Pain Assessment & Management Flashcards
(52 cards)
Discuss whether pain is common in cancer patients
- 30-40% with early disease
- 75-90% with advanced cancer
- ⅓ >2 different pains
- Can be controlled in 80% of pts using stepwise approach
*NOTE: 65% dying from non-malignant disease also experience pain
Remind yourself of key aspects of a pain history
- Site (localised, diffuse)
- Quality
- Intensity
- Timing (onset, duration, breakthrough or incident pain)
- Aggravating factors
- Relieving factors
- Symptoms associated (be sure to ask about power, sensory loss, parasthesia)
- Impact on life (ADLs, sleep)
- ICE (what pt thinks it is, what they are concerned about, any expectations they have)
Describe the pathophysiology of each of the following types of pain:
- Nociceptive
- Neuropathic
- Visceral
- Somatic
- Incident
- Nociceptive pain: caused by the detection of noxious or potentially harmful stimuli (e.g. mechanical, thermal, chemical) by the nociceptors around the body
- _Neuropathic pain:_pain occurring due to damage or disease of nerves (CNS or PNS)
- Visceral pain: pain from internal organs in thoracic or abdominal cavity
- Somatic pain: pain from nociceptors that are located in skin and deep musculoskeletal tissues. Can be superficial (skin) or deep (muscles, bone, tendons/ligaments)
- Incident pain: pain associated with a particular activity or movement (e.g. coughing, walking etc…)
*NOTE: 40% of pain is mixed
Compare nociceptive and neuropathic pain in terms of presentation (focus on features in neuropathic pain that aren’t present in nociceptive)
- Burning
- Shooting
- Stinging
- Paraesthesia
- Numbness
- Allodynia
- Less likely to respond to traditional painkillers
Compare visceral and somatic pain (both superficial and deep) in terms of presentation
Visceral
- Poorly localised
- Crampy, squeezing type pressure, dull, achy
- Referred pain
- Associated nausea, vomiting, sweating
Somatic
- Superficial: sharp, well localised, pulsatile
- Deep: ache, not as well localised as superficial (but usually more so than visceral)
What is end of dose failure pain?
Pain due to effects of analgesia wearing off; occurs around same time every day (if pt is on round the clock analgesia)
For each of the following pain descriptions, suggest a possible cause
(image taken from NICE palliative care pain section)
State some factors that:
- Increase
- Decrease
… pain sensation
State some potential sources of pain in a cancer pt
- Direct effects of the tumour (for example infiltration of pain-sensitive structures)
- Treatment associated with the cancer (for example surgery, chemotherapy, radiation treatment).
- Pain related to procedures (for example dressing changes, change of position).
- A condition not directly related to the cancer (for example infection, pre-existing osteoarthritis).
Describe the WHO pain ladder
State some examples of non-opioids
- Paracetamol
- NSAIDs
State some examples of weak opioids
- Co-codamol
- Codeine phosphate
- Dihydrocodeine
- Tramadol
State some examples of strong opioids
- Fentanyl
- Oxycodone (synthetic morphine, more expensive)
- Morphine
- Diamorphine (more soluble than morphine)
- Methadone
- Buprenorphine
State some examples of adjuvants
Variety of drugs belonging to different classes:
- Amitriptyline (TCA)
- Pregabalin (anticonvulsant)
- Gabapentin (anticonvulsant)
- Duloxetine (SNRI)
- Topical therapies e.g. capsaicin
- Bisphosphonates
- Steroids e.g. dexamethasone
What must you always co-prescribe to cancer pts who are taking NSAIDs and/or steroids?
PPI
If a pt had GI risk but no CV risk what NSAIDs could you prescribe?
Cox-2 inhibitors e.g. celecoxib, etoricoxib
Remind yourself how NSAIDs work- particularly in inflammatory pain
- Inhibition of prostaglandin synthesis by the enzyme cyclooxygenase which catalyses the conversion of arachidonic acid to the various prostaglandins that are the chief mediators of inflammation
- Prostagladins, particularly PGE2, sensitise nociceptive fibre nerve endings to other inflammatory mediators (such as bradykinin)
- It is the other inflammatory mediators that are sending the ‘pain signals’ not the prostaglandin itself
- Hence if have pain caused by these inflammatory mediators then NSAIDs will be more effective against pain
Remind yourself how opioids work
State some common side effects of opioids
- Constipation
- N&V (transient)
- Drowsiness (transient)
- Dry mouth
- Rash
- Pruritis
- Urinary retention
- Confusion
State some contraindications to opioids
- Respiratory depression
- Comatosed pts
- Head injury (mask symptoms & interfere with pupillary response)
- Raised ICP
- At risk of paralytic ileus
*Contraindications according to BNF
State some side effects of NSAIDs
- GI ADRs (dyspepsia, nausea, peptic ulceration, perforatin)
- Renal ADRs (renal failure/AKI)
- Others may include:
- Hypersensitivity
- Rash
State some contraindications to NSAIDs
MOST related to GI disorders:
- Active GI bleeding
- Active GI ulceration
- Hx GI bleeding related to NSAIDs
- Hx GI perforation related to NSAIDs
- Hx recurrent GI haemorrhage
- Hx recurrent GI ulceration
- Severe HF
- Varicella infection
What adjuvants can you use for neuropathic pain?
NICE updated their guidance on the management of neuropathic pain in 2013:
- First line: amitriptyline, duloxetine, gabapentin or pregabalin
- if the first-line drug treatment does not work try one of the other 3 drugs
- in contrast to standard analgesics, drugs for neuropathic pain are typically used as monotherapy, i.e. if not working then drugs should be switched, not added
- tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
- topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
State some common side effects of amitriptyline
- Confusion
- Hypotension
- Drowsiness
- Dry mouth
- Constipation