Analgesia & Anaesthesia

Question 1

What are the pathways of pain?

Answer 1

• Spinothalamic tracts
• Lateral= pain and temperature
• Tested with neuro tip

Question 2

Describe the neurobiology of pain/ destination of lateral spinothalamic C fibers

Answer 2

1. Reticular Activating System (spinoreticular fibers, 85%, arousal- wake up)
2. Superior Colliculi (spinorectal fibers, orientating response= controlling eye movements, look at where pain is coming from)
3. Hypothalamus (spinohypothalamic fibers, autonomic response, fight or flight)
4. Thalamus, Insula, Angular Cingulate Cortex, (somatotopic map of visceral organs) PFC (interoceptive cognitive model)
5. PB, Amygdala (emotional response- motivational in limbic system)
6. Thalamus, S1, S2 (localisation)

Question 3

How is pain processed in the cerebellum?

Answer 3

PAG (periaqueductal grey)– THE VOLUME KNOB

5HT (serotonin) release
5HT travels in CSF downwards and triggers endogenous opioid release in dorsal horn spinal cord interneurons

Endogenous opioids reduce incoming pain pathway activity via opioid receptors (mu, kappa, delta)

starts to fail in motion controls when overloaded with sensory information e.g. Shaking during pain or loss of fine motor skills with chronic pain

Question 4

What are the peripheral sources of pain?

Answer 4

Tissue Damage, typically acute

Inflammatory cascade mediators (Prostanoids, Arachidonic acid)

Question 5

How do we treat peripheral pain?

Answer 5

‘simple analgesia’ – paracetamol

NSAIDs & Aspirin

Opioids

Question 6

What are the sources of central pain?

Answer 6

• Chronic/ neurogenic= centralisation (volume up all the time)
• Psychic pain

Question 7

What are the treatments of central pain?

Answer 7

Neuropathic pain agents
Anticonvulsants / TCAs
SSRIs
Opioids

CBT
Mindfulness / Meditation
Yoga, Physical therapy

Question 8

What are the types of anaesthesia?

Answer 8

• General= whole body loss of consciousness, movement and pain
• Local= specific targets

Question 9

What are the stages of general anaesthetics?

Answer 9

-Induction= period of consciousness to unconsciousness
-Excitement= depression of inhibitory neurones in CNS= involuntary movement, increase in heart rate, blood pressure and respiratory rate
=Surgical anaesthetic, gradual loss of muscle tone and reflexia, regular breathing
=Medullary paralysis/ overdose, cardiac and respiratory failure

Question 10

Mechanism of action at macroscopic level for General

Answer 10

• Thalamus and RAS =reversible loss of consciousness
• Hippocampus, amygdala and PFC= amnesia
• Spinal cord= immobility and analgesia

Question 11

Groups of General Anaesthetics based on relative abilities to produce analgesia, loss of consciousness and immobility

Answer 11

-Intravenous= Etomidate, Propofol, barbiturates
=Unconsciousness better than immobility or analgesia so induction phase, GABA(A) receptors
-IV ketamine and inhalation Nitrous oxide, xenon and cyclopropane
=Significant analgesia, maintenance phase, selectively inhibit NMDA receptors in spinal cord, 2-pore-domain K+ channel opening
-Halogenated volatile= halothane, enflurane, isoflurane, sevoflurane, desflurane
=immobility, unconsciousness by GABA different to group 1, 2-pore-domain K+ channel, NDMA inhibitors

Question 12

What are the side effects of Group 1 drugs?

Answer 12

• Etomidate= adrenal suppressant, transient skeletal muscle movement
• Propofol= respiratory depression and hypotension
• Barbiturates= apnoea, respiratory depression, cough, bronchospasms

Question 13

What are the side effects of Group 2 drugs?

Answer 13

• Ketamine= hypertension, tachycardia, hypersalivation, emergence phenomena (delirium, hallucination)
• Nitrous Oxide and cyclopropane= dizziness, nausea, vomiting
• Xenon= no significant side effects

Question 14

What are the side effects of Group 3 drugs?

Answer 14

Dose dependent reduction in blood pressure and cardiac output

• Halothane= cardiac arrhythmias, hepatic toxicity
• Sevoflurane= renal toxicity

Question 15

What drug does not fit these Groups?

Answer 15

Dexmedetomidine

• No respiratory depression
• Presynaptic alpha 2 adrenergic receptors sub type 2A
• Inhibits release norepinephrine, terminating propagation of pain signals and light sedation

Question 16

What are the side effects of Dexmedetomidine?

Answer 16

• Bradycardia
• Hypotension
• Transient hypertension due to weak peripheral alpha 1 receptor agonist activity

Question 17

How do local anaesthetics work?

Answer 17

• Transient loss of sensory perception without unconsciousness
• Pass through neuronal membrane, bind to receptor at voltage gated sodium channel to prevent sodium influx to stop initiation of AP

Question 18

Examples of local anaesthetics

Answer 18

Bupivacaine
Lidocaine
Mepivacaine
Procaine
Ropivacaine
Tetracaine

Question 19

What are the side effects of local anaesthetics?

Answer 19

Blurry vision, light-headedness

Cardiac arrhythmias and seizures

Question 20

Describe periaqueductal grey matter

Answer 20

• Collection of grey matter that sits around the brainstem around the cerebral aqueduct
• ‘Volume dial’ with regards to pain perception - controls how much information is coming in - tolerance control
• Cells release 5HT (serotonin)
• 5HT diffuses in CSF down towards spinal cord where it interacts with dorsal horn spinal cord interneurons - which release endogenous opioids
• Endogenous opioids reduce incoming pain pathway activity via opioid receptors (mu, kappa, delta)