Experience of pain Flashcards

1
Q

What is Pain - IASP

A
  • An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.
  • Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and social factors.
  • Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurons.
  • Through their life experiences, individuals learn the concept of pain. A person’s report of an experience as pain should be respected.
  • Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being.

Pian is a vital function of the ns. It provides the body with a warning of potential or actual injury. It has a sensory and emotional experience.

  • Verbal description is only one of several behaviours to express pain; inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain.
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2
Q

WHat is Nociception

A

Nociception = describes the neural processes involved in producing the sensation of pain

A basic nociceptive system is found in all vertebrates, but in higher primates the system has evolved into a complex organisation of peripheral and central pathways. Projections to higher centres in the brain produce an integrated, abstract representation of pain, prompting appropriate action.

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3
Q

2 dimensions of pain

A
  1. Sensory/discriminative: allowing us to locate tissue damage = Carried along newer tracts to sensory cortex
  2. Affective/aversive: unpleasant and emotional = affective compoennt travels centrally along ancient spinal cord pathways to \old brain’ centres in the brain.

(the anatomy of the different components of the pain pathway reflects there’s 2 different dimensions

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4
Q

SIgnficiance of ‘potential’ tissue damage in pain definition

A

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.

The fact that pain may be described in terms of tissue damage when there is no actual damage present, reminds us of the complexity of the system, and the non-linear relationship between stimulus and intensity of pain.

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5
Q

Pain Physiology:

A
  • Pain is part of the somatosensory system which conveys information about physical
  • stimuli from the periphery to the brain.
  • It includes stimulus modalities of touch, temperature, proprioception and pain.
  • All of these stimulus modalities share a common neural pathway from the periphery to the brain.
  • Peripheral receptor -> 1st order neuron -> 2nd order neuron -> 3rd order neuron
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6
Q

Nociceptors - what do they respond to and the types

A
  • Nociceptors are polymodal: they respond to a variety of mechanical, thermal and chemical stimuli.
  • Nociceptors have a HIGH threshold for mechanical and thermal stimulation (activated by extreme pressure or temperature).
  • Aδ nociceptors: Fast pain. Initiatates fast withdrawal reflex.
  • C nociceptors: ‘Slow’ dull throbbing pain, associated with inflammation, promotes immobilisation of injured body part.

Visceral nociceptors: similar to Adelta and C found in the periphery, but respond to distention and ischameia rather than uctting or thermal damage.

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7
Q

Pathway of neuronss in pain physiology

A

peripheral receptor -> 1st order neuron -> 2nd order neuron-> 3rd order neuron

  • The first order neuron in the nociceptive pathway is the primary afferent.
  • The cell body of the primary afferent is found in the dorsal root ganglion. The central
  • Process of the 1y afferent projects into the dorsal horn. Sensory neurons are classified according to fibre diameter.
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8
Q

Spunal cord primary and secondary afferents image

A
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9
Q

Rexed Laminae in the spinal cord

A
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10
Q

First order neurones synapsing with second one

A
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11
Q

Tracts in spinal cord section

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12
Q

Primary ascending pain pathways

A
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13
Q

Thir dorder neurons in pain pathway

A
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14
Q

Secondary Ascending Pain pathway

A
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15
Q

what types of pain are there?

A
  • Acute
  • Nociceptive
  • Nociplastic
  • Referred
  • Rebound
  • nEUROPATHIC
  • chRONIC
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16
Q

nociceptive pain def

A

IASP: Pain that arises from actual or threatened damage to non-neural tissue and i due to the activation of nociceptors

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17
Q

Neuropathic pain

A

Pain caused by a lesion or disease of the somatosensory nervous system.

Neuropathic pain is a clinical description (and not a diagnosis) which requires a demonstrable lesion or a disease that satisfies established neurological diagnostic criteria

Central neuropathic pain = Pain caused by a lesion or disease of the central somatosensory nervous system.

Peripheral neuropathic pain = Pain caused by a lesion or disease of the peripheral somatosensory nervous system.

18
Q
A
19
Q

Nociplastic Pain

A

Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.

Note: Patients can have a combination of nociceptive and nociplastic pain

20
Q

Acute vs chronic pain def

A

Acute pain implies a painful condition with a rapid onset or of a short duration.

Chronic pain is referred to as a painful condition persisting beyond the normal time of healing.

21
Q

Aspects of pain

A
22
Q

Measurement of pain

A
  • Structured pain assessment using a variety of validated measures is important in diagnosis of pain, direct treatment and evaluate it.
  • Assessment of acute pain severity is crucial for effective pain management and to reduce the risk of chronicity.
  • The multidimensional character of chronic pain requires specialized tools for elucidation of sensory components and also cognitive and psychological dimensions.
  • Specialized scales can be used in many settings as screening tools to support diagnosis of neuropathic pain, the essential first step in its treatment, and for assessment of pain at the extremes of age.
23
Q

Measurement of Acute Pain

A

Most scales used in the acute pain setting are unidimensional and are designed

for the assessment of pain intensity and degree of pain relief.

Visual analogue scale (VAS)- gold standard

Numeric rating scale (NRS) - 0-10

Categorical verbal rating scale (VRS)- describe

24
Q

Visual analogue scale - measurement acute pain

A

Visual analogue scale (VAS)

  • Considered the ‘gold standard’
  • Particularly used in pain related research
  • 100mm unmarked line with standardized wording at each end “No pain’ and ‘Worst Pain imaginable’
  • Does not give instant rating
  • Requires explanation to patient
  • Not be useful when level of understanding is impaired.
25
Q

Numerical Rating Scale (NRS) - measurement acute pain

A

Uses an 11 point scale:

0-No Pain to 10- Worst Pain

26
Q

Verbal rating scale (VRS) in acute measurmeent pain

A

Uses words to describe the magnitude of pain None, mild, moderate, severe

Quick, simple tool with high validity as a measure of pain intensity But, less precise and less sensitive than VAS
Language can be a barrier to correct administration

27
Q

Wong-Baker Faces Pain rating scale

A
28
Q

FLACC Behavioural Pain Scale

A

Patients awake: observe at least 2-5 mins, observe legs + body uncovered, reposition patient or observe activity, assess body for tenseness and tone and initiate consoling interventions if needed.

Patients asleep: Observe 5+mins, observe legs and body uncovered, if possible reposition patient, and touch the body and assess for tenseness or tone.

Assessment of Behaviour Score:

0 = Relaxed and Comfortable

1-3 = Mild Discomfort

4-6 = Moderate Pain

7-10 = Severe discomfort/pain

29
Q

Multidimensia pain scales:

A
30
Q

Screening tools of rneuropathic pain

A

Leeds Assesment of Neuropathic Signs and Symptoms (LANSS) pain scale

Doleur Neuropathique questionnaire (DN4)
PainDETECT
Neuropathic Pain Score (NPS)

All of these are used as screening tools for neuropathic pain—however, there is no conclusion which is best for clinical practice.

Pain caused by a lesion or disease of the somatosensory nervous system.

31
Q

SOCRATES for pain

A
32
Q

Types words to describe pain

A
33
Q

Treatment of Pain: Eg Postoperative pain management

A
  • Surgery is one of commonest treatment offered by NHS, over half surgery carried out on an ambulatory basis.
  • Post-op analgesia is suboptimal in more than half of patients undergoing surgery
  • Pain management should begin in the pre-assessment stage. It is important to identify patients who are likely to experience difficult pain control postoperatively.
  • Education is of crucial importance. It can reduce patient and carer anxiety, develop realisti expectations, and improve compliance with post discharge pain management.
  • Patients often do not take adequate pain medication due to lack of information or misunderstandings.
  • Need to take into account attiitudes and beliefs, and patients capacity to comply with treatments.
  • In general patients should be instructed to take regular analgesics for at least 3 days after surgery.
  • The first postoperative analgesia dose should be taken before the effects of any intraoperative analgesia have worn off.
  • Minimally invasive surgical techniques should be used where possible.
  • Regional anaesthesia techniques, or local anaesthetic infiltration have an important role.
  • Multimodal analgesia regimes should be prescribed.

*

34
Q

Treatment of Pain - Drug treatmenta (Eg psotop)

A

Drug treatments.

Wherever possible regional (peripheral or neuraxial) or local anaesthetic (infiltration) techniques,

plus:

  1. Paracetamol
  2. Nonsteroidal antiinflammatory agents (NSAIDs) 3. Opioids

‘Adjuvants’

  1. NMDA antagonists
  2. Gabapentinoids
  3. Clonidine, dexmedetomidine
  4. Dexamethasone
  5. Othera
35
Q

Opioids

A
  • Opium and its derivatives have been use for centuries.The major active ingredient of opium was discovered and named Morphine in 1799.
  • The opioid system comprises 4 types of receptors: μ- (MOP), δ- (DOP), κ-opioid and nociceptin (NOP).
  • All opioid receptors have selective endogenous peptides. Analgesia is elicited principally via MOP receptors.
  • Act both pre- and postsynaptically to produce analgesia.
  • Presynaptically they block calcium channels on nociceptive afferent nerves to inhibit release of neurotransmitters eg substance P and glutamate which contribute to nociception.
  • Postsynaptically opioids open potassium channels, which hyperpolarizes cell membranes.
  • Mu, kappa & delta opioid receptors mediate analgesia at spinal and supraspinal sites.
  • Some opioids also result in weak serotonin reuptake inhibition, or by increasing intrasy serotonin through inhibition of GABAergic presynaptic inhibitory interneurons on serotoninergic neurons (Eg Tramadol, Codeine, Oxycodone, Fentanyl).
  • Some opioids also have activity at NMDA receptors (Methadone)
36
Q

Opioid dependence

A
  • Opioids represent one class of analgesics that play an essential role in pain management.
  • However, their use has become controversial.
  • With the growth in opioid prescribing in the last two decades rising rates of morbidity and mortality associated with their use have become a topic of public health importance.
  • It has been said that the escalating number of deaths observed related to opioid prescriptions have caused a trending decline in life expectancy that has not been observed since World War I
  • There are many different definitions of persistent opioid use currently in use. This makes it difficult to define the and investigate the problem.
    Many emotive terms are use, eg: ‘opioid crisis’ and ‘opioid epidemic’
  • We have a responsibility to identify high risk patients and provide relevant multidisciplinary support to help to prevent future opioid misuse in our patients.
37
Q

NSAIDS

A

The main MOA is blockade of the production of prostaglandins
inhibition of cyclooxygenase (COX) enzymes needed for prostaglandin synthesis.

Aspirin is the only NSAID that binds irreversibly to COX, the others are reversible inhibitors. Other examples of NSAIDs include Ibuprofen, Diclofenac, Naproxen

38
Q

Congenital Insensitivity to Pain (CIP)

A

Patient lacks the ability to perceive physical pain.

  • From birth, affected individuals never feel pain in any part of their body when injured.
  • People with this condition can feel the difference between sharp and dull and hot and cold, but cannot sense, for example, that a hot drink is burning their tongue. This lack of pain awareness often leads to an accumulation of wounds, bruises, broken bones, and other health issues that may go undetected.
  • Young children with congenital insensitivity to pain may have mouth or finger wounds due to repeated self-biting, and may also experience multiple burn-related injuries.

CIP is caused by a mutation in the SCN9A gene cause.

CIP. The SCN9A gene provides instructions for making one part (the alpha subunit) of the NaV1.7 sodium channel responsible for transport sodium ions into cells (vital for signal transmission).

NaV1.7 sodium channels are found in nociceptors.
The NaV1.7 channel is also found in sensory neurons of the olfactory system.

  • These repeated injuries often lead to a reduced life expectancy in people with CIP. Many people with CIP also have a complete loss of the sense of smell (anosmia).
39
Q

Causes of CIP - Congenital insensitivity to pain

A
  • CIP is caused by a mutation in the SCN9A gene cause.
  • CIP. The SCN9A gene provides instructions for making one part (the alpha subunit) of the NaV1.7 sodium channel responsible for transport sodium ions into cells (vital for signal transmission).
  • NaV1.7 sodium channels are found in nociceptors.
  • The NaV1.7 channel is also found in sensory neurons of the olfactory system.
40
Q

Some effects of Congenital insensitivity to pain

A