1.
PRESENTED TO: PRESENTED BY:
Mrs. Vinay Kumari Amandeep Kaur
Associate Professor Roll No. 1915703
Medical Surgical Nursing M.Sc. (N) 2nd Year

2.
Algesia (pain)
 It is an ill-defined, unpleasant sensation,
usually evoked by an external or internal
noxious stimulus.
1. "Pain" is defined by IASP(International
association for the study of pain): "an
unpleasant sensory and emotional experience
arising from actual or potential tissue damage
or described in terms of such damage“

3.
P
a
i
n

4.
 Margo Mc Caffery (1968)first defined pain:
"whatever the person experiencing says it is,
existing whenever he says it does.”
 Analgesia: Absence of pain in response to
stimulation which would normally be painful
(e.g. using drugs)
 Nociceptor: A sensory receptor of the
peripheral (somatosensory nervous system)
that transmits noxious stimuli to CNS.

5.
 Noxious stimulus: A stimulus that is
damaging or threatens damage to normal
tissues (chemical, mechanical, thermal)
 Pain threshold: The minimum intensity of a
stimulus that is perceived as painful.
 Neuropathic pain: Pain caused by a lesion
or disease of the nervous system.

6.
Factors affecting pain perception
PAIN
EXPERIENCE
AGE

7.
PAIN PATHWAY

8.
Gate control theory of pain

9.
 Gate control theory was described by Melzack and
Wall in 1965.
 This theory explains about a pain-modulating system
in which a neural gate present in the spinal cord can
open and close thereby modulating the perception of
pain.
 The gate control theory suggests that psychological
factors play a role in the perception of pain.

10.
 It also suggests 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.

11.
Centers in CNS
 The three systems located in the spinal cord
act to influence perception of pain
 The substantia gelatinosa in the dorsal horn,
 The dorsal column fibers
 The central transmission cells.

12.
The dorsal column fibers

13.
The central transmission cells/neuron

14.
 The dorsal horn is responsible for passing on
information which can be interpreted as pain.
This area is referred to as the 'gate' as it prevents
the brain from receiving too much information
too quickly. DORSAL HORN of
spinal cord grey
matter

15.
Neurons involved in pain conduction
1. Primary: from the
‘nociceptors’/ peripheral
nerve fibre to the dorsal
horn of the spinal cord.
2. Secondary: from the dorsal
horn to the thalamus.
3. Tertiary: from thalamus to
cortex and awareness.
Tertiary
Neuron
Secondary
Neuron
Primary
Neuron
Nociceptors

16.
Mechanism:
Trauma Receptors A-delta
C fibers
Afferent Pathway
Thalamus
Reticular Formation
PAG(periaqueductal gray)
Cortex
Higher centers
“ouch”
“mommy”

17.
Phases of pain perception
2. Conduction
•After noxious stimulus conduction
of action potential will occur
3 5
4
5
4
32
3

18.
Nerve fibers Involved
 The smaller, unmyelenated A (delta) and C nerve
fibers sense pain such as sharp burning and aching
feelings.
 Larger, myelenated A (beta) skin nerves which carry
senses of touch, heat, cold and pressure.
 The A (beta) nerves are faster, and also have priority
which effectively blocks out the pain messages to the
brain and closes the gate.
 Stimulation of the large-diameter fibers (A-Fibers)
inhibits the transmission of pain (closing the gate)

19.
 Stimulation of the Small-diameter fibers (C-Fibers)
stimulates the transmission of pain (opening the Gate)
 When the gate is closed, signals from small diameter
pain fibers do not excite the dorsal horn transmission
neurons.
 When the gate is open pain signals excite dorsal horn
transmission cells.
 The gating mechanism is influenced by nerve impulses
that descend from the brain

20.
 Factors which influence opening and closing
the gate are:
 The amount of activity in the pain fibers.
 The amount of activity in other peripheral fibers
 Messages that descend from the brain.

21.
Gate may be closed by:
 Physical Pain - Analgesic Remedies
 Emotional Pain - Being in a ‘good’ mood
 Behavioral Factors - Concentrating on things
other than the injury
 Relaxation and Contentment –
 Mental factors: - work, T.V., book,
 Activity - Taking exercise,
 counter-stimulation- heat, massage, acupuncture

22.
Gate is opened by
 Physical Factors - Bodily injury
 Emotional Factors - Anxiety & Depression
 Behavioral Factors - Attending to the injury and
concentrating on the pain
 Lack of Activity –
 Mental Factors –

23.
TYPES OF PAIN/CLASSIFICATION
Diagnostic classification
 A. Nociceptive pain,
 B. Neuropathic pain,
 C. Idiopathic pain.

24.
A. Nociceptive pain
 I. Somatic: well localized; e.g. skin, bones
 II. Visceral: poorly localized; e.g. organs
It is due to the activation of nociceptors at the site of
tissue damage. These types of pain can Results by
mechanical, chemical, or thermal stimulus, such as
surgery, traumatic injury, and inflammatory
processes.
It is divided into either
1. Somatic: localized pain in skin, bones or muscles,
joint. Or
2. Visceral: poorly localized (may be referred to other
areas)located in organs, characterized by having
deep pressure like squeezing.

25.
B. Neuropathic pain
I. Central: Localized and diffused; burning, stabbing
pain e.g. CNS
II. Peripheral: localized neuropathies
 Results from damage of afferent nerve fibers,
characterized by burning, stabbing, electrical
numbing, radiating shooting pain. Either to CNS,
or to peripheral which further divides into
polyneuropathy, or mononeuropathy (e.g. diabetic
neuropathy)

26.
C. Idiopathic pain
1. Usually in head, shoulders, or pelvic areas.
2. Results of non-specific origin, due to stress,
anxiety, depression, or cold pressure e.g. head,
shoulders, abdomen, and pelvic areas.

27.
PAIN CLASSIFICATION
CLINICAL TYPES
1. Acute pain
2. Chronic pain

28.
2. Pain classification
Clinical types
Acute pain Chronic pain
 Results from noxious
stimuli that activates
nociceptors neuron
 It accompanies surgery,
traumatic injury, tissue
damage, and inflammatory
processes.
 Self-limited, resolves over
days to weeks, but can
persist for 3 months
 Treatment is short term
and curative
 Results from: nociceptors,
visceral, or somatic
 It accompanies chronic
disease, untreated condition.
 Unresolved as long as
underlying cause is present.
 Treatment goal oriented,
multidisciplinary
approaches.

29.
TREATMENT OF PAIN :-ANALGESICS
1. Non-Opioids,
2. Opioids,
3. Adjuvants.

30.
1. NON-OPIOIDS

31.
Non-steroidal Anti-inflammatory Drugs
(NSAIDs)
Cox-1, cox-2 Inhibitors
 Ketorolac (Toradol)- inj. Ibuprofen (Advil, Neurofen, Brufen)
200-400mg PO, 4-6hrly
 Diclofenac Na/K (Voltaren, Olfen, Cataflam)75mgPO twice/day
 Mefanemic acid (Ponstan):- in acute pain-500mg PO, once/day
 Naproxen (Naprosyn)500mgPO 8hrly
Cox-2 Inhibitors
 Celebrex (Celecoxib)100-200mg PO twice/day
 Etoricoxib (Arocoxia)
 Meloxicam (Mobic)

32.
NSAIDS MECHANISM OFACTION

33.
Cox-1 inhibitors
 Ketorolac (Toradol):
 Postoperatively for max 5 days
 Reduce amount of opioid requirement, reduce
S.E’s
 Dose= 15 – 30 mg IV / IM Q6hrs

34.
 Cox-2 inhibitors:
 Effective anti-inflammatory in arthritis
 Carry cardiovascular risk warning
 Less GI S.E’s

35.
Side effects:
 Prolong bleeding time
 Gastric erosions/ ulceration/ perfusion
 Affect kidney function:
-Water / electrolyte balance
-Interfere with diuretics/antihypertensive
-Renal injury / nephrotic syndrome

36.
2. OPIOIDS / NARCOTIC ANALGESICS

37.
OPIOIDS / NARCOTICANALGESICS
Opium a dark brown, resinous material obtained from poppy (Papaver
somniferum) capsule. It contains two types of alkaloids.
Phenanthrene derivatives
 Morphine (10% in opium) 15 to 30 mg orally every 4 hours as needed
 Codeine (0.5% in opium) 15 to 60 mg up to every 4 hours as needed
 Thebaine (0.2% in opium),
(Nonanalgesic)
Benzoisoquinoline derivatives
 Papaverine (1%) } Nonanageslc
(30 to 60 milligrams (mg) injection)
 Noscapine (6%)} Nonanageslc
 (50 mg8 hourlyPO)

38.
MORPHINE
 Morphine is the principal alkaloid in opium
and still widely used. Therefore, it is described
as prototype.
(a first or preliminary version from which other forms are
developed.)

39.
Mechanism of action

40.
PHARMACOLOGICAL
ACTIONS
a.) CNS
Morphine has site specific depressant and stimulant actions
in the CNS by interacting primarily with the I-l opioid
receptor as a full agonist. The depressant actions are:
1. Analgesia Morphine is a strong analgesic.
2. Sedation which is different from that produced by
hypnotics is seen. Drowsiness and indifference to
surroundings as well as to own body occurs without motor
in-coordination, ataxia or apparent excitement (contrast
alcohol). Higher doses progressively induce sleep and
coma. Morphine has no anticonvulsant action.

41.
Con…
3. Mood and subjective effects These are
prominent. Morphine has a calming effect; there
is loss of apprehension, feeling of detachment,
lack of initiative, limbs feel heavy and body
warm, mental clouding and inability to
concentrate occurs.
4. Respiratory centre Morphine depresses
respiratory centre in a dose dependent manner;
rate and tidal volume are both decreased: death in
poisoning is due to respiratory failure.

42.
Con…
5. Cough centre: It is depressed; more sensitive
to morphine than respiratory centre.
6. Temperature regulating centre: It is
depressed; hypothermia occurs in cold
surroundings.
7. Vasomotor centre: It is depressed at higher
doses and contributes to the fall in BP.

43.
b). NEURO-ENDOCRINE
1. Hypothalamic influence on pituitary is reduced.
2. As a result FSH, LH, ACTH levels are lowered, while
prolactin and GH levels are raised (these are under
predominant inhibitory control).
3. The sex hormone and corticosteroid levels are
lowered in the short term, but tolerance develops in
the long term.
4. Only few chronic abusers suffer from loss of libido,
impotence, menstrual irregularities and infertility.
5. Morphine can release ADH and reduce urine volume.

44.
c). CVS
 Morphine causes vasodilatation due to:
1. histamine release.
2. depression of vasomotor centre.
3. direct action decreasing tone of blood vessels.
 There is a shift of blood from pulmonary to systemic circuit due
to greater vasodilatation in the latter. Therapeutic doses cause
little change in the BP of recumbent normovolaemic patient.
Postural hypotension and fainting do occur due to impairment of
vascular reflexes. Morphine has little direct effect on heart; rate
generally decreases due to stimulation of vagal centre, but may
increase reflexly if the BP falls. Cardiac work is consistently
reduced due to decrease in peripheral resistance. Intracranial
tension tends to rise as a consequence of CO2 retention leading
to cerebral vasodilatation.

45.
d). GIT
 Constipation is a prominent feature of morphine action.
Several factors contribute:
1. Action directly on intestines and in CNS increases tone and
segmentation but decreases propulsive movements. Tone of
duodenum and colon may be increased to the level of spasm.
2. Spasm of pyloric, ileocaecal and anal sphincters.
3. Decrease in all gastrointestinal secretions: reduction in
transfer of water and electrolytes from mucosa to the lumen.
Absorption of fluid is increased due to stasis.
4. Central action causing inattention to defecation reflex. No
tolerance develops to this action: addicts remain chronically
constipated.

46.
e). OTHER SMOOTH MUSCLES
1. Biliary tract:- Morphine causes spasm of sphincter of
Oddi → intrabiliary pressure is increased → may cause
biliary colic.
2. Urinary bladder:- Tone of both detrusor and sphincter is
increased → urinary urgency and difficulty in
micturition. Contractions of ureter are also increased.
3. Uterus:- The action is clinically insignificant, may
slightly prolong labour.
4. Bronchi:- Morphine releases histamine which can cause
bronchoconstriction. This is of no consequence in normal
individuals, but can be dangerous in asthmatics.

47.
PHARMACOKINETICS
1. The oral absorption of morphine is unreliable because of high
and variable first pass metabolism; oral bioavailability is
1/6th to 1/4th of parenterally administered drug.
2. About 30% is bound to plasma proteins.
3. Concentration in liver, spleen and kidney is higher than that
in plasma. Only a small fraction enters brain rather slowly.
4. Morphine freely crosses placenta and can affect the foetus
more than the mother.
5. It is primarily metabolized in liver by glucuronide
conjugation.
6. Effect of a parenteral dose lasts 4--6 hours.
7. Elimination is almost complete in 24 hours and morphine is
noncumulative.
8. Small amounts may persist due to enterohepatic circulation.

48.
ADVERSE EFFECTS
 Nausea and vomiting
 Constipation
 BP may fall, especially in hypovolaemic patient.
 Irritable movement
 Psycho mimetic effects
 Sedation
 Broncho-constriction
 Respiratory Depression
 Acute morphine poisoning

49.
 Acute morphine poisoning
 It is accidental, suicidal or seen in drug abusers.
In the non-tolerant adult, 50 mg of morphine I.M.
produces serious toxicity. The human lethal dose
(amount of dose that can cause death) is
estimated to be about 250 mg. Manifestations are
extensions of the pharmacological action.

50.
Symptoms:-
 Stupor or coma, (impaired consciousness)
 flaccidity, (lack of muscle tone, deep tendon
reflexes)
 shallow and occasional breathing,
 cynosis,
 pinpoint pupil,
 fall in BP and shock
 convulsions may be seen in few patients,
 pulmonary edema occurs at terminal stages,
 death is due to respiratory failure.

51.
Treatment: consists of
1. Respiratory Support (positive pressure respiration also
decreases pulmonary edema formation)
2. Maintenance Of B.P. (I.V. fluids, vasoconstrictors).
3. Gastric Lavage should be done with potassium permanganate
to remove unabsorbed drug. Lavage is indicated even when
morphine has been injected; being a basic drug it is partitioned
to the acid gastric juice, ionizes there and does not diffuse back
into blood.
4. Specific antidote: Naloxone 0.4-0.8 mg I.V. repeated every 2-
3 min till respiration picks up, is the preferred specific
antagonist because it does not have any agonistic action and
does not per se depress respiration.

52.
3. ADJUVANTS

53.
ADJUVANTS
“An adjuvant is a pharmacological or immunological agent
that modifies the effect of other agents.”
Adjuvant may be added to a vaccine to modify the immune
response by boosting it such as to give a higher amount
of antibodies and a longer-lasting protection, thus
minimizing the amount of injected foreign material.
Or
“An adjuvant is a substance that is added to a vaccine to
increase the body's immune response to the vaccine.”

54.
a) In other words, adjuvants help vaccines work better.
b) Some vaccines made from weakened or dead germs
contain naturally occurring adjuvants and help the
body produce a strong protective immune response.
c) However, most vaccines developed today include just
small components of germs, such as their proteins,
rather than the entire virus or bacteria.
d) These vaccines often must be made with adjuvants to
ensure the body produces an immune response strong
enough to protect the patient from the germ he or she
is being vaccinated against.

55.
Agents used to induce analgesic effect indirectly
 Local anesthetics
 Antidepressants
 Anticonvulsants
 Corticosteroids
 Muscle relaxants
 Anti histamines

56.
Local anesthetics gain access to the inner
axonal membrane by
1. traversing sodium channels while they are
more often in an open configuration
2. passage directly through the plasma
membrane
3. Block initiation and propagation of action
potential

57.
Sequence of clinical anesthesia
• Sympathetic block (vasodilatation)
• Loss of pain and temperature sensation
• Loss of proprioception
• Loss of touch and pressure sensation
• Loss of motor function

58.
Antidepressant for nerve pain
 They found that the older class of antidepressants called
tricyclics can provide significant pain relief.
These include medications such as
• Amitriptyline(10-25 mg PO qHS; 10-400 mg PO qHS
dose range for migraine headache),
• Imipramine(50-100 mg PO qDay),
• Clomipramine(25 mg PO qDay),
• Desipramine, and
• Nortriptyline.
Anticonvulsant drugs were also shown to alleviate
neuropathic pain.

59.
Antidepressan con…
Tricyclic antidepressants enhance the descending
inhibitory system by preventing the cellular
reuptake of serotonin and norepinephrine.
Higher level of serotonin and norepinephrine in the
synaptic cleft inhibit the transmission of
nociceptive signals in the CNS.

60.
Anticonvulsants
Affects peripheral nerves and central nerves in
several ways, including sodium channel
modulation, central calcium channel modulation
and changes in excitatory amino- acids and other
receptors.
Effective in neuropathic pain and prophylactic
treatment of migraine headache.

61.
Corticosteroids
These drugs which includes:-
 Dexamethazone,
 Prednisone,
 Methylprednisone
Are used for the management of acute and chronic cancer pain,
pain secondary to spinal cord compression, and inflammatory
joint pain syndromes.
Mechanism of action are unknown but may be due to the ability of
corticosteroids to decrease edema and inflammation.
They may decrease activation of inflammed neuron.
Because of this effect, corticosteroids are usefull when injected
epidurally for acute or sub-acute disk herniation.

62.
Two adjuvants, aluminum and monophosphoryl lipid A,
are used in some U.S. vaccines.
Aluminum gels or aluminum salts are vaccine ingredients that
have been used in vaccines since the 1930s. Small amounts
of aluminum are added to help the body build stronger
immunity against the germ in the vaccine. Aluminum is one
of the most common metals found in nature and is present in
air, food, and water. The amount of aluminum present in
vaccines is low and is regulated by the U.S. Food and Drug
Administration (FDA).
Monophosphoryl lipid A has been used since 2009 in one
vaccine in the US, Cervarix. This immune-boosting
substance was isolated from the surface of bacteria. It has
been tested for safety in tens of thousands of people and
found to be safe.

63.
Only some vaccines contain adjuvants.
Aluminum is present in U.S. childhood vaccines that
prevent
Hepatitis A,
Hepatitis B,
Diphtheria-tetanus-pertussis (dtap, tdap),
Haemophilus influenzae type b (hib),
Human papillomavirus (HPV) and
Pneumococcus infection.
Monophosphoryl lipid A is included in one
Human papillomavirus (HPV) vaccine, Cervarix.

64.
Research input
Mechanisms of Action of Adjuvants
 Sunita Awate,1,2 Lorne A. Babiuk,3 and George
Mutwiri1,2,*
Abstract
Adjuvants are used in many vaccines, but their
mechanisms of action are not fully understood.
Studies from the past decade on adjuvant
mechanisms are slowly revealing the secrets of
adjuvant activity. In this review, we have
summarized the recent progress in our understanding
of the mechanisms of action of adjuvants.

65.
Adjuvants may act by a combination of various
mechanisms including formation of depot, induction
of cytokines and chemokines, recruitment of immune
cells, enhancement of antigen uptake and
presentation, and promoting antigen transport to
draining lymph nodes. It appears that adjuvants
activate innate immune responses to create a local
immuno-competent environment at the injection site.
Depending on the type of innate responses activated,
adjuvants can alter the quality and quantity of
adaptive immune responses. Understanding the
mechanisms of action of adjuvants will provide
critical information on how innate immunity
influences the development of adaptive immunity,
help in rational design of vaccines against various
diseases, and can inform on adjuvant safety.

66.
NeurologicalAnalgesia
 There are certain drugs that are mainly used for
neurologic and psychiatric conditions but they
can also relieve neuropathic pain, which occurs
without any external pain triggers like heat or
sharp points.
 Neuropathic anlagesia drugs include the
antidepressant amitriptyline (Elavil) and the
anticonvulsant gabapentin (Neurontin).

67.
Analgesics used in neurological conditions
 The opioid analgesics relieve pain by binding to opioid receptors in
the central nervous system.
They are also known as narcotics. Popular ones are
-Morphine,
-Fentanyl, and
-Oxycodone.
These drugs act as agonists to produce the effect of analgesia.
Opioids give relief for moderate to severe pain.
However, there is also the risk for potential addiction in some patients.
Narcotics are stronger analgesics.
They are used when pain is too severe to be controlled by NSAID
analgesics.
All narcotic analgesics are prescription medications.

68.
NURSING CARE OF THE PATIENT IN PAIN
 NURSING DIAGNOSIS: Pain
 GOAL: Relief of pain or decrease in intensity of
pain

69.
 Nursing Interventions
1. Reassure patient that you know pain is real and will assist
him or her in dealing with it.
2. Use pain assessment scale to identify intensity of pain.
3. Assess and record pain and its characteristics: intensity,
location, quality, frequency, and duration.
4. Administer balanced analgesic agents as prescribed to
promote optimal pain relief.
5. Administer pain medication around-the-clock, as ordered.

70.
Con..
6. Provide comfort measures, such as back massage, positioning,
linen changes, and oral or skin care.
7. Teach noninvasive techniques to control pain, such as
relaxation, guided imagery, distraction, and cutaneous
stimulation.
8. Explain the role of sleep and the importance of being well
rested.
9. Document severity of patient’s pain on chart.
10. Instruct patient and family about potential side effects of
analgesic agents and their prevention and management.

71.
Conclusion
 Pain motivates the individual to withdraw from
damaging situations, to protect a damaged body part
while it heals, and to avoid similar experiences in the
future. Most pain resolves once the noxious stimulus
is removed and the body has healed. Analgesics are
helpful in relieving pain as well as other
complications like inflammation.

72.
REFERENCES
BOOKS
 Mosbey’s drug guide for nurses. Edition:-9th . P.-198-203.
 Medications , How do analgesics work on pain? , Craig C.
Freudenrich and Discovery Fit & Health , Retrieved August 02,
2012
INTERNET
 Analgesics Research & Articles, Analgesics, Retrieved August
02, 2012
 http://www.bookrags.com/research/analgesics-woc
 https://www.cdc.gov/vaccinesafety/concerns/adjuvants.html

73.
THANK YOU…..