In this presentation I have tried to explain in brief about pain management, different types of pain, its diagnostic criteria, its physiology, and its treatment approaches both pharmacological and non pharmacological
this topic explains the nature of pain, signs and symptoms of pain, different types of pain, factors influencing pain, assessment of pain and pharmacological and non pharmacological management of pain.
this topic explains the nature of pain, signs and symptoms of pain, different types of pain, factors influencing pain, assessment of pain and pharmacological and non pharmacological management of pain.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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The prostate is an exocrine gland of the male mammalian reproductive system
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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2. Is an unpleasant sensory and
emotional experience associated with
actual and potential tissue damage, or
described in terms of such damage.
(American Pain
Society[APS],2003;Gordon,2002)
PAIN
3. 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.
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.
4. Pain threshold- least amount of stimuli that is needed for a
person to label sensation as pain.
Pain tolerance- maximum amount of painful stimuli that a person
is willing to withstand without seeking avoidance of the pain or
relief.
Hyperalgesia and Hyperpathia- used interchangeably to denote
heightened response to a painful stimuli.
Allodynia-non-painful stimuli produce pain
Dysesthesia- an abnormal unpleasant sensation felt when
touched, caused by damage to peripheral nerves
5. IMPORTANT
IMPLICATIONS
Pain is physical and emotional experience,
not all in the body or all in the mind.
It is in response to actual or potential tissue
damage, so there may not be abnormal lab
or radiographic reports despite real pain.
Pain is described in terms of such damage.
6.
7. ON THE BASIS OF LOCATION
Classifications of pain based on where it is
in the body may be useful in determining
the client’s underlying problems or needs.
Complicating the categorization of pan by
location is the fact that some pains
radiate(spread or extend) to other areas.
8. • 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.
2 . P a i n c l a s s i f i c a t i o n
CLINICAL CLASSIFICATION
9. ON THE BASIS OF INTENSITY
Classified using a standard 0(no pain) to
10 (worst possible pain) scale.
Mild pain- rating of 1-3
Moderate pain- rating of 4-6
Severe pain- reaching 7-10 and is
associated with worst outcome.
10. DIAGNOSTIC CLASSIFICATION
A. Nociceptive pain
I. Somatic: well localized; e.g. skin, bones
II. Visceral: poorly localized; e.g. organs
B. Neuropathic pain
I. Central: Localized and diffused; burning,
stabbing pain e.g. CNS
II. Peripheral: localized neuropathies
C. Idiopathic pain
usually in head, shoulders, or pelvic areas
11.
12. PHYSIOLOGY OF PAIN
How pain is transmitted and perceived is
a complex in part because of the nature
of the fully integrated constantly changing
structure of the central nervous system,
and the symphony of chemical mediators,
only a fraction of which are understood.
13. NOCICEPTION
The peripheral nervous system includes
primary sensory neurons specialized to detect
mechanical, thermal or chemical conditions
associated with potential tissue damage.
The signals, when these nociceptors are
activated, must be transduced and transmitted to
the spine and brain where signals are modified
before they are ultimately understood or “felt”.
4 physiologic processed involved ( transduction,
transmission, perception, and modulation)
14. TRANSDUCTION
During this stage, noxious stimuli ( with
potential to injure tissue) trigger the release
of biochemical mediators (prostaglandins,
bradykinin, serotonin, histamine, substance
P) that sensitize nociceptors.
Noxious or painful stimulation also causes
movement of ions across cell membranes,
which excites nociceptors.
15. Pain medication can work during this phase
by blocking the production of
prostaglandin(e.g., ibuprofen or aspirin) or by
decreasing the movements of ions across the
cell membrane (e.g., local anesthetic) . topical
analgesic capsaicin ( Zostrix) depletes the
accumulation of subtance P and blocks
transduction.
16. TRANSMISSION
Includes 3 segments.
First segment- pain impulse travels from the
peripheral nerve fibers to the spinal cord.
Second segment- transmission from the spinal
cord and ascension via spinothalamic tracts, to the
brain stem and thalamus.
Third segment- involves transmission of signals
between thalamus to the somatic sensory cortex
where pain perception occurs.
17. Pain control can take place during this
second process. Opoids (narcotic
analgesics) block the release of
neurotransmitters, particularly
substance P, which stops the pain at the
spinal level. Capsaicin may also deplete
substance P that could inhibit the
transmission of pain signals.
18. MODULATION
Often described as “descending System”
Occurs when neurons in the thalamus
and brain stem send signals down to the
dorsal horn of the spinal cord. These
descending fibers release substances
such as endogenous opoids, serotonin,
and norepinephrine which can inhibit the
ascending noxious(painful) impulses in
the dorsal horn.
19. PERCEPTION
Is when the client becomes conscious
of the pain. Pain perception is the
sum of complex activities in the
Central Nervous System that may
shape the character and intensity of
pain perceived and ascribe meaning
to the pain.
22. If pain is inadequately controlled,
what are the consequences?
Anxiety
Family
worries
Depression
Sleep
disturbances
Impaired
ambulation
Medication
worries
Increase
hospitalization
and costs
23. GATE-CONTROL THEORY
According to Melzack and Wall’s gate theory,
small diameter(A-delta,or C) peripheral nerve
fibers carry signals of noxious stimuli to dorsal
horn , where these signals are modified when
they’re exposed to substantia gelatinosa.
Peripherally, large diameter (A-delta) nerve
fibers, which typically send messages of
touch, or warm or cold temperature, have am
inhibitory effect on substantia gelatinosa and
may activate descending mechanism or inhibit
transmission of pain impulses.
24. Higher centers in the brain, esp. those
associated with affect and motivation,
are capable of modifying the substantia
gelatinosa and influence the opening or
closing of gates.
25. RESPONSE TO PAIN
• The body’s response to pain has both physiologic and
psychological aspects.
• The sympathetic Nervous System responds, resulting in
fight-or-flight response, with noticeable increase in pulse
and blood pressure. The person may hold his breath or
have short, shallow breathing,
26. • Pain interferes with sleep, affects appetite and lowers
quality of life for clients and their family members.
• Natural response is to stop activity, tense muscles, and
withdraw from the pain-provoking activities which
reduced mobility that may produce muscle atrophy and
painful spasm.
• Uncontrolled pain impairs immune function, which slows
healing and increase susceptibility to infections and
dermal ulcers. This short, shallow breathing that
accompanies pain produces atelectasis, lowers circulating
oxygen and increase cardiac load.
27. Factors affecting Pain
Ethnic and cultural values
Developmental stage
Environment and support people
Past-pain experience
Meaning of pain
PAIN
EXPERIENCE
AGE MEANING
OF PAIN
ATTENTION
SexAnxiety
Pain
Control
CULTURE
30. • Obtain a Pain History
Allow the client to describe the pain to establish a trust
relationship between you and the client
Discover the effects of pain on the client's quality of life
Assess for emotional and spiritual distress and coping abilities
Ask about previous pain experience and what measures have
been effective as well as those who have not
Use WHAT’S UP format or PQRST or OLDCART in assessing pain
31. • W – where is the pain? Be specific. Use drawing of body if
necessary
• H – how does the pain feel? Is it shooting, burning, dull, sharp?
• A – aggravating and alleviating factors. What makes the pain
better? Worse?
• T – timing. When did the pain start? Is it intermittent? Continuous?
• S – severity. How bad is the pain on a 0 to 10 (0 to 5; faces) scale
• U – useful other data. Are you experiencing any other symptoms
associated with the pain or pain treatment? Itching, nausea,
sedation, constipation?
• P – perception. What is the client’s perception of what caused the
pain?
32. • P – provoked
• Q- quality
• R – region/radiation
• S – severity
• T - timing
33. • O – onset
• L – location
• D – duration
• C – characteristic
• A – aggravating factors
• R – radiation
• T – treatment
34. Daily Pain Diary
• For clients who experience chronic pain
• May help the client and nurse identify pain
patterns and factors that exacerbate or
mediate pain
• The record can include: time or onset of
pain, activity before pain, pain-related
positions or behaviors, pain intensity level,
use of analgesics or other relief measures,
duration of pain, time spent in relief
activities.
35. Visual Analogue Scales
• Useful in assessing the intensity of pain
• Includes a horizontal 10cm line, with
anchors indicating the extremes of pain
• The client is asked to place a mark
indicating where the current pain lies on
the line
• Left: none or no pain
• Right: severe or worst possible pain
36. Faces Pain Scale
• This instrument has six faces depicting expressions that range from
contented to obvious distress
• The client is asked to point to the face that most closely resembles
the intensity of his or her pain
41. Pharmacological Treatment of Pain
NSAIDs
Ketorolac (Toradol):
• Postoperatively for max 5 days
• Reduce amount of opioid requirement, reduce S.E’s
• Dose= 15 – 30 mg IV / IM Q6hrs
Cox-2 inhibitors:
• Effective anti-inflammatory in arthritis
• Carry cardiovascular risk warning
• Less GI S.E’s
42. Pharmacological Treatment of Pain
NSAIDs
Side effects:
Prolong bleeding time
Gastric erosions/ ulceration/ perfusion
Affect kidney function:
_ Water / electrolyte balance
_ Interfere with diuretics/ antihypertensive
_ Renal injury / nephrotic syndrome
43. Pharmacological Treatment of Pain
Opioids
Morphine
Oral, Rectal, IV, IM, SC, pca,
Epi,
Equianalgesic potency
10 mg IM
Meperidine
(Pethidine)
IV, IM, pca, Epi 75 mg
Fentanyl
IV, Epi, pca, Transdermal
patches, sublingual lollipops
100 mcg
Codeine
(Solpadeine: codeine
8mg/Aceta./caffeine)
Oral, Rectal, IV, IM. 130 mg
Hydromorphone
Oral, IV, SC, IM, Rectal, pca 1.5 mg
Tramadol
(Tramal)
Oral, IV, IM, SC 100 mg
44. Opioids / Narcotic analgesics
Morphine: Gold standard opiate
Bolus: 2-5 mg slowly over 5min (Q 1-3 hrs).
CI: 1mg/hr titrated to the desired analgesic effect.
IM; 5-10 mg (Q3-4 hrs).
SC: not recommended in repeated dose.
Meperidine: used in acute pain only, alternative for morphine
intolerance.
limited use due to toxic metabolite, sedative, and emetic effect.
Fentanyl: 100 times more potent, rapid onset of action
given bolus, CI, oral, patches.
Tramadol:
Acts on opioid & non-opioid receptors (moderate pain)
Show poor analgesic effect as compared to morphine.
45.
46. Opioids Side Effects
Nausea and vomiting
Constipation
Pruritis
Irritable movement
Psychomimetic effects
Sedation
Broncho-constriction
Respiratory Depression
N.B: If respiratory depression/sedation develops, the nurse must
be familiar with administration of Naloxone, which will
reverse the effect . Naloxone is diluted (0.4 mg in 10 mL NS)
every 1-2 min until the patient's respiratory status improves
and the patient starts to arouse.
47. 3. Pharmacological Treatment of Pain
Adjuvants
Agents used to induce analgesic effect indirectly
• Local anesthetics
• Antidepressant
• Anticonvulsants
• Corticosteroids
• Muscle relaxants
• Anti histamines
50. Choice of Drugs in Treatment of Acute /
Chronic Pain
1) Severity of pain
2) Routes of administration
3) Patient information
4) Pharmacokinetic of drug
5) Patient’s preference
51.
52. NON - PHARMACOLOGIC
Non-pharmacological pain
management is the management
of pain without medications. This
method utilizes ways to alter
thoughts and focus concentration
to better manage and reduce pain.
Methods of non-pharmacological
pain include:
53. Bed Rest
The use of prolonged bed rest in the treatment of
patients with neck and low back pain and associated
disorders is without any significant scientific merit. Bed
rest supports immobilization with its deleterious effects
on bone, connective tissue, muscle, and psychosocial
well-being. For severe radicular symptoms, limited bed
rest of less than 48 hours may be beneficial to allow for
reduction of significant muscle spasm brought on with
upright activity. Patients should be instructed to avoid
resting with the head in a hyperflexed or extended
position. The proactive approach emphasizes activity
modification as opposed to bed rest and immobilization.
54. Manipulation and Mobilization
Manipulative treatment is commonly used in the
treatment of patients with neck pain and
associated disorders. Many different types of
manual treatment exist, including soft tissue
myofascial release, muscle energy/contract-relax,
and high-velocity low-amplitude manipulation. Soft
tissue myofascial release may include various
techniques, including effleurage, pétrissage,
friction, and tapotement. It has been shown to
improve flexibility, decrease the perception of pain,
and decrease the levels of stress hormones.
55. Traction
Cervical traction is a therapeutic modality that can be
administered with the patient in the supine or seated position.
Traction may reduce neck pain and works through a number of
mechanisms including passive stretching of myofascial
elements, gapping of facet joints, improving neural foraminal
opening, and reducing cervical disc herniation. It has been
found to reduce radicular symptoms in individuals with
confirmed radiculopathy and localized neck pain in individuals
with cervicogenic pain and spondylosis.Cervical traction may
be initiated during physical therapy with the patient properly
instructed in home use. It is not a stand-alone treatment
modality and should be done in conjunction with range-of-
motion (ROM) exercises, appropriate strengthening, and
correction of postural issues.
56. Therapeutic Modalities
Therapeutic modalities should be
considered an adjunct to an active
treatment program in the management of
acute low back pain. They should never be
used as the sole method of treatment. The
prescribing physician should first be aware
of all indications and contraindications for
a prescribed modality and have a clear
understanding of each modality and its
level of tissue penetration.
57. Transcutaneous Electrical Nerve
Stimulation
Transcutaneous electrical nerve stimulation (TENS) has been
used to treat patients with various pain conditions, including
neck and low back pain. Success may be dictated by many
factors, including electrode placement, chronicity of the
problem, and previous modes of treatment.TENS is
generally used in chronic pain conditions and not indicated
in the initial management of acute cervical or lumbar spine
pain.Overall, research is limited in regard to the isolated use
of TENS in the treatment of patients with acute cervical and
lumbar spine disorders, though it has been used in
combination with ROM exercises, spray and stretch, and
myofascial release.
58. Superficial Heat
Superficial heat can produce heating effects at a depth
limited to between 1 cm and 2 cm. Deeper tissues are
generally not heated owing to the thermal insulation of
subcutaneous fat and the increased cutaneous blood flow
that dissipates heat. It has been found to be helpful in
diminishing pain and decreasing local muscle spasm.
Superficial heat, such as the hydrocollator pack, should be
used as an adjunct to facilitate an active exercise program. It
is most often used during the acute phases of treatment
when the reduction of pain and inflammation are the
primary goals.
59. Cryotherapy
Cryotherapy can be achieved through the use of ice, ice
packs, or continuously via adjustable cuffs attached to
cold water dispensers. Intramuscular temperatures can
be reduced by between 3 °C and 7 °C, which functions to
reduce local metabolism, inflammation, and pain.
Cryotherapy works by decreasing nerve conduction
velocity, termed cold-induced neuropraxia, along pain
fibers with a reduction of the muscle spindle activity
responsible for mediating local muscle tone. It is usually
most effective in the acute phase of treatment, though it
can be used by patients after their physical therapy
sessions or their home exercise program to reduce pain
and the inflammatory response.
60. Exercise
Correction of posture may be the simplest technique to
relieve symptoms in patients with nonspecific neck or
low back pain, though it is extremely difficult to change
habits. The physician should instruct patients to assume
their worst postural “slump position” with forward
protrusion of the head, flexion of the neck, rounding of
the shoulders, and increased thoracic kyphosis and
reversed lumbar lordosis while sitting. Next, the
physician should instruct patients to correct these
postural abnormalities through retraction and extension
of the head, retraction of the shoulders, extension of the
thoracic spine, and return of the lumbar lordosis.
61. Electrical Stimulation
High-voltage pulsed galvanic stimulation has been used in
acute neck pain to reduce muscle spasm and soft tissue
edema. It is commonly used despite the lack of hard
scientific evidence for its efficacy. Its effect on muscle
spasm and pain is thought to occur by its counterirritant
effect on nerve conduction and a reduction in muscle
contractility. Use of electrical stimulation should be limited
to the initial stages of treatment, such as the first week
after injury, so that patients may quickly progress to more
active treatment that includes restoration of ROM and
strengthening. Electrical stimulation often may be
combined with ice or heat to enhance its analgesic effects.