Week 4 - Prerequisite knowledge Flashcards

(61 cards)

1
Q

What is pain?

A

A sensory and emotional experience linked to actual or potential tissue damage

The person in pain is the authority on it—pain exists when and where they say it does.

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2
Q

What are the four stages of how pain is generated and carried?

A
  • Transduction
  • Transmission
  • Perception
  • Modulation

These stages describe the process from tissue injury to the brain’s interpretation of pain.

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3
Q

What happens during the transduction stage of pain?

A

Tissue injury releases chemicals (e.g., prostaglandins, bradykinin) that nociceptors convert into an electrical signal

This is the first stage in the pain pathway.

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4
Q

What is the role of A-delta fibres in pain transmission?

A

Thinly myelinated, fast; sharp, localised pain; usually acute

They carry the initial sharp pain signal to the brain.

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5
Q

What is the role of C fibres in pain transmission?

A

Unmyelinated, slow; dull, diffuse, persistent pain

They carry the longer-lasting, aching pain signal.

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6
Q

What is the Gate Control Theory?

A

A dynamic ‘gate’ in the substantia gelatinosa regulates traffic from ascending pain fibres and descending brain signals

Touch input can close the gate, while strong nociceptive input opens it.

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7
Q

What are the two main classifications of pain by time course?

A
  • Acute pain
  • Persistent (chronic) pain

Acute pain has a sudden onset, while persistent pain lasts beyond expected healing time.

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8
Q

What is nociceptive pain?

A

Tissue pain via normal nociceptor processing

It can be somatic (skin/muscles/bones/joints) or visceral (organs).

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9
Q

What is neuropathic pain?

A

Nerve injury/dysfunction; burning, tingling, electric-shock-like

It may respond poorly to opioids.

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10
Q

What is catastrophising in the context of pain?

A

A cognitive style of magnifying threat and feeling helpless about pain

It is linked to worse outcomes and measured by the Pain Catastrophising Scale (PCS).

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11
Q

What are some tools used to assess acute pain?

A
  • NRS (0-10)
  • VAS
  • Verbal Rating Scale
  • PQRST / OPQRSTUV

These tools help gauge pain intensity and characteristics.

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12
Q

What is the Behavioural Pain Assessment Scale used for?

A

To rate face, restlessness, tone, vocalisation, consolability (0-10 total)

It is used when a person cannot self-report pain.

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13
Q

What is the Functional Activity Score (FAS)?

A

A score that ties pain to function by asking the person to perform a relevant activity

It grades the activity from A (no limitation) to C (severe).

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14
Q

What are some multidimensional tools for assessing persistent pain?

A
  • Brief Pain Inventory (BPI)
  • McGill Pain Questionnaire (MPQ/SF-MPQ)
  • DN4 (neuropathic screening)
  • PCS (catastrophising)
  • PASS (pain anxiety)

These tools provide a broader understanding of pain beyond intensity.

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15
Q

What is the bottom line for effective pain management?

A

Great pain management starts with great assessment: be holistic, suspend assumptions, and believe the patient’s report

This approach ensures a comprehensive understanding of the patient’s pain experience.

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16
Q

What is McCaffery’s dictum regarding pain?

A

“Pain is whatever the experiencing person says it is, existing whenever they say it does.”

Guides validation and assessment.

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17
Q

Define the difference between pain and nociception.

A

Nociception = neural processing of noxious stimuli; pain = conscious sensory + emotional experience (requires brain appraisal).

Understanding this distinction is crucial for pain management.

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18
Q

What is the difference between protective and non-protective pain?

A
  • Acute pain is typically protective (alerts to harm)
  • Persistent pain often becomes non-protective and maladaptive

This distinction helps in understanding pain management strategies.

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19
Q

Differentiate between afferent and efferent pathways.

A
  • Afferent = ascending sensory input to CNS
  • Efferent = descending motor/modulatory output from brain to spinal cord/periphery

These pathways are essential for understanding pain signaling.

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20
Q

Name the key CNS structures involved in pain.

A
  • Thalamus (relay/switch)
  • Limbic system (affect/meaning)
  • Reticular formation (arousal)
  • Cortex (discrimination/attention)

Each structure plays a role in the perception and processing of pain.

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21
Q

List the chemical mediators involved in transduction.

A
  • Prostaglandins
  • Bradykinin
  • Histamine
  • Serotonin
  • Substance P
  • H⁺/K⁺/Na⁺ flux → nociceptor depolarisation

These mediators are crucial for the initiation of pain signaling.

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22
Q

Describe the clinical feel of A-δ vs C fibres.

A
  • A-δ = sharp/pricking, well-localised
  • C = dull/aching/burning, diffuse, lingering

Understanding these fibre types aids in pain assessment.

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23
Q

What is the role of A-β fibres in pain gating?

A

Non-noxious touch/pressure fibres; stimulate inhibitory interneurons in dorsal horn → ‘rubbing it’ can reduce pain.

This mechanism is important for pain modulation.

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24
Q

What is the dorsal horn substantia gelatinosa?

A

Site of ‘gate’ integration of small pain fibres, large touch fibres, and descending inhibitory signals.

This area is critical for the modulation of pain signals.

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25
Name the **descending inhibitory transmitters**.
* Endorphins/enkephalins (opioid receptors) * Serotonin * Noradrenaline ## Footnote These transmitters help dampen pain transmission in the spinal cord.
26
Differentiate between **hyperalgesia** and **allodynia**.
* Hyperalgesia = increased pain to painful stimulus * Allodynia = pain to normally non-painful stimulus (often neuropathic) ## Footnote These conditions reflect different pain processing mechanisms.
27
What is the difference between **peripheral** and **central sensitisation**?
* Peripheral: sensitised nociceptors at injury site * Central: spinal/brain neurons become hyperexcitable (‘wind-up’) ## Footnote Understanding these concepts is crucial for treating chronic pain.
28
What role does **NMDA/glutamate** play in pain?
Noxious input releases glutamate → NMDA receptor activation contributes to central sensitisation and opioid resistance. ## Footnote This mechanism is significant in chronic pain conditions.
29
Give examples of **somatic superficial** vs **deep pain**.
* Superficial: laceration, burn * Deep: muscle spasm, bone metastasis, post-op wound pain ## Footnote These examples illustrate the different types of somatic pain.
30
What are the hallmarks of **visceral pain**?
* Poorly localised * Cramping/squeezing * Autonomic features (N/V/diaphoresis) * Referred pain * Cutaneous hyperalgesia ## Footnote Recognizing these features is important for diagnosis.
31
Explain the **referred pain mechanism**.
Convergence of visceral and somatic afferents onto same spinal neurons → brain mislocalises source. ## Footnote This phenomenon complicates the diagnosis of pain.
32
Define **cutaneous hyperalgesia**.
Increased skin sensitivity over an affected viscus (e.g., abdominal wall tenderness with visceral pathology). ## Footnote This condition is often seen in visceral pain syndromes.
33
Describe the descriptors of **neuropathic pain**.
* Burning * Shooting * Electric shock * Pins/needles * Painful numbness * May have allodynia and hyperalgesia ## Footnote These descriptors help in identifying neuropathic pain.
34
What are common **neuropathic aetiologies**?
* Post-stroke * MS * Spinal cord injury * Diabetic polyneuropathy * Nerve entrapment * Post-herpetic neuralgia ## Footnote These conditions are often associated with neuropathic pain.
35
Describe the **cancer pain patterning**.
Often mixed mechanisms (nociceptive + neuropathic), persistent background with breakthrough episodes. ## Footnote Understanding this pattern is essential for effective pain management.
36
What are the features of **breakthrough pain (BTP)**?
* Transient exacerbation despite controlled baseline * Rapid onset/short duration * Often needs rapid-onset rescue ## Footnote Recognizing BTP is crucial for effective pain management.
37
Define **intractable pain**.
Severe, relentless pain not relieved by standard medical/surgical/nursing measures; major functional/psych impact. ## Footnote This type of pain poses significant challenges for treatment.
38
What are the basics of **phantom limb pain**?
Pain perceived in a missing limb; neuropathic features; related to cortical reorganisation and ectopic activity. ## Footnote This phenomenon illustrates the complexity of pain perception.
39
What is **somatoform (somatic symptom) pain**?
Pain with prominent psychological/behavioural maintenance; diagnosis of exclusion; avoid stigmatising language. ## Footnote This type of pain requires sensitive handling in clinical settings.
40
How does **context/meaning** affect pain perception?
Threatening meaning increases pain; benign/valued meaning (e.g., labour) can reduce perceived intensity. ## Footnote This highlights the psychological aspects of pain.
41
What are the effects of **attention/expectation** on pain?
* Hyper-attention and negative expectancy (nocebo) amplify pain * Positive expectancy (placebo) can reduce pain ## Footnote These effects are important in pain management strategies.
42
List the **harmful effects of unrelieved pain** on the cardiovascular system.
* ↑HR * ↑BP * ↑cardiac workload * Hypercoagulability → ↑cardiovascular event risk ## Footnote Understanding these effects is crucial for comprehensive pain management.
43
What are the **harmful effects of unrelieved pain** on the respiratory system?
* Shallow breathing * ↓lung volumes * Atelectasis * Secretion retention * Pneumonia risk * Impaired cough ## Footnote These effects highlight the importance of effective pain management.
44
Describe the **harmful effects of unrelieved pain** on the endocrine/metabolic system.
* ↑Cortisol/catecholamines/ADH/RAAS → insulin resistance and hyperglycaemia * Catabolism ## Footnote These metabolic changes can complicate recovery.
45
What are the **harmful effects of unrelieved pain** on the gastrointestinal/genitourinary systems?
* ↓Gastric emptying and motility → ileus/constipation * Urinary retention * Fluid/electrolyte issues ## Footnote These complications can lead to significant morbidity.
46
List the **harmful effects of unrelieved pain** on the musculoskeletal & immune systems.
* Spasm * Immobility * Deconditioning * VTE risk * Stress-mediated immunosuppression and delayed healing ## Footnote These effects underscore the need for effective pain management.
47
What are the **harmful effects of unrelieved pain** on neuropsychological aspects and quality of life?
* Anxiety * Sleep loss * Low mood * Hopelessness * Poorer recovery and participation ## Footnote These psychological impacts can hinder overall recovery.
48
How do **acute** vs **persistent pain** differ in vital signs?
* Acute often shows sympathetic signs * Persistent pain often shows normal vitals due to parasympathetic balancing ## Footnote This difference is important for clinical assessment.
49
What is included in the **minimum data set** for acute assessment?
* Location/character * NRS at rest & movement * Functional task (FAS) * Aggravating/relieving * Vitals * Plan & review time ## Footnote This data set is essential for effective pain management.
50
What is the **rule of thumb** for reassessment timing?
* Oral analgesic: check 30–60 min * IV: 15–30 min * Regional: per protocol * Document time and effect ## Footnote Timely reassessment is crucial for effective pain management.
51
How is the **Functional Activity Score (A/B/C)** used?
Test a relevant task (e.g., cough, sit-stand); A = no limitation, B = mild–moderate, C = severe; compare to baseline. ## Footnote This score helps in assessing functional impact of pain.
52
What items are included in the **Behavioural Pain Assessment Scale**?
* Face * Restlessness * Muscle tone * Vocalisation * Consolability ## Footnote Each item is scored 0–2, with a total score of 0–10 to track pain interventions.
53
What domains are assessed in the **Brief Pain Inventory (BPI)**?
* Severity now/worst/least/average (24 h) * Interference: general activity, walking, work, relations, mood, sleep, enjoyment ## Footnote This inventory helps in understanding pain impact on daily life.
54
What is the value of the **McGill Pain Questionnaire (MPQ)**?
Profiles sensory/affective qualities and totals; useful when quality guides mechanism and targeting. ## Footnote This tool aids in comprehensive pain assessment.
55
What are examples of **neuropathic screeners**?
* DN4 (≥4 suggests neuropathic) * Leeds Neuropathic Scale ## Footnote These screeners are used alongside history/exam for diagnosing neuropathic pain.
56
What is the clinical impact of **catastrophising**?
Higher PCS predicts higher pain/disability and poorer treatment response; target with CBT/ACT and education. ## Footnote Addressing catastrophising is crucial for effective pain management.
57
What does the **QUESTT framework** involve in pediatrics?
* Question child * Use scale * Evaluate behaviour/physiology * Secure parent input * Take cause into account * Take action/evaluate ## Footnote This framework ensures comprehensive assessment in children.
58
What are the details of the **FLACC scale**?
Face, Legs, Activity, Cry, Consolability (0–2 each) for non-verbal/young children; max 10; repeat to track change. ## Footnote This scale is useful for assessing pain in non-verbal children.
59
How should the **FACES scale** be used?
Explain faces show ‘how much you hurt right now’; child points to matching face; recommended for ≥3 years. ## Footnote This scale helps children express their pain levels.
60
What caution should be taken regarding **paediatric physiology**?
Vitals/colour/sweat can reflect fear or sepsis; never use physiological signs in isolation—combine with behaviour/self-report. ## Footnote This approach ensures accurate assessment in children.
61
What must be included in **documentation** for pain assessment?
* Tool used and scores (rest/movement/FAS) * Descriptors * Function impact * Interventions + times * Effect/side effects * Next review * Goals ## Footnote Comprehensive documentation is essential for continuity of care.