when we look at the humunculus, do the upper and lower limbs relate to the medial or lateral aspects?

A
  • lower = medial (closer to longitudinal fissure)
  • upper = lateral
56
Q

The 3rd orders neurons that are involved in pain synapse with second order neurons at the medulla and then travel to the primary somatosensory cortex. However, there is an additional 3rd order neuron that does not travel to the somatosensory cortex that provides emotional stimulus. Where do these neurons travel to in the brain to provide emotional stimulus?

A
  • limbic system
  • cingulate cortex
  • prefrontal cortex
57
Q

The delivery of pain is transmitted along the ascending spinothalamic tract. However, there is also the descending tracts. These descending tracts are able to regulate pain, what does this regulation actually mean?

A
  • descending tracts can be inhibitory or excitatory muscles as required
58
Q

The delivery of pain is transmitted along the ascending spinothalamic tract. However, there is also the descending tracts. These descending tracts are able to regulate pain (both inhibitory or excitatory. One of these is the Periaqueductal gray matter (PAG), where is this located?

A
  • grey matter located in the midbrain
  • surrounds the cerebral aqueduct, also called the aqueduct of sylvius (conduit joining 3rd and 4th ventricles)
59
Q

The delivery of pain is transmitted along the ascending spinothalamic tract. However, there is also the descending tracts. These descending tracts are able to regulate pain (both inhibitory or excitatory. One of these is the Periaqueductal grey matter (PAG), which is grey matter located in the midbrain around the cerebral aqueduct (conduit joining 3rd and 4th ventricles). What is the function of PAG?

A
  • input is received from the higher cortical regions
  • signal is transmitted to the rostral ventromedial medulla (RVM), a cell nuclei
  • RVM projects information about pain to the dorsal horn
60
Q

The Periaqueductal gray matter (PAG) and Rostral ventromedial medulla (RVM) are really important in pain modulation. Why is PAG specifically really important in pain management?

1 - able to induce pain
2 - able to inhibit pain
3 - able to initiate recovery at the site of pain

A

2 - able to inhibit pain
- stimulation of PAG results in immediate and profound analgesia

61
Q

What are serotonergic receptors?

A
  • receptors sensitive to serotonin (5-HT)
62
Q

What is the main function of serotonin?

1 - stimulates pain
2 - associated with cognitive function
3 - stabilises moor, feeling, happiness and well being
4 - contributes to sound and speech

A

3 - stabilises moor, feeling, happiness and well being

63
Q

The Periaqueductal grey matter (PAG) transmit signals to the Rostral ventromedial medulla (RVM). PAG stimulation specifically has been shown to inhibit pain. Signals from the PAG and RVM transmits to the dorsal horn (which is where 1st order afferent neurons synapse with 2nd order neurons and transmit pain to somatosensory cortex), where it is able to modulate pain through the release of serotonin (5-HT). What does 5-HT bind with that can excite in order to inhibit pain?

1 - gamma neurons
2 - alpha neurons
3 - type Ia and II fibres
4 - interneurons

A

4 - interneurons

64
Q

The Periaqueductal grey matter (PAG) transmit signals to the Rostral ventromedial medulla (RVM), which in turn transmits signals to the dorsal horn, where it is able to modulate pain through the release of serotonin (5-HT). 5-HT excites interneurons and is able to inhibit pain. How is it able to do this?

1 - block 2nd order synapsing with 1st order neuron
2 - release endogenous opioid peptides that inhibit 2nd order neurons
3 - inhibit 1st order neurons in the dorsal ganglia
4 - bind to and inhibit 1st order neurons

A

2 - release endogenous opioid peptides that inhibit 2nd order neurons
- 2nd order neurons do not transmit their signal, through the spinal cord, thus no pain is felt

65
Q

What is the mechanism of action of opioids?

A
  • able to bind with K+ receptors on post synapse causing hyperpolarisation
  • able to bind with and inhibit Ca2+ receptors inhibiting release of neurotransmitters from pre-synapse
66
Q

The Periaqueductal grey matter (PAG) transmit signals to the Rostral ventromedial medulla (RVM), which in turn transmits signals to the dorsal horn, where it is able to modulate pain through the release of serotonin (5-HT). 5-HT excite interneurons and is able to inhibit pain. What 3 endogenous opioid peptides are inhibitory interneurons able to release that can inhibit the spinothalamic tract?

A

1 - Enkephalins
2 - Endorphins
3 - Dynorphins

ALL END IN INS

67
Q

Endogenous opioid peptides (Enkephalins, Endorphins and Dynorphins) are released by interneurons in the dorsal horn of the spinal cord, where the 2nd order neuron synapses with the 1st order neuron. Why are these endogenous opioid peptides so important?

A
  • able to inhibit pain
  • bodies natural opioid system
  • for example when we exercise we get a release of Endorphins, which makes us feel good
68
Q

Endogenous opioid peptides (Enkephalins, Endorphins and Dynorphins) are released by interneurons in the dorsal horn of the spinal cord, where the 2nd order neuron synapses with the 1st order neuron, and inhibit pain. Which 2 brain regions are able to activate the endogenous opioid peptides?

1 - limbic structures and sensory cortex
2 - limbic structures and visual cortex
3 - limbic structures and frontal cortex
4 - limbic structures and motor cortex

A

1 - limbic structures and sensory cortex

69
Q

Endogenous opioid peptides (Enkephalins, Endorphins and Dynorphins) are released by interneurons in the dorsal horn of the spinal cord, where the 2nd order neuron synapses with the 1st order neuron, and is able to inhibit pain. The limbic structures and sensory cortex is able to activate the endogenous opioid peptides, but which tract specific to pain can also activate them?

A
  • spinothalamic tract, specifically then pinomesencephalic fibres
70
Q

What are the 3 opioid receptors called?

A

1 - Mu
2 - Delta
3 - Kappa

71
Q

Exogenous opioid medication (codeine/morphine) can be used to act in the same manner as endogenous opioids. Keeping in mind that opioids act on the CNS, which types of pain are they able to treat from the figure below?

1 - nociceptive, inflammatory, dysfunctional
2 - nociceptive, dysfunctional, neuropathic
3 - dysfunctional, inflammatory, neuropathic
4 - nociceptive, inflammatory, neuropathic

A

4 - nociceptive, inflammatory, neuropathic

72
Q

NSAIDs are able to act on inflammation, pain and fever. In the figure below, which types of pain can NSAIDs be used to treat?

1 - nociceptive and inflammatory
2 - nociceptive and dysfunctional
3 - dysfunctional and neuropathic
4 - nociceptive and neuropathic

A

1 - nociceptive and inflammatory

73
Q

Paracetamol is able to act on pain and fever, predominantly in the CNS. In the figure below, which type of pain can Paracetamol be used to treat?

1 - nociceptive
2 - neuropathic
3 - dysfunctional
4 - inflammatory

A

1 - nociceptive

74
Q

Adjuvant medications (antidepressants (TCAs) are Anti-epileptic medication (carbamazepine, gabapentin) are those that we can use to “add on” to help in the treatment of pain. What is the only sort of pain can these be used to treat in the figure below?

1 - nociceptive
2 - neuropathic
3 - dysfunctional
4 - inflammatory

A

1 - neuropathic
- modulate neurotransmission in the CNS

75
Q

Can pathological dysfunctional pain be treated with medication?

A
  • no
  • nothing to treat

NSB! (53 decks)

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