Non Surgical Pain Flashcards
common chronic pain conditions (4)
lumbar radiculopathy
facet arthroplathy
SI joint dysfunction
occipital neuritis
material released after trauma includes (8)
potassium plasma RBC/WBC's clotting factors peptides prostaglandins inflammatory cells
materials released after trauma are through to enhance
activation of membrane channels (Na/Ca/etc)
release of these two things cause vascular leaking leading to swelling
substance p
calcitonin
pain response without tissue injury
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
if you sit on a thumb tack, describe the a fiber and c fiber response
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
pain response with tissue injury
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
pain response with nerve injury description
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
evolution of chronic pain (5)
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)
what encompasses a windup or “enhanced spinal response”
- neurotransmitters (3)
- cell effected
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
during the windup or enhanced spinal response, what encompasses the loss of central inhibition mechanisms
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
what happens to glycine and GABA in chronic pain
they transition from inhibitory to excitatory
what are the effects of NSAIDS
antipyretic, anti inflammatory, analgesia
aceta has little anti inflammatory activity
NSAID MOA
inhibits prostaglandin production from arachidonic acid by acetylation of cyclooxygenase
MOA of COX1
contributes to hemostasis and platelet aggregation
protects the gastric mucosa via prostacyclin production
MOA of COX2 (4)
produces inflammation
contributes to fever (cytokines)
stimulates pain sensation
supports prostacyclin anti coagulation activity
both are present peripherally and in the CNS
NSAID PK: absorption
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
NSAID PK: peak concentration
1-4 hours
NSAID PK: distribution
weakly acidic, highly plasma bound, lipophilic, only unbound portion is effective
NSAID PK: elimination
hepatic oxidation and conjugation
less than 10% renal elimination
some active metabolites
propionic acid NSAID examples (2)
naproxen (aleve)
ibuprofen (advil, motrin)
(naproxen) aleve COX selectivity, half life, elimination
non selective
half life of 14 hours
renal excretion
ibuprofen (advil, motrin) cox selectivity, peak, protein binding, anti inflammatory dose
non selective
peaks in 1-2 hours
highly bound to plasma
anti inflammatory effective at doses >1600mg/day
acetic acid NSAID examples (3)
diclofenic (voltaren) (COX2)
indomethacin (non selective)
ketorolac (toradol) (non selective)
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
indomethacin COX selectivity, SE to be aware of
non selective
high GI side effects
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
anthranilic acid NSAID example, selectivity, half life
meloxicam (Mobic)
COX2 selectivity at lower doses <15mg
half life 15-20 hours
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???
two brand names for acetaminophen include
paracetamol (Tylenol)
Propocetamol (IV tylenol)
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
what is a use for IV tylenol (propocetamol)
reduced postop narcotic consumption
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
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
effects of stimulating the Mu receptors include (6)
analgesia respiratory depression euphoria sedation decreased GI motility dependence
effects of stimulating the kappa receptors include (6)
spinal analgesia sedation dyspnea dependence dysphoria respiratory depression
effects of stimulating the delta receptors include (4)
psychomimetic effects
dusphoria
increase release of dopamine stimulating pleasure centers
insignificant analgesic effects
opioid side effects include
constipation nausea pruritis sedation respiratory depression endocrine
metabolites can produce
hyperalgesia
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
oxymorphone opioid type, primary action, metabolites specs
synthetic opioid
primary action: mu (respiratory depression) and some delta activity (psychomimetic)
metabolites are active mu agonists
hydrocodone opioid type, activity, brand names, combined with what
synthetic opioid
mu, some kappa (dysphoria)
brand names: vicodin, lortab
combined with aceta
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
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
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.
is opioid therapy a good long term solution for chronic pain
no, bro. no.
corticoid steroids commonly used in pain management include (3)
triamcinolone (kenalog)
betamethasone (celestone)
methylprednisolone (depo-medrol)
(these are all long acting)
what can happen if you inject particulate steroids in vasculature
particulates can cause spinal infarct
all steroids can have some mineralocorticoid effects including (2)
sodium retention and insulin resistance
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
steroid side effects: long term use issues (3)
hyperpigmentation
myopathy
osteoporosis
do topical agents require systemic absorption
no
how do topical anesthetics help treat chronic pain
stops peripheral transmission
non pharmaceutical ways to increase sleep
mechanical aids (pillows, positioning)
natural aids (valerian, melatonin)
exercise (stretching)
biofeedback
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
how do anticonvulsants help with pain
pain changes sensory processes. helps with fibromyalgia (functional pain), trigeminal neuralgia (most effective).
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
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)
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
the two dimensions of perceptive pain include
sensory discrimination in dorsal and sensory cortex (causes perception of pain)
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
most common cause of pain and disability
lumbar radicular syndrome
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
targeted lumbar radiculopathy: L4
anterior part of the thigh, knee, and medial calf. weak knee extension and diminished patellar reflex
targeted lumbar radiculopathy: L3/L2
similar alterations in sensation of thigh
targeted lumbar radiculopathy: S1
posterior thigh, calf, and plantar surface of foot
treatment options for lumbar radicular syndrome: inter laminal esi
blind or with imaging (fluoro or US)
catheter or without
lower risk
lowest results
treatment options for lumbar radicular syndrome: transforaminal ESI
imaging (fluoro/CT and contrast required)
highest risk
best results
treatment options for lumbar radicular syndrome: caudal esi
imaging recommended
catheter recommended for lumbar
most versatile
good results
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
the purpose of a facet joint
to stabilize the spine, problems most frequently are lumbar and thoracic, but it can be cervical
symptoms of facet arthropathy (zygapophyseal joint)
focal pain over joint, no significant radiculopathy, no neurological deficit, pain exaggerated on twisting movement
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
purpose of sacroiliac joint
shock absorption for the spine, along with the job of torque conversion
SI joint syndrome symptoms
pain in superior medial buttock, lateral buttock, radiation to the hip and groin
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
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
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
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
occipital neuritis definitive dx
symptomatic. definitive dx is injection, often unilateral but can be bilateral
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
