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Y2 medical pathophysiology > Pain > Flashcards

Pain Flashcards

1
Q

Define pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

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2
Q

What are the purposes of pain?

A
  • Prevents further tissue damage.
  • Initiated escape/ withdrawal/ protective reflexes and behaviours
  • Promotes avoidance behaviour
  • Immobilisation of damaged tissue to aid in recovery process
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3
Q

Does the brain feel pain?

A

The brain does not contain nociceptors and therefore cannot experience pain.

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4
Q

How does a headache occur?

A

Pain receptors are in the Meninges which cause the headache sensation. When the meninges become inflamed, or you experience pain in this are, this is what causes the headache.

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5
Q

Why don’t you have pain receptors in the brain?

A

Nociceptors are present to help avoidance behaviour. There is no real scenario where avoidance of using the brain would be helpful because in any scenarios such as infection or trauma to the brain, this is likely to be fatal and so there is no need to have nociceptors in the brain.

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6
Q

What are nociceptors?

A

Receptors preferentially sensitive to noxious stimulus or to a stimulus which would become noxious if prolonged.

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7
Q

What is meant by the term noxious?

A

Harmful, poisonous or very unpleasant to normal tissues.

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8
Q

What are the types of noxious stimulus?

A

Chemical
Thermal
Mechanical

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9
Q

What type of nociceptors are sensitive to noxious chemical stimuli and where are these found?

A

Sensitive to polymodal nociceptors found on C-fibres.

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10
Q

What type of nociceptors are sensitive to noxious thermal stimuli and whereare these found?

A
  • Sensitive to polymodal nociceptors found on C-fibres.

- Chemothermal nociceptors which are found in A-delta neurones.

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11
Q

What type of nociceptors are sensitive to noxious mechanical stimuli and where are these found?

A
  • Sensitive to polymodal nociceptors found on C-fibres.
  • Chemothermal nociceptors which are found in A-delta neurones.
  • Mechanoreceptor found in A-delta neurones.
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12
Q

What is nociceptive pain?

A

A warning device which is activated to impending damage to an organism.

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13
Q

What activates nociceptive pain?

A

Noxious stimulus acting on specialised high-threshold sensory apparatus (nociceptors) found in the skin, muscle and viscera.

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14
Q

What are nociceptors in terms of their structure?

A

Free sensory nerve endings that respond to a variety of noxious stimuli that cause or have the potential to cause tissue damage.

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15
Q

What effect do non-noxious stimulus have and what receptors do they activate?

A

They activate low threshold afferent receptors which eventually leads to the processing of innocuous signals to the CNS.

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16
Q

What is meant by the term innocuous?

A

Non-harmful

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17
Q

What effect do noxious stimulus have and what receptors do they activate?

A

High intensity stimulus activate low threshold afferent receptors and the high threshold nociceptors. This is then processed in the CNS to produce a physiological pain.

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18
Q

What causes rate of conduction alone nerve axons to vary?

A
  • Diameter of the nerve axon

- Myelin sheath or not

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19
Q

How does myelin sheath affect the conduction rate along nerve axons?

A

Myelin sheath increases rate of conduction as the action potentials can jump by saltatory condition between gaps in the myelin sheath called Nodes of ranvier.

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20
Q

Describe the classifications of nerve fibres.

A

Classified as A, B or C.
A fibres are large and myelinated.
C fibres are small and unmyelinates.

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21
Q

Describe fast pain; how this is stimulated, what receptors are triggered , what is the function of this and what fibres are used.

A

Stimulation of high threshold thermo/mechanical nociceptors triggers fast pain which is usually conducted by A-delta fibres. This has a protective function such as withdrawing from a harmful situation.

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22
Q

Describe slow pain; how this is stimulated, what receptors are triggered , what is the function of this and what fibres are used.

A

Slow pain is responsible for the delayed pain sensation that occurs after tissue injury. This is caused by activation of high threshold polymodal pain receptors which activate slow conduction via un-myelinated C-fibres.
The purpose of this is to encourage healing by eliciting behaviour to protect the damaged area.

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23
Q

What are the 3 sources of pain?

A
  • Cutaneous
  • Somatic
  • Visceral
24
Q

What is cutaneous pain?

A

Injury to the skin and superficial tissues.

25
Q

Describe the concentration of receptors in cutaneous pain, where these receptors are and the effect this has.

A

Cutaneous nociceptors below the skin at high concentrations allow production of well-defined localised plan.

26
Q

Describe the concentration of receptors in somatic pain and the effect this has and the localisation of this pain.

A

Low concentrations of nociceptors produces a dull, poorly-localised pain. This may be local or referred to another part of the body.

27
Q

What is somatic pain?

A

Injury to ligaments, tendons, bonds, blood vessels and nerves.

28
Q

Describe the concentration of receptors in visceral pain and the effect this has.

A

Very low concentration of nociceptors causes longer, aching pain.

29
Q

Describe the localisation of visceral pain.

A

It is difficult to localise so may refer to an area unrelated to the injury site

30
Q

What is Ruch’s hypothesis?

A

Convergence of visceral and somatic pain receptors converge on the same spinal cord pain-transmitting neurones on the skin surface.

31
Q

What are the different types of headaches?

A

Tension, thunderclap, cluster, hyping, cold stimulus

32
Q

What is the most common type of headache?

A

Tension type

33
Q

Describe tension type headaches

A

Pain radiating from the neck, back, eyes and rest of the body.

34
Q

Describe the pathophysiology of tension headaches.

A

Thought to involve muscle tension, anxiety and depression.

35
Q

Describe cluster headaches.

A

Attacks occur in cyclical patterns or clusters, potentially over a period of weeks. to months with remission periods.

Painful but not life threatening.

36
Q

Describe thunderclap headaches.

A

Sudden onset and very severe headaches.

May be a sign of severe underlying issues.

37
Q

Describe hyping headaches.

A

Occur in the elderly, particularly at night and last for up to one hour

38
Q

Describe cold stimulus headaches.

A

Ingestion of cold food/drink results in a rapid onset short duration headache which subsides spontaneously.

39
Q

What severe underlying issues do headaches sometimes indicate?

A 
Hypertension 
Glaucoma
Eye strain
Anaemia
Fever
Brain tumour
Infections 
Hemorrhagic strokes
Cranial/ cervical vascular disorders
Head/neck trama
Substance withdrawal
Psychiatric disorder
40
Q

Why may individuals suffer pain in different ways?

A

Varying genetic components

Cultural components

41
Q

Describe the difference in the biological function of acute nociceptive pain and chronic neuropathic pain

A

Acute has biological function and chronic does not.

42
Q

Describe the difference in the onset of acute nociceptive pain and chronic neuropathic pain

A

Acute - recent onset

Chronic - delayed onset

43
Q

Describe the difference in the duration of acute nociceptive pain and chronic neuropathic pain

A

Acute - finite duration (days to weeks)

Chronic - persists beyond acute (months to years)

44
Q

What is hyperalgesia?

A

Exaggerated pain which is an increased response to a stimulus which is normally painful.

45
Q

What is allodynia?

A

Tenderness and production of pain in an injured tissue by a stimulus which is normally innocuous.

46
Q

What causes acute pain and what is its purpose?

A

Usually results from tissue damage, infection or inflammation and alters the body after injury or malfunction to cause protective mechanisms which prevent further damage.

47
Q

What are some of the classifications of pain?

A

Nociceptive
Neuropathic
Mixed origin
Psycopathic

48
Q

How do cancers cause pain?

A

By compressing other tissues, activating the nociceptors. Or by invading other tissues.

49
Q

What are pain mediators and why may this occur?

A

They cause sensitisation to pain. This is as a result of tissue damage, inflammation of ischaemic changes in tissue.

50
Q

What is central sensitisation?

A

Prolonged activation of a neurone which leads to strengthening of the synapse and this then results in a painful sensation from an innocuous synapse.

51
Q

What are the 2 different mechanisms of peripheral sensitisation?

A

1) Something happens to the neurone. The neurone the fires action potentials when no stimulus is present. This causes a pain sensation and response.
2) Release of neuropeptides leads to sensitisation of adjacent sensory terminals. This leads to the sensory terminals in response to innocuous stimuli and triggering a pain sensation.

52
Q

What happens if axonal damage occurs?

A

If you damage a neurone, the downstream axon degenerates and other neurones may take over. Certain amounts of regrowth of the stump of the damaged neurone can occur resulting in neuroma formation.

53
Q

What issues do neuromas cause?

A

Shooting pains
Hyperalgesia
Allodynia

54
Q

What possible ways are there to modify the pain response?

A
  • Endogenous analgesia systems which modulate pain levels.
  • Supplementation with drugs.
  • Inhibitory connection between A-beta fibres and C-fibres.
  • TENs (Transcutaneous electrical nerve stimulation)
55
Q

How does- TENs (Transcutaneous electrical nerve stimulation) work?

A

Electrical signals are used to mimic touch and therefore try to reduce pain.
Pain gates are closed stimulating A beta fibres and causing supraspinal inhibition. This triggers endorphin release.

Y2 medical pathophysiology (12 decks)

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