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What is the definition of pain?

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It is important to note that pain has 2 components a peripheral (i.e. sensory) and a central (i.e. emotional) one. Therefore you cannot be in pain when unconscious, but you may still be able to respond to noxious stimuli.


What is chronic pain?

This is pain persisting beyond 6 months duration or beyond the time for normal tissue healing.


What neuronal pathway transmits painful stimuli?

Spinothalamic tract - decussates at the level it enters before ascending to the thalamus.


Describe the pain pathway?

Pain is transmitted by the spinothalamic tract. First order nociceptive neurones have there cell bodies in the DRG and make synaptic connections in Rexed layer I. Axons from layer I decussate in the anterior white commissure, at roughly the same (if not within 1 or 2) spinal levels that they enter. From here they ascend in the lateral spinothalamic tract to the ventroposterolateral (VPL) nucleus and ventroposteroinferior (VPI) nucleus of the thalamus. These serve as a relay station for third order neurones to the primary somatosensory cortex.


What are the types of somatosensory pain transmitting neurones?

- A delta fibres: mechanoreceptors and nociceptors
- C fibres (unmyelinated): mechanoreceptors and nociceptors
- B fibres: sympathetic preganglionic fibres
- A beta fibres: cutaneous touch and pressure


Do A beta fibres normally respond to pain?

No. A beta fibres only respond to noxious stimuli under abnormal conditions. They are also more resistant to local anaesthetic blockade than A delta or C fibres. This explains how patients under spinal or epidural anaesthesia may sense touch and movement but not pain and temperature.


Which somatosensory fibres are most sensitive to local anaesthetics?

C fibres are more easily blocked by local anaesthetics, so it is possible to remove the sensation of pain (and temperature) leaving light touch/ movement intact.


What is somatic pain?

Somatic pain can be classified as i) cutaneous, superficial or peripheral pain, or ii) deep pain.

Cutaneous/ superficial/ peripheral pain is well localised and has 2 components. A first pain that is transmitted by fast myelinated A delta fibres, and has a sharp pricking quality. This is followed by second pain, which is transmitted by unmyelinated C fibres that has a burning sore quality due to tissue damage.

Deep pain may be poorly localised and may be diffuse.


How is visceral pain transmitted?

Visceral pain (i.e. pain from organs) is poorly localised and often referred surface areas innervated by the same spinal segment (e.g. diaphragmatic pain --> shoulder tip). Visceral pain is typically transmitted by visceral afferent fibres that travel with autonomic nerves to the CNS.


What is the difference between acute and chronic pain transmission?

Acute pain is transmitted via glutamate acting at NMDA and AMPA receptors.

Chronic pain acts via substance P and other mediators (e.g. NO) which affects gene regulation.


What is the gate control theory of pain?

The gate control theory of pain states that incoming nociceptive stimuli entering the dorsal horn of the spinal cord can be modulated by the activity of an interneurone. This inhibitory interneurone is activated by non-nociceptive signals from A delta or A beta fibres. These signals are carried by the dorsal column medial lemniscus pathway and so interrupt ascending pain transmission.

TENS machines make use of this principle.


What is the maximum dose of an NSAIDs that patients can receive?

Ibuprofen = 400mg PO, QDS
Diclofenac = 50mg PO, 8 hourly

Note that ibuprofen and diclofenac cannot be administered IV.

They are contraindicated in patients with:
- peptic ulceration
- bronchospasm (esp. aspirin)
- renal failure*

NSAIDs can cause renal failure particularly if the patient is hypotensive because prostaglandins preserve afferent arteriolar blood flow during hypotension (when renal perfusion pressure decreases).


What are opioids?

Opioids are defined as compounds with effects that are antagonised by naloxone. There are both endogenous opioids (endorphins, dynorphins and enkephalins) and synthetic opioid analgesics.

Opioid analgesics are drugs that mimic endogenous opioid peptides by causing prolonged activation of opioid receptors (usually mu receptors).


Where are endogenous opioids produced and how do they work?

Primary afferent nociceptive fibres synapse in lamina I and II of the dorsal horn of the spinal cord. Second order neurones transmit pain information to the somatosensory cortex via the thalamus.

The activity of second order neurones is modulated by inhibitory inputs. These include local interneurones which release opioid peptides (mainly dynorphin) and descending enkephalinergic, noradrenergic and serotonergic fibres which originate in the brainstem and are themselves activated by opioid peptides.

Opioids released by the PAG activates the nucleus raphe magnus. This in turn activates enkephalingeric and serotonergic outflow from this nucleus. Noradrenergic release comes from the locus coeruleus.


What are "weak opioids"?

Weak opioid analgesics are used in mild to moderate pain. They may cause dependence and are subject to abuse.

Examples are codeine, and dihydrocodeine.
Codeine (methylmorphine) is well absorbed orally but has very low affinity for opioid receptors. About 10% of the drug is demethylated in the liver to morphine which is responsible for the analgesic effect. Side effects (vomiting, constipation, sedation) limit the possible safe dosage to levels that produce much less analgesia than morphine.


What is the maximum daily dosage of dihydrocodeine?

30mg PO, PRN 4-6 hourly (max 120mg) or QDS

Dihydrocodeine and codeine are equipotent when given orally - when dihydrocodeine is given by injection it is twice as potent as codeine.


What is the WHO analgesic ladder?

This is a stepwise approach to administering analgesia.
Step 1 = non opioid - e.g. paracetamol, NSAIDs
Step 2 = weak opioid - e.g. codeine for mild to moderate pain + non opioid
Step 3 = strong opioid - e.g. morphine + non opioid

Note that adjuvants (e.g. anticonvulsants and antidepressants) can be given at any stage if required


What are the side effects of opioid analgesics?

The side effects of opioid analgesics can be divided into central and peripheral effects.

Central effects:
- analgesia
- euphoria
- sedation
- respiratory depression
- depression of vasomotor centre (causing postural hypotension)
- miosis because of 3rd nerve nucleus stimulation (except pethidine, which has a weak atropine like activity)
- nausea and vomiting (due to CTZ activation)
- cough suppression

Peripheral effects:
- constipation
- biliary spasm
- constriction of the sphincter of Oddi
- histamine release, vasodilation and itching (morphine only)


How is morphine metabolised?

Morphine is metabolised in the liver by conjugation with glucaronic acid to form morphine-3-glucuronide, which is inactive, and morphine-6-glucuronide, which is a more potent analgesic than morphine itself.


What is the maximum daily dose of morphine?

This somewhat depends on the formulation.
- Morphine sulphate oral solution (Oramorph) 10mg/5ml can be given 5-10ml PO, PRN 2 hourly

- Morphine - 10mg IV/IM/ S, PRN 4 hourly (max 60mg)

The dosing interval in both of these needs to be reduced in renal impairment.


What is diamorphine?

Diamorphine (heroin, diacetylmorphine) is more lipid soluble than morphine and therefore has a more rapid onset of action when given by injection. The higher peak levels result in more sedation than that caused by morphine.


What is methadone and when is it used?

Methadone has a long duration of action and is less sedating than morphine. It is used orally for maintenance treatment of heroin or morphine addicts.


What is pethidine? What does it interact with?

Pethidine is another strong opioid analgesic. It has a rapid onset of action but its short half life makes it unsuitable for the control of prolonged pain. Pethidine is metabolised by the liver and at high doses, a toxic metabolite can accumulate and cause convulsions. Pethidine interacts seriously with MAOIs causing delirium, hyperpyrexia, and convulsions or respiratory depression.


What is buprenorphine?

Buprenorphine is a partial agonist at mu receptors. It has a slow onset of action, but is an effective analgesic following sublingual administration. It has a much longer duration of action than morphine, but may cause prolonged vomiting. Respiratory depression is rare, but if it occurs it is difficult to reverse with naloxone because buprenorphine dissociates very slowly from receptors.


When are fentanyl, alfentanil and remifentanil used? How are they metabolised?

These are all potent, highly lipid soluble rapidly acting mu opioid receptor agonists. They are given IV to provide analgesia during maintenance anaesthesia.

Low doses of fentanyl and alfentanil are short acting due to rapid redistribution, but higher doses saturate the tissues and their actions are more prolonged.

Fentanyl and alfentanil are metabolised by the liver, but remifentanil is metabolised by tissue and blood esterases and has a constant half life even after prolonged infusion.

Fentanyl can be given as transdermal patches, especially if oral opioids cause intolerable nausea and vomiting.


What is Tramadol? Outline its mechanism of action?

Tramadol is a strong opioid (note than some sources will quote it as a weak opioid). It acts centrally at opioid receptors but also has non opioid properties as well. These include serotonin release, and inhibition of synaptic reuptake of serotonin and noradrenaline.

Tramadol should be used with caution in patients with epilepsy.


What is the maximum daily dose of tramadol?

50-100mg PO, PRN 4-6 hourly (max 400mg) or QDS.


What are co-analgesics and when are they used?

Co-analgesics are combined oral preparations of paracetamol + weak opioid. They have improved efficacy over each individual component alone and can improve compliance in patients who require analgesia at step 2 (weak opioid + non opioid).

- Co-dydramol = dihydrocodeine 10, 20 or 30mg in combination with paracetamol 500mg
- Co-codamol = codeine 8, 15 or 30mg in combination with paracetamol 500mg
- Co-proxamol = dextropropoxyphene in combination with paracetamol (**NO longer licensed in the UK**)


What is the maximum daily dose of co-codamol?

30/500 = 1-2 tablets PO, PRN 4-6 hourly (max 8 tablets)

It is important to remind the patient that they should not take any more paracetamol if taking co-codamol. The maximum safe paracetamol daily dose is 4g in 24 hours.