Pain Flashcards
What are classifications of pain?
Duration= acute/chronic Pathophysiology= neuropathic/nociceptive
What is nociceptive pain?
- Regulated by opioidergic system -Acute nociceptive pain subsides when damage resolves
- Chronic pain persists may lead to neuropathic/mixed pain
Describe the analgesic ladder
- Non-opioid (NSAIDs, aspirin)
- Opioid for mild-moderate pain & non-opioid (Codeine, tramadol)
- Opioid for moderate-severe pain & non-opioid, freedom from cancer pain (morphine, methadone)
What is the mechanism of action for non-opioids for acute pain?
- NSAIDs/COX-2 inhibitors act peripherally
- Paracetamol has central activity
- Efficacy in acute pain management & control of nociceptive pain
What is the mechanism of action for opioids for acute pain?
- Activate endogenous analgesic system
- Stimulate receptors in limbic system to eliminate pain
- Affects descending pathway modulating pain perception
- Acts at 2 sites
- Presynaptically pain signal transmission is inhibited
- Postsynaptic membrane hyperpolarised, decreasing the probability of ap generation
- Main efficacy in nociceptive pain
What is the mode of action and any side effects for NSAIDs?
MA= inhibition of cyclooxygenase, prostaglandin synthesis decreases -SE= GI irritation/bleeding, renal toxicity, drug interactions, CV effects
What is the mode of action and any side effects for paracetamol?
MA= Inhibition of central prostaglandin synthesis SE= risk of toxic liver damage
What are side effects of opioids?
- Nausea
- Vomiting
- Constipation
- Dizziness/vertigo
- Somnolence
- Dry skin/pruritus
- Respiratory depression & hypoxia
What is epidural analgesia used for?
-Postop: thoracic, abdo, lower limb surgery, labour, chronic
What are the benefits of epidural analgesia?
- High quality pain relief
- Improved pulmonary function
- Reduced sepsis & chest infection
- Reduced cardiac morbidity
- Reduced vascular graft failure
- Reduced incidence of DVT
When is a celiac plexus block used?
- Pancreatic carcinoma
- Upper abdominal neoplasia
Describe neuropathic pain
- Spont pain &hypersensitivity associated with damage/lesion of NS
- Intense pain accompanied b other pain phenomena
- Persistent & recurrent
- Associated with severe comorbidity & poor QOL
- post herpetic neuralgia, pain after CVA, post-op, painful diabetic neuropathy, trigeminal neuralgia
What features suggest neuropathic pain?
- Pain different from everyday pain
- Pain in area of sensory loss
- Paroxysmal/spontaneous pain
- Allodynia (pain from non painful stimuli)
- Hyperalgesia (inc pain in response to painful stimuli)
- Dysaesthesias (unpleasant abnormal sensations)
What drug therapy is there for neuropathic pain?
-NSAIDs
-Antidepressants
-Anticonvulsants
-Opioids
-Membrane stabilising drugs
Topical drugs
What is the mechanism of action and side effects of antidepressants?
MA= Inhibition of neuronal reuptake of noradrenaline & serotonin SE= Dry mouth, insomnia, inc appetite, constipation, abnormal heart rate/rhythm, somnolence
What is the mechanism of action and side effects of anticonvulsants?
MA= Gabapentin: binds to presynaptic voltage-dependent Ca channels, pregabalin: interacts with special N-type Ca channels, Carbamazepine: blocks Na+, Ca2+ channels SE= sedation, dizziness, ataxia, nausea, weight gain, peripheral oedema
What are the types of nociceptors?
- Unmyelinated C fibres
- thinly myelinated Ad fibres
What modalities do nociceptors respond to?
- Mechanical
- Thermal
- Chemical (histamine)
What neurotransmitter is released by pain afferents?
Glutamate
Neurons in the dorsal horn express what neuropeptide?
Substance P receptor (NK1) and project to the thalamus
What can hyperalgesia be?
- Spontaneous pain
- Reduced threshold for pain
- Increased intensity of painful stimuli
Describe first & second pain
1st=Fast, A-delta fibres, sharp/ pricking, rapid, easily localised, short time, mechanical/thermal
2nd=Slow, C-fibres, dull ache/ burning, poorly localised, persistent, polymodal, slow onset
Where are nociceptors found?
- Periphery as free nerve endings
- Branched, unmyelinated in dermis
How does hyperalgesia occur?
1) Tissue damage/inflammation
2) Release of prostaglandins, bradykinin, histamine
3) Sensitize peripheral nociceptors that express heterogenous receptors/ion channels
4) Transmission of impulses via A-delta & C sensory afferents to dorsal horn
5) Projection to brain via ascending pathways
6) Experience sensory/emotional hyperalgesia
Give the sub modality, position and fibre type of thermoreceptive & nociceptive afferents
- Warm= C, deep epidermis
- Cold=A-delta, deep epidermis
- Nociceptive= either C or A-delt, superficial epidermis
Where do nociceptive fibres have their cell bodies?
- Dorsal root ganglion
- Travel up/down in zone of lissauer
- Innervates substantia gelatinosa
Describe the components of the ascending pain pathway
- Lateral spinothalamic tract
- Spinoreticulothalamic tract
- Anterior spinothalamic tract (to RF and periaqueductal grey matter)
- Contralateral pathway at the level of the spinal cord
What occurs in a unilateral spinal cord injury/lesion?
- Brown sequard syndrome
- Dissociated sensory loss
- Loss of pain on opposite side
- Loss of sensory on the same side
What does the VPM & VPL of the thalamus innervate?
VPM= face VPL= rest of body
