Narcotics and

Analgesics
 Pain

 Universal, complex,
subjective experience
 Number one reason
people take
medication
 Generally is related to
some type of tissue
damage and serves as
a warning signal
 Scope of the Problem

 Increases as Baby Boomers age

 25 million people suffer acute pain
related to surgery or injury
 Chronic pain affects 250 million
Americans
 Is a multibillion dollar industry
 Much ignorance exists about this
complaint
Gate Control Theory of
Pain
 Gate control theory of
pain is the idea that
physical pain is not a
direct result of activation
of pain receptor neurons,
but rather, its perception is
modulated by interaction
between different neurons
 Gate Control Theory of
Pain
 Nerve fibers (A delta (fast
channels)) and C fibers
(slow channels) transmit
pain impulses from the
periphery
 Impulses are intercepted
in the dorsal horns of the
spinal cord, the substantia
gelatinosa
 In this region, cells can be
inhibited or facilitated to
the T-cells (trigger cells)
Gate Control Theory of Pain
cont.

 When cells in the

substantia gelatinosa
are inhibited, the ‘gate’
to the brain is closed
 When facilitated, the
‘gate’ to the brain is
open
 Gate Control Theory of
Pain
 Similar gating
mechanisms exist in the
nerve fibers descending
from the thalamus and
the cortex. These areas
of the brain regulate
thoughts and emotions.
Thus, with a pain stimulus,
one’s thoughts and
emotions can actually
modify the pain
experience.
 Pathophysiological
Response
 Tissue damage activates free
nerve endings (nociceptors)
of peripheral nerves
 Pain signal is transmitted to
the spinal cord,
hypothalamus, and cerebral
cortex
 Pain is transmitted to spinal
cord by A-delta fibers and C
fibers
 Pathophysiological
Response
 A-delta fibers transmit fast,
sharp, well-localized pain
signals
 C fibers conduct the pain
signal slowly and produce
poorly localized, dull, or burning
type of pain
 Thalamus is the relay station for
incoming stimuli, incl. pain
 Pain Fibers and Pathways
 A delta fibers found in the skin
and muscle, myelinated,
respond to mechanical
stimuli. Produce intermittent
pain.
 C fibers distributed in the
muscle as well as the
periosteum and the viscera.
These fibers are unmyelinated,
conduct thermal, chemical
and strong mechanical
stimuli. Produce persistent
pain.
 Inhibitory and Facilitatory
Mechanisms
 Neurotransmitters—
chemicals that exert
inhibitory or excitatory
activity at post-synaptic
nerve cell membranes.
Examples include:
acetylcholine,
norepinehprine, epinephrine,
dopamin, and serotonin.
 Neuromodulators—
endogenous opiates.
Hormones in brain. Alpha
endorphins, beta endorphins
and enkephalins. Help to
relieve pain.
 Opioid Receptors

 Opioid receptors—
binding sites not only
for endogenous
opiates but also for
opioid analgesics to
relieve pain. Several
types of receptors:
Mu, Kappa, Delta,
Epsilon and Sigma.
 Mu Receptors

 Location: CNS incl.

brainstem, limbic
system, dorsal horn
of spinal cord
 Morphine sulfate
and morphine
sulfate agonists bind
to Mu receptors
 Sources of Pain

 Nociceptive—free
nerve endings
that receive
painful stimuli
 Neuropathic –
damaged nerves
 Narcotic Analgesics
 Relieve moderate to severe pain
by inhibiting release of Substance P
in central and peripheral nerves;
reducing the perception of pain
sensation in brain, producing
sedation and decreasing
emotional upsets associated with
pain/
 Substance P's most well-known
function is as a neurotransmitter
and a modulator of pain
perception by altering cellular
signaling pathways. Additionally,
substance P plays a role in
gastrointestinal functioning,
memory processing, angiogenesis,
vasodilation, and cell growth and
proliferation.
 Narcotic Analgesics

 Can be given orally, IM, sub q, IV or

even transdermal
 Orally are metabolized by liver,
excreted by kidney—caution if
compromised
 Morphine and meperidine produce
metabolites
 Widespread effects: CNS, Resp., GI
 Narcotics—Mechanisms of
Action

 Narcotics are strong drugs that are sometimes

used to treat pain. They are also called opioids.
 Bind to opioid receptors in brain and SC and even
in periphery
 Indications for Use

 Before and during surgery

 Before and during invasive
diagnostic procedures
 During labor and delivery
 Tx acute pulmonary edema
 Treating severe, nonproductive
cough
Contraindications to Use

 Respiratory depression
 Chronic lung disease
 Chronic liver or kidney disease
 BPH
 Increased intracranial pressure
 Hypersensitivity reactions
Changing Philosophy on
Pain
 Undermedicated
 Titrate to comfort
 Management
Considerations
 age-specific considerations
 Morphine often drug of choice—non-ceiling.
Other nonceiling drugs include: hydromorphone,
levorphanol and methadone
 Use non-narcotic when able
 Combinations may work by different mechanisms
thus greater efficacy (e.g. Tylenol w/codeine)
 Of the three groups of analgesics – opioids,
nonopioids, and coanalgesic drugs, only the
morphine-like opioids have no analgesic ceiling.
In other words, higher doses increase analgesia
and only adverse effects limit how high the dose
can be
 Route selections

 Oral preferred
 IV most rapid—PCA allows self
administration. Basal dosage. More
effective, requires less dosing.
 Epidural, intrathecal or local injection
 Can use rectal suppositories or
transdermal routes
 Dosage

 Dosages of narcotic analgesics should be

reduced for clients receiving other CNS
depressants such as other sedative-type
drugs, antihistamines or sedating
antianxiety medications
 Scheduling

 Give narcotics before encouraging turning,

coughing and deep breathing in post-surgical
patients
 Automatic stop orders after 72h
 In acute pain, narcotic analgesics are most
effective when given parenterally and at start of
pain
 Individual Drugs

 Agonists have activity on mu and kappa opioid

receptors
 Agonist/antagonists have agonist activity in some
receptors; antagonists in others. Have lower abuse
potential than pure agonists; because of
antagonism—can produce withdrawal symptoms
 Antagonists are antidote drugs
 Agonists
 Alfenta (alfentanil)—short duration
 Codeine – for pain, cough, diarrhea
 Sublimaze or Duragesic (Fentanyl)—
short duration
 Dilaudid (hydromorphone)
 Demerol (meperidine)—preferred in
urinary and biliary colic, less resp.
depression newborns
 Morphine
 OxyContin
 Darvon (propoxyphene)
 Ultram (tramadol)
 Methadone
 Agonists/Antagonists

Have lower abuse potential than pure agonists

 Buprenex (buprenorphine)
 Nubain (nalbuphine)
 Talwin (pentazocine)
 Stadol (butohanol)—also in nasal spray
 Antagonists

 Revex (nalmefene)—longer duration of action

than Narcan
 Narcan (naloxone)
 ReVia (naltrexone)-used in maintenance of
opiate-free states in opiate addicts
Dietary and Herbal Supplements

 Zostrix (capsaicin)—from cayenne peppers;

topical indicated for post-herpetic neuralgia,
neuropathic pain=Substance P
 Cancer
 Give on a regular schedule
 Oral, rectal and transdermal are
preferred over IV
 Oxycodone and a non-narcotic
analgesic may have addictive effects.
 Oxycodone may cause serious or life-
threatening breathing problems
 MS or other for severe pain
 Long acting for chronic pain with fast
acting meds for “break-through pain”
 May use TCAs, anti-emetics, stool
regimen
Management of Withdrawal
Symptoms

 Methadone- is a powerful drug used for pain relief

and treatment of drug addiction.
 Clonidine (norepinephrine)
 Gradually decrease dosing so not to cause
withdrawal s/s
Analgesic,Antipyretic, and Anti-
inflammatory Drugs
 Mechanism of action—inactivate cyclo-oxygenases,
enzymes required for the production of
prostaglandins
 The prostaglandins are a group of lipids made at
sites of tissue damage or infection that are involved
in dealing with injury and illness. They control
processes such as inflammation, blood flow, the
formation of blood clots and the induction of labour.
 ASA and traditional NSAIDs inhibit both COX 1
(cyclooxeginase 1) and COX 2
 COX 1 is present in all tissues esp. GI, kidneys,
endothelial cells and in platelets
 COX-1 maintains the normal lining of the stomach
and intestines, protecting the stomach from the
digestive juices
 Cox 1 cont.

COX-1 generates prostaglandins that are involved in

the protection of gastrointestinal mucosa, while
COX-2 generates prostaglandins that mediate
inflammation and pain in sites throughout the
body
Prostaglandins important in:
1. Protection of kidneys and stomach
2. Regulate vascular tone and platelets in CV
system
 COX 2

 Found in brain, bone, kidneys, GI tract, and the

female reproductive system
 Overall, prostaglandins produced by COX 2 are
associated with pain and inflammation
 Actions of the COX’s

 also known as prostaglandin G/H

synthase 1,
 Act on hypothalamus to decrease
response to pyrogens and reset the
thermostat
 Prevent prostaglandins from increasing
the pain and edema produced by other
substances released by damaged cells
 COX 1-Antiplatelet activity for life of
platelet—7-10 days plus interfere w/blood
coagulation and increase risk for
bleeding
 Indications for Use
 Treat mild to moderate pain or inflammation
 Musculoskeletal disorders; HA; dysmenorrhea,
minor trauma and surgery
 Low dose ASA for risk of MI or stroke
 Celebrex is indicated for familial polyposis
 This medication is a nonsteroidal anti-
inflammatory drug (NSAID), specifically a COX-2
inhibitor, which relieves pain and swelling
(inflammation)
 Contraindications to Use
 PUD
 GI or bleeding disorders
 Hypersensitivity reactions
 Impaired renal function
 If allergic to ASA
 In children, ASA contraindicated in
presence of viruses=Reye’s syndrome
 Reye's syndrome, a child's blood sugar level
typically drops while the levels of ammonia
and acidity in his or her blood rise. At the
same time, the liver may swell and develop
fatty deposits. Swelling may also occur in
the brain, which can cause seizures,
convulsions or loss of consciousness
 Celebrex if allergic to sulfonamides
 Reye’s Syndrome

 Seen in children under 15 after an

acute viral illness
 Results in encephalopathy, fatty
infiltration of the liver, pancreas,
kidneys, spleen, and lymph nodes
 Cause is unknown
 Contraindications

 Toradol (ketorolac tromethamine) is a

nonsteroidal anti-inflammatory drug (NSAID) that
is used to treat moderately severe pain and
inflammation,
 Toradol (ketoralac) not used in labor and delivery
or during any major surgery
 OTC preps contraindicated in alcoholics due to
possible liver damage
 Aspirin (ASA)

 Home remedy for headaches, colds, influenza

and other respiratory infections
 For fever
 For inflammation
 ASA and COX 2 are ok, COX 2 have little effect on
platelet function
 ASA cont.
 Poisoning can occur with large doses.
Saturate the metabolic pathway, slow
elimination and cause drug
accumulation
 If overdose, measure serum levels
 Recognize s/s: N/V, fever, fluid and lyte
deficiencies, tinnitus, decreased hearing,
hyperventilation, confusion, visual
changes>>>>delirium, stupor and coma
 ASA salicylism

 Gastric lavage
 Activated charcoal
 IV bicarbonate so more rapid excretion
 hemodialysis
 NSAIDS

 Propionic acid derivatives such as

ibuprofen, ketoprofen (Orudis), naproxen
and fenoprofen (Nalfon)
 Acetic acid derivatives include
indomethacin (Indocin), sulindac (Clinoril)
and tolmetin (Tolectin)---these drugs have
more severe adverse reactions than the
proprionic acid derivatives
 NSAIDS

 IV indomethacin is approved for the tx of

patent ductus arteriosus in premature
infants.
 Remember: patent ductus is a
communication between the pulmonary
artery and the aorta
 NSAIDS

 Toradol (ketoralac) is used only for pain. Is the only

NSAID that can be given by injection. Use limited
to 5 days as can cause bleeding.
 Oxicam drugs include Mobic (meloxacam) and
Feldene (piroxicam)
 Celebrex (celecoxib)
 Affect bleeding only while drug is still in the system
Effects of Nonsteroidals on Other
Drugs

 Decrease effects of Angiotensin-

converting-enzyme inhibitors (ACEI), beta
blockers and diuretics
 Affect sodium and water retention
 Inhibit renal prostaglandin synthesis
 Acetaminophen
(Paracetamol)
 This drug is used to treat mild to moderate
pain (from headaches, menstrual periods,
toothaches, backaches, osteoarthritis, or
cold/flu aches and pains)
 Equal in effectiveness to ASA in analgesic
and antipyretic effects
 Lacks anti-inflammatory actions
 Ethanol induces drug-metabolizing enzymes
in liver. Resulting rapid metabolism of
acetaminophen produces enough toxic
metabolite to exceed glutathione. Need
glutathione to inactivate toxic metabolites. P.
114
Acetaminophen Poisoning
 Toxicity occurs with 20g or more.
 Creates toxic metabolite that is
inactivated by glutathione.
 OD supply of glutathione is depleted
and toxic metabolite damages liver
cells
 Not to exceed 4g/day
 Treatment—gastric lavage, charcoal,
antidote is Mucomyst (acetylcysteine).
Provides cysteine, a precursor to
glutethione.
 Drugs used in Gout and
Hyperuricemia

 Zyloprim (allopurinol)—
prevents or treats
hyperuricemia
 Uric acid is formed by purine
metabolism and an enzyme
xanthine oxidase. Allopurinol
prevents formation by
inhibiting xanthine oxidase.
 Antigout Medications

 Colchicine—used to treat or prevent

acute attacks of gout. Drug of choice
for acute attacks. Decreases
inflammation by affecting leukocytes.
 Benemid (probenecid) increases
urinary excretion of uric acid. Not
effective in acute attacks.
 Anturane (sulfinpyrazone) uricosuric
similar to Benemid. Not for acute
attacks.
 Guidelines for Treating
Gout
 Maintenance drugs are Zyloprim,
Benemid and Anturane
 Colchicine needed for several weeks to
prevent acute attacks while serum levels
are being lowered
 Need high fluid intake, alkaline urine to
prevent renal calculi
Drugs Used for Migraines

 Selective serotonin 5-HT1 receptor

agonists
 Increase serotonin in the brain
 Constrict blood vessels
 Contraindicated in patient’s with history
of MI,, angina, uncontrolled htn.
Drugs used for migraines

 Drugs vary in onset with sub q sumatriptan

acting the most rapidly and starting
within 10 minutes; most clients get relief
within 1-2 hours
 Drugs are metabolized in the liver by
monoamine oxidase or by cytochrome
p450 enzymes; sub q administrations
causes more adverse effects than the
oral drugs
 Migraine Meds

 Ergotamine tartrate—ergot alkaloid used

only in tx of migraine
 Work by constricting blood vessels
 Most effective when given sublingual or
by inhalation
 Contraindicated in pregnancy, htn, PVD,
CAD, renal or hepatic disease and even
in severe infections
 Guidelines for Treating
Migraine
 Start out with acetaminophen, aspirin, or
other NSAIDs
 Moderate to severe migraines,
sumatriptan or other related drugs are
useful
 For severe and frequent migraines,
prophylaxis is indicated. Use ASA and
NSAIDs.
Guidelines for Treating migraines

 For menstrual migraines, start tx one week

before and during menses
 Other drugs indicated for tx include beta
adrenergic blocking agents such as
Inderal
 Guidelines for Treating
Arthritis
 Control pain and inflammation
 Rest, exercise,and PT
 Osteoarthritis—COX1, COX2,
glucosamine, intraarticular injections of
corticosteroids or hyaluronic acid
(Synvisc) to act as shock absorber
 Rheumatoid Arthritis

 NSAIDs
 Corticosteroids
 Immunosuppressants—methotrexate
 Enbrel, Remicade and Arava. Affect
tumor necrosis factor and other
cytokines.
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