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2.1 T2: Sensory inputs and motor outputs > T2 L12: Physiology of pain 2 > Flashcards

T2 L12: Physiology of pain 2 Flashcards

1
Q

What is the definition of acute and chronic pain?

A

Acute <3months

Chronic >3 months

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2
Q

What causes acute pain

A

Tissue injury or inflammation. When the injury site recovers, the pain stops

Eg. following surgery, musculoskeletal injury, burn, headache, visceral pain

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3
Q

Which type of pain is caused by excitation of nociceptors?

A

Acute pain

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4
Q

What is the effect of bradykinin and NGF on pain?

A

They reduce the threshold of heat-activated channels (TRPV1) so cause pain

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5
Q

What is the effect of prostaglandins on pain?

A

They reduce the threshold of sodium channels so cause pain

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6
Q

What is hyperalgesia?

A

An increased sensitivity to feeling pain and an extreme response to pain

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7
Q

What are the sites of action of acute pain treatment?

A

PNS (at the site of injury)
CNS
Both

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8
Q

What is the drug Lidocaine for?

A

Also known as Lignocaine

It is applied to the skin to reduce pain

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9
Q

How does Lidocaine work?

A

It prevents nociceptors firing by blocking sodium channels

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10
Q

How do NSAID’s work?

A

They reduce the inflammatory response by inhibiting prostaglandin synthesis so that the sodium channel threshold can’t decrease

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11
Q

How does paracetamol work?

A

It exact mechanism in not known

It inhibits COX enzymes enzymes in the CNS so there is no prostaglandin formation. It acts on the serotonergic pathway

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12
Q

How do topical capsasin treatments work on reducing pain?

A

They are TRPV1 agonists so they persist opening of the TRPV1 channels causing a calcium overload so the nociceptor stops working

Too much calcium causes mitochondrial overload

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13
Q

How do opioids work to reduce pain?

A

They agonise the endogenous opioid system

They work on the spinal cord, disinhibit the brainstem, and inhibit nociceptor channels peripherally

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14
Q

What type of drug is Tramadol?

A

An opioid

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15
Q

What is the gate control theory of pain?

A

The pain cause by nociceptors can be reduced by the simultaneous activation of low threshold mechanoreceptors (alpha/beta fibres)

Rubbing or blowing on the pain will reduce it

It’s modulation of pain at the spinal cord level

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16
Q

What is the mechanism of gate theory?

A

Stimulation of alpha/beta fibres at injury site activates interneurons in the dorsal horn, which inhibit spinothalamic neurones

The C fibres inhibit inhibitory interneurons (opening of the gate)
Alpha/beta fibres activate inhibitory interneurons (closes gate)

17
Q

What % of population does chronic pain affect?

A

20-50%

18
Q

Which type of pain is both nociceptive and neurpathic?

A

Chronic pain

19
Q

What are some causes of neuropathic pain?

A 
Compression
Traction
Sever
Hypoxia
Demyelination
Tumour
Neuroinflammation
20
Q

How may patients describe neuropathic pain?

A 
Burning
Numbness
Shooting pains
Pins and needles 
Aching
Hypersensitivity
21
Q

What happens to nerve at the site of injury?

A

The damaged nociceptor tips fire spontaneously because there is an accumulation of transported ion channels at the site

22
Q

What is central sensitisation?

A

Increase in responsiveness of nociceptors withing the CNS

Normal inputs begin to produce abnormal responses due to reduced threshold for activation

23
Q

What is the mechanism behind reduced threshold for activation in the CNS?

A

There is alteration of channels and causes insertion of more channels so neurones fire more easily

24
Q

What is Allodynia?

A

Extreme sensitivity to touch

25
Q

What is the mechanism behind allodynia?

A

Central sensitisation

Non-noxious alpha/beta fibres are normally non-function but in allodynia, they synapse onto 2nd order spinothalamic neurones

26
Q

Why is chronic pain difficult to treat?

A

Because it’s not easily reversed

27
Q

What are some current neuropathic pain treatments?

A
  • Drugs: tricyclic antidepressants, anticonvulsants, and topical capsacin or Lidocaine because they have analgesic properties
  • Acupuncture
  • Physical therapies: manipulation of tissues, pacing
  • Psychological therapies: CBD
  • Surgery: spinal cord stimulator
28
Q

What is acupuncture?

A

Thin needles are inserted into the body to relieve pain

29
Q

How do tricyclic antidepressants work as analgesia?

A

Eg. Amitriptyline, Duloxetine

They act centrally on the descending inhibitory pathways to inhibit reuptake or serotonin and noradrenalin

30
Q

How do anticonvulsants work as analgesia?

A

Eg. Pregablin, Gabapentin, Carbamazepine

They are proposed to act in the spinal cord to reduce excitability by blocking calcium or sodium channels

31
Q

What is the first line of treatment for neuropathic pain?

A

Amitriptyline, Duloxetine, Pregabalin, Gabapentin

32
Q

What is the second-line of treatment for neuropathic pain?

A

Switch drugs or combine them

33
Q

What is the third-line of treatment for neuropathic pain?

A

Refer patients to a specialist pain service and consider oral tramadol for when there are flare ups

Along with the second-line of treatment, topical Lidocaine could also be considered

34
Q

How does placebo analgesia work?

A

It has been shown to treat neuropathic pain by activating the descending inhibitory pathway because we think it works

35
Q

What are complementary alternative medicines (CAM’s)?

A

Eg. Acupuncture, massage therapy, homeopathy, hypnosis

36
Q

What goes wrong in the body to cause neuropathic pain?

A
  • Peripheral terminals: peripheral sensitisation
  • Axon: Increased firing of primary afferents
  • Dorsal root ganglia: changes in protein synthesis
  • Dorsal horn/spinal cord: Central sensitisation
  • Brain: Changes in brain activation patterns

2.1 T2: Sensory inputs and motor outputs (14 decks)

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