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Medical Pathophysiology > Week 3 - Neurobiology of pain > Flashcards

Week 3 - Neurobiology of pain Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the purpose of pain?

A

To promote avoidance behaviour

Prevents further tissue damage

Initiates withdrawal behaviours/reflexes

Immobilisation of damaged tissue to aid in recovery process

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2
Q

Do we feel pain in the brain?

A

No.
We feel pain when the signals reach our brain.

Also, the brain does not contain nociceptors, so can’t experience pain.

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3
Q

What is the meninges?

A

3 membrane layers around the brain that DO contain nociceptors, so that’s why we can sometimes feel pain in our head.

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4
Q

What is pain caused by?

A

It is caused by the transmission of impulses from the site of tissue damage along pain nerve fibres towards the central nervous system.

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5
Q

What is a noxious stimulus?

A

A stimulus in the environment that can cause damage to normal tissues.

E.G. fire

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6
Q

What are the types of noxious stimuli?

A

Chemical
Thermal
Mechanical

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7
Q

What are nociceptors?

A

They are receptors that are sensitive to noxious stimuli or a stimulus which would become noxious if prolonged.

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8
Q

Is there just one type of pain receptor?

A

No.
There are many types of receptors that are sensitive to different types of pain.

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9
Q

What is the sensory processing pathway from a low intensity (non-noxious) stimuli?

A

Low-intensity non noxious stimulus > low threshold afferent > processing in CNS > innocuous sensation

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10
Q

What is the sensory processing pathway from a high intensity noxious stimuli?

A

High intensity noxious stimuli > nociceptor > high afferent threshold > processing in CNS > painful sensation

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11
Q

How is information transmitted from the nociceptor?

A

Nociceptor activated > Info enters into spinal cord > reflexes activated > info travels to thalamus directly via spinothalamic tract and indirectly via spinoreticular tract producing a stress response.

The limbic system produces an emotional response.
Info is also sent to somatosensory cortex to localise pain.

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12
Q

What can increase rate of conduction in the axon?

A

Larger nerve diameter
Myelination of the nerve fibre

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13
Q

What is saltatory conduction?

A

This is where the action potential jumps between the nodes of ranvier.

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14
Q

What are the different types of nerve fibres?

A

A Fibre - large and myelinated.

B fibre

C fibre - small and unmyelinated.

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15
Q

What is fast (first) pain?

A
  1. You can get it when there is a stimulation of HIGH THRESHOLD thermo/mechano nociceptors which results in fast pain.
  2. transmitted by fast conducting A-delta fibres.
  3. Result in protective function - removal/withdrawal from harm.
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16
Q

What is slow (second) pain?

A
  1. It is the activation of high threshold polymodal pain receptors which activate slow conducting unmyelinated C-fibres.
  2. It is responsible for delayed pain sensation that occurs after tissue injury.
  3. encourages healing by eliciting behaviour to protect the damaged area.
17
Q

What are the other types/sources of pain?>

A

Cutaneous pain
Somatic pain
Viscera pain

18
Q

What is cutaneous pain?

A

Injury to skin/superficial tissues

Nocicetors at below skin at high concentrations allow for well defined LOCALISED pain sensation.

19
Q

What is somatic pain?

A

Injury to ligaments, tendons, bones, blood vessels, nerves.

Low concentration of nociceptors produces dull, poorly localised pain.

Longer pain duration than cutaneous pain.

20
Q

What is visceral pain>?

A

Pain in bodies organs or internal cavities.

VERY LOW concentration of nociceptors, so pain is very difficult to localise - may refer to area unrelated to injury site.

21
Q

What is Ruch’s hypothesis?

A

It states that visceral and somatic pain receptors come together on the same spinal cord pain-transmitting neurons.

For example, it’s why when you have a heart attack, you feel pain in your left arm.

22
Q

what is tension type headache

A

pain radiating from neck, back, eyes, rest
of body

Unknown precise pathophysiology – may
involve muscle tension, anxiety, depression

23
Q

what is thunderclap headache

A

Sudden onset and very severe
headache

may be a sign of a severe underlying issue

24
Q

what is a Cluster headache

A

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

Despite being very
painful, not life threatening

25
Q

what are Hypnic Headaches

A

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

26
Q

what are Cold Stimulus Headaches

A

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

27
Q

what complex sensations can pain v=be a response to

A

behavioural dimensions
emotional dimensions
sensory dimensions

28
Q

what is pain based on

A

the interaction of peripheral pain receptors, central processing and modifying factors

29
Q

how can pain be quantified

A

validated questionnaires: hospital anxiety & depression (HAD), pain locus of control (PLC), brief pain inventory (BPI), McGill pain questionnaire (MPQ)

physical evidence: pallor, sweating, high BP, tachycardia, nausea, vomiting, fainting, dizziness, Anxiety, fear etc

30
Q

what is the time course of pain response

A

seconds- fast/slow pain sensations, inflammation develops

minutes/hours- Inflammation, hyperalgesia, allodynia

hours/weeks/months- Hyperalgesia/allodynia disappear, tissue repair occurs

if persists for months/years= chronic issue

31
Q

What is hyperalgesia?

A

An increased response to a stimulus which is normally painful.

32
Q

What is allodynia/

A

It is when you feel pain in tissue from a stimulus which is normally innocuous (non-noxious)

33
Q

What are the 4 classifications of pain/

A

Neuropathic
Nociceptive
Mixed origin
Psychogenic

34
Q

What is neuropathic pain/

A

It is pain for no reason.
The pain becomes the pathology usually via damage to the CNS/PNS

35
Q

what are pain mediators and what do they do

A

they sensitise us to pain

they are released from when tissues are damaged, inflammation provoking the chemical stimulation of nerves

36
Q

what chemical stimulations are included in pain mediations

A

bradykinin, prostaglandins, seratonin and histamines

37
Q
A

Medical Pathophysiology (11 decks)

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