What are classifications of pain?
Duration= acute/chronic Pathophysiology= neuropathic/nociceptive
What is nociceptive pain?
Describe the analgesic ladder
What is the mechanism of action for non-opioids for acute pain?
What is the mechanism of action for opioids for acute 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?
What is epidural analgesia used for?
-Postop: thoracic, abdo, lower limb surgery, labour, chronic
What are the benefits of epidural analgesia?
When is a celiac plexus block used?
- Upper abdominal neoplasia
Describe neuropathic pain
What features suggest neuropathic pain?
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?
- thinly myelinated Ad fibres
What modalities do nociceptors respond to?
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?
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?
- 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