OBJECTIVES

At the end of the presentation students will have a

clearer understanding of:
 Terms associated with analgesia.
 The physiology of pain.
 Classification of analgesics
 Mechanism of action of various analgesics.
 Clinical uses, contraindications, side effects and drug
interactions of various analgesic agents.
 DEFINITIONS

ANALGESIA: Lack of sensitivity to pain without loss of

consciousness.

 ANALGESIC: A drug that relieves pain.

 PAIN: A state of localized or generalized discomfort that

ranges from mild distress to acute agony.

Blackwell’s Dictionary of Nursing 1994

 HOW DO WE
EXPERIENCE PAIN
PAIN PATHWAY
 CLASSIFICATION OF ANALGESICS

OPIOIDS NON-OPIOIDS

Synthetic Natural NSAID’s Salicylates Acetaminophen

Pethidine Morphine Voltaren Aspirin Panadol

 OPIOIDS
•Opioid analgesics interact with four major receptors, mu,
kappa, sigma and delta, that exist in and outside the CNS.
 OPIOID RECEPTORS
mu receptors Kappa receptors Delta receptors Sigma
receptors
Analgesia Analgesia Analgesia Hallucination

Respiratory Respiratory Modulation of Dysphoria

depression depression hormone and
neurotransmitter Seizures
Euphoria Miosis
Increased
Slowed GI transit Sedation irritability

Modulation of Psychotomimetic Respiratory

hormone and effects stimulation
neurotransmitter
release Slowed GI transit Mydriasis.
 TYPES OF OPIOIDS
There are three main types of opioids, namely:

1. Full Agonists. These pure opioid drugs bind tightly to

mu receptor sites, producing maximum pain inhibition.
2. Mixed agonists-antagonists. These drugs can act like
opioids and relieve pain when given to persons who
have not taken pure opioids. They can block the mu
receptor site and activate the kappa receptor site.
3. Partial agonists. Have a ceiling effect in contrast to a
full agonist. These drugs block the mu receptors or are
neutral at that receptor but bind to kappa receptor site.
 CLASSIFICATION OF FULL AGONISTS
Full Agonists can further be broken down as:
STRONG AGONISTS: example morphine,
pethidine and fentanyl

MODERATE AGONISTS: oxycodone

WEAK AGONISTS: example codeine

EXAMPLES OF OTHER GROUPS OF OPIOIDS

PARTIAL AGONISTS: buprenorphine

MIXED AGONIST-ANTAGONISTS: pentazocine
and nalbuphine
 STRONG OPIOID AGONISTS (morphine)
• Used primarily to relieve moderate to severe pain, by
binding to the mu and delta receptors.
• It targets areas involved with regulation of pain,
perception, respiration, and affective behaviour.
•Drug of choice for persons with pain from
myocardial infarction, pulmonary edema, and
dyspnoea from acute left ventricular failure.
•Also decreases the cough reflex.
•Terminal illness
•Pre and post operative medication.
 UNDESIRED CLINICAL RESPONSES AND SIDE
EFFECTS
•Dizziness
•Mental clouding
•Dysphoria
•Sometimes delirium
•Respiratory depression
•Nausea, vomiting and constipation
•Tolerance, physical and psychologic dependence.
• Urinary effects ( urinary retention)
UNDESIRED/ SIDE EFFECTS CONTINUED

•Relaxation of uterus which may delay labour

•Postural hypotension (depression of vasomotor center)
•Urticaria and skin rashes
•Bronchoconstriction
•miosis
•Convulsions at high doses
 CONTRAINDICATION/ CAUTION

 Clients with head injury or increased intracranial

pressure.
Severe liver and kidney impairment.
Clients with reduced blood volume.
Previous hypersensitivity to opioids.
After surgical anastomosis of the GI tract.
Pregnancy
Asthmatics
METABOLISM AND EXCRETION
Morphine is
• metabolized in the liver
•Conjugation with glucuronic acid
•most excreted through the kidneys in urine.
•A small percentage is excreted in faeces.
•Half-life of 2.5 – 3 hours
•Only traces found in the body after 48 hours.
 DRUG-DRUG INTERACTIONS

• Additive CNS depression with phenothiazines.

• Increased hypotension with tricyclic
antidepressants.
• Severe and immediate hypertension, respiratory
depression and rigidity with MOA inhibitors.
• Enhanced analgesic effect with amphetamines.
• Alcohol, barbiturates, and other CNS depressants
should be avoided.
Meperidine (Demerol)

 Meperidine is reported to have the most pronounced

anti-shivering properties.
Analgesic efficacy similar to that of morphine
Faster onset but shorter duration of action than
morphine.
Often used for labor and post-operative pain.
Less cough suppressant activity and constipation than
morphine.
Is about one sixth as potent as morphine.
CODEINE
•Effects similar to those of morphine.
•used to treat mild-moderate pain and as a cough
suppressant.
•Usually administered orally.
•Less addictive than morphine at therapeutic doses.
•Less side effects than morphine.
BUPRENORPHINE (PARTIAL AGONIST)
 Is a partial agonist at the mu receptors and an
antagonist at kappa receptors.
Is long acting and quite potent.
N.B. A dose of 0.3mg IM has analgesic effects
equivalent to those of 10mg of morphine.
Peak effects occur in one hour, analgesic action
sustained for up to six hours.
Has low potential for abuse.
Effective in the detoxification and maintanance of
heroin users.
Is available combined with a mu opioid antagonist to
help prevent its diversion for illicit intravenous abuse.
 PENTAZOCINE (TALWIN)
•Used to relieve moderate to severe pain.
•Used for postoperative medication and as a supplement
to surgical anaesthesia.
•Acts at the kappa receptor sites.
•Duration of action three hours.
•Available as injectible and oral forms.
•Causes nausea, vomiting, dizziness and euphoria.
•Safe use in pregnancy has not being established.
 NON-OPIOID ANALGESICS
Drug type Pharmacologic effects Adverse effects
Salicylates: •Analgesia: GI:
used to reduce mild to moderate pain increased GI
•Aspirin by inhibiting PG synthesis. PG sensitize ulceration & bleeding
nerve endings to action of chemicals
•Diflunisal that mediate pain sensations
Bleeding:
prolonged bleeding
•Antipyretic: time due to aspirin
used to lower body temperate by binding to platelets,
causing peripheral vasodilation and reducing platelet
sweating. Reset thermoregulatory adhesiveness
centre Does not reduce body
temperature below normal (98.6°F)

•Anti-inflammatory:
Reduces pain, redness & swelling of
 NON-OPIOID ANALGESICS
Drug type Pharmacologic effects Adverse effects

SALICYLATES Anticoagulation: more Contraindications:

CONTINUED specifically antiplatelet Persons:-
•With renal, hepatic
Inhibit cyclo-oxygenase or GI disease.
leading to inhibition of • on anticoagulant
thromboxane formation and therapy
reduce platelet aggregation •last trimester of
Inhibition of prostaglandin pregnancy.
synthesis. Small doses are •In teens or children
used to prevent recurrence of because of Reye's
strokes and myocardial syndrome.
infarctions. •Caution in
Pharmacokinetics: asthmatics,
Rapidly absorbed from the cardiovascular
stomach & small intestine, disease, coagulation
then widely distributed to disorders, ulcers
most body tissues. and fluid retention
Metabolized in the liver, then problems.
excreted by the kidneys.
 NON-OPIOID ANALGESICS
Drug type Pharmacologic effects
NSAIDs Analgesia:
NSAIDs are used to reduce
•Voltaren mild to moderate pain.
Antipyretic:
•Ibuprofen
NSAIDs are used to lower body
temperate & treat a fever by
•Naprosyn causing peripheral vasodilation
and sweating.
Anti-inflammatory:
Reduces pain, redness &
swelling of inflamed areas by
inhibition of prostaglandin
synthesis, vasodilation and
increasing capillary
permeability.
Adverse effects
GI:
increased GI ulceration &
bleeding
CNS:
increased drowiness, sedation,
confusion, headache, vertigo,
strange dreams
Bleeding:
prolonged bleeding time due to
NSAIDs binding to platelets,
reducing platelet adhesiveness
Allergy:
symptoms ranging from mild
rash to anaphylactic shock
 NON-OPIOID ANALGESICS
Drug type Pharmacologic effects Adverse effects
NSAIDs Anticoagulation: Similar to salicylates.
CONTINUED Reduces blood clotting by inhibition of
prostaglandin synthesis. Small doses
are used to prevent recurrence of
strokes and myocardial infarctions .

Pharmacokinetics:
NSAIDs absorbed from the stomach &
small intestine, then widely distributed
to most body tissues. Metabolized in
the liver, then excreted by the kidneys.

Mechanism:
Works by blocking prostaglandin
synthesis in the peripheral nerves &
the hypothalamus portion of the brain.
 NON-OPIOID ANALGESICS
Drug type Pharmacologic effects Adverse effects

ACETAMINOPHEN Analgesia: •Very few adverse reactions.

acetaminophen is used to reduce • Does not cause GI irritation
•Tylenol mild to moderate pain. & bleeding.
•Extremely high doses over
•Panadol Antipyretic: long time periods may lead to
acetaminophen is used to lower body hepatoxicity and
•Paracetamol temperate & treat a fever by causing nephrotoxicity
peripheral vasodilation and sweating.
Does not reduce body temperature
below normal (98.6°F)

Pharmacokinetics:
Acetaminophen is absorbed from the
stomach & small intestine, then
distributed to body tissues.
Metabolized in the liver, then
excreted by the kidneys.
 NON-OPIOID ANALGESICS
Drug type Pharmacologic effects
ACETAMINOPHEN Mechanism:
CONTINUED Exact mechanism not known,
but believed to work in the
CNS, not the peripheral
nervous system.
Analgesic and antipyretic
actions & weak anti-
inflammatory
Adverse effects
Contraindication:
•Patients with alcoholism, or
hepatic disease because of
hepatoxicity. Antidote
acetylcystine
•In renal disease

It is a weak prostaglandin
inhibitor.
 SCENARIO ONE
Mr. Chin is a new patient to your practice with headaches. At his first
appointment you inform him you would like to ask him some questions
about the medical history form he just completed. During the interview
you find out he has a history of peptic ulcer disease and is on medication
to treat it. He takes ranitidine, 150mg., at bedtime for his ulcer and
occasional acetaminophen for pain. He drinks socially, usually wine or
beer.
Is there anything else you need to know before you begin his treatment?
Is acetaminophen an appropriate pain medication for Mr. Chin to take
for pain control? Justify answer.
 REFERENCES
Iowa Sate University. (2008). Analgesic Classification. Author. Retrieved from
http:/www.lar.iastate.edu/index.

Katzung, B.G. (2007). Basic and Clinical Pharmacology. New York: McGraw Hill Co.
Kozier, B., Erb, G., Berman, A., and Burke, K. (2000). Fundamentals of Nursing.
New Jersey: Prentice-Hall Inc.

Pinnell, N.L. (1996). Nursing Pharmacology. Philadelphia: W.B. Saunders Company.