Lec: pain Flashcards
Define pain
Pain: unpleasant sensory + emotional experience associated with tissue damage
What is the purpose of pain?
Allow wound repairing + recoveryTAB
What are the negative impacts of pain on cardiovascular system?
Increased HR, BP, risk of ischaemic heart disease
How does pain adversely affect the central nervous system?
Increase risk of anxiety, depression, sleep impairments
Does pain stimulate cough?
No, pain inhibits cough and promotes hyperventilation
Can pain cause any GI symptoms?
Nausea and vomiting
Can pain cause any genitourinary symptoms?
Urinary retention and uterine inhibition
How does pain adversely affect the musculoskeletal system?
Muscle restlessness, immobility (increased risk of deep vein thrombosis)
Is pain a catabolic or anabolic process?
Catabolic stress response: increased cortisone, glucagon, growth hormone, catecholamines; reduced anabolism (insulin, testosterone); reduced plasminogen (increase risk of coagulation - DVT)
Define nociception
The mechanism of detecting presence of noxious stimuli (mechanical, chemical, thermal)
What are the 4 processes of nociception?
Transduction - transmission - modulation - perception
Explain transduction of nociceptive pathway.
Noxious stimuli damage tissue, this is converted/transduced into an electrical signal by a peripheral nociceptor found in skin, muscle, bone, internal organs, vessels, not the brain.
Nociceptive pain is sensed and transmitted by 2 types of nerve fibres. Compare and contrast these 2 fibres.
Ad: myelinated, fast conduction velocity, high threshold of activation (higher than Ab, lower than C), respond to mechanical + thermal stimuli (cold), responsible for localised, sharp, primary pain, reflex withdrawal; not abolished by morphine.
C: unmyelinated, slow conduction velocity, high threshold of activation, respond to all three stimuli (heat), responsible for dull, throbbing, diffuse, prolonged pain, produce spasm; abolished by morphine
Describe the second process in the nociceptive pathway.
Impulses travel along axons of Ad + C fibres toward spinal cord. In the spinal cord, they synapse differently.
- Ad fibres
i. Ad fibres enter dorsal horn and synapse in lamina I
ii. neurons from lamina I cross midline via ventral white commissure
iii. these neurons enter the contralateral side and go up the cord in spinothalamic tract to thalamus
iv. in the thalamus, they synapse in ventroposterolateral nucleus.
v. from thalamus, they travel to somatosensory cortex, where pain is identified. - C fibres
i. C fibres enter dorsal horn and ascend in Lissauer’s tract to 1-2 spinal segment above level of entry.
ii. C fibres synapse on the interneurons (excitatory: glutamate, inhibitory: GABA, glycine) in lamina II
iii. the interneuron travel down to lamina V
iv. from lamina V, fibres decussate and ascend up spinoreticular tract
v. fibres synapse in reticular formation of medulla, nucleus raphe and locus coeruleus
vi. finally these fibres synapse in thalamus and cingulate cortex.
All these connections activate descending analgesic pathway
What is the purpose of modulation in nociceptive pathway?
Once pain has been sensed and danger averted, pain sensation needs to be depressed to allow normal, painless tissue repairing
Where are the 2 sites of modulation?
- Periphery: gate-control theory
2. Brain/brainstem: top-down/conditioned pain modulation/descending analgesic pathway
Describe the gate-control theory.
occurs when 1st order neurons synapse with 2nd order neurons in dorsal horn
- in the absence of input from C fibres, tonically active inhibitory interneuron suppresses pathway of pain
- with strong pain, C fibres stops the inhibitory pathway, allowing strong signal to be sent to brain
- touch/non-painful stimuli through Ab fibres can stimulate inhibitory interneuron, reducing painful stimuli
Gate-controlled theory is when Ab fibres control the transmission of pain in dorsal horn. This forms the basis of TENS (Transcutaneous Electrical Nerve Stimulation)
Draw a flow-chart explaining the mechanism of top-down regulation/descending analgesic pathway.
Amygdala + thalamus => activate PAG of midbrain, which activate locus coerulus and nucleus raphe.
- locus coerulus inhibit pain with NorA
- nucleus raphe inhibit pain with 5-HT and endogenous opioid enkephalin
Name 3 excitatory neuropeptides and outline its functions
Glutamate, aspartate, substance P; facilitate + amplify pain in ascending spinothalamic tract
Outline the last step in nociceptive pathway.
Perception: cerebral cortical response to nociceptive signals
What is chronic pain hypersentivity?
A hallmark feature of chronic pain, a result of altered nervous system response at central and peripheral locations.
Define hyperalgesia.
Enhanced pain result from tissue damage and release of endogenous chemicals, which either activate nociceptors directly or sensitise nociceptors and reduce their threshold.
Define allodynia.
Pain from a stimulus that is not normally painful.
Is primary hyperalgesia (at site of injury) peripheral or central sensitisation?
Peripheral sensitisation
Explain peripheral sensitisation/primary hyperalgesia.
Tissue inflammation release mediators that either activate (K+, 5-HT, H+, ATP, bradykinin, histamine, adenosine) nociceptors or sensitise (PG, NO, ROS, CGRP,leukotrienes, substance P, noradrenaline) nociceptors by reducing nociceptor threshold
Explain central sensitisation/secondary hyperalgesia
Increase in excitability of neurons, mediated by activation of NMDA receptors in dorsal horn neurons. characterised by expanded receptor field and painful responses to normally innocuous stimuli (Ab).
Reduction in inhibitory interneuron GABA and glycine
Reduction in CPM (Conditioned Pain Modulation) NorA and 5-HT
Briefly outline the classification of pain
- Acute vs Chronic (>3mth)
- Cancer vs non-cancerous
- Nociceptive (tissue damage) vs neuropathic (nerve damage)
Compare and contrast two types of nociceptive pain
Somatic (skin, muscles, bones): localised, dermatomal radiation, sharp, aching pain, constant or incidental, rarely associated symptoms
Visceral (internal organs): vaguely distributed, diffused radiation, dull, cramp pain, periodic, associated with nausea, sweating, HR and BP
Give three causes of neuropathic pain.
Diabetic neuropathy
Post-stroke/surgical pain
Lumbar radicular pain
describe as shooting, burning, tingling, numbness
List the possible sources of lower back pain (5)
disc: bulge, rupture;
vertebrae: OA, lumbar instability
joint: facet joint, sacroiliac joint
muscle: paravertebral muscle, gluteal muscle
ligament: ant. and post. longitudinal ligament laxity
Herniation of disc/lumbar radicular pain can compress nerve roots. Is this neuropathic or nociceptive pain?
Both. compression of nerve root activate peripheral nociceptors (nociceptive pain) and inflame nerve roots (neuropathic pain).
Thus a combo of constant ache, throbbing pain and shooting, burning pain.
Describe the assessment of pain -brief pain inventory.
pain severity + functional impairment assessed
Describe pain treatment (6Ps)
- Preventatives: back exercise, good care, acute pain control
- Pathology: treat underlying problems
- Physical therapies: maintain activity, physio, TENS
- Pharmacology: paracetamol/NSAIDs; codine/dihydrocodeine/dextropropoxyphene; tramadol; morphine (oxycodone, fentanyl, methadone)
NSAID bad for GI, renal, asthma, bone healing and bleeding; paracetamol bad for hepatic
codeine metabolised to morphine by CYP2D6, can be genetic variant, deficiency + codeine use lead to respiratory depression - Procedural: regional analgesia
- Psychological: education, distraction
Give 2 examples of the neuropathic analgesic adjuvants.
Anti-depressants: amitriptyline
Anti-convulsants: gabapentin
Anti-arrhythmias: lidocaine
Name the 4Ps yellow flags of pain
Progressive pathology
Passive: believe pain and activity are harmful; sickness behaviour; overprotective family; lack of support
dePression
Problems: social withdrawal, work problem, financial problem, legal compensations
Non-specific lower back pain is common due to trauma or work-related physical exertion; it is characterised by tension, pain and stiffness. It is often self-limiting. When certain reg flag symptoms show up, doctors might suspect serious spinal diseases including malignancy, fx, sacroillitis. What are these red flags?
Weight loss, fever, PMH, anatomical changes, history of trauma, cauda equina syndrome, <20yr, >50yr old, persistent pain + serious cause, worse at certain times, saddle anaesthesia, urinary incontinence
