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Pain Kim Baily RN, MSN, PhD
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
Whatever the person says it is and existing whenever the person says it does (Margo McCaffery)
Physiology
o Nociception
 Noxious stimuli activation of primary afferent nerves (PANs)
 Nociceptors sense and transmit pain signals
o Gate Control Theory
 Pain transmitted to the dorsal horn of the spinal cord (substantia gelatinosa)
 Cells act as a gate which can be either opened or closed
 Gates are influenced by stimulatory or inhibitory signals from either the periphery or
higher centers in the CNS
 Brain does not perceive pain while it is occupied with other sensory input
 Massage, vibration, pressure, heat, cold, non-drug
o Transduction
 Noxious stimuli – pressure, heat, and chemical activate primary afferent Nociceptors
 Tissue damage leads to release of chemicals around the Primary Afferent Neuron
(PAN)
 Bradykinin, histamine, prostaglandins, substance P
 Local inflammatory response
o Transmission
 Projection to CNS
 Different types of fibers cause different sensations
 A - fast large myelinated fibers = sharp, well localized and distinct pain
 C fibers – very small, slow unmyelinated dull – poorly localized, persistent
aching, burning sensation, diffuse nature, slow onset,
 Processing in dorsal horn
 Substantia gelatinosa - dorsal horn act as gate
 Pain impulses then cross spinal cord from dorsal horn (via interneurons) and travel via
either of two pathways to higher levels of CNS
 Spinothalamic tract (STT)
 Spinoreticular tract (SRT)
 Transmitters can facilitate or inhibit transmission to a second neuron in the dorsal
horn synapses
 Perception of pain is based on the modulation ascending pathways and descending
inhibitory pathways
 Drugs which cause membrane stabilization inactivate sodium channels, prevent action
potential - Prevent transmission
 E.g. lidocaine, bupivacaine
 Anti seizure drugs
o phenytoin (dilantin).
o gabapentin (Neurontin)
Referred pain
o Not clearly understood
o Pain transmission may be carried by fibers that also carry info from distance anatomical
locations  referred pain
o Same spinothalamic tracts
o Related embryological dermatomes
Endorphins (from endogenous and morphine)
o These are the body’s pain relievers, (natural opioids)
o
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Descending (efferent) pathways from thalamus and midbrain carry inhibitory impulses which
prevent the release of neurotransmitters associated with pain e.g. substance P and
prostaglandins
Pain Perception
o Pain Perception – Conscious experience of discomfort occurs when the pain threshold is
reached.
o Pain Threshold – Point at which sufficient signals reach the brain
o Pain Tolerance – Point at which individual withdraws or asks to have the stimulus stopped
Classification of Pain
o Nociceptive
o Neuropathic pain
o Acute versus Chronic
o Somatic, Visceral or Superficial
o Phantom limb pain
Pain Assessment
o Onset, Pattern, Quality/nature, Intensity, Location, Duration, Relief,See text for pain
assessment tools
o Special consideration for Older Adult,Cognitively Impaired
Nurses Attitudes About Pain
o Silent suffering – most valued response to pain in US.
o Nurses tend to be “stoic and non-verbal”
o “When in pain, nurses expect people to stay calm and avoid complaining, screaming or
crying”
o YOU bring your own attitudes with you
o Power!!
o Patient is at the mercy of the nurse
o Respect clients response to pain
o Never stereotype a person based on culture
o Facts
 Nurses commonly under-medicate patients who don’t appear to be in pain
 Patients with chronic pain don’t have predictable VS changes
 Over time, undermedication  fear and depression
 Patients with chronic pain don’t develop tolerance to pain
 Nurses more willing to medicate if obvious physical reasons for pain
Vital Signs
o VITAL SIGNS ARE NOT A RELIABLE INDICATOR OF PAIN
Pain Management
JCAHO
APA
Standards for the Relief of Acute Pain and Cancer Pain
WHO Analgesic Ladder
o Mild pain
 Low doses on nonopioid drugs
o Intermediate pain or pain not well controlled with nonopioid
 Combine nonopioid with low-dose opioid
 Adjuvants
o Severe pain
 Higher doses of opioids
Equianalgesic dose
o Dose of drug to produce the same effect as:
o Standard 10 mg morphine IM
Scheduling
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Prevention is the key
Continuous versus PRN medication
Additional dose for breakthrough pain
Step 1 Non-opioids
o NSAIDs/Acetaminophen – see Chapter 24
o Adjuvants e.g.
 Tricyclic antidepressants
 Amphetamines
 Selective serotonin reuptake inhibitors
 Antiseizure medications
 Membrane stabilizers
Step 2
o Moderate Pain (4 to 6) or pain that persists with Step 1 drugs
o Moderate opioid analgesics
o Codeine
 PO and Parenteral Route
 Tylenol #2, Tylenol #3, Tylenol #4 (pg 1144)
 Continuation of step 1 drugs
 Adjuvants
Step 3
o Moderate to Severe Pain (7-10)
o Or moderate pain uncontrolled by step 2 meds
o Opioids e.g. morphine – (Davis C68-70)
o May continue step 2 meds
o Adjuvants
o Morphine (Roxanol) *
 0.05 to 0.1 mg/kg every 2 hours
 Oxycodone, methadone and fentanyl
o Combination Drugs
 Hydrocodone (Davis pg 510) PO Route only
 Vicodin = Hydrocodone and Acetaminophen
Opioids
o Bind to opioid receptors in NS
o Mimic descending inhibitory system by to endogenous endorphin receptors in brain,
brainstem, spinal cord and peripheral tissues
o Inhibit A-delta and C fibers (inhibit AP)
o Therapuetic uses of Opioids
 Relief of pain
 Renal colic, MI, terminal CA
 Relief depends on opioid and receptor
 Anti-tussive
 Balanced anesthesia
 Pulmonary edema
 Diarrhea
o Routes of Administration
 Oral, Sublingual, Transmucosal, Transdermal, Infusion
Agonist/Antagonist Opioids
Opioids bind to different receptors
Pentazocine
o Agonist to kappa receptors
o Blocks mu receptors
o Use cautiously in patients with mu dependence
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Drug Interactions
o Alcohol, sedative, hypnotics, anesthetics
o Tricyclic anti-depressants, phenothiazines and anticholinergics
o No dose ceiling for agonist drugs
Adverse Reactions
o Decreased respirations
o Biggest risk with first dose
o Opioid naïve patients
o Sedation
o Cough suppressant
o Itching, rash, hemodynamic changes
o Light-headed and orthostatic hypotension
o N/V, constipation
Addiction
Tolerance
Physical dependence
o Withdrawal
Psychological dependence
Opioid Abstinence Syndrome
o Anxiety
o Irritability
o Chills, hot flashes
o Tears, rhinorrhea
o Sweating
o Abdominal cramps, N/V
Combination Drugs
o Vicodin *
 Hydrocodone (5mg) and acetaminophen (500mg)
Opioid Antagonists
Narcan * – Naloxone hydrochloride
Merperidine (Demerol)
o Known neurotoxicity
o Normeperidine  seizures
Patient Controlled Analgesia
Loading dose (bolus)
o MS 5 mg
Continuous infusion
o Hourly rate MS 0.5-1.0 mg/hr
Bolus
o 1mg
Lock out period
o Q 6 minutes
Hourly limit
o 10 mg
Opioids - Summary
o Look at effect not dose
o Give the next dose before the last wears off
o Relieve pain before it starts
o There is no maximum dose for morphine
o UNRELIEVED PAIN IS UNACCEPTABLE
Nonopioids: Used to treat
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Fever
Inflammation
o Vascular responses
 Vasoconstriction/Vasodilation
 Increased blood flow
 Increased permeability  swelling
o Cellualar
 WBCs  phagocytosis
Pain
Migraine headache
Prostaglandin Synthesis
o Arachidonic Acid Pathway
NSAIDs Includes:
o Salicylates
o Prostaglandin Synthetase Inhibitors
70 million prescriptions per year
o 5% all prescriptions
NSAIDs - Pharmacotherapeutics
o Anti-inflammatory
 Lupus, Rheumatoid arthritis
o Analgesic
o Antipyretic
o Anti-platelet (not all NSAIDs)
Salicylates
o Analgesia, Antipyretic, Anti-inflammatory
o Anti-thrombolytic
Aspirin has irreversible effects
Adverse reactions:
o Salicylism – mild toxicity
o Salicylate poisoning
o Excessive bleeding
o Caution in patients with liver and renal disease
NSAID - PGIs
o COX I
 Ibuprofen
o COXll Inhibitors
 Was thought to have safer profile
 Prevents of loss of gastric PGs – protects gastric lining
 Celebrex (Many now not available – Vioxx)
Adverse Reactions
o CV, GI
o Few available on the market
Acetominaphen (Tylenol)
o Para-aminophenol Derivative
o Synthetic – nonopioid
o Exact mechanism unknown
o Analgesic and Antipyretic
o Not anti-inflammatory
Phenazopyridine (Ppyridium)
o Azo dye
o Local analgesic effect on the urinary tract
o Relieves pain
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Corticosteroids
Adrenal Medulla  epi and norepi
Cortex
o Glucocorticoids
o Mineralocorticoids
o Sex hormones
Hypothalamic-pituitary-adrenal feedback
o CRH – corticotrophin- releasing hormone from hypothalamus
o ACTH from ant pituitary
o Cortisol from adrenal cortex
Corticosteroids medications
o Used as replacement therapy for inadequate adrenal cortex function
o Addison’s disease
o Anti-inflammatory, antiallergenic and immunosuppressive
Addison’s disease
o Hypoglycemia
o Anorexia
o N/V
o Flatulence
o Diarrhea
o Hyper-pigmentation of the skin
o Anxiety
o Depression
o Loss of mental acuity
o Addisonian crisis – Adrenal crisis
 Severe hypotension
 Hyponatremia
 Dehydration
 Hyperkalemia
 Malaise
 Muscle weakness/pain
 Cardiac arrhythmias
Prednisone
Replacement of adrenal cortex hormones
Anti-inflammatory
o Suppress the redness, edema, heat and tenderness associated with inflammation
Antiallergenic
o Immunosuppression
Unlabeled uses
o COPD, Duchenne’s muscular dystrophy and TB pleurisy.
Prednisone A/R
**** Steroid therapy compromises the immune system and makes the patient vulnerable to infection
******Suppression of tissue repair
Page 985 Cushing’s Syndrome
o Redistribution of fat – from arms and legs to face, between shoulders, and around waist “Moon face”
o Increased aldosterone  water retention + muscle weakness because K+ 
Corticosteroid-withdrawal syndrome
o Use longer than 2 weeks suppresses hypothalamic feedback axis
o Sudden withdrawal  Adrenal insufficiency
o See symptoms above
o Read planning and intervention, minimizing A/r and family education page 992