Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MD4001 > Pain > Flashcards

Pain Flashcards

1
Q

Why is it important for medical students to know about pain ?

A
  • Really common symptom
  • Access to pain relief is thought by many to be a human right
  • As an FY1 you will be required to (prevent) Recognise, Assess and Treat pain effectively
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define pain.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the function of pain ?

A

Protective function, minimises damage by warning body that tissues/cells are getting damaged, or that a structure is not getting enough blood supply (e.g. myocardium).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Identify the main kinds of pain.

A 
IMMEDIATE PAIN (transmitted by A delta fibers) 
PERSISTING PAIN (transmitted by C fibers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens following immediate pain ?

A

WITHDRAWAL REFLEX
-Polysynaptic reflex
E.g. Foot injury

APs to nerves which will travel along spinal cord in dorsal horn.
Will then synapse to cause withdrawal of the limb by activating flexors + by relaxing extensors in limb involved + by
activating extensors and relaxing flexors of opposite leg to prepare it to take up weight of the whole body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give an example of pain where C fibers may be involved.

A

Polyneuropathy in diabetes, causing loss of sensation to the feet. Due to inability to sense, get repeated trauma to foot which then gets infected.

–> Chronic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the general neural pathways of pain in the spinal cord/brain.

A
  • Primary afferents (first oder neuron) from periphery synapse in dorsal horn of spinal cord.
  • Second order neurons decussate and ascend in spinothalamic tract to thalamus.
  • Third order neuron projects from thalamus to somatosensory cortex.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a nociceptor ?

A

Free nerve endings in the skin and viscera (especially in tissues which can become distended/ischemic/ damaged thermally/chemically /mechanically).

HOWEVER, only respond at extremes of stimuli, where stimuli will cause damage to tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which types of nerve fibers are involved in pain ?

A
  • A-delta (temperature and pain)

- C (temperature and pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Rank the following by velocity of transmission:

  • A beta
  • A delta
  • C
A

1) A beta
2) A delta
3) C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Identify the main differences between A delta and C fibers.

A

A-delta fibres:

  • Myelinated, thinner
  • Faster conduction (6-30 m/s)
  • Sharp, localised pain
  • Minority of nociceptor
  • Polymodal (but usually mechanical and thermal)
  • Not usually visceral

C fibers:

  • Unmyelinated
  • Dull, achy, throbbing, diffuse pain
  • Majority of nociceptors
  • Slow conduction (0.5-2 m/s)
  • Polymodal (thermal, mechanical, chemical stimuli)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the management of pain associated with C fibers ?

A

Imobilise limbs, imobilise joints (to allow healing, esp fracture healing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Identify the main steps in the physiology of pain (i.e. how noxious stimulus comes from periphery of body to be perceived brain as pain).

A
  1. Transduction
    • Conversion of a noxious stimulus (heat, mechanical, chemical) into an action potential in a nociceptor
    • Pain sensation may extend beyond actual assault
    • Primary hyperalgesia effect (when tissue damaged, nerve endings are bathed in chemicals released from damaged tissue, so sensations that may not have been previously perceived can become painful e.g. sunburn under hot water)
    (through recruitment of sleeping C fibers)
  2. Transmission
  3. Modulation
  4. Perception
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Identify examples of thermal, mechanical, and chemical stimuli which may be involved in transduction.

A
  • Heat: >450C or less that 150C
  • Chemical: K+, ATP (both of these intracellular, if cell is damaged and empty its contents, K+ activates nociceptors), Bradykinin, histamine (released by inflammatory response in tissue damage), Substance P (generated by nociceptor itself and released at synapses, when AP is getting transmitted up to brain + also releases in retrograde fashion and bathes nociceptors, and sensitises them to other stimuli)
  • Mechanical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do nociceptors adapt ? Why is this useful ?

A

Nociceptors do NOT adapt (unlike other nerve endings).
Rather than adapting (so that brain ignores it), they get more sensitive and transmit more APs, and your brain perceives pain as getting worse.

USEFUL because protective mechanism, body has to move if sitting in uncomfortable position and foot gets ischemic, and if don’t do anything gets MORE sore so forces you to do something about it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which nerve fibers are involved in transduction phase of pain ? Which modalities to they respond to ?

A

• Nociceptors are free nerve endings of A-delta and C afferent fibres, responding to stimuli (polymodal) that will potentially damage tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Identify the main chemical mediators of pain, as well as their source and effect on nociceptor.

A

MEDIATORS

  • K+ (Damaged cells, activates nociceptors)
  • Protons (Hypoxic cells, activates nociceptors)
  • Serotonin (platelets, activates nociceptors)
  • Bradykinin (plasma kininogen, activates nociceptors)
  • Histamine (mast cells, activates nociceptors)
  • Prostanoids (damaged cells, sensitisation)
  • Leukotrienes (damaged cells, sensitisation)
  • Substance P (primary afferents, sensitisation)
  • CGRP (primary afferents, sensitisation)
  • Glutamate (primary afferents, sensitisation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Explain why MIs are painful.

A

Ischemia (eg MI, sitting awkwardly so supply to leg cut off), organ involved
become hypoxic an lactic acid is produced, so activates nociceptors and
cause pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is it clinically important that pain and temperature run together ?

A

When doing an anesthetic block, instead of testing pain to make sure block is working, can test using temperature sense (e.g. can you feel this ice as cold).
If cannot perceive ice cube as cold, pretty certain that pain is blocked too.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Identify the excitatory substance, and receptors involved in transmission (second step of pain physiology).

A

Transmission between first and second order neurons

No single excitatory substance
• Glutamate (main one)
• SubstanceP
• CGRP

No single “pain receptor” but glutamate binds to:
• AMPA (when this one gets flooded and noxious stimulus continues, then gets to NMDA receptors and wakes them up)
• NMDA (sleeping but important!)
• G-protein couple receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Identify the main components of the anterolateral system, including where they terminate and their main function.

A

SPINOTHALAMIC

1) Paleo-spinothalamic
- Terminates in the dorsomedial (DM) and intra laminar areas (only provide generalised location for pain)

2) Neo-spinothalamic
- Terminates in the ventral posterior lateral nucleus (VPL, which is somatotopic so there IS local discrimination along this pathway)

SPINOMESENCEPHALIC
-“Terminates in the periaqeductal grey of the midbrain (area that is important to inhibiting or controlling pain sensations)”

SPINORETICULAR
-“Teriminates in the reticular formation in the brainstem. The spinoreticular tract is thought to be important in directing attention toward painful stimuli”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What kind of fibers does the neospinothalamic, and paliospinothalamic tract contrain respectively ?

A

NEO
-Adelta fibers

PALIO
-C fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where does modulation of pain occur ?

A

Modulation of pain occurs at the dorsal horn.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Identify the main mechanisms of modulations of pain at the dorsal horn.

A

3 mechanisms of descending inhibition

  • GABA and glycinergic interneurons
  • Descending inhibition PAG-RVM-DH (stimulates GABA release)
  • Endogenous opioids (e.g. encephalins, released at dorsal horn and minimize transmission of pain upwards to thalamus)

ALSO
• Higher order brain function (distraction, serotonin, NA all have impact at that synapse in dorsal horn)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the gate control theory.

A

Damage results in AP sent along nociceptor into dorsal horn.
If provide mechanical stimulation to same area, will travel through A-beta fibers, and will therefore transmit APs faster than A-delta fibers, so travel along the fiber and stimulate inhibitory neurons, resulting in presynaptic inhibition of pain information, so mechanoreceptors will stimulate target cell as opposed to the nociceptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Identify a clinical applicaiton of the gate control theory.

A

Transcutaneous electrical nerve stimulator sometimes used for patients suffering from neuropathic pain post-shingles or secondary to diabetes, also in the early stages of labor.

Overall effect is to block noxious stimulus.

27
Q

Identify the main aspects of response to pain. Why do different people react differently to an identical stimulus ?

A

Two aspects:

  1. Earliest “Ow!” response
  2. Fine distinction, interindividual variation (modulated by past experience)
28
Q

Define pain perception. What factors influence this ?

A

End result, where neuronal activity becomes a conscious experience.

Past experience, current situation, understanding, all modulate that conscious experience (somatosensory cortex).

29
Q

Describe the effects of reticular system and limbic systems on pain perception.

A
  • Reticular system elicits an autonomic response (thus patients with chest patient may also have nausea, sweating…)
  • Limbic system links perception of pain with mood
30
Q

Describe the relationship between a chronic condition on depression and anxiety.

A

Chronic condition can lead to depression and anxiety

31
Q

What type of receptor is responsible for detecting visceral pain ? What do these receptor respond to ?

A

• Visceral nociceptors (usually C fibers) respond to distension or ischaemia

32
Q

Describe the neural pathway emerging from visceral nociceptors (i.e. for visceral pain). What is the clinical implication of this ?

A

VISCERAL PAIN

  • Visceral primary afferents will activate multiple second order neurones (unlike somatic, one nociceptor activates one second order neuron)
  • C vibers from viscera converge on second order neurones with somatic input (e.g. second order neuron may also be getting A-delta fiber from shoulder, so pain may refer to the shoulder)

REFERRED PAIN (convergence)

33
Q

What is the main difference between somatic, and visceral pain ?

A

Visceral pain more diffuse (less well localised)

34
Q

Which visceral pain may refer to the shoulder tip ?

A

Gall bladder and diaphragm

35
Q

Identify the main associated features of pain.

A 
Associated features (remember Autonomic NS)
• Sweating
• Pallor
• Nausea
• Tachycardia
• Hypertension
36
Q

What are the main principles of management of pain ?

A

Preparation and Prevention
Recognise
Assessment
Treatment

37
Q

Describe prevention and preparation for pain.

A

• Anticipation and simple adjustments (e.g. damaged hand take ring off due to incoming swelling, elevate hand, ice packs to minimize swelling)
• Distraction
• Education (e.g. if patient with shoulder pain had relative with similar pain who had MI, reassure them if appropriate that’s it’s only Musculoskeletal)
• Challenge misconceptions (that all pain is bad)
• Re-branding:
-“pain should be too strong a word but you will be tender”
-“you shouldn’t feel pain but you will feel heavy, heavy pressure”
• Patient control (“raise a hand if you want me to stop”)
• Ametop, EMLA (topical local anesthetics, can be used in venapuncture, arterial blood gases, wait 30 mins after application)

38
Q

How may you recognise that a patient has pain ? What groups of patients may this be more challenging in ?

A

THROUGH
• History (patient tells you)
• Observation (way patient is moving, behaving e.g. non verbal patient need to observe for any changes in behavior/mood)
• Physiological parameters (acute pain- tachyC, hyperT)
• Autonomic symptoms (pale, sweaty, nauseated)

MORE CHALLENGING IN FOLLOWING GROUPS

  • Children- 2 and under non-verbal
  • Elderly with dementia- difficulty to express fact they have pain
  • Learning disability- may be non-verbal
39
Q

Identify a way to assess a patient with pain.

A

SOCRATES
+ Impact of the pain…what does it stop the patient doing
+ Treatment history (compliance, S-E, benefits)
+ Psycho-social history and awareness of yellow flags

40
Q

Identify red flags in pain.

A

Back pain and temperature

Woken up in middle of night with back pain

41
Q

Describe the effect of comorbidities on management of pain.

A 
May affect cause of pain
Affects prescription (renal impairment- avoid NSAIDS, opioids)
42
Q

What are yellow flags in the context of pain ?

A

Things which are likely to make acute pain become chronic pain

43
Q

Identify any limitations of the universal pain assessment tool. What is the max score ?

A

Maximum score is 15.

Limitations: pain is multidimensional and this scale is very unidimensional

44
Q

Describe treatment of pain.

A
  • Identify and manage the underlying cause
  • WHO ladder of pain
  • Involve non-pharma treatments if appropriate
45
Q

What is the aim of the WHO ladder ?

A
  • Developed for cancer pain
  • Emphasises oral treatment
  • Treats nociceptive pain
  • May need other medications for neuropathic pain
46
Q

Define nociceptive pain. How might it be described by a patient ?

A

A pain arising as a direct consequence of a lesion or a disease affecting the somatosensory system

• Difficult to describe…shooting, lancinating, stabbing

47
Q

How common is neuropathic pain ?

A

Fairly common (3-18%)

48
Q

State management for neuropathic pain.

A

Tricyclics (e.g. Amitriptyline) and Anticonvulsants (e.g. Gabapentinoids)

49
Q

Identify some causes of neuropathic pain.

A

Traumatic (phantom limb pain) Diabetic neuropathy (absence of sensation can cause feet damage)
Postherpetic neuralgia Trigeminal neuralgia
Post-stroke pain

50
Q

Identify possible findings upon examination in a patient with neuropathic pain.

A

Changes in colour (e.g. of limb)

Changes in sensation

51
Q

Identify the main clinical features of neuropathic pain.

A

POSITIVE PHENOMENA
⚪Spontaneous pain (pain without stimulus)
-Continuous (cutaneous, deep, visceral)
-Paroxysmal

⚪Evoked pain (pain with stimulus, which is usually non-noxious)

  • Allodynia (qualitative abnormalities: mechanical, which can be dynamic or static, and thermal)
  • Hyperalgia (quantitative abnormalities)
  • Hyperpathia (spatial and temporal abnormalities)

AUTONOMIC DYSFUNCTION
⚪Vasomotor (vascular dysfunction)
⚪Sudomotor (sweat and hair dysfunction)

NEGATIVE PHENOMENA
⚪Sensory loss (thermal, vibration, soft touch)

52
Q

Define paraesthesia, and dysaesthesia.

A

PARA: abnormal sensation, whether spontaneous or evoked
DYS: unpleasant abnormal sensation, whether spontaneous or evoked

53
Q

Define allodynia.

A

Pain due to stimulus that does not normally provoke pain

54
Q

Define hyperpathia.

A

Painful syndrome characterised by abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased treshold.

55
Q

Define neuralgia.

A

Pain in the anatomical distribution of a nerve or nerves.

56
Q

Define chronic pain. How common is this ?

A

Pain persisting beyond the usual healing time of the acute injury (usually beyond three months (12 weeks))

Common

57
Q

How may chronic pain impact on society ?

A

• Significant socio-economic burden (e.g. time off work)

58
Q

Describe the pathophysiology behind chronic pain.

A

Peripherally
• Prolonged inflammatory response results in decreased pain threshold in primary afferents
• Increased production of substance P and CGRP (and sensitising nociceptor)
• Recruitment of NMDA receptors
• Wakes up WDR
• “wind-up” phenomenon

Spinal cord
• Changes in gene and receptor expression in DRG and dorsal horn neurons

59
Q

Identify and describe a model to describe perception of pain by patients.

A

Refer to graph on slide 41.

Fear-Avoidance Model:

INJURY
↓
PAIN EXPERICENCE
↓
PAIN CATASTROPHIZING (input also from negative affectivity and threatening illness information)
↓
PAIN-RELATED FEAR
↓
AVOIDANCE+HYPERVIGILANCE
↓
DISUSE, DEP, DISABILITY
↓
PAIN EXPERIENCE

or

INJURY 
↓
PAIN EXPERIENCE
↓
NO FEAR
↓
CONFRONTATION
↓
RECOVERY

Example:
Bad cycle: Injury to my L arm, have past experience of relative
having heart attacks and pain radiating to L shoulder,
think you might have an MI, and be dying. Focus on it a lot, get scared, notice every-time it changes,
stop using your arm (because every time use it, it causes pain and makes you aware of it) which makes it sorer, decrease in mood and down that spiral.

Good cycle: If patient has been educated earlier on, reassured
appropriately earlier on, no fear, happy it’s simply musculoskeletal pain, happy by using limb they won’t do any harm, confrontation
and use of the limb and eventually recovery

60
Q

Identify modifiable, and non-modifiable risk factors for chronic pain.

A

MODIFIABLE

  • Past experience of pain (that site and others)
  • Anxiety and Depression
  • Catastrophizing beliefs
  • Surgical approach (some can minimise chronic pain post-op)
  • Attitudes (patients that passively want to be cured more likely to enter chronic pain cycle than patients who are actively engaging in physio, yoga etc. to help pain)
  • Communication

NON-MODIFIABLE

  • Gender (female)
  • Age (older, although for some surgeries e.g. inguinal hernia, opposite trend with younger males tending to get more chronic pain while in mastectomy older more likely)
  • Genetic prediposition
  • Lower socio-economic status
  • Occupational factors (if unhappy at work and perceive lack of support in work, can be a maintaining factor)
  • History of abuse (e.g. women’s refuge)
  • Compensation (if benefiting from pain, unlikely to resolve until legal resolve)
61
Q

Identify the main features of complex regional pain syndrome.

A
  • Severe continuous neuropathic pain
  • Abnormal sensation (either evoked positive symptoms of neuropathic pain, or negative phenomena and decreased sensation)
  • Vasomotor change (e.g. different color)
  • Sudomotor change (i.e. increased or decreased sweatiness)
  • Motor / trophic change (e.g. hair changes)
  • Regionally restricted e.g. hand
  • Disproportionate to the trauma (e.g. after fracture which would take 6 w, get this syndrome instead)
62
Q

Describe appearance of a hand affected by CRPS.

A 
Brawny discoloration
Shiny skin
Cyanotic fingers 
Brittle ridged fingernails
Swollen hand
63
Q

Describe diagnostic criteria of CRPS.

A

Budapest Criteria

  1. Patients must report continuing pain disproportionate to the trauma
  2. Patients must report at least one symptom in three of the four following categories:
    (a) Sensory: hyperalgesia (that is, exaggerated pain to a painful stimulus, such as pinprick) and/or allodynia (that is, pain elicited by a normally non-painful stimulus, such as light touch)
    (b) Vasomotor: skin colour and/or temperature changes/asymmetry
    (c) Sudomotor/oedema: swelling and/or sweating changes or asymmetry
    (d) Motor/trophic: weakness, tremor, dystonia, decreased range of motion and/or trophic changes/asymmetry involving nails, skin and/or hair
  3. Patients must display one sign in two of the categories above
  4. Signs and symptoms must not be better explained by another diagnosis.

MD4001 (74 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions