Pain Management Flashcards
What is Pain?
unpleasant, uncomfortable sensation that usually indicates tissue damage
• Primarily a protective mechanism - allows us to have an awareness of tissue damage and takes steps to correct it
• Most common symptom prompting people to seek healthcare
• Memory of pain can help us avoid potentially harmful events in the future - triggers behavioural and emotional reactions influenced by past or present experience
*Ineffective pain management may greatly impair quality of life and ability to perform activities of daily living
All sensations result from the same sequence of events (5)
All sensations result from the same sequence of events:
1. stimulus 2. detection of stimulus 3. generation of receptor and action potential 4. neurons carry a signal to the brain 5. brain integrates the signal into conscious perception
Loeser Pain Model
Nociception: Stimuli that act on peripheral pain receptors to give activity in nerve fibres
Pain: Perception of the sensation of pain
Suffering: The negative emotional response generated in the higher nervous system
Pain Behaviour: Verbal/nonverbal expressions that convey to the outside world that the patient is in pain
Types of nociceptors
- Mechanical receptors: respond to mechanical damage such as cutting, crushing or pinching
- Thermal receptors: respond to extreme temperatures, especially heat
- Polymodal receptors: respond to all kinds of damaging stimuli including chemicals released from injured tissue
2 afferent pain perception pathways
- Myelinated delta fibres (fast pain pathway)
- Unmyelinated C fibres (slow pain pathway)
- Mechanical and Thermoreceptors: Fast and slow afferent fibres; transmitted over myelinated delta fibres (30 m/sec, fast) for acute localised pain
- Polymodal Nociceptors: carried by unmyelinated C fibres (12 m/sec, slow) for slow-burning pain
Transduction process and higher level processing of pain
Transduction Process:
• Pain impulses conducted to the SC via the dorsal root (1st order neurons) => synapse with interneurons (2nd order neurons)
• @ Dorsal horn (central terminalis) of SC, nociceptive fibres release substance P and glutamate that activate spinothalamic neurons - transmit impulses to the thalamus
Higher-level Processing of Pain: NT involvement of substance P and glutamate
• Substance P: activates ascending pathways transmitting signals to higher brain levels for processing
*Different brain regions process different aspects of the painful experience:
• Thalamus: identifies the perception of pain
• Somatosensory cortex: localises the pain
• Reticular formation: increases the level of alertness and the hypothalamus
• Limbic system: augments behavioural and emotional responses
• Glutamate: principal excitatory NT acting on the dorsal horn; permeability change = permits Ca2+ entry into the dorsal horn = AP generation = increase neuron excitability = transmission of pain messages; Results in hyperexcitability and exaggerated sensitivity of an injured part *Descending analgesic pathway – Inhibition of pain transmission
CNS contains a built-in pain suppressing system: ——— in the midbrain and the ———– (involved in descending inhibitory modulation):
- Stimulation of these centres = release of the ------- ------ from the descending pathway = bind with opiate receptors at the synaptic knob of the afferent pathway pain fibre = inhibits release of --------- -- = block pain signal - Morphine binds to the same opiate receptor’s analgesic properties
CNS contains a built-in pain suppressing system: periaqueductal grey (PAG) in the midbrain and the rostral ventromedial medulla (RVM) (involved in descending inhibitory modulation):
- Stimulation of these centres = release of the endogenous opiates from the descending pathway = bind with opiate receptors at the synaptic knob of the afferent pathway pain fibre = inhibits release of substance P = block pain signal - Morphine binds to the same opiate receptor’s analgesic properties
What are the 3 types of pain? Explain each of them
· Acute Pain: pain of recent onset and probable limited duration; usually has an identifiable temporal and causal relationship to injury or disease
· Chronic Pain: persistent or recurring pain that continues for a long time; serves no purpose and causes suffering; commonly persists beyond the time of healing of an injury, and frequently there may not be any clearly identifiable cause
- Often appears out of proportion to any observable injury
- Involves a permanently sensitised dorsal horn leading to hyperalgesia, a poor/impaired descending pathway or exaggerated afferent pain impulse
- Risk factors: genetics, psychosocial status, past pain experience, culture, personal belief, life stressors
*Approximately one in five (~20%) Australians suffer from chronic pain
· Neuropathic Pain: damage, injury or dysfunction of nerves due to trauma, surgery, disease or chemotherapy
- Described as burning, painful, cold or electric shocks and may be associated with tingling, pins and needles, numbness or itching
How does endogenous analgesia work?
CNS has its own system for relieving pain: suppresses pain signal from peripheral nerves = opioid peptides (endorphins, enkephalins, dynorphins) interact with opioid receptors = inhibits perception of pain signals
What is the “Gate Control Theory of Pain”?
· Interneuronal connections (pain and sensory pathways) passing through the neural gate in the SC
· Simultaneous firing of the 2 pathways “closes the gate” on pain transmission = perception of touch only = suggests that non-painful input closes the “gates” to painful input travelling to the CNS
· Provided a basis for various methods - massage, heat pack, rubbing, buzzy bee, acupuncture
Pain management (3)
· Analgesia: multimodal approach that incorporates NSAIDs, paracetamol, baclofen and/or anxiolytics in conjunction with opioids = effective and reduces risk for opioid adverse effects
· Pre-emptive analgesia: multimodal approach prior to incision reduces pain relief requirements postoperatively
· Peripheral nerve block: continuous analgesia with LA
What is the WHO analgesic ladder (3 concepts)?
- ‘By mouth’ – injections not necessarily better
- ‘By the clock’ – respect pharmacokinetics – steady-state level
- ‘By the ladder’ – three classes (NSAIDs, paracetamol, opioids)
What is the 3 step -step analgesic protocol based on intensity as a guideline for treating pain (opioids and non-opioids)?
- Mild Pain: non-opioid analgesic may be prescribed; if necessary, an adjuvant agent may be used to promote the pain-relieving effect
- Moderate Pain: weak opioids (codeine tramadol) with/out non-opioid analgesics and with/out adjuvants
- Severe and Persistent Pain: potent opioids (morphine, methadone, fentanyl, oxycodone, oxymorphone) with/out non-opioid analgesics and with/out adjuvants (muscle relaxants, antidepressants, anti-epileptic, Botox)
*Nonopioid analgesics are drugs that relieve pain without causing the loss of consciousness and are used for acute, chronic pain and neuropathic or bone pain
What are some non-pharmacological treatments to pain?
Can address both physical and psychological factors; RICE for injuries, massage, physiotherapy, psychological counselling, education and reassurance
What are some non-opioid analgesics?
relieve pain by mechanisms largely or completely unrelated to opioid receptors; do not cause respiratory depression, physical dependence, or abuse
• Aspirin (non-selective NSAID; analgesic, antipyretic, anti-inflammatory and antiplatelet drug)
- Prevents synthesis of prostaglandins by non-competitively inhibiting both forms of cyclo-oxygenase (COX) 1 and COX‑2
- Common adverse effects: dyspepsia, vomiting, GI ulceration or bleeding, asymptomatic blood loss, increased bleeding time, headache, dizziness and tinnitus (common with high doses)
• Paracetamol: analgesic effect is not fully determined
- May be related to inhibition of central prostaglandin synthesis and modulation of inhibitory descending serotonergic pathways
- Common adverse effect: hepatotoxicity
