2. OBJECTIVES:
By the completion of this section the students will
be able to: Describe the neural mechanism for
pain at the level of Spinal cord.
Review the definitions of Analgesic, Narcotic and
Antagonistic.
List characteristics of Opioid analgesics in terms
of mechanism of action, indications for use and
major adverse effects.
Explain why higher doses of opioid analgesics are
needed when the drugs are given orally. Discuss
principles of therapy for nursing process for using
opioid analgesics.
3. Discuss signs and symptoms of opioid overdose, its
withdrawal and treatment of each.
Illustrate client teaching regarding safe and
effective use of opioid analgesics.
Discuss the nursing care, including client
teachings associated with narcotics.
Differentiate between non-narcotic and narcotic
analgesics
4. Pain
Definition:
It is an unpleasant sensation that often indicates tissue
damage and impels the person to remove the cause of the
damage.
(Abrams, 2001).
4
5. Chemical Mediators are released (e.g., Bradykinin, serotonin,
Prostaglandin)
Stimulate Pain receptors (Nociceptors) located peripherally
throughout the body
Nerve impulse of pain sent to spinal cord Neurotransmitter
(Substance P) passes the message along to next
neuron
Pain impulse reaches the brain
Pain is sensed
NeuralMecha
5
nismof Pain Sensation
Tissue damage
6.
7.
8. ReceptorsinCNS Responsible
for Analgesia
🞇 Mu and Kappa receptors in CNS are responsible for
pain control or analgesia.
Effects produced by the activation of Mu
receptors are: Analgesia, Decreased GI motility,
RespiratoryDepression, Sedation, Physical
dependence
Effects produced by the activation of Kappa
receptors are: Analgesia, Decreased GI motility,
and Sedation
7
9. Endogenous Opioids
🞇 These are naturally occurring neurotransmitters in
the central nervous system, which reduce pain
sensation by acting on mu and kappa receptors
🞇 T
hey also inhibit the release of substance P;
inhibition of substance P reduces the transmission
of pain impulses in central nervous system, thus
reducing pain sensation.
For e.g. Endorphins, Dynorphins.
8
10. Analgesic Drugs
Analgesics:
These are the medications used to relieve pain.
(Kee, 2006).
Types ofAnalgesics:
🞇 Opioid or NarcoticAnalgesics:
🞇 These drugs act on the brain (CNS) and reduce the appreciation
of moderate to severe pain
Non Steroidal Anti Inflammatory Drugs (NSAIDs)/Non-
NarcoticAnalgesics:
🞇 These drugs reduce inflammation and release of inflammatory
mediators at peripheries, thus reducing onset of the neural
mechanism of pain sensation by nerve fibres
9
11.
12.
13. Opioids withdrawl sym
What are suspected opioid withdrawal symptoms?
Withdrawal symptoms might include headaches,
changes in blood pressure, rapid heart rate,
sweating, nausea, vomiting, and tremors.
14.
15. Difference b/w Narcotic and Non-
Narcotic Analgesics
Narcotic Non-Narcotics (NSAIDs)
Acts mostly on the Central
Nervous System
Acts on Peripheral nervous
system at the pain receptor sites.
Suppress moderate to severe
Pain as well as it suppresses
respiration and coughing by
acting on medulla of the
brainstem.
Suppress mild to moderate pain.
Performs Analgesic, Anti-pyretic
and Anti-inflammatory actions.
Effective for severe pain during
and after surgeries, during
invasive diagnostic procedures,
L&D etc.
Effective for dull, throbbing pain
of inflammation, minor abrasions,
mild to moderate arthritis.
10
16.
17. Opioid/Narcotic Agents
Complete OpioidAgonists:
These drugs act as complete agonists to endogenous
opioids, and thus they act on and stimulate both mu and
kappa receptors. These are the most potent analgesics.
E.g. Morphine, Pethadine, Fentanyl
Partial OpioidAgonist-Antagonists:
These agents have agonist activity at kappa receptors and
antagonist activity at mu receptors. Therefore, though
they are not as potent analgesics as complete opioid
agonists; however, these have fewer side effects. E.g.
Pentazocine
(Abrams, 2001)
11
18. Narcotic/Opioid Analgesics
Mechanism ofAction:
Opioid Drugs bind to Mu, Kappa receptors
Stimulation of Mu and Kappa receptors
Prevents release of substance P (responsible for pain impulse
transmission in CNS)
Transmission of nerve impulses related to pain suppressed
Decreased Pain sensation
12
20. Narcotic/Opioid Analgesics
Indications: These drugs are usually given to prevent and
relieve acute & chronic pain when other measures and milder
drugs are ineffective.
Pre, Intra and Post-Op surgical patients.
Invasive diagnostic procedures (Angiograms,
Endoscopic examination).
GI disorders (abdominal cramps, pain).
Angina (Chest pain)
Burns and other traumatic injuries.
Cancer
Renal colic
14
22. Narcotic/Opioid Analgesics
Side Effects:
Respiratory depression (Respiratory center depression)
Nausea & vomiting (CTZ stimulation)
Pupillary constriction/ pin point pupils (esp. with Morphine)
CNS Depression (sedation, drowsiness, decrease mental
activity)
Hypotension (Stimulation of Vagus nerve)
Decreased GI motility (Constipation)
Urinary Retention (Sphincter spasm)
Bradycardia (Stimulation of Vagus nerve)
Physiologic & Psychological dependence.
16
23. Narcotic/Opioid Analgesics
Oral doses of drug undergoes hepatic bypass (liver
metabolizes 75% of the drug); therefore mostly given
through I/V or I/M routes in controlled doses
It crosses the blood brain barrier to produce analgesic effects.
17
25. Narcotic/Opioid Analgesics
Patient controlled IntravenousAnalgesia (PCIA):
🞇 The device consist of a syringe of diluted drug connected to an
IV line and infusion pump.
🞇 The client controls the release of narcotic analgesic,
depending on the amount of pain.
🞇 The syringe delivers the predetermined dose when the client
pushes a button connected with the PCIA
device and placed it on clients hand.
🞇 A lock out mechanism on PCIA machine
prevents the client from constantly pushing
the button and causing drug overdose.
🞇 Examples of drugs given through PCIA:
Pethidine, Morphine & Tramadol.
19
26.
27. Diagnosis anTreatment of Opioid
Overdosage
Diagnosis and Treatment of Opioid Overdosage
Intravenous injection of naloxone dramatically
reverses coma due
to opioid overdose but not that due to other CNS
depressants.
Use of the antagonist should not, of course, delay
the institution
of other therapeutic measures, especially
respiratory support. (See
also The Opioid Antagonists, below, and Chapter
58.) The growing epidemic of prescription opioid
use and opioid-related adverse
28. drug reactions has been accompanied by an even
greater increase
in heroin-related deaths in the United States from
2010 to 2014.
For this reason, attention is being directed to
make naloxone via
intramuscular and intranasal routes widely
available, including as
over-the-counter formulations.
29. In general, the oral route is preferred because of ease
of administration and good oral bioavailability of
most opioids. In addition to the scheduled dosage of
an opioid, extra "rescue" doses (5 to 10% of the total
daily opioid dosage) should be available to the
patient for breakthrough pain.
30. Opioid Antagonists
🞇 Narcotic antagonists reverse the analgesic and
depressant effects of narcotic agonists by
displacing the agonists from their receptor sites
E.G. Nalaxone.
🞇 These are used in case of opioid overdose
(Abrams, 2001).
20
31. Narcotic/Opioid Analgesics:
Nursing Process
Assessment:
Assess type of Pain, its location & duration.
Obtain medical history related to any
disorders contraindicated for the therapy.
Assess Vital signs and urinary output.
Assess any substance abuse history,
dependence or withdrawal symptoms.
Check doctor’s order for the method of
Opioid administration either IV, PCIAor IM.
21
32. Narcotic/Opioid Analgesics
🞇 Assess for Drug interactions:
🞇 CNS Depressants (Alcohol, antipsychotics, antihistamines
etc.)--- Increased effect.
🞇 Diuretics (Morphine can reduce the efficacy of diuretics)
🞇 NarcoticAntagonists--- decreased effect.
Assess for the safety measures including keeping
side rails up and instructing the patient to avoid
activity till 30-60 min after Opioid administration.
22
34. Narcotic/Opioid Analgesics
Nursing Interventions:
Administer the narcotic before pain reaches its peak to maximize the
effectiveness of the drug.
Monitor V/S (HR, BP, Respiratory rate and effort) at frequent
intervals to detect alterations.
Record client’s urine output.
Check bowel sounds for decreased peristalsis. Dietary changes (high
fiber diet, increased fluids) may be required.
Check for Pupillary changes. Pinpoint pupils indicate Morphine
overdose.
Have Naloxone available as an antidote and emergency equipment
at bedside if Opioid overdose occurs.
Validate child’s and adult’s doses before administration.
Administer anti-emetic (drugs that prevent vomiting) along with
opioids, as prescribed.
24
35. Narcotic/Opioid Analgesics
Patient Teaching:
Instruct client to take medicines as prescribed, and not to increase
the dose or its frequency.
Encourage client not to use alcohol or CNS depressants with
narcotic analgesics.
Discourage client for driving or operating any machinery while
drowsiness, after taking narcotic analgesics.
Encourage for high fiber diet such as whole grain cereals, fruits &
vegetables, drink 2-3 quarts of fluid daily to prevent constipation.
Suggest non-pharmacological measures to relieve pain .
25
36.
37. Non-Narcotic/Non-Opioid
Analgesics
The non-narcotic analgesics are less potent than narcotic
analgesics, and are not addictive. E.g. NSAIDs,
Acetaminophen
(Kee , 2006).
Most NSAIDs have analgesic, anti-pyretic and anti-
inflammatory action i.e. relieve pain, fever and inflammation.
These drugs act by suppressing the formation of prostaglandin,
which increases the nociceptors’sensitivity to pain.
Aspirin is the prototype of this group.
26
38. Non-Narcotic/Non-Opioid
Analgesics
Mechanism ofAction:
Aspirin and other NSAID’s inhibit the enzyme cycloxygenase
(COX 1 & 2), needed for the synthesis of prostaglandin.
It triggers pain,
fever and
inflammation
Inhibition
Decreased
pain &
It Protects stomach lining,
Promotes platelets aggregation (blood
Clotting)
Inhibition
Loss of stomach lining protection
leading to GI ulcer, Increased bleeding tendency.
inflammation,
fever
27
42. Non-Narcotic/Non-Opioid Analgesics:
Aspirin
Important aspects while administeringAspirin:
1. Used as an analgesic, anti-inflammatory, antipyretic
or anti-platelet.
2. Enteric coated aspirin is slowly absorbed.
3. Administer aspirin with meals to reduce gastric
irritation.
4. Monitor Platelet count (150-450)
5. Manifestations of Aspirin overdose include: Nausea,
vomiting, Fever, Fluid electrolyte imbalance,
tinnitus, drowsiness, confusion and hyperventilation.
31
43. Non-Narcotic/Non-Opioid Analgesics:
Acetaminophen
Acetaminophen is not an NSAID.
It is a weak inhibitor of prostaglandin, and
decreases pain and fever. Does not have anti-
inflammatory properties.
It does not cause gastric distress and not involved
in platelet aggregation.
Preferred for children <12 years of age.
Adverse effects are uncommon but overdose may
result in dangerous liver damage.
Examples:
Tylenol, Panadol.
32
44. Assessment:
Obtain medical history for any disorders
contraindicated for medicine.
Assess the severity of pain.
Assess V/S, inflammation or edema
Assess for allergic reactions toAspirin or
NSAID’s
Non-Narcotic/No
33
n-Opioid Analgesics:
Nursin
g Process
45. Nursing Interventions:
Administer NSAID’s with food or full glass of water to
reduce GI irritation.
Observe for therapeutic effects.
Check Liver enzymes, Renal Function test results.
Instruct the client about Live damage can
occur with continuous use of acetaminophen.
Check serum Acetaminophen level (5-20 ug/ml).
Toxic level is between 50 ug/ml and 200 ug/ml
considered as hepatotoxicity.
Non-Narcotic/Non
34
-Opioid Analgesics:N
u
r
s
ing
Process
46. References
Abrams,A.C. (2001). Clinical drug therapy:
rationales for nursing practice. (5th.ed.).
Philadelphia: Lippincott
Kee, J. Hayes, E. (2006). Pharmacology: A nursing
process approach. (4th ed.). New York: Saunders
Lilley, L.L. Aucker, R.S. (2001). Pharmacology and
the nursing process. (3rd ed). Philadelphia:
Mosby
Mosby, T. (2002). Clinical Nursing, 5th ed.Mosby,
Inc.
McCuistion, L.E. Gutierrez, K.J. (2002).
Pharmacology. USA: Saunders
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