WEEK 5 (PAIN)

• What are the pain pathways?

  1. TRANSDUCTION
  2. TRANSMISSION
  3. PERCEPTION
  4. MODULATION
• What are VISCERAL and SOMATIC pain?

  VISCERAL:

  • deep tissue
  • cramping, aching, difficult to localise
  • may radiate
  • C-FIBRES

  SOMATIC:

  • superficial
  • sharp, stabbing
  • easily localised
  • A-DELTA FIBRES
• What is the definition of PAIN?

  An unpleasant sensory and/or emotional experience caused by actual or potential tissue damage (physical + chemical)
• What are the different types of pain?

  PHYSIOLOGICAL

  • nociceptive: impulses sent to the brain to signal the presence of a stimulus that has or may cause pain.
  • inflammatory: occurs with inflammation, and promotes heightened sensory sensitivity following tissue damage

  PATHOLOGICAL

  • neuropathic: damage to the nervous system, neuronal dysfunction + abnormal firing of impulses to the brain
  • chronic: persistent pain despite resolution of initial injury, structural changes to the nervous system
• What is TRANSDUCTION?

  • nociceptors are activated by noxious stimuli
  • depolarisation of free endings of C-FIBRES + A-DELTA of primary afferent neurons
  • Mechanical, chemical or thermal
  • A-delta fibres are throughout skin (have small receptive fields + myelinated = fast and sensitive)
  • C-fibres are on organs and visceral tissues (wide receptive fields and unmyelinated = slow and not sensitive)
  • high activation threshold, needs intense stimulation to generate AP
  • membranes of nociceptors have proteins + voltage ion channels = convert energy into AP = electrical impulse
• What is TRANSMISSION?

  • movement of APs, conducted along fibres to dorsal horn

  THREE STAGES:

  1. site of transduction to the dorsal horn in the spinal cord
  2. from spinal cord to brain stem
  3. through connections between thalamus, cortex + higher levels of the brain
• What is PERCEPTION?

  • pain becomes more than a pattern of APs when it reaches the brain
  • end result of neuronal of the neuronal activity of pain transmission
  • pain becomes a conscious multidimensional experience

  1. affective (motivational)
  2. sensory (localise)
  3. emotional (upsetting, stressful)
  4. behavioural

  • multiple cortical areas
  • integration of sensations, emotions + cognition
• What is MODULATION?

  • changing the impacts of painful stimulus in the brain that aims to reduce the effects of pain through activation of inhibitory and/or excitatory processes within the CNS
  • gate control theory = noxious stimuli activates C-fibre or A-delta fibres
  • descending/ascending modulatory pathways (DMPP)= release of excitatory or inhibitory transmitters to reduce pain
• What is REFERRED PAIN?

  • perception of pain that is different location to original stimulus
  • visceral organs do not have A-delta innervation
  • C-fibres converge in the same area as nerves from peripheries = brain localises the pain at the peripheries rather than the organ
• What are the 5 ways to provide analgesia?

  1. pharmacological
  2. reassurance
  3. distraction
  4. splinting
  5. positioning
• What are the differences between MORPHINE + FENTANYL?

  MORPHINE:

  Peak effect: 15min

  Duration: 2-4hr

  Histamine: more

  Lipid solubility: less

  FENTANYL:

  Peak effect: 2-3min

  Duration: 30min

  Histamine: less

  Lipid solubility: more
• Why is it better to have less histamine release?

  Mast cells contain opiate receptors = when opiates administered it can cause the release of histamine which causes vasodilation and cause cardiac output to significantly drop
• How do opioids affect the body?

  Delta, Kappa, and Mu receptors

  BRAIN:

  • pain perception
  • emotion
  • reward
  • addiction
  • activation of descending inhibitory controls

  BRAIN STEM:

  • affect breathing = resp depression

  SPINAL CORD:

  • inhibition of neurotransmitter release from primary afferent terminals in dorsal horn

  PERIPHERAL NEURONS:

  • inhibition of neurotransmitter release

  GI TRACT:

  • inhibition of peristalsis
• What are opioid SIDE EFFECTS?

  NEUROLOGICAL:

  • sedation
  • euphoria
  • addiction
  • anxiolysis
  • miosis

  CARDIOVASCULAR:

  • bradycardia
  • vasodilation (increases PNS + histamine)

  RESP:

  • resp depression
  • apnoea (desensitised to CO2)

  GI:

  • constipation
  • nausea + vomiting

  CONTINUED USE:

  • down regulation of opioid receptors = body becomes used to new baseline = becomes tolerant

  SUPRATHERPEUTIC DOSES:

  • excessive activation of new receptors in the brain can decrease glutamate and noradrenaline release = dysregulates SNS and PNS
• What is KETAMINE?

  • inhibits NMDA receptors = slow/stop large volumes of APs in the SC and brain
  • analgesia = modulation of pain receptors occurs safely with doses <0.5mg/kg
  • has dissociative and anaesthesia purposes
• What are KETAMINE PHARMACODYNAMICS?

  • designed to give as an anaesthetic
  • stimulates increased heart and resp activity

  1. supraspinal NMDA receptor antagonist
  2. activity of delta opioid receptor
  3. augments MU receptor functions
  4. stimulates catecholamine = increases CO
• What are the adverse effects of KETAMINE?

  • hallucinations
  • anxiety
  • dizzy
  • nausea
  • vomiting