Week 7 Flashcards
What 5 examples of Pain syndromes?
- Bone (worse on weight bearing)
- Nerve (burning/shooting/tingling)
- Liver (upper right quadrant)
- RIP (headache and/or nausea)
- Colic (cramping pain)
What are the 3 steps in managing chronic pain according to WHO
AND
what drugs may be used for each?
Step 1 - Non-opioid
(aspirin, paracetamol or NSAID)
Step 2 - Weak opioid
(codeine +/- non-opioid)
Step 3 - Strong opioid
(morphine +/- non-opioid)
+/- Adjuvant for all steps
What are the Indications, Actions, and Cautions of Morphine?
Indications
Moderate to severe pain / dyspnoea (breathlessness)
Action
Opioid receptor agonist (u-receptors). Centrally acting
Cautions
Longlist in BNF; including renal impairment and elderly; Avoid in acute respiratory depression
By what methods may Opioids be administered?
Oral / Rectal
Parenterally - im/sc injections
Delivery via syringe driver over 24h
What should you do when starting Strong opioids (step 3)?
- Stop any ‘Step 2’ weak opioids
- Titrate immediate release strong opioid
- Convert to modified release form
- Monitor response and side-effects
What are the 2 types of Opioid release in BNF?
Modified (slow) release
and
Immediate release
What are 3 examples of Modified release in opioids
AND
what are some examples of drugs used for these?
- ‘Background’ pain relief
- Twice daily prep at 12h intervals (Filnarine)
- Once daily prep at 24h intervals (MXL)
When are Imediate release opioids used
AND
what are some drug examples?
- ‘Breakthrough’ pain
- As required (PRN)
Oramorph liquid / Sevredol tabs
What is Diamorphine and what are some differences between in and Morphine?
Heroin
- Semi-synthetic morphine derivative
- More soluble than Morphine -> smaller vol needed
- Can be used for parenteral administration (injection / syringe driver)
What are some OTHER opioids than just Morphine?
Oxycodone
- second line opioid
- less hallucinations, itch, drowsiness, confusion
Fentanyl patch
- second line opioid
- lasts 72h
- only use in stable pain
- useful if oral and sc routes not available
- useful if persistent side-effects w/ morphine / diamorphine
What are some side effects of opioids?
- N&V
- Constipation
- Dry mouth
- Billary spasm
How do you manage Constipation as a result of opioid side-effects?
- Stimulant & softening laxative
- Senna / Bisacodyl + Docusate
- Magrogol e.g. laxido / movicol
- Or Co-Danthramer alone
How do you manage Nausea as a result of opioid side-effects?
- Antiemetic
- Metoclopramide
- Haloperidone (QT interval)
What are some signs of Opioid Toxicity?
- Pin point pupils
- Shadows edge of visual feild
- Increasing drowsiness
- Vivid dreams / Hallucinations
- Muscle twitching / Myoclonus
- Confusion
- Rarely, resp depression
What issues would require Adjunct Medication and what drus would be used for such?
Liver capsule pain / RIP
- Steroids (e.g. Dexamethasone)
- Remember to consider gastroprotection
Neuropathic pain
- Amitriptyline / Gabapentin / Carbamazepine
Bowel / Bladder spasm
- Buscopan (hyoscine butylbromide)
Bone Pain / Soft tissue infiltration
- NSAIDs / Radiotherapy for bony metastases
What are the functions of Syringe Drivers?
- Delivery over 24h - usually sc
- Useful when oral route inappropriate
- Often useful for rapid symptom control
- Multiple medications can be added
- Stigma of being on a ‘pump’
What is the deffinition of Psycho-spiritual distress?
The impaired ability to experience and integrate meaning and purpose in life through connections with self, others, nature, or a higher power
Why is Psycho-spiritual distress important?
May magnify the intensity of physical symptoms
When may Psycho-spiritual distress occur?
- at Diagnosis
- at Home after treatment
- upon Disease progression
- at Terminal phase
How do you manage Psycho-spiritual distress?
- Encourage hope, purpose and meaning
- Respect religious / cultural needs
- Affirming patients humanity
- Protecting patient’s dignity, self worth and identity
What percentage of greif is Non-complex compared to Complex / unresolved?
90-94%
to
6-10%
What may an individual dealing with greif WANT from the NHS?
Medication
(Antidepressants / Benzodiazepines)
Sick line
Counselling
What may an individual dealing with greif NEED from the NHS?
Support and space to be heard
What are the Peripheral aspects of pain?
- Nociceptive receptors
- Nociceptive activation
- Nociceptive fibres
- Sensitisation of receptors
Describe Nociceptive nerves
They have free unspecialised nerve endings with ‘pain’ channels inserted in the membrane
What is the most common Nociceptor nerve?
Transient Receptor Potential family of channels (TRP)
What are Nociceptor nerves sensitive to?
- O2
- pH osmolarity
- Valinoids (spice)
- Heat
What can Nociceptive receptors be sensitised by?
- Substance P
- Bradykinins
- Serotonin
- pH
- ATP
- NO
What is the Composition of the Nociceptive receptors
AND
What does this Allow?
Composed of a 6 unit trans-membrane portion and a ‘basket’ of regulatory complex in the cytoplasm
Allows Ca2+ & Na+ into the cell
What physical stimuli will Activate Nociceptive receptors?
Temperature
- Extreme heat and extreme cold open ‘Transient receptor potential vanilloid’ (TRPV) channels inserted in the membrane
- Allows Na2+ & Ca2+ entry and so depolarises cell to give action potential
Mechanical
- Actual mechanism still unknown. Presumed to be a form of insensitive mechanoreceptor which allows Na entry when activated
Chemical
- Apart from TRPV receptors, it’s largely unknown but chemical transmission can cause sensitisation of pain receptors
What specifically does each molecule do to sensitize nociceptors?
Calcitonin gene regulated peptide (CGRP) and Substance P (SP)
- Recruit silent receptors which increase summation in dorsal horn
Histamine
- Causes hyperalgesia (more pain than normal) through its effects on nerve endings
Bradykinin
- Activates pain fibres directly and causes increase in protaglandins
Tissue damage
- Produces H ions which give muscle ache (weight lifting)
Protaglandin E2
- Aspirin and other NSAIDs act to inhibit this enzyme
What are the two main types of Nociceptive fibres?
Aδ fibres
- Myelinated
- Sharp 1st pain
- Mechanical pinching
- Extreme hot or cold
C fibres
- Unmyelinated
- Aching 2nd pain (diffuse)
- Mechanical pinching
- Thermal and chemical stimuli (polymodal)
Upon stimulation, what NTs do nociceptive fibres release?
- Glutamate
- Substance P
- CGRP (Calcitonin gene-related peptide)
What are some signs of nociceptor activation?
Substance P and CGRP release is responsible for 3 signs:
- Calor (heat)
- Rubor (redness)
- Tumor (swelling)
1 & 2 caused by local hyperaemia (increased blood flow) and 3 is by plasma extravasation (leaking out of veins)
What are the differences between the Paleo-spinothalamic and Neo-spinothalamic pathways?
Paleo-spinothalamic
- Synapses at Dorsal Medial intralaminar portion of thalamus
- Undiscriminating system
- Finally synapses at Limbic system association cortices
Neo-spinothalamic
- Synapses at Vental-posterolateral portion of thalamus
- Discriminating system
- Finally synapses at Primary somatosensory cortex
Where do Nociceptive fibres first synapse in the spinal cord?
Ipsilateral Dorsal Horn
What are the two types of ascending axons for nociceptive fibres?
Nociceptive specific
- C and Aδ only
Wide dynamic range neurons (WDR)
- Any sensory input including pain, can fire in a graded fashion based on C fibre frequency of input (higher pain = higher input)
How do AMPA receptors interact with NMDA receptors?
NMDA recpectors are normaly closed due to Mg2+ Block.
AMPA receptors (once stimulated by Glutamate) allow Ca2+ into the cell which then depolarises.
This releases the Mg2+ block, activating NMDA receptors
What is Central sensitisation - Wind up?
Long term sensitisation of post synaptic neurons in the dorsal horn
Mediated by WDR neurons which, when firing at high frequency, open NMDA channels
The inflow of calcium causes nuclear expression resulting in increased Na channels and a blockade of K channels
The net result is a resting potential closer to threshold and a more sensitive cell
This effectively amplifies the pain signal
What are the three main goals of dorsal horn Wind up?
Priority salience
- You’ll notice it more than normal
Protection
- Prevent futher injury
Memory
- Increased duration of stimuli increases the chance of consolidation
Describe the Gate theory of pain management
C fibres both stimulate the WDR neuron AND inhibit the inhibitory neuron from Aβ fibres that would normal inhibit the WDR. This increase the pain signal
By rubbing the area around the source of pain, you activate a stronger signal in the Aβ inhibitory neuron, therefore decreasing the activation of WDR neuron.
Describe Descending analgesia in the contex of pain management
Periaqueductal gray matter creates inhibition of incoming pain signals at the cord level, aswell as the presence of encephalin-secreting neurons that supress pain signals in the cord
Describe the Endogenous opioid system
These are a group of NTs called:
- Endorphins
- Encephalins
- Dynorphins
Work at opiate receptors and are present at all levels of the pain pathways, therefore doses of opiates can act simultaneously at all levels of the pain pathway providing high efficacy
What would electrical stimulation of the PAG result in?
A strong analgesic effect
(Blocked by Nalaxone)
List some examples of the types of pain
- Chronic / Acute
- Nociceptive / Neuropathic / Phantom limb
- Maladaptive
- Viceral
- Referred
- Sharp / Ache
- Headache
- Complex regional pain syndrome
Describe the characteristics of Nociceptive pain
Results from conditions such as:
- Sprains
- Bone fractures
- Burns, bumps, bruises
- Inflamation
Pain stops when the problem is healed
Responds well to painkillers such as opioids
What are the 3 types of Chronic pain?
- Nociceptive pain
- Neuropathic pain
- Central maladaptation
Describe the characteristics of Neuropathic pain
Pain persists beyond healing process of damaged tissues and may include:
- Hyperalgesia (strong reaction to weak pain signal)
- Allodynia (painful reaction to non painful stimuli like a light touch on sunburn)
- Summation (repeated low innocuous stimuli causing increasing intensity of response)
- Parasthesias (tingling without stimuli)
- Dysthesias (burning / shooting pain without stimuli)
This type of pain is hard to treat and is caused by maladaptation of the dorsal horn wind up and sensitisation systems
What is Central maladaptation?
A type of sensitisation that can lead to long term changes in the structure of synapses in the dorsal horn or the spinal cord
Increases in Ionotropic glutamate receptors (NMDA) cause a sensitivity in second order neurons which then more readily send pain signals to the thalamus
A second component is where descending modulation of the inhibitory interneurons becomes maladapted. This can lead to a reduction in inhibition of WDR neurons and so a dis-inhibition of the second order neurons
List some symptoms of Complex regional pain syndromes
- Severe continuous neuropathic pain
- Abnormal sensation
- Vasomotor change
- Sudomotor change
- Motor / trophic change
- Regionally restricted e.g. hand
- Disproportionate to the trauma
What is the Budapest criteria?
Used to diagnose Complex regional pain syndromes
1) Patients must report continuing pain disproportionate to the trauma
2) Patients must report at least one of the following symptoms:
- Sensory: hyperalgesia
- Vasomotor: skin colour or temp changes
- Sudomotor / oedema: swelling or weating changes
- Motor / trophic: weakness, tremor, dystonia, decreased range of motion or trophic changes
3) Patients must display one sign in two of the above catagories
4) Signs and symptoms must not be better explained by another diagnosis
How does Referred pain work?
Viceral sensory fibres and Skin sensory fibres synapse at the same location in the dorsal horn
In the Gate control theory, what ‘opens’ and ‘closes’ the gate?
Opens
- Inactivity / poor fitness
- Poor pacing
- Anxiety / depression / hopelessness
- Worrying about the pain (cognitive)
Closes
- Appropriate use of medication
- Massage / relaxation
- Heat / cold
- Positive coping strategies
- Exercise
Describe the Biopsychosocial model of pain
Views illness as a dynamic and reciprocal interaction among biological, psychological and sociocultural variables that shape a person’s response to pain