Non Surgical Pain Flashcards

1
Q

common chronic pain conditions (4)

A

lumbar radiculopathy
facet arthroplathy
SI joint dysfunction
occipital neuritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

material released after trauma includes (8)

A
potassium
plasma
RBC/WBC's
clotting factors
peptides
prostaglandins
inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

materials released after trauma are through to enhance

A

activation of membrane channels (Na/Ca/etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

release of these two things cause vascular leaking leading to swelling

A

substance p

calcitonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what happens to glycine and GABA in chronic pain

A

they transition from inhibitory to excitatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the effects of NSAIDS

A

antipyretic, anti inflammatory, analgesia

aceta has little anti inflammatory activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

NSAID MOA

A

inhibits prostaglandin production from arachidonic acid by acetylation of cyclooxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MOA of COX1

A

contributes to hemostasis and platelet aggregation

protects the gastric mucosa via prostacyclin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

NSAID PK: peak concentration

A

1-4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

NSAID PK: distribution

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

NSAID PK: elimination

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

propionic acid NSAID examples (2)

A

naproxen (aleve)

ibuprofen (advil, motrin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

(naproxen) aleve COX selectivity, half life, elimination

A

non selective
half life of 14 hours
renal excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

acetic acid NSAID examples (3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
diclofenic (voltaren) cox selectivity, elimination, toxicity considerations, risk associated with it
COX2 selective hepatic toxicity transdermal use effective without systemic toxicity increased risk of thrombotic event
26
indomethacin COX selectivity, SE to be aware of
non selective | high GI side effects
27
ketorolac (toradol) COX selectivity, potency, SE
non selective up to 800 times more potent than ASA can impair renal function, limit dose to 3-5 days
28
anthranilic acid NSAID example, selectivity, half life
meloxicam (Mobic) COX2 selectivity at lower doses <15mg half life 15-20 hours
29
Celecoxib (Celebrex) selectivity, elimination, considerations, uses
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???
30
two brand names for acetaminophen include
paracetamol (Tylenol) | Propocetamol (IV tylenol)
31
paracetamol (tylenol) MOA, considerations, potential toxicity, toxic dose
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
32
what is a use for IV tylenol (propocetamol)
reduced postop narcotic consumption
33
acetylsalicylic acid (aspirin) COX selectivity, properties, SE's
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
NSAID SE's include
``` 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
effects of stimulating the Mu receptors include (6)
``` analgesia respiratory depression euphoria sedation decreased GI motility dependence ```
36
effects of stimulating the kappa receptors include (6)
``` spinal analgesia sedation dyspnea dependence dysphoria respiratory depression ```
37
effects of stimulating the delta receptors include (4)
psychomimetic effects dusphoria increase release of dopamine stimulating pleasure centers insignificant analgesic effects
38
opioid side effects include
``` constipation nausea pruritis sedation respiratory depression endocrine ```
39
metabolites can produce
hyperalgesia
40
oxycodone opioid type, primary action, metabolite specs, brand names
synthetic opioid primary action is dysphoria on kappa receptors metabolites have anti sedative effects brand names include oxycontin and roxocodone
41
oxymorphone opioid type, primary action, metabolites specs
synthetic opioid primary action: mu (respiratory depression) and some delta activity (psychomimetic) metabolites are active mu agonists
42
hydrocodone opioid type, activity, brand names, combined with what
synthetic opioid mu, some kappa (dysphoria) brand names: vicodin, lortab combined with aceta
43
hydromorphone opioid type, receptor activity, brand name, way it can be utilized
synthetic opioid Mu and Kappa activity (dysphoria) brand name: dilaudid may be used intrathecally
44
methadone opioid type, receptor activity, metabolite activity, DOA, uses, SE
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
tramadol opioid strength, analogue, spec
considered a weak opioid analogue of codeine considered non addictive, but it can be. seen as safer than opioids but it is not.
46
is opioid therapy a good long term solution for chronic pain
no, bro. no.
47
corticoid steroids commonly used in pain management include (3)
triamcinolone (kenalog) betamethasone (celestone) methylprednisolone (depo-medrol) (these are all long acting)
48
what can happen if you inject particulate steroids in vasculature
particulates can cause spinal infarct
49
all steroids can have some mineralocorticoid effects including (2)
sodium retention and insulin resistance
50
steroid side effects: frequent (2), infrequent (6)
fluid retention, hyperglycemia with increased insulin requirements HTN, amenorrhea, hypokalemia, exacerbation of CHF, anaphylactoid/hypersensitivity reactions, adrenal suppresion
51
steroid side effects: long term use issues (3)
hyperpigmentation myopathy osteoporosis
52
do topical agents require systemic absorption
no
53
how do topical anesthetics help treat chronic pain
stops peripheral transmission
54
non pharmaceutical ways to increase sleep
mechanical aids (pillows, positioning) natural aids (valerian, melatonin) exercise (stretching) biofeedback
55
pharmacological pain adjuncts: antidepressants.
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
how do anticonvulsants help with pain
pain changes sensory processes. helps with fibromyalgia (functional pain), trigeminal neuralgia (most effective).
57
NMDA role in chronic pain
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
what has ketamine been studied/used for
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
muscle relaxants for chronic pain
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
the two dimensions of perceptive pain include
sensory discrimination in dorsal and sensory cortex (causes perception of pain)
61
lumbar radicular syndrome causes, purpose of tx, symptoms, imaging
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
most common cause of pain and disability
lumbar radicular syndrome
63
targeted lumbar radiculopathy: L5 | where would you expect someone to complain of pain
buttock and anterolateral aspect of leg to calf, mid foot and great toe. difficulty heel walking, with weakness of ankle and toe extension
64
targeted lumbar radiculopathy: L4
anterior part of the thigh, knee, and medial calf. weak knee extension and diminished patellar reflex
65
targeted lumbar radiculopathy: L3/L2
similar alterations in sensation of thigh
66
targeted lumbar radiculopathy: S1
posterior thigh, calf, and plantar surface of foot
67
treatment options for lumbar radicular syndrome: inter laminal esi
blind or with imaging (fluoro or US) catheter or without lower risk lowest results
68
treatment options for lumbar radicular syndrome: transforaminal ESI
imaging (fluoro/CT and contrast required) highest risk best results
69
treatment options for lumbar radicular syndrome: caudal esi
imaging recommended catheter recommended for lumbar most versatile good results
70
red flags (7)
<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
the purpose of a facet joint
to stabilize the spine, problems most frequently are lumbar and thoracic, but it can be cervical
72
symptoms of facet arthropathy (zygapophyseal joint)
focal pain over joint, no significant radiculopathy, no neurological deficit, pain exaggerated on twisting movement
73
definitive dx of facet arthropathy (zygapophyseal joint)
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
purpose of sacroiliac joint
shock absorption for the spine, along with the job of torque conversion
75
SI joint syndrome symptoms
pain in superior medial buttock, lateral buttock, radiation to the hip and groin
76
SI joint syndrome definitive diagnosis
provocative (stress) maneuvers are the best diagnostic tools. studies suggest three (+) tests yield the best results. faber-patrick, gaenslens, yeomans, dillet, shear, others
77
SI joint syndrome technique and results
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
purpose of occipital nerve
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
occipital neuritis symptoms
headaches that originate in the neck and radiate along the occipital skull to the top of the head and later to ear
80
occipital neuritis definitive dx
symptomatic. definitive dx is injection, often unilateral but can be bilateral
81
occipital neuritis technique and results
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