Chapter 24: Pain Flashcards
Major contributors to the onset of pain
arthritis, back pain, cancer, headache
most common prescription meds used for pain relief
NSAIDs
Acute pain
nocioceptive pain that is a result of actual or pending tissue damage
duration is short
resolves with healing
chronic pain
Perception is a function of a person’s personality and character traits, cultural/ethnic backgound, presence of support systems, work/home satisfaction, and motivation
lasts longer than 3 months
cause is hard to identify
removing barriers that render pain management ineffective
stigma attached to certain medications like morphine
patient prefernce on strength
provider concerns about DEA reprisal
consequences of poorly managed pain
impaired function and quality of life
depression
polypharmacy from treated manifestations of pain (agitation, etc)
uncontrolled acute pain leading to chronic pain
properly assess pain before prescribing any drug
detailed history and physical
idetify the source of the pain
discuss realistic goals
re-examine and adjust therapy as needed
remeber the goal of using medications to manage acute pain
restore function as soon as possible
prevent the development of chronic pain syndrome
use different prescribing algorythms for mild, moderate, and severe acute pain
mild - NSAIDs and acetominophen with adjunct medications like capscaicin creams or topical salicylates (Ben-gay)
moderate - hydrocodone/APAP, hydrocodone/ibuprofen, oxycodone/APAP, or codeine
severe - pure opiates with dosages limited to less than 200mg morphine equivalent/day
use different algorythm when prescribing for chronic pain
usually requires adjunctive use of other medications for neuropathic component
comes about through hyperstimulation of NMDA receptors
remeber there is a role for adjunctive medications
drugs used to manage pain but whose primary action is ot analgesia
medications used to treat pain are generally grouped into what 2 categories
opioid and nonopioid
opiates
naturally occuring opium alkaloids or synthetic derivatives of them
multiple opiate receptor types throughout body to relieve pain
function as either agonists, partial agonists, or antagonists at one or more types of receptors
which opiate receptors are most snesitive and most important for managing general anethesia
Mu1 and Mu2
conscientious prescribing of opiates
equivalencies of using one opiate over another are approximate
when switching from oral to subQ or IV use 70-75% of dose
dose may be decreased d/t limited cross-tolerance
appropriate dose is the one that relieves pain with least side effects
schedule around the clock, not prn, especially for chronic pain
treatment of myoclonus reltaed to pain medication
change opioid or treat with lorazepam
typica dose of Narcan for overdose
0.2-0.8mg IV
up to 2mg is often given
prototype agent for antagonist agonist opiate analgesics
Morphine
morphine mechanism of action
have activity at pre- and post-synaptic mu receptors as well as pre-synaptic kappa and delta receptors
reduces neurotransmitter release from nociceptive primary afferent terminals
antagonist agonist opiate analgesic (morphine)
pharmacokinetics
- Absorption: oral, subQ, and IV absorbed well. Fentanyl not given orally because it is broken down by mucosal and hepatic P450 and 3A4
- Distribution: widely into CNS and other tissues, especially lipophillic
- Metabolism: morphine/hydromorphone by glucuronidation, fentanyl by P450 and 3A4, most others by P450 2D6 isoenzyme
- Excretion: urine
- Half-life: 2-3 hours, prolonged with hepatic impairment
opiate adverse reactions
- CV: ortho hypotension, decreased BP
- DERM: occasional allergic rash/pruritus
- EENT: visual changes
- GI: constipation, n/v, abdominal cramps, dry mouth
- GU: urine retention
- META: decreased appetite, increased urine glucose
- NEURO: sedation, diaphoresis, flushing, somnolence, dizziness
- PUL: overdose=respiratory depression with skeletal muscle flaccidity, cold/clammy skin, cyanosis, extreme somnolence progressing to seizures, stupor, coma, death
opiate interactions
anything that causes respiratory depression
medications that prolong QT interval if using methadone or buprenorphine
mixed/partial agonist-antagonist analgesics
4 available agents
buprenorphine (Buprenex, Subutex)
pantazocine (Talwin)
nalbuphine (Nubain)
butorphanol (Stadol)
can precipitate withdrawal symptoms in patients taking chronic opiates
clinical use of buprenorphine
alters emotional perception of pain
sed as an alternative to methadone in opioid detox because of slow dissociation from mu receptor
antagonist at delta and kappa receptors
low analgesi activity
clinical use for pentazocine (Talwin) and nalbuphine (Nubain)
treat mod-severe pain
higher rate of hallucinations, nightmares, and anxiety than other opioids
Talwin is used as a supplement to surgical anethesia or pre-surgical sedative
clinical use of butorphanol (Stadol)
available as nasal spray and IV
treat mod-severe pain (migraines)
supplement anethsesia
pain during labor
synthetic opiate antagonists
bind to same opioid receptors as morphine but with higher affinity so it blocks effects of opioid
precipitates withdrawal symptoms in opioid-dependency
no effect on non-addicts
naloxone (Narcan)
fast onset (minutes)
will antagonize post-op analgesics
Narcan mechanism of action
high affinity for mu sites
antagonistic effects at delta and kappa sites
clinica use of Narcan
opioid overdose
Narcan pharmacokinetics
- Absorption: very poor from GI tract, well absorbed when given SC or IV
- Distribution: rapidly to all tissues, crosses placenta
- Metabolism: glucuronide conjugation in the liver
- Excretion: urine
- Half-life: 1-2 hours
Narcan adverse reactions
- CV: HTN, hypotension, v-fib, tachycardia
- GI: n/v
- MISC: severe opiate withdrawal
methylnaltrexone (Relistor)
no risk for abuse/dependency
peripherally acting mu opioid receptor antagonist
does not cross blood brain barrier
Relistor clinical uses and contraindication
treats opioid induced constipation (counteracts opioid effects like constipation and itching without effecting analgesia because it doesn’t cross the blood brain barrier)
contraindicated in GI obstruction
Relistor pharmacokinetics
- Absorption: admin SC w/ peak concentration in 30 minutes
- Distribution: moderate
- Metabolism: slightly via methylation in the liver
- Excretion: 85% unchanged, half in urine, half in feces
- Half-life: 8 hours
Reistor adverse reactions
- DERM: hyperhidrosis
- GI: abdominal pain, gas, nausea, severe and/or persistent diarrhea
- NEURO: dizziness
nalmefene (Revex) and naltrexone (ReVia, Trexan)
similar chemical structures
used to decrease craving for opioids
naltrexone: used in “rapid detox” for opiate addicts and alcoholics
nalfmefene: long-acting injectable used to prevent alcoholic from relapsing
examples of nonopiate analgesics
tramadol (Ultram)
ziconotide (Prialt)
tapentadol (Nucynta)
tramadol (Ultram)
centrally acting synthetic agent with analgesic properties
used for mod-moderatly severe pain
can be subject to abuse
tramadol (Ultram) mechanism of action
binds to mu receptors in CNS and
inhibits reuptake of serotonin and norepinephrine
to modify the acending pathways of pain
tramadol pharmacokinetics
- Absorption: good absorption through GI tract
- Deistribution: widely
- Metabolism: liver
- Excretion: urine
- Half-life: 6-8 hours
tramadol adverse effects
- CV: flushing
- DERM: rash
- EENT: burry vision, miosis
- GI: nausea, constipation
- MISC: flu-like symptoms
- NEURO: dizziness, headache, insomnia, somnolence, weakness, and possible seizures
tramadol contraindications
seizure disorders or concomittent use with medications that lower seizure threshold
ziconotide (Prialt)
used for severe chronic pain when IT (intrathecal) therapy is warranted
administered directly into CSF
for patients who are intolerant of or refractory to other treatments
Prialt mechanism of action
blocks excitatory neurotransmitter release and reduces their sensitivity to painful stimuli
Prialt contraindications
history of psychosis, schizophrenia, clinical depression, bipolar disorder and seizures
Prialt pharmacokinetics
- Absorption: administered directly into CSF
- Distribution: 50% bound to protein
- Metabolism: by several enzymes inmultiple organs degrade it to peptide fragments and free amino acids
- Excretion: urine
- Haf-life: 2.9-6.5 hours
Prialt adverse reactions
- EENT: abnormal vision
- GI: nausea, anorexia
- NEURO: dizziness, confusion, headache, hypertonia, ataxia, somnolence, unsteadiness, memory impairment
most severe are hallucinations, suicidal idation, new/worsening depression ans seizures
Tapentadol
similar to tramadol
similar to oxycodone inits ability to relieve severe pain, but very inexpensive
NSAIDs
several available with similar pain alleviating effects and adverse reaction profiles
NSAID mechanism of action
- inhibit COX, resulting in decresed formation of prostaglandin precursors (PGE2, prostacyclin, and thromboxane) and an inhibition of phospholipids
- may also inhibit lipoxygenase
- extent of inhibition varies with each chemicla category
- produces vasodilation by acting on the heat-regulation center of the hypothalamus
Clinical uses of NSAIDs
pain relief
reduce inflammation
reduce fever
NSAID contraindications
active peptic ulcers
chronic inflammation of the GI tract
GI bleeding
history of ulceration
history of sensitivity to ASA or other NSAIDs
NSAID pharmacokinetics
- Absorption: rapidly from GI tract
- Distribution: 90% via protein binding
- Metabolism: in liver to water soluble metabolite
- Excretion: urine
- Half-life: most are 2-4 hours
NSAID adverse reactions
- CV: edema
- DERM: itiching, rash
- ENDO: fluid retention
- GI: abdominal pain. cramps, heartburn, constipation, gas, decreased appetite
- NEURO: dizziness, headache, nervousness
NSAID interactions
inhibits alpha blockers, ACE inhibitors, ARBs, beta blockers, and diuretics
decreased platelet aggregation with anticoagulants
decreased clearance with aminoglycosides
GI bleed with corticosteroids
NSAID conscientious considerations
watch for hypersensitivity reactions and renal impairment
do not use in last trimester
stop one week before elective surgery
high doses do not increase effect
ASA properties
analgesic, antipyretic, anti-inflammatory, antiplatelet
higher doses required for anti-inflammatory effect
ASA antiplatelet effect
significantly reduces risk of MI and CVA
mearurable prolongation of bleeding time
inhibitory platelt aggregation effect lasts up to 8 days
ASA mechanism of action
inhibits prostaglandin and thromboxane synthesis
salicylism
mild, chronic salicylate intoxication after repeated administration of high doses
symptoms: headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation, n/v, occasional diarrhea
IMMEDIATE treatment required
treatment of salicylism
gastric lavage
activated charcoal to absorb drug left in stomach
ASA and Reye’s syndrome
association exists in children
no ASA under 16yo
acetominophen mechanism of action
exact site and mechanism not known
possibly inhibits nitric oxide pathway mediated by multiple neurotransmitter receptors, most notable substance P and NMDA
blocks production and release of PGEs into CNS and blocks their effects in the heat-regulating areas of the anterior hypothalamus
clinical uses of acetominophen
analgesic, antipyretic, mild arthritis, analgesic in those taking anticoagulants or children (not associated with Reyes syndrome)
acetominophen contraindications
liver disease
allergy
acetominophen conscientious considerations
risk for hepatotoxicity in malnourished and alcohol abusers
any drug that increases action of liver enzymes may nullify effect
safe in pregnancy and lactation
