Pain Flashcards

0
Q

Why do you get referred pain?

A

Visceral fibres converge on the spinal-cord second order neurones and are shared by somatic nociceptors fibres so they converge

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1
Q

Define pain

A

Unpleasant, sensory and emotional experience associated with actual or potential tissue damage

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2
Q

What do you get with somatic pain in terms of different responses?

A

Pain elicits sensation with autonomic, somatic endocrine and emotional responses so you get release of cortisol, eyes dilating, increased BP etc

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3
Q

Define nociception

A

Non-conscious neuronal traffic originating with trauma or potential tissue trauma

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4
Q

What is the difference between the threshold and tolerance of pain?

A

Everyone has the same threshold
Tolerance people differ in and it increases with age it may also depend on physiological, psychological and emotional factors

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5
Q

What the ascending tracts for pain?

A

The spinothalamic tract with the lateral in particular

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6
Q

What are the stages of nociception?

A

Transduction which is the activation of nociceptors
Transmission which is relay of action potentials to the CNS
Modulation by other peripheral nerves or CNS mechanisms
Perception is the final result

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7
Q

What are the different types of nociceptors?

A

Mechanical which have A delta fibres
Thermal which is also A delta fibres
Polymodal which is C fibres which is both mechanical and thermal

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8
Q

Explain about unmyelinated C fibres.

A

These are unmyelinated and slow and have capacitance they carry pain and temperature sensation and are responsible for dull and throbbing pain

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9
Q

Explain about A delta fibres

A

These are myelinated so are responsible for fast transmission of pain they don’t have a capacitance and they also carry pain and temperature they are responsible for fast, sharp and stabbing sensation

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10
Q

What lamiae is the nucleus proprius?

A

IV and V

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11
Q

What factors are released with tissue damage?

A

Histamine, prostaglandins, bradykinin, serotonin, potassium, hydrogen and substance P.
Substance P is released from nerve endings and increases the permeability of capillaries so contributes to inflammation. It also causes mast cells to release histamine causing activation of nociceptors and an action potential.
It works via a positive feedback mechanism.

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12
Q

How do NSAID’s produce their analgesic effects?

A

Cox 1 inhibitors therefore decrease prostaglandins therefore decrease activation of nociceptors.

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13
Q

What is thalamus, the limbic system and the hypothalamus responsible for in terms of pain?

A

Thalamus carries information on location and intensity
The limbic system is responsible for the emotional response
The hypothalamus is responsible for the stress response.

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14
Q

What is congenital analgia?

A

A congenital condition in which no pain is felt at all
It is incredibly dangerous because there is no protective mechanism from painful stimuli which can result in significant tissue damage.
E.g. placing your hand on a hot radiator and not realising -> would lead to burns

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15
Q

Why do we get acute pain?

A

It is a survival mechanism in order to protect our bodies from severe harm

16
Q

What is the definition of chronic pain?

A

Pain or discomfort persisting continuously or intermittently for three months or more

17
Q

What are the 2 main types of pain?

A

Nociceptive

Neuropathic

18
Q

Explain the gate control theory of pain

A

C and A delta fibres synapse with either lamina I or V to the transmission neurone.
Lamina II is the gate which is open or closed and sets the pain threshold this then it goes onto a transmission neurone the thalamus

19
Q

Explain the pathophysiology of hyperalgesia and allodynia

A

Hyperalgesia is increased pain at a normal threshold
Allodynia is increased sensitivity to pain where a normal person would not feel pain at all.
Chronic pain stimulates nerves which become hypersensitive
There is excess glutamate release, and excess NMDA receptor activation which results in wind up which is the basis of these two conditions.
This can lead to receptive field expansion and hyperexcitsbility of neurones

20
Q

What is chronic pain often due to?

A

Nociceptors
Neuropathic
Mixed pain
It involves changes in the spinal cord such as increased calcium and sodium channels and also wind up the brain also remaps

21
Q

What is neuropathic pain caused by?

A

Nerve damage

It is pain of neuronal origin and very difficult to treat

22
Q

After you prefer nerve injury, sensation occurs which can lead to any of what?

A

D crease threshold of nociceptor activation
Increased receptive field expansion
Allodynia
Hyperalgesia
Hyperpathia
Emergence of spontaneous activity due to sodium channel up-regulation

23
Q

Explain phantom limb pain

A

This is a pain felt by amputees.
The nerve ending is still present and it also has a part still in the homunculus.
Therefore sensation can still travel to brain
The homunculus however, can remap and therefore you can get sensation in the phantom limb by stimulating other parts of the body for example touching the lip can sometimes lead to phantom limb pain because more area is given to the lip in the homunculus.

24
Q

What are the two types of complex regional pain syndrome?

A

Type one where there is no identifiable lesion

Type two where there is an identifiable nerve lesion

25
Q

Explain the epidemiology of complex regional pain syndrome

A

It tends to occur in about the fourth decade
It is 2 to 3 times more common in females
It usually involves a single limb at first
There is usually 30 months before diagnosis and after symptom onset.

26
Q

What is complete regional pain syndrome caused by?

A
Minor trauma
Bone fracture
Surgery
Stroke
MI
27
Q

What are the signs and symptoms of complex regional pain syndrome?

A

Oedema, redness, clammy extremities, allodynia, hyperalgesia, trophic effects, contractures, atrophy, burning pain

28
Q

What is the mechanism of complex regional pain syndrome?

A

An original injury is carried to the brain
The pain impulse then triggers the sympathetic nervous system which returns to the site of injury
The sympathetic impulse triggers inflammation and vasospasm leading to oedema and increased pain
The pain triggers another cycle

29
Q

What are the three stages of complex regional pain syndrome?

A

1 acute
2 dystrophic
3 atrophic

30
Q

What is cancer pain caused by?

A

Neuropathic due to invasion
Nociceptive due to inflammation
Drugs for example methotrexate

31
Q

What are the effects of opioids?

A
Nausea
Vomiting
Euphoria
Analgesia
Respiratory depression
Itching
Constipation
32
Q

What are the three types of opioid receptors and what type of receptor are they?

A

Mu, Delta, kappa

They are GPCR and inhibit neurotransmitter release

33
Q

Where are opioid receptors found?

A

Myenteric plexus which is why they cause constipation
Hippocampus which is why they cause memory loss
The brainstem which is why they cause respiratory depression
The heart, vas deferens, spinal-cord, thalamus and hypothalamus, cortex

34
Q

Give some examples of weak opioids

A

Tramadol
Codeine
Dihydrocodeine

35
Q

Give some examples of strong opiods

A
Morphine
Oxycodone
Hydromorphone
Diamorphine
Fentanyl
36
Q

What can you give for opiod insensitive pain?

A

Antidepressants
Anticonvulsants
Local anaesthetics
Spinal analgesia