Pain management Flashcards
What is acute pain?
Acute pain has a recent onset and generally occurs as a result of an event e.g. surgery, sickle cell crisis, trauma.
In acute pain, symptoms tend to decrease over time.
What is chronic pain?
Chronic pain can develop over a period of time and lasts longer than 3 months. Includes neuropathic pain and may or may not have a specific cause.
In chronic pain, symptoms tend to worsen with time.
We need to try and prevent acute pain from becoming chronic.
What is nociceptive pain?
Stimulation of nociceptors which are sensory receptors found on nerve fibres that transmit the pain stimulus to the spinal cord and brain.
Many different neurotransmitters are involved in transmission of the pain signal including GABA, noradrenaline and serotonin.
Somatic pain occurs when there is activation of pain receptors in muscles, bones and skin.
Visceral pain occurs when internal organs become injured or inflamed.
Usually more of an ache in a vague location.
Acute pain is generally nociceptive in origin and has a recent onset in the order of hours to days.
What is neuropathic pain?
Occurs as a result of damage to neural tissue such as nerve dysfunction, compression or injury and includes:
Phantom limb pain. Neuropathy. Trauma. Central pain – linked to stroke or spinal cord injury. Neuralgia.
Presents with symptoms including:
Tingling.
Burning.
Hypersensitivity to touch.
Muscle weakness.
Specific types of neuropathic pain include:
Allodynia – pain caused by a stimulus that wouldn’t usually cause pain.
Hyperalgesia – severe pain from a stimulus that would normally only cause slight pain.
Paresthesia – pain in the absence of a stimulus experienced as painful ‘pins and needles’ or electric shock sensations.
How can back pain be treated?
Most commonly it is acute and can be managed with NSAIDs with or without a weak opioid along with an attempt to maintain physical activity.
If it becomes chronic it is much more difficult to manage and becomes associated with co-morbidities such as depression, anxiety and disability.
Why is paracetamol used for pain management?
Mechanism of action still not completely understood but does inhibit prostaglandin synthesis in the CNS.
Regular paracetamol 4g daily is a good basis for pain management.
It is analgesic and antipyretic but not anti-inflammatory.
Combination preparations with low dose weak opioids are not shown to provide greater pain relief but can cause side effects and dependence or addiction.
Greater pain relief can only be achieved when adequate doses of each are used but can cause additional side effects.
Why is aspirin used for pain management?
Low doses (75mg) are used for their antiplatelet effect, whilst higher doses (300-900mg) can be used for some types of pain.
Indicated for headache, musculoskeletal pain, dysmenorrhoea and pyrexia.
Can be particularly useful for migraine in some patients.
Significant GI related side effects limit long term use at analgesic doses.
Why is nefopam used for pain management?
Useful for persistent pain that is unresponsive to other non opioids including dental, musculoskeletal and cancer pain.
Centrally acting analgesic that is distinct from opioids and does not cause respiratory depression.
Mechanism of action is unclear but leads to inhibition of dopamine, noradrenaline and serotonin reuptake thereby inhibiting pain signal transmission.
Has significant sympathomimetic and antimuscarinic side effects.
Why are NSAIDs used for pain management?
When used regularly at full dosage, they have analgesic and anti-inflammatory activity therefore are more appropriate for conditions with an inflammatory component.
Differences in anti-inflammatory activity between the drugs is small but there is significant variation in how patients respond to, and tolerate the drugs.
Pain relief can be achieved by one week but it can take up to three weeks for the full anti-inflammatory effect to be achieved.
Useful for treatment of both short term musculoskeletal and chronic diseases (e.g. arthritis) associated with pain and inflammation.
Also useful in dysmenorrhea and bone metastases (breakdown of bone leads to prostaglandin release – link to palliative care).
Useful in chronic low back pain but alongside other measures such as exercise and psychological therapies.
What are the risks of using selective NSAIDs?
These include celecoxib and etoricoxib.
They are as effective as non-selective NSAIDs in terms of analgesia and anti-inflammatory action.
Risk of serious upper GI events is lower with COX-2 selective inhibitors as compared to the non-selective NSAIDs.
Risk of cardiovascular events is higher than for some non-selective NSAIDs.
What is the mechanism of action of NSAIDs?
Reduce production of prostaglandins via inhibition of cyclo-oxygenase (COX) enzymes.
Different NSAIDs have different selectivity for different types of COX which influences their cardiovascular and GI risk profile.
What is the role of COX-1?
Present in nearly all cells.
Leads to production of prostaglandins that are involved in GI protection, platelet aggregation and renal function.
Action of NSAIDs on COX-1 leads to GI, renal and cardiovascular side effects.
What is the role of COX-2?
Normally absent from cells but produced rapidly in response to an inflammatory stimulus.
Activation of COX-2 leads to production of prostaglandins involved in producing inflammation, pain and fever.
Action of NSAIDs on COX-2 leads to analgesic and anti-inflammatory activity.
How would you choose the correct NSAID?
Start with one that carries a lower risk (e.g. ibuprofen), at the lowest recommended dose and only use one oral NSAID at a time.
Combinations of NSAIDs and low dose aspirin (for antiplatelet effect) increases the risk of GI side effects so is not recommended and should only be used if absolutely necessary.
Some patients, especially those with e.g. rheumatoid arthritis, may be dependent on NSAIDs despite the associated risks.
Patients at risk of GI ulceration should receive gastroprotective cover e.g. a PPI.
Excessive alcohol also increases the risk of GI haemorrhage associated with NSAIDs.
How do opioids work?
Opioid peptides are neurotransmitter molecules involved in pain signaling.
Opioid receptors are found in CNS and periphery and opioid peptides bind to these receptors and suppress pain signals. Naturally occurring opioid peptides include the endorphins.
Opioid drugs mimic the actions of the natural ligands for the opioid receptors and thereby decrease the transmission of painful stimuli.
