wk 7- pain Flashcards
most common site of pain in the foot
toes and forefoot
pain is
unpleasant sensory and emotional experience with actual or percieved tissue damage
models for understanding pain
gare control theory- spinal cord has a neural gate that can modulate pain signals, things that open and close the gate
neuromatrix model- memories of past experiences, attention, meaning and anxiety
3 systems for pain perception
- afferent pathways- take pain signals to the spinal cord
- CNS-
neospinothalamic tract carries sharp and intense acute pain signals
paleospinothalamic tract carries dull and burning pain signals - efferent pathways- module pain sensation
how does tissue injury cause pain
production of arachidonic acid, COX catalyses to produce prostaglandins, causing depolarization of adjacent nociceptors. acute pain is result
what can modulte pain in the medulla and travelling down efferent fibres in the spinal cord
noradrenaline and serotonin
therefore, TCA, SSRI, SNRI can be used as treatment for pain management as they increase levels of NA and seratonin
what neuropeptides inhibit pain transmission in spinal cord and brain
beta lipotropin
enkophalin
dynorphin
stimulate opiod receptors on plasma membranes of afferent neurons and inhibit release of excitatory neurotransmitters
types of pain
inflammatory
pathologic
nociceptive
what is acute pain
short, less than 30 days
identifiable pathology
predictable prognosis
treatment- analgesics
what is chronic pain
daily pain for 3 months or more in the past 6 months
pathology may be unclear
unpredictable prognosis
treatment multidisciplinary
nociceptive v neuropathic pain
NOCI
- sharp, dull, aching, radiates
-detection of tissue damage from noxious stimuli
-treated with NSAIDs and Opiods
NEURO
-burning, tingly, sensory changes
-lesion or dysfunction in CNS
1. trigeminal neuralgia (sciatica)
2. postherpetic zoster pain (peripheral)
3. thalamic pain (central)
-resistant to NSAIDS
-treated with TCA, anticonvulsants, sodium channel blockers, IV local anaestheic
types of nociceptive pain
acute or chronic
types of neuropathic pain
central or peripheral
what type of pain is fibromylagia
nociplastic
what is chronic pain differetiated into?
cancer and non cancer pain
what is the physiology of chronic pain
- lowered endorphin levels
- increased C neruon stimulation
- pain neurons more likely to depolarise
- regenerating peropheral nerves may produce spontaneous impulses
- loss of pain inhibitiion mechanisms in spinal cord
6 changes in dorsal root ganglia, causing reorganisation of nociceptive neurons
underlying maladaptive neural changes, resulting in continued perception of pain
4 major types of chronic pain
- central - lesion/dysfunction in CNS
- Non neuropathic pain- myalgia, myositis (non canerous and reuslt of nerve damage)
- neuropathic pain - trauma/disease of peripheral nerves
- psychogenic pain - disorder related
what is nociplastic pain
altered/abnormal function of the nociceptive pathways or cerebral cortex in the absence of nociceptive stimulus or neuropathic lesion
example: fibromyalgia
what are examples of inflammatory pain
rhematoid arthritis
gout
seronegative arthropathies
what gout drugs can a podiatrist prescribe
colchine
what NSAIDs can pod prescribe
celecoxib
diclofenac
ibuprofen
meloxicam
naproxen
sulindac
indometacin
simple analegesics pods can prescribe
aspirin
paracetamol
opiods pods can prescribe
codeine phosphate
corticosteroids pods can prescribe
dexamethasone
betamethasone
methylprednisolone
traimcinolone
acute pain treatment mild-sev
- NSAIDs with/wo paractemol
- opioids
pain1-3 (mild): paracetamol with or without NSAIDS
pain4-6(mod): paracetamol and weak opiod (codeine)
pain7-10(sev): paracetamol and strong opioid (morphine)
what is paracetamol
analgesic
antipyretic
mild anti inflammatory
MOA paracetamol
not fully understood
indications for paracetamol
mild - mod pain
what is paracetamol contraindicated in
infants less than 1 month
hepatic impairment
renal impairment
allergy
result of cox 1 and 2 inhibition by NSAIDs
bleeding
gastrointestinal ulcers
reduced renal function
increased sodium retention
reduced inflammation, fever and pain
decreased vasodilation
increased production of TXA2
NSAIDs half life
generally 2-3 hours
NSAIDs adverse effects
GI bleeding
renal/hepatic disturbances
rash
cardiovascular risk (MI)
asthma 3-11% suffer aspirin/NSAID intolerance asthma
what drugs interact with NSAIDs
alcohol
anticoag
antacids
antihypertensives
cyclosporin
diuretics
lithium
MTX
nsaids
sulfonylureas
what conditions do NSAIDs interact with
blood pressure
liver/kidney function
inflammatory response
coagulation
acid/base balance
triple whammy/ acute renal failure
ace inhibitor dilates the efferent arteriole and reduces GFR
duiertics reduce plasma volume and GFR
NSAIDs constrict blood flow into the glomerulus via the afferent arteriole and reduce GFR
GRF is how much blood kidneys filter each minute
what NSAID drugs are first line for inflammatory joint disease
- ibuprofen
2.fenbrufen
3.naproxen
less side effects
aspirin is
first line for mild-mod pain
other than children under 16
ibuprofen is
first choice for inflammatory conditions
mild-mod pain
fenbrufen/naproxen/diclofenac is
alternative to ibuprofen
indometacin is
anti inflammatory, less analgesic action but serious side effects
what drugs are cox 2 inhibitors
celecoxib
lumiracoxib
etoricoxib
topical NSAIDS are
diclofenac (voltaren)
ketoprofen
piroxicam
are topical NSAIDs systemically absorbed?
yes
increased local side effects too
codeine is a what
opiod receptor agonist
moa of codeine
molecules bind to opioid receptors which inhibit release of substance P
5-10% metabolised into morphine which mimics enkephalins and endorphins
indications of codeine
moderate to severe nociceptive pain, cough suppression, sedation/sleep
contraindications of codeine
allergy
respiratory depression
constipation
addiction
CYPD6 deficiency - cannot metabolise into morphine
are opioids metabolised by everyone?
7% of caucasians and 2% of asians cannot metabolise codeine to morphine
codeine precautions
hepatic/renal impairment
drug abuse
respiratory depression
GI tract injury
pregnancy
adverse effects of codeine
nausea
vomiting
drowsiness
dizziness
constipation
respiratory depression
euphoria
rashes
what drugs do codeine interact with
CNS depressants (anti convulsants)
what amount of codeine is considered S4/S8
30MG OR MORE
what is 1.5mg of codeine in combination with paracetamol considered with scheduling
S4
how many opioid receptors are there
17, all are responsible for different effects in the body
codeine binds to which receptor
prodrug that binds to mu
analgesic properties depend on conversion to morphine that also binds to mu with much greater affinity
where can steroid injections be injected into
joints, soft tissue, bursa, around tendon, proximal to nerve
steorid injections are usually combined with
LA
what steroids are long lasting and short lasting
long- acetate based
short- phosphate based
what can steroids do to normal blood levels?
increase blood glucose levels
increase blood pressure
Moa of glucocorticoids
hormones that bind to glucocorticoid receptors
main functions of glucocorticoids
immunosuppression
anti inflammation
adverse effects of GCS
immunodeficiency
skin fragility (particularly with acetate based forumlas)
osteoporosis
moon face
cushingoid appearance
weight gain
growth failure
menstrual cycle changes
mood changes
suppression of pituitary adrenal axis
flares within the first 24 hours of injection
radiuclopathy is
nerve root compression
mononeuropathy is
a local nerve compression/damage
polyneuropathy is
multiple peripheral nerves are damaged
commonly caused by
diabetic neuropathy
alcohol induced neuropathy
infections
when treatment neuropathies why is finding the cause so important
depends if compressive neuropathy or degeneration of nerve
more likely to use cortisone injections for compressive neuropathy
what is the aim of chronic pain management
restore function and quality of life, hard to eliminate pain completely
for chronic non cancer/non neuropathic pain what treatments are used
step ladder
NSAIDS/paracetamol
opioids
for chronic non cancer/ but neuropathic pain what treatment?
TCA (amitryptyline)
antiepileptics (gabapentin, pegabalin)
for these doses are lower than depression/epilepsy
diabetic peripheral neuropathy- SNRI (duloxetine)
what should patient education cover?
condition and treatment approach
drug treatment
reason why they’re taking drug
expectations after therapy
adherence
step ladder including cortisone
paracetamol
NSAID
opioid
cortisone
7-10 days of care then refer
treatment for acute soft tissue injury
- paracetamol
- NSAID s2 -s4
- opioid - codeine ESM
non drug
- PEACE AND LOVE
-orthoses/footwear
referral-
1. stronger pain relief
2. surgery
treatment for chronic conditions (OA, tendinopathy, plantar fasciopathy)
non drug-
-PEACE and LOVE
-orthoses/footwear
drug-
1. paracetamol
2. NSAID s2-s4
3. opioid- codeine
4. cortisone injection
referral-
1. long term pain relief
treatment for acute on chronic flares (synovitis, bursitis, tensosynovitis, inflammatory flares)
- paracetamol
- NSAID up to s4
- opioid - codeine
- cortisone injection
non drug-
1. PEACE and LOVE
referral-
1. disease modifying drugs
2. surgery
3. long term pain relief
treatment for nociplastic pain (chronic/unresponsive pain, non specific pain)
pod
- non drug, supportive
referral-
1. TCA, Ketamiline
treatment for neuropathic pain (mono neuropathy, peripheral neuropathy)
- paracetamol
- NSAID
- cortisone injection
non drug-
1. offload/footwear
2. manage skin
referral-
1. surgery
2. antidepressants, anticonvulsants
treatment for gout
up to 5 days
for acute flare
1. NSAID
2. colchine
referral
1. long term urate lowering medication
2. management
why is neuropathic pain resistant to standard analgesics
different type of pain, non inflammatory it needs medication that act on the CNS to inhibit the pain
what contributes to the development of chronic pain
- depression/anxeity/mood
- multimorbidities
- not correcting acute pain early
what information do you need to give the patient when prescribing a drug
- how to take it
- common side effects
- stop taking if you have an allergy, seek emergency if anaphylaxis
- that it’s short term
- not on PBS
side effects of blood pressure medication
falls
fluid retention
