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N934 Adv Principles Fa 21 > Non Surgical Pain > Flashcards

Non Surgical Pain Flashcards

1
Q

common chronic pain conditions (4)

A

lumbar radiculopathy
facet arthroplathy
SI joint dysfunction
occipital neuritis

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2
Q

material released after trauma includes (8)

A 
potassium
plasma
RBC/WBC's
clotting factors
peptides
prostaglandins
inflammatory cells
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3
Q

materials released after trauma are through to enhance

A

activation of membrane channels (Na/Ca/etc)

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4
Q

release of these two things cause vascular leaking leading to swelling

A

substance p

calcitonin

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5
Q

pain response without tissue injury

A

escape response consistent with intensity of stimulation
removal of stimulation terminates sensation and response
sensation is specific to a site of potential injury
initial sensation is sharp, followed by a dull sensation

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6
Q

if you sit on a thumb tack, describe the a fiber and c fiber response

A

a fibers: quickest to respond, sharp sensation
c fibers: if you dont remove yourself from the object, a fibers are transmitting less and c fibers transmit more, which is more of a dull pain

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7
Q

pain response with tissue injury

A

pain persists after removal of stimulus. stimulating injured tissue cause an intense response (hyperalgesia), lower threshold of stimulation required to elicit an adverse response, has both localized sensation and referred sensation

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8
Q

pain response with nerve injury description

A

ongoing unpleasant pain sensation usually referred to the dermatome innervated by the injured nerve (hyperalgesia)- pain greater than expected.
increased pain sensation with touch (allodynia). pain that should not be painful

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9
Q

evolution of chronic pain (5)

A

associated with nerve injury response (not always but mostly)
failure to treat nerve and tissue injury effectively
occult inflammation
failure of tissue healing
persistent inflammation
(any or all of these may result in a windup)

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10
Q

what encompasses a windup or “enhanced spinal response”

  • neurotransmitters (3)
  • cell effected
A

repetitive stimulation releases glutamate, neurokinin, substance P which overwhelms the magnesium block
channels are opened, proteins couple with receptors producing long lasting calcium release
glial cell dysfunction in dorsal horn can be appreciated
loss of central inhibition mechanisms

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11
Q

during the windup or enhanced spinal response, what encompasses the loss of central inhibition mechanisms

A

there is an increased intracellular calcium, release of arachidonic acid (irritant), creation of cyclooxygenase, cox synthesizes prostaglandins, which reduces glycine and GABA mediated inhibition, negative impact on NMDA receptors (stimulates them), promoting dorsal horn excitability

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12
Q

what happens to glycine and GABA in chronic pain

A

they transition from inhibitory to excitatory

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13
Q

what are the effects of NSAIDS

A

antipyretic, anti inflammatory, analgesia

aceta has little anti inflammatory activity

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14
Q

NSAID MOA

A

inhibits prostaglandin production from arachidonic acid by acetylation of cyclooxygenase

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15
Q

MOA of COX1

A

contributes to hemostasis and platelet aggregation

protects the gastric mucosa via prostacyclin production

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16
Q

MOA of COX2 (4)

A

produces inflammation
contributes to fever (cytokines)
stimulates pain sensation
supports prostacyclin anti coagulation activity
both are present peripherally and in the CNS

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17
Q

NSAID PK: absorption

A

PO in stomach and small intestines
food delays absorption
IV administration may not reduce negative gastric effects
topical absorption has advantages of local targeted effect

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18
Q

NSAID PK: peak concentration

A

1-4 hours

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19
Q

NSAID PK: distribution

A

weakly acidic, highly plasma bound, lipophilic, only unbound portion is effective

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20
Q

NSAID PK: elimination

A

hepatic oxidation and conjugation
less than 10% renal elimination
some active metabolites

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21
Q

propionic acid NSAID examples (2)

A

naproxen (aleve)

ibuprofen (advil, motrin)

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22
Q

(naproxen) aleve COX selectivity, half life, elimination

A

non selective
half life of 14 hours
renal excretion

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23
Q

ibuprofen (advil, motrin) cox selectivity, peak, protein binding, anti inflammatory dose

A

non selective
peaks in 1-2 hours
highly bound to plasma
anti inflammatory effective at doses >1600mg/day

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24
Q

acetic acid NSAID examples (3)

A

diclofenic (voltaren) (COX2)
indomethacin (non selective)
ketorolac (toradol) (non selective)

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25
Q

diclofenic (voltaren) cox selectivity, elimination, toxicity considerations, risk associated with it

A

COX2 selective
hepatic toxicity
transdermal use effective without systemic toxicity
increased risk of thrombotic event

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26
Q

indomethacin COX selectivity, SE to be aware of

A

non selective

high GI side effects

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27
Q

ketorolac (toradol) COX selectivity, potency, SE

A

non selective
up to 800 times more potent than ASA
can impair renal function, limit dose to 3-5 days

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28
Q

anthranilic acid NSAID example, selectivity, half life

A

meloxicam (Mobic)
COX2 selectivity at lower doses <15mg
half life 15-20 hours

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29
Q

Celecoxib (Celebrex) selectivity, elimination, considerations, uses

A

only highly selective COX2 inhibitor available in the US
hepatic elimination
does not interfere with platelet aggregation like other COX2’s
colon polyp tx, cancer, mental illness???

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30
Q

two brand names for acetaminophen include

A

paracetamol (Tylenol)

Propocetamol (IV tylenol)

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31
Q

paracetamol (tylenol) MOA, considerations, potential toxicity, toxic dose

A

MOA inhibition of prostaglandin synthesis, weak anti inflammatory effects. poor COX inhibition
no effect on platelet function or gastric mucosa
potential hepatic toxicity, toxic dose 200mg/kg

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32
Q

what is a use for IV tylenol (propocetamol)

A

reduced postop narcotic consumption

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33
Q

acetylsalicylic acid (aspirin) COX selectivity, properties, SE’s

A

nonselective, long term antipyretic and anti inflammatory properties, permanent inhibition of COX, significant platelet response via thromboxane inhibition, significant long term side effects including bleeding and ulcers and reyes syndrome in children

34
Q

NSAID SE’s include

A 
gastric mucosa SE's being most prevalent
dyspepsia
decreased renal function
hepatic SE's
aceta hepatotoxicity (threshold 125mg/kg?)
increased plt aggregation at high doses
decreased plt aggregation at low doses
35
Q

effects of stimulating the Mu receptors include (6)

A 
analgesia
respiratory depression
euphoria
sedation
decreased GI motility
dependence
36
Q

effects of stimulating the kappa receptors include (6)

A 
spinal analgesia
sedation
dyspnea
dependence
dysphoria
respiratory depression
37
Q

effects of stimulating the delta receptors include (4)

A

psychomimetic effects
dusphoria
increase release of dopamine stimulating pleasure centers
insignificant analgesic effects

38
Q

opioid side effects include

A 
constipation
nausea
pruritis
sedation
respiratory depression
endocrine
39
Q

metabolites can produce

A

hyperalgesia

40
Q

oxycodone opioid type, primary action, metabolite specs, brand names

A

synthetic opioid
primary action is dysphoria on kappa receptors
metabolites have anti sedative effects
brand names include oxycontin and roxocodone

41
Q

oxymorphone opioid type, primary action, metabolites specs

A

synthetic opioid
primary action: mu (respiratory depression) and some delta activity (psychomimetic)
metabolites are active mu agonists

42
Q

hydrocodone opioid type, activity, brand names, combined with what

A

synthetic opioid
mu, some kappa (dysphoria)
brand names: vicodin, lortab
combined with aceta

43
Q

hydromorphone opioid type, receptor activity, brand name, way it can be utilized

A

synthetic opioid
Mu and Kappa activity (dysphoria)
brand name: dilaudid
may be used intrathecally

44
Q

methadone opioid type, receptor activity, metabolite activity, DOA, uses, SE

A

synthetic Mu agonist, NMDA antagonism involved as well.
analgesic properties like morphine but no metabolites
long acting
used for patients with morphine allergies
cardiotoxic

45
Q

tramadol opioid strength, analogue, spec

A

considered a weak opioid
analogue of codeine
considered non addictive, but it can be. seen as safer than opioids but it is not.

46
Q

is opioid therapy a good long term solution for chronic pain

A

no, bro. no.

47
Q

corticoid steroids commonly used in pain management include (3)

A

triamcinolone (kenalog)
betamethasone (celestone)
methylprednisolone (depo-medrol)
(these are all long acting)

48
Q

what can happen if you inject particulate steroids in vasculature

A

particulates can cause spinal infarct

49
Q

all steroids can have some mineralocorticoid effects including (2)

A

sodium retention and insulin resistance

50
Q

steroid side effects: frequent (2), infrequent (6)

A

fluid retention, hyperglycemia with increased insulin requirements
HTN, amenorrhea, hypokalemia, exacerbation of CHF, anaphylactoid/hypersensitivity reactions, adrenal suppresion

51
Q

steroid side effects: long term use issues (3)

A

hyperpigmentation
myopathy
osteoporosis

52
Q

do topical agents require systemic absorption

A

no

53
Q

how do topical anesthetics help treat chronic pain

A

stops peripheral transmission

54
Q

non pharmaceutical ways to increase sleep

A

mechanical aids (pillows, positioning)
natural aids (valerian, melatonin)
exercise (stretching)
biofeedback

55
Q

pharmacological pain adjuncts: antidepressants.

A

serotoninergic inhibitory properties (SSRI and SNRI)
complimentary to pain medications
may take days to weeks to be effective so they are not appropriate for acute pain
some are not effective for pain relief
increased compliance and mood reported

56
Q

how do anticonvulsants help with pain

A

pain changes sensory processes. helps with fibromyalgia (functional pain), trigeminal neuralgia (most effective).

57
Q

NMDA role in chronic pain

A

use of NMDA antagonist is being studied due to sustained chronic pain promoted by the NMDA receptor system
critical in synaptic plasticity, a cellular mechanism for learning and memory. may play a role in alzheimers disease and schizophrenia

58
Q

what has ketamine been studied/used for

A

low dose has been studied for the tx of complex regional pain syndrome (CRPS)
preemptive tx may be effective to prevent postop pain hypersensitivity (.25mg/kg)

59
Q

muscle relaxants for chronic pain

A

they have significant SE’s, should not be used as first line, should used only for a limited time.
good evidence for use with myofascial or low back pain.
most effective if used in combination with NSAIDS

60
Q

the two dimensions of perceptive pain include

A

sensory discrimination in dorsal and sensory cortex (causes perception of pain)

61
Q

lumbar radicular syndrome causes, purpose of tx, symptoms, imaging

A

causes: various discogenic, osteogenic, neurogenic. associated nerve root inflammation
purpose of treatment: to reduce nerve root pressure caused by inflammation
symptoms: pain, paresthesia and/or numbness following a particular dermatomal distribution, diminished reflexes. increased pain with straight leg raises
imaging: plain film xrays are of little value, MRI is most valuable but many false positives

62
Q

most common cause of pain and disability

A

lumbar radicular syndrome

63
Q

targeted lumbar radiculopathy: L5

where would you expect someone to complain of pain

A

buttock and anterolateral aspect of leg to calf, mid foot and great toe. difficulty heel walking, with weakness of ankle and toe extension

64
Q

targeted lumbar radiculopathy: L4

A

anterior part of the thigh, knee, and medial calf. weak knee extension and diminished patellar reflex

65
Q

targeted lumbar radiculopathy: L3/L2

A

similar alterations in sensation of thigh

66
Q

targeted lumbar radiculopathy: S1

A

posterior thigh, calf, and plantar surface of foot

67
Q

treatment options for lumbar radicular syndrome: inter laminal esi

A

blind or with imaging (fluoro or US)
catheter or without
lower risk
lowest results

68
Q

treatment options for lumbar radicular syndrome: transforaminal ESI

A

imaging (fluoro/CT and contrast required)
highest risk
best results

69
Q

treatment options for lumbar radicular syndrome: caudal esi

A

imaging recommended
catheter recommended for lumbar
most versatile
good results

70
Q

red flags (7)

A

<20 y/o, rule out congenital issues
>50, r/o malignancy, AAA
short term, <3mo look for more serious etiology
recent trauma
any signs of infection
unrelated pain
incontinence, bilateral neurological symptoms that excludes pain

71
Q

the purpose of a facet joint

A

to stabilize the spine, problems most frequently are lumbar and thoracic, but it can be cervical

72
Q

symptoms of facet arthropathy (zygapophyseal joint)

A

focal pain over joint, no significant radiculopathy, no neurological deficit, pain exaggerated on twisting movement

73
Q

definitive dx of facet arthropathy (zygapophyseal joint)

A

local injection of medial branch nerve MBNB or intra articular is only true diagnostic, but can have false positive and block is not typically therapeutic for long term. ablative therapy is next step

74
Q

purpose of sacroiliac joint

A

shock absorption for the spine, along with the job of torque conversion

75
Q

SI joint syndrome symptoms

A

pain in superior medial buttock, lateral buttock, radiation to the hip and groin

76
Q

SI joint syndrome definitive diagnosis

A

provocative (stress) maneuvers are the best diagnostic tools. studies suggest three (+) tests yield the best results. faber-patrick, gaenslens, yeomans, dillet, shear, others

77
Q

SI joint syndrome technique and results

A

imaging is recommended for best results. 22g spinal needle, 1cc steroid of choice with anesthestic 2cc in small joint. results are usually good. ablation possible

78
Q

purpose of occipital nerve

A

artists from C2/C3, exit the skull and runs perpendicular to the nuchal ridge providing sensor input for the C2/C3 facet joints and occipital area of the skull

79
Q

occipital neuritis symptoms

A

headaches that originate in the neck and radiate along the occipital skull to the top of the head and later to ear

80
Q

occipital neuritis definitive dx

A

symptomatic. definitive dx is injection, often unilateral but can be bilateral

81
Q

occipital neuritis technique and results

A

blind technique, inject lateral to midline along nuchal ridge (safest). some prerfer using imaging and injecting at C2 and C3. but this is high risk. blind technique uses anesthetic and steroid. 3-5cc.
long term results good for post concussive HA, atypical migraine, ablation possible if injection results positive but limited

N934 Adv Principles Fa 21 (23 decks)

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