Chapter 24: Pain Flashcards Preview

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Flashcards in Chapter 24: Pain Deck (68):



Major contributors to the onset of pain



arthritis, back pain, cancer, headache




most common prescription meds used for pain relief







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


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






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 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)


  • 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







similar to tramadol

similar to oxycodone inits ability to relieve severe pain, but very inexpensive







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






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





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