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YR3S2- clinical therapeutics > wk 7- pain > Flashcards

wk 7- pain Flashcards

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1
Q

most common site of pain in the foot

A

toes and forefoot

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2
Q

pain is

A

unpleasant sensory and emotional experience with actual or percieved tissue damage

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3
Q

models for understanding pain

A

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

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4
Q

3 systems for pain perception

A
  1. afferent pathways- take pain signals to the spinal cord
  2. CNS-
    neospinothalamic tract carries sharp and intense acute pain signals
    paleospinothalamic tract carries dull and burning pain signals
  3. efferent pathways- module pain sensation
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5
Q

how does tissue injury cause pain

A

production of arachidonic acid, COX catalyses to produce prostaglandins, causing depolarization of adjacent nociceptors. acute pain is result

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6
Q

what can modulte pain in the medulla and travelling down efferent fibres in the spinal cord

A

noradrenaline and serotonin

therefore, TCA, SSRI, SNRI can be used as treatment for pain management as they increase levels of NA and seratonin

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7
Q

what neuropeptides inhibit pain transmission in spinal cord and brain

A

beta lipotropin
enkophalin
dynorphin

stimulate opiod receptors on plasma membranes of afferent neurons and inhibit release of excitatory neurotransmitters

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8
Q

types of pain

A

inflammatory
pathologic
nociceptive

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9
Q

what is acute pain

A

short, less than 30 days
identifiable pathology
predictable prognosis
treatment- analgesics

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10
Q

what is chronic pain

A

daily pain for 3 months or more in the past 6 months
pathology may be unclear
unpredictable prognosis
treatment multidisciplinary

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11
Q

nociceptive v neuropathic pain

A

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

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12
Q

types of nociceptive pain

A

acute or chronic

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13
Q

types of neuropathic pain

A

central or peripheral

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14
Q

what type of pain is fibromylagia

A

nociplastic

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15
Q

what is chronic pain differetiated into?

A

cancer and non cancer pain

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16
Q

what is the physiology of chronic pain

A
  1. lowered endorphin levels
  2. increased C neruon stimulation
  3. pain neurons more likely to depolarise
  4. regenerating peropheral nerves may produce spontaneous impulses
  5. 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

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17
Q

4 major types of chronic pain

A
  1. central - lesion/dysfunction in CNS
  2. Non neuropathic pain- myalgia, myositis (non canerous and reuslt of nerve damage)
  3. neuropathic pain - trauma/disease of peripheral nerves
  4. psychogenic pain - disorder related
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18
Q

what is nociplastic pain

A

altered/abnormal function of the nociceptive pathways or cerebral cortex in the absence of nociceptive stimulus or neuropathic lesion

example: fibromyalgia

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19
Q

what are examples of inflammatory pain

A

rhematoid arthritis
gout
seronegative arthropathies

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20
Q

what gout drugs can a podiatrist prescribe

A

colchine

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21
Q

what NSAIDs can pod prescribe

A

celecoxib
diclofenac
ibuprofen
meloxicam
naproxen
sulindac
indometacin

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22
Q

simple analegesics pods can prescribe

A

aspirin
paracetamol

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23
Q

opiods pods can prescribe

A

codeine phosphate

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24
Q

corticosteroids pods can prescribe

A

dexamethasone
betamethasone
methylprednisolone
traimcinolone

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25
acute pain treatment mild-sev
1. NSAIDs with/wo paractemol 2. 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)
26
what is paracetamol
analgesic antipyretic mild anti inflammatory
27
MOA paracetamol
not fully understood
28
indications for paracetamol
mild - mod pain
29
what is paracetamol contraindicated in
infants less than 1 month hepatic impairment renal impairment allergy
30
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
31
NSAIDs half life
generally 2-3 hours
32
NSAIDs adverse effects
GI bleeding renal/hepatic disturbances rash cardiovascular risk (MI) asthma 3-11% suffer aspirin/NSAID intolerance asthma
33
what drugs interact with NSAIDs
alcohol anticoag antacids antihypertensives cyclosporin diuretics lithium MTX nsaids sulfonylureas
34
what conditions do NSAIDs interact with
blood pressure liver/kidney function inflammatory response coagulation acid/base balance
35
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
36
what NSAID drugs are first line for inflammatory joint disease
1. ibuprofen 2.fenbrufen 3.naproxen less side effects
37
aspirin is
first line for mild-mod pain other than children under 16
38
ibuprofen is
first choice for inflammatory conditions mild-mod pain
39
fenbrufen/naproxen/diclofenac is
alternative to ibuprofen
40
indometacin is
anti inflammatory, less analgesic action but serious side effects
41
what drugs are cox 2 inhibitors
celecoxib lumiracoxib etoricoxib
42
topical NSAIDS are
diclofenac (voltaren) ketoprofen piroxicam
43
are topical NSAIDs systemically absorbed?
yes increased local side effects too
44
codeine is a what
opiod receptor agonist
45
moa of codeine
molecules bind to opioid receptors which inhibit release of substance P 5-10% metabolised into morphine which mimics enkephalins and endorphins
46
indications of codeine
moderate to severe nociceptive pain, cough suppression, sedation/sleep
47
contraindications of codeine
allergy respiratory depression constipation addiction CYPD6 deficiency - cannot metabolise into morphine
48
are opioids metabolised by everyone?
7% of caucasians and 2% of asians cannot metabolise codeine to morphine
49
codeine precautions
hepatic/renal impairment drug abuse respiratory depression GI tract injury pregnancy
50
adverse effects of codeine
nausea vomiting drowsiness dizziness constipation respiratory depression euphoria rashes
51
what drugs do codeine interact with
CNS depressants (anti convulsants)
52
what amount of codeine is considered S4/S8
30MG OR MORE
53
what is 1.5mg of codeine in combination with paracetamol considered with scheduling
S4
54
how many opioid receptors are there
17, all are responsible for different effects in the body
55
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
56
where can steroid injections be injected into
joints, soft tissue, bursa, around tendon, proximal to nerve
57
steorid injections are usually combined with
LA
58
what steroids are long lasting and short lasting
long- acetate based short- phosphate based
59
what can steroids do to normal blood levels?
increase blood glucose levels increase blood pressure
60
Moa of glucocorticoids
hormones that bind to glucocorticoid receptors
61
main functions of glucocorticoids
immunosuppression anti inflammation
62
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
63
radiuclopathy is
nerve root compression
64
mononeuropathy is
a local nerve compression/damage
65
polyneuropathy is
multiple peripheral nerves are damaged commonly caused by diabetic neuropathy alcohol induced neuropathy infections
66
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
67
what is the aim of chronic pain management
restore function and quality of life, hard to eliminate pain completely
68
for chronic non cancer/non neuropathic pain what treatments are used
step ladder NSAIDS/paracetamol opioids
69
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)
70
what should patient education cover?
condition and treatment approach drug treatment reason why they're taking drug expectations after therapy adherence
71
step ladder including cortisone
paracetamol NSAID opioid cortisone 7-10 days of care then refer
72
treatment for acute soft tissue injury
1. paracetamol 2. NSAID s2 -s4 3. opioid - codeine ESM non drug - PEACE AND LOVE -orthoses/footwear referral- 1. stronger pain relief 2. surgery
73
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
74
treatment for acute on chronic flares (synovitis, bursitis, tensosynovitis, inflammatory flares)
1. paracetamol 2. NSAID up to s4 3. opioid - codeine 4. cortisone injection non drug- 1. PEACE and LOVE referral- 1. disease modifying drugs 2. surgery 3. long term pain relief
75
treatment for nociplastic pain (chronic/unresponsive pain, non specific pain)
pod - non drug, supportive referral- 1. TCA, Ketamiline
76
treatment for neuropathic pain (mono neuropathy, peripheral neuropathy)
1. paracetamol 2. NSAID 3. cortisone injection non drug- 1. offload/footwear 2. manage skin referral- 1. surgery 2. antidepressants, anticonvulsants
77
treatment for gout
up to 5 days for acute flare 1. NSAID 2. colchine referral 1. long term urate lowering medication 2. management
78
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
79
what contributes to the development of chronic pain
1. depression/anxeity/mood 2. multimorbidities 3. not correcting acute pain early
80
what information do you need to give the patient when prescribing a drug
1. how to take it 2. common side effects 3. stop taking if you have an allergy, seek emergency if anaphylaxis 4. that it's short term 5. not on PBS
81
side effects of blood pressure medication
falls fluid retention
82

YR3S2- clinical therapeutics (12 decks)

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