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YR3S2- clinical therapeutics > wk 7- pain > Flashcards

wk 7- pain Flashcards

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
Q

acute pain treatment mild-sev

A
  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)

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26
Q

what is paracetamol

A

analgesic
antipyretic
mild anti inflammatory

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27
Q

MOA paracetamol

A

not fully understood

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28
Q

indications for paracetamol

A

mild - mod pain

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29
Q

what is paracetamol contraindicated in

A

infants less than 1 month
hepatic impairment
renal impairment
allergy

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30
Q

result of cox 1 and 2 inhibition by NSAIDs

A

bleeding
gastrointestinal ulcers
reduced renal function
increased sodium retention
reduced inflammation, fever and pain
decreased vasodilation
increased production of TXA2

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31
Q

NSAIDs half life

A

generally 2-3 hours

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32
Q

NSAIDs adverse effects

A

GI bleeding
renal/hepatic disturbances
rash
cardiovascular risk (MI)
asthma 3-11% suffer aspirin/NSAID intolerance asthma

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33
Q

what drugs interact with NSAIDs

A

alcohol
anticoag
antacids
antihypertensives
cyclosporin
diuretics
lithium
MTX
nsaids
sulfonylureas

34
Q

what conditions do NSAIDs interact with

A

blood pressure
liver/kidney function
inflammatory response
coagulation
acid/base balance

35
Q

triple whammy/ acute renal failure

A

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
Q

what NSAID drugs are first line for inflammatory joint disease

A
  1. ibuprofen
    2.fenbrufen
    3.naproxen

less side effects

37
Q

aspirin is

A

first line for mild-mod pain
other than children under 16

38
Q

ibuprofen is

A

first choice for inflammatory conditions

mild-mod pain

39
Q

fenbrufen/naproxen/diclofenac is

A

alternative to ibuprofen

40
Q

indometacin is

A

anti inflammatory, less analgesic action but serious side effects

41
Q

what drugs are cox 2 inhibitors

A

celecoxib
lumiracoxib
etoricoxib

42
Q

topical NSAIDS are

A

diclofenac (voltaren)
ketoprofen
piroxicam

43
Q

are topical NSAIDs systemically absorbed?

A

yes

increased local side effects too

44
Q

codeine is a what

A

opiod receptor agonist

45
Q

moa of codeine

A

molecules bind to opioid receptors which inhibit release of substance P

5-10% metabolised into morphine which mimics enkephalins and endorphins

46
Q

indications of codeine

A

moderate to severe nociceptive pain, cough suppression, sedation/sleep

47
Q

contraindications of codeine

A

allergy
respiratory depression
constipation
addiction
CYPD6 deficiency - cannot metabolise into morphine

48
Q

are opioids metabolised by everyone?

A

7% of caucasians and 2% of asians cannot metabolise codeine to morphine

49
Q

codeine precautions

A

hepatic/renal impairment
drug abuse
respiratory depression
GI tract injury
pregnancy

50
Q

adverse effects of codeine

A

nausea
vomiting
drowsiness
dizziness
constipation
respiratory depression
euphoria
rashes

51
Q

what drugs do codeine interact with

A

CNS depressants (anti convulsants)

52
Q

what amount of codeine is considered S4/S8

A

30MG OR MORE

53
Q

what is 1.5mg of codeine in combination with paracetamol considered with scheduling

A

S4

54
Q

how many opioid receptors are there

A

17, all are responsible for different effects in the body

55
Q

codeine binds to which receptor

A

prodrug that binds to mu

analgesic properties depend on conversion to morphine that also binds to mu with much greater affinity

56
Q

where can steroid injections be injected into

A

joints, soft tissue, bursa, around tendon, proximal to nerve

57
Q

steorid injections are usually combined with

A

LA

58
Q

what steroids are long lasting and short lasting

A

long- acetate based
short- phosphate based

59
Q

what can steroids do to normal blood levels?

A

increase blood glucose levels
increase blood pressure

60
Q

Moa of glucocorticoids

A

hormones that bind to glucocorticoid receptors

61
Q

main functions of glucocorticoids

A

immunosuppression
anti inflammation

62
Q

adverse effects of GCS

A

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
Q

radiuclopathy is

A

nerve root compression

64
Q

mononeuropathy is

A

a local nerve compression/damage

65
Q

polyneuropathy is

A

multiple peripheral nerves are damaged
commonly caused by
diabetic neuropathy
alcohol induced neuropathy
infections

66
Q

when treatment neuropathies why is finding the cause so important

A

depends if compressive neuropathy or degeneration of nerve

more likely to use cortisone injections for compressive neuropathy

67
Q

what is the aim of chronic pain management

A

restore function and quality of life, hard to eliminate pain completely

68
Q

for chronic non cancer/non neuropathic pain what treatments are used

A

step ladder
NSAIDS/paracetamol
opioids

69
Q

for chronic non cancer/ but neuropathic pain what treatment?

A

TCA (amitryptyline)

antiepileptics (gabapentin, pegabalin)

for these doses are lower than depression/epilepsy

diabetic peripheral neuropathy- SNRI (duloxetine)

70
Q

what should patient education cover?

A

condition and treatment approach

drug treatment

reason why they’re taking drug

expectations after therapy

adherence

71
Q

step ladder including cortisone

A

paracetamol
NSAID
opioid
cortisone

7-10 days of care then refer

72
Q

treatment for acute soft tissue injury

A
  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
Q

treatment for chronic conditions (OA, tendinopathy, plantar fasciopathy)

A

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
Q

treatment for acute on chronic flares (synovitis, bursitis, tensosynovitis, inflammatory flares)

A
  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
Q

treatment for nociplastic pain (chronic/unresponsive pain, non specific pain)

A

pod
- non drug, supportive

referral-
1. TCA, Ketamiline

76
Q

treatment for neuropathic pain (mono neuropathy, peripheral neuropathy)

A
  1. paracetamol
  2. NSAID
  3. cortisone injection

non drug-
1. offload/footwear
2. manage skin

referral-
1. surgery
2. antidepressants, anticonvulsants

77
Q

treatment for gout

A

up to 5 days
for acute flare
1. NSAID
2. colchine

referral
1. long term urate lowering medication
2. management

78
Q

why is neuropathic pain resistant to standard analgesics

A

different type of pain, non inflammatory it needs medication that act on the CNS to inhibit the pain

79
Q

what contributes to the development of chronic pain

A
  1. depression/anxeity/mood
  2. multimorbidities
  3. not correcting acute pain early
80
Q

what information do you need to give the patient when prescribing a drug

A
  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
Q

side effects of blood pressure medication

A

falls
fluid retention

82
Q
A

YR3S2- clinical therapeutics (12 decks)

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