Pharmacology Of Pain Management

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chronic pain

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persists > 3-6 months

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pain meds

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opiods
alpha-2 agonists
local anesthetics
anti-inflammatory drugs

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4 stages of nociception

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transduction
transmission
perception
modulation

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nocieptive nerve terminals

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respond to noxious stimuli & inflammatory mediators(histamine, serotonin, bradykinin, prostaglandins, ATP, H+, nerve growth factor, TNF-alpha, endothelins, interluekins

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local anesthetics block

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transmission

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modulation

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involves descending inhibition
midbrain triggers release of NE, serotonin, and endogenous opoids to reduce pain transmission

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endogenous opiod

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endorphins, dynorphins, and ekephalins
inhibit pain transmission and perception
stimulated by exercise & stress to prevent pain from being able to escape a dangerous situation

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strong agonist opiods

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alfentanil
fentanyl
heroin
meperidine
methadone
morphine
oxycodone
remifentanil
sufentanil

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moderate/low opioid agonists

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codeine (anti-tussive)
prpoxyphene

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opioid antagonists

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nalmefene
noloxone
naltrexone

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opioid receptor types

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mu, delta, kappa
level of analgesia
mu>delta>kappa

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activation of kappa receptors

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can produce hallucinogenic effects

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opioids derived from opium

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morphine - poor PO effectiveness (metabolized to codeine)

codeine - high anti-tussive potency, good PO effectiveness, added to APAP/NSAIDs for additive analgesia w/no increase in AEs

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dihydromorphone

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diluadid
semisynthetic narcotic
high potency
good CSF:plasma ration

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oxycodone

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semisynthetic narcotic
10x potency of codeine
oxycontin is CR dosage form

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fentanyl

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synthetic opioid agonist
derivatives: sulfentayl, alfentayl, remifentanyl
100x more potent than morphine
IV for anesthesia

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Etorphine

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synthetic opioid agonist in veterinary medicine
extremely potent & always packaged with a potent antagonist, diprenorphine

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methadone

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synthetic opioid agonist
long plasma t1/2
used in tx of narcotic dependence

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buprenorphine

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busprenex
partial opioid agonist at mu receptor
used in opiate detoxification
causes littler sedation, hypotension and respiratory depression even at high doses

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opiate detoxificat

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methadone - available only at specialized clinics
buprenorphine - less severe & shorter withdrawal symptoms than methadone, can be used to office-based detoxification or maintenance

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Butorphanol & Nalbuphine

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preoperative meds to relieve moderate-severe pain
have ceiling effect for respiratory depression
effective for migraine HDs (few peripheral AEs)

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opoid adverse effects

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sedation
respiratory depression (reduces sensitivity to respiraotry centers to CO2 in brain stem)
constipation
nausea
miosis
urinary retention

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AEs with no tolerance to opioids

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constipation
miosis

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naloxone

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opioid antagonist
short t1/2
poor PO absorption
reverse herion effects

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targin

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oxycodone + naloxone (used to tx chronic pain)
lower gi AEs

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suboxone

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buprenorphine + nalaoxone
-used for tx of addiction

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COX 2

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produces PGs from arachidonic responsible or inflammation & paint

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COX 1

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produces PGs from archiodonic responsible for maintenance & protection of GI tract

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celecoxib

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selective cox-2 inhibitor
decreased GI effects
increase risk of heart attack, thrombosis, and stroke

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migraine pathophysiology theories

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1) inappropritate contraction and dilation of brain blood vessels, leaky vessels release inflammatory mediators (substance P)
2)abnormal central processing of sensory information

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activation of 5HT-1 receptors

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causes vasoconstriction
lead to development of sumatriptan to tx migraine HDs
GPCR
decreases levels of cAMP

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5-HT3

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only sertonin receptor that is a ligand gated ion channel (Na+/K+, excitatory) rest are GPCRs

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sumitriptan MOA

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B, D, and F subtypes of 5HT1 are found to be involved in a migraine
sumatriptan binds to D subtype

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triptans MOA

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bind to 5HT which are Gi coupled (activate K+ & inhibit Ca2+ pre & post-synaptically) leading to inhibition of nueronal excitability and inhibition of inflammatory mediator release

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modulation occurs in

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spinal cord
thalamus
cortex

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faster conduction w/

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more myelination
bigger diameter
transmit inital intense pain, fibers w/small diameters & less myelin transmit chronic dull pain

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nerve growth factor

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inflammatory mediator released by macrophages
indirectly activates ion channels resulting in pain

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most prominent excitatory nuerotransmitter

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glutamate

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substance P

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activates new signals in secondary neurons in dorsal horn

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reticular formation is suppressed when

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you have chronic pain or tired

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eipural opioids

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can number certain areas of body without brain side effects

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gating mechanism

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can attenuate pain going up to the brain
in spinal cord & procesing circuits in brain
stimulation of locus cerlues releases NE - flight/fight response - decreased pain transmission

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alpha-2 adrenergic blockers MOA

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receptors coupled to Gi
increase K+ efflux - hyperpolarization - inhibits glutamate relase
inhibit Ca2+ - reduction in nuerotransmisstion

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nueropathic pain in DMs

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damage to nerve fibers causes them to fire without noxious stimuli

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alpha-2 adrenergic receptors

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can be activated by serotonin
why TCAs can be sued to tx chronic fatigue syndrome in MS/fibromyalgia/chronic pain

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cymbalta MOA

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increase NE in synaptic space which activates alpha-2 adrenergic receptors to tx fibromyalgia

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lyrica MOA

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inhibits Ca2+ channels in alpha-2 receptors to tx fibromyalgia

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Peptide nuerotransmitter

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made as protiens and stored in vesicles assembled in golgi appartus
cleaved in vesicle at nerve terminal into actual peptide

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synthetic opoids are

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piperidine derivatives (6-membered righ w/nitrogen)

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Fentanyl is more potent than

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morphine
can't take advantage of extra potency due to respiratory depression

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opoids can cause

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loss of consciousness at higher doses
nausea
constipation (opoid receptors in GI tract)
convulsions (uncontrolled excitation indirectly by binding to opiod receptors on GABA nuerons thus preventing their release)
antitussive
miosis
urinary retention

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need to wean off opoids or

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could have life-threatening convulsions

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opoid addiction

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changes in brain circuits
bind to opiod receptors on GABA nuerons inhibitng GABA release which increases dopamine release (normally inhibited by GABA) which causes reward

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morphine

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gold standard to which other opiods are compared
active metabolite is more potent (can accumulate renal damage)
not effective PO unlike codeine

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heroin

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replaces hydroxyls with acetyls groups on morphine making it more lipophillic

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methadone

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NMDA receptor antagonist
more potent than morphine
eurphoria & reward circuit are acitvated by NMDA receptors
used to tx addiction