Pain

nMost common reason people seek health care

nTissue damage activates free nerve endings (pain receptors)

nGenerally indicates tissue damage

Pain

nDefined as whatever the patient says it is

nIt exists whenever he or she says it does

Gate Theory
Pg 122 Fig 9-1

nInjury results in release (from the tissues) of

nBradykinin

nHistamine

nProstoglandins

nAction potential along nerve fiber

nActivates pain receptor

nEnter the spinal cord via the dorsal horn

nIf impulses can be stopped here…pain stops

 

Gate Theory

nBrain can evaluate, identify and localize pain

 

Bradykinin

nStrongest pain producing substances

nMay be involved in acute pain

nProstglandins increase sensitivity to pain

nChemical mediators activate and sensitize pain receptors or stimulate the release of pain producing substances

 

 

Endogenous Analgesia

nActivated by nerve signals or by morphine-like substances entering the brain

nOpiate receptors

nEndogenous peptides

Pain Treatment

nOften UNDER treated

nCancer pain management in particular

nNot aimed at prevention of addiction

nPatient comfort

nTolerance may occur

Pg 123 (do not confuse with addiction)

 

 

Opiod Analgesics

nModerate to severe pain

nReduction of pain sensation

nSedation

nDecreases emotional upset

nMost are schedule II

Opioid Analgesics

nOral, IM, SQ, & IV

n PO requires high doses

nPrevent or relieve acute or chronic pain

nBind to opioid receptors in the brain and spinal cord and activate the endogenous system

 

 

nAgonist-binds to a receptor site and causes a response

nPartial agonist-binds to a receptor and causes only limited actions

nAntagonist-bind to a receptor and produce no response

Agonists
Prototype: Morphine Sulfate

nMorphine and morphine like drugs

nActivity at Mu, Kappa, & ??? Delta receptors

nSevere & Chronic Pain

nIV, IM, SQ, Suppository, Epidural,&, PO

nImpaired kidney function may cause prolonged drug action and accumulation

nNonceiling drug

Prototype:
Codeine

n PO onset 15-30 minutes duration 4-6 hours

nNaturally occurring opium alkaloid

nANTI-TUSSIVE

nAnalgesic

nMilder adverse effects than morphine

nMay be combined with Acetaminophen

 

Contraindications

nRespiratory depression

nChronic lung disease

nLiver or kidney disease

nProstatic hypertrophy

nIncreased ICP

Agonist/Antagonist
Prototype: Nalbuphine (Nubain)

nAgonist activity at some sites and antagonist at others

nLow abuse potential

nPotent analgesics

nMay produce withdrawal symptoms in those with opiate dependence

nSynthetic

Opioid Antagonist
Prototype: Naloxone (Narcan)

nReverse or block analgesia, respiratory depression

nOnset within minutes and last 1-2 hours

nShorter duration than opioids

nMay give repeated injections

 

Withdrawal
Pg 125

nAnxiety, aggressiveness, restlessness, lacrimation, rhinorhea, perspiration, pupil dilation, piloerection, elevated body temp, diarrhea, BP

nBegin within few hours of last dose

nEarly recognition and treatment key

Side Effects & Assessments

nRespiratory depression

nHypotension

nN & V

nConstipation

nMonitor respirations

nOrthostatic pressures

nBP

nBowel regimen

Teaching

nNo Etoh

nDo not increase dose (unless Rx’d)

nStay in bed 30-60 minutes after receiving

nNo heavy machinery

nHigh fiber foods & increase fluids

Non Opioid Analgesics

Analgesic, Antipyretic, &

Anti-inflammatory Drugs

 

nAcetylsalic Acid (Aspirin)

nAcetominophen (Tylenol)

nIbuprofen (Motrin)

 

Prototype
Acetominophen

nDoes not cause N & V or GI bleeding

nDoes not interfere with clotting

nLacks anti-inflammatory activity

nMetabolized in liver

nAlters pain perception

 

Side Effects

nHepatic necrosis (Acute overdose)

nNephropathy (Chronic overuse)

nLiver toxicity increase with alcohol ingestion!

 

Mucolytic
Prototype: Acetylcysteine (Mucomyst)

nAntidote to Acetaminophen overdose

nGive PO

nMust be given within 24 hours

nBad smell

n17 doses

nPg 132

Activated Charcoal

May be given for an overdose of Acetaminophen

Other NSAIDS

Arachidonic Acid Pathway

nReleased after injury

nMetabolized

nBoth paths result in inflammation and pain

GI Distress

nProstaglandins maintain the integrity of stomach

nInhibition sets up

nUlceration

nGI bleeds

nMisoprostol

 

Prototype
ASA (Aspirin)

nInhibits the synthesis of prostaglandins

nNon selective COX inhibitor

nAntiplatelet and Antipyretic

nPrevent sensitization of pain receptors to various chemical substances

Contraindications

nPUD

nGI or other bleeding disorders

nHypersensitivity

nImpaired renal function

nChildren with viral infections (pg 671)

nIntoxication  (table 42-2)

Prototype
Ibuprofen (Motrin)

nAnti-inflammatory agent

nOTC

nMay be better tolerated than aspirin but work in a similar fashion

nHypersensitivity may occur in people with allergy to aspirin

nContraindications similar to ASA (except Reye’s)

Selective COX-2 Inhibitor
Prototype: Celecoxib (Celebrex)

nDesigned to relieve pain, fever,  and inflammation

nFewer side effects than older NSAIDS

nContraindicated with ulcers, GI bleeds, asthma, severe renal impairment, & allergy to other NSAIDS

Feverfew

nRelieves HA, fever, and menstrual irregularities

nCan increase bleeding with aspirin, dipyridamole, warfarin

nContraindicated in pregnant patients, breastfeeding, and children < 2 y/o

 

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