Transcript Analgetics - TMA Department Sites

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 postsynaptic 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, producting
sedation and decreasing emotional
upsets associated with pain
Narcotic Analgesics
 Can be given orally, IM, sub q, IV or
even transdermally
 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
 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
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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—nonceiling. 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)
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
 Sublimaze or Duragesic (Fentanyl)—short
duration
 Dilaudid (hydromorphone)
 Demerol (meperidine)—preferred in urinary
and biliary colic, less resp. depression
newborns
 Morphine
 OxyContin
Agonists cont.
 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