College of Nursing
Allied Hospital, Faisalabad Medical University,
Faisalabad
Assignment of Pathophysiology
Submitted by :
Anam Shahzadi
Izza Javed
Submitted to :
Mam Tallat ul Nisa
Mam Kaneez um Farwa Kaausar
Topic :
Endogenous Analgesic Mechanism
Objectives
Upon completion of this assignment and clinical application,
the nurse will be able to:
• Define pain and endogenous analgesia
• Explain pain pathway
• Describe endogenous analgesic mechanism
• Discuss neurotransmitters involved
• Explain gate control and descending pathway
• Describe clinical importance and nursing points
Table of Contents
Introduction / Definition
Anatomy of Pain Pathways
Types of Pain
Causes / Risk Factors
Pathophysiology
Signs & Symptom
PAIN
1. Introduction / Definition
Pain is an important protective mechanism of the body. Proper assessment and
management help improve patient comfort and recovery.
2. Anatomy of Pain Pathways
2.1 Nociceptors
Free nerve endings activated by mechanical, thermal, and chemical stimuli.
2.2 Afferent Nerve Fibers
Aδ fibers: fast, sharp, localized pain
C fibers: slow, dull, burning, chronic/visceral pain
2.3 Spinal Cord & Ascending Tracts
Neospinothalamic tract: fast sharp pain
Paleospinothalamic tract: slow chronic pain with emotional response
2.4 Brain Centers
Thalamus and somatosensory cortex process pain, while PAG, hypothalamus, and
reticular formation help modulate it.
Figure 1: Nociceptive Pain Pathway — from tissue injury to cortical perception
3. Types of Pain
3.1 Acute vs. Chronic Pain
Acute pain: Short-term pain from injury or illness with autonomic
responses
Chronic pain: Lasts >6 months, linked with psychological effects and no
autonomic signs
3.2 Cutaneous & Deep Somatic Pain
Cutaneous: Sharp, well-localized skin pain
Deep somatic: Diffuse pain from muscles, joints, or bones
3.3 Visceral Pain
Poorly localized pain from internal organs, often cramping or aching.
3.4 Referred Pain
Pain felt at a different site sharing the same spinal segment (e.g., heart pain felt in
left arm).
Figure 2: Classification of Pain by Duration, Location, Origin, and Quality
4. Causes / Risk Factors
Acute Pain Causes
Trauma (fractures, burns, injuries)
Surgery or medical procedures
Infections (e.g., appendicitis, otitis media)
Myocardial ischemia/infarction
Chronic Pain Causes
Musculoskeletal disorders (arthritis, back pain)
Cancer or nerve compression
Neuropathy (diabetic, post-herpetic, HIV)
Central sensitization after injury
Risk Factors
Age extremes, female gender, prior trauma
Diabetes, vascular disease, cancer
Psychological, cultural, and socioeconomic factors
5. Pathophysiology
Pain pathophysiology follows a sequential cascade from injury to perception and
modulation:
PATHOPHYSIOLOGY OF PAIN — STEP-BY-STEP FLOW
▼
STEP 1 TISSUE INJURY / NOXIOUS STIMULUS
▼
Release of chemical mediators: Bradykinin,
STEP 2 Prostaglandins, Histamine, Substance P, Serotonin,
ATP
▼
NOCICEPTOR ACTIVATION — Free nerve endings
STEP 3
threshold lowered (Peripheral Sensitization)
▼
ACTION POTENTIAL transmitted via: • Aδ fibers
STEP 4 (fast, sharp pain — 6–30 m/s) • C fibers (slow, dull
pain — 0.5–2 m/s)
▼
DORSAL HORN (Spinal Cord) — Glutamate &
Substance P released → 2nd-order neuron
STEP 5
activation → WINDUP phenomenon → Central
Sensitization
▼
ASCENDING TRACTS: • Neospinothalamic tract →
Fast, sharp, localized pain → Somatosensory
STEP 6 Cortex • Paleospinothalamic tract → Slow, diffuse,
chronic/visceral pain → Thalamus → Limbic
system
▼
THALAMUS → Relays to Somatosensory Cortex &
STEP 7 Limbic System → PAIN PERCEPTION: localization,
intensity, quality, affective response
▼
STEP 8 DESCENDING MODULATION — PAG → Raphe
nuclei (Serotonin) + Locus Coeruleus
(Norepinephrine) → Enkephalinergic interneurons
in dorsal horn → PAIN INHIBITION
6. Signs & Symptoms
Acute Pain
Pain ≥4/10, guarding, facial grimacing
Tachycardia, hypertension, sweating, pupil dilation
Anxiety, restlessness, reduced gut motility
Chronic Pain
Pain >6 months, depression, irritability, social withdrawal
Sleep disturbance, fatigue, low appetite/libido
Neuropathic features (paresthesia, allodynia), minimal autonomic signs
Altered Pain Sensitivity
Hyperalgesia: increased pain response
Allodynia: pain from non-painful stimuli
Hyperpathia: delayed but exaggerated pain
Hypoesthesia/Anesthesia: reduced or absent sensation
Endogenous Analgesic Mechanisms
It is the natural pain control system of the body that suppresses or blocks pain
impulses by releasing endogenous opioids and activating inhibitory pathways.
Components of the Endogenous Analgesic System
1. Periaqueductal Gray (PAG)
Located in the midbrain around the cerebral aqueduct.
Acts as the main control center for pain inhibition.
Receives pain signals from higher brain centers.
Activates descending inhibitory pathways to reduce pain transmission.
2. Nucleus Raphe Magnus
Located in the medulla of the brainstem.
Receives signals from the PAG.
Releases serotonin, which helps suppress pain signals.
Sends descending fibers to the spinal cord.
3. Dorsal Horn of Spinal Cord
First relay station for pain signals entering the spinal cord.
Descending fibers from PAG and nucleus raphe magnus act here.
Inhibitory interneurons block transmission of pain impulses from Aδ and C
fibers.
Reduces the pain signal traveling to the brain.
4. Endogenous Opioids
Natural pain-relieving chemicals of the body.
Include:
o Endorphins
o Enkephalins
o Dynorphins
Bind to opioid receptors (μ, δ, κ) and inhibit pain transmission.
Produce analgesia without external drugs.
Mechanisms Steps
Mechanism of Endogenous Analgesic System
Step 1: Activation of Periaqueductal Gray (PAG)
When pain occurs, pain signals reach the brain and activate the PAG in the
midbrain. PAG acts as the main pain control center and starts the descending pain
inhibitory pathway.
Step 2: Stimulation of Brainstem Nuclei
The PAG sends signals to the nucleus raphe magnus in the medulla. These nuclei
release neurotransmitters like serotonin and norepinephrine, which travel
downward toward the spinal cord.
Step 3: Inhibition at the Dorsal Horn
Descending fibers reach the dorsal horn of the spinal cord and activate inhibitory
interneurons. Endogenous opioids (endorphins, enkephalins) are released, blocking
Substance P and pain transmission from Aδ and C fibers. As a result, fewer pain
signals reach the brain, producing analgesia.
Gate Control Theory of Pain
The Gate Control Theory was proposed by Ronald Melzack and Patrick Wall in
1965.
It explains how pain signals are controlled at the spinal cord level before reaching
the brain.
Definition
Gate Control Theory states that a “gate” mechanism in the dorsal horn of the
spinal cord (substantia gelatinosa) regulates whether pain signals are allowed to
pass to the brain or are blocked.
Main Components
1. Small Diameter Fibers (Pain Fibers)
These fibers carry pain impulses.
Aδ fibers → fast, sharp pain
C fibers → slow, dull, burning pain
Function
They open the gate and increase pain transmission.
2. Large Diameter Fibers (Touch Fibers)
Aβ fibers
Function
Carry touch, pressure, vibration sensations and close the gate by activating
inhibitory interneurons.
3. Substantia Gelatinosa (Gate)
Located in the dorsal horn of spinal cord.
Acts like a control gate.
Function
Determines whether pain signals continue to the brain or get blocked.
4. Transmission (T) Cells
Second-order neurons in spinal cord.
Function
Transmit pain impulses upward through the spinothalamic tract to the brain.
Mechanism of Gate Control Theory
Step 1: Pain Stimulus
A painful stimulus (injury, burn, cut) activates nociceptors.
Step 2: Small Fibers Open the Gate
Aδ and C fibers carry pain signals to the dorsal horn and stimulate T-cells.
This opens the gate, allowing pain signals to travel to the brain.
Step 3: Large Fibers Close the Gate
When touch or rubbing occurs, Aβ fibers become activated.
These fibers stimulate inhibitory interneurons in substantia gelatinosa.
Step 4: Inhibition of Pain Transmission
The inhibitory interneurons suppress T-cell activity and block pain impulses from
small fibers.
Step 5: Reduced Pain Perception
Fewer pain signals reach the brain, so pain sensation decreases.
Simple Example
When you accidentally hit your hand, you immediately rub the area.
Rubbing activates Aβ touch fibers, which close the gate and reduce pain.
Clinical Importance
Basis of Pain Relief Methods
TENS (Transcutaneous Electrical Nerve Stimulation)
Massage therapy
Rubbing injured area
Heat and cold therapy
Acupuncture
Advantages
Explains why psychological and touch factors affect pain.
Explains effectiveness of non-drug pain therapies.
Introduced concept of pain modulation.
Limitations
Cannot fully explain chronic or phantom pain.
Pain perception also involves emotional and cognitive brain processes.
Clinical Importance of Endogenous Analgesic System
Opioids in Pain Management: Opioid drugs (morphine, codeine) act on
opioid receptors similar to endogenous opioids to reduce pain.
Stress-Induced Analgesia: During severe stress or trauma, the body
releases endorphins that temporarily suppress pain.
Placebo Effect: Belief in treatment can activate endogenous opioid
pathways and reduce pain perception.
Chronic Pain Treatment: Understanding endogenous analgesia helps
develop therapies for chronic pain control.
Basis of Non-Drug Therapies: Techniques like acupuncture, TENS, exercise,
and meditation stimulate endogenous opioid release.
Nursing Management of Pain
Assess pain regularly using pain scale.
Administer prescribed analgesics on time and correctly.
Use non-pharmacological methods like positioning, heat/cold therapy, and
relaxation techniques.
Provide emotional support and reassurance to reduce anxiety.
Maintain a calm and comfortable environment.
Educate the patient about pain reporting and medication use.
Monitor and evaluate pain relief after interventions.
NANDA Nursing Diagnosis of Pain (Points Form)
Acute Pain (Problem-Focused)
o Related to tissue injury
o Evidenced by verbal report of pain, guarding, facial grimacing
Chronic Pain (Problem-Focused)
o Related to long-term disease condition
o Evidenced by persistent pain, fatigue, sleep disturbance
Risk for Chronic Pain (Risk Diagnosis)
o Related to untreated or poorly managed acute pain
o Related to nerve damage or prolonged inflammation
Readiness for Enhanced Comfort (Health Promotion)
o Patient expresses desire to improve comfort and pain control
o Willing to use pain management strategies
Chronic Pain Syndrome (Syndrome Diagnosis)
o Related to long-term physical and psychological effects of pain
o Includes functional impairment and emotional distress
Summary
Pain is a complex and individualized experience influenced by physical,
psychological, and cultural factors. Nociceptors detect harmful stimuli and
transmit signals to the brain through nerve pathways. Pain may be acute or
chronic, and can be nociceptive or neuropathic. The body controls pain through
endogenous analgesic mechanisms involving endorphins, enkephalins,
dynorphins, and descending inhibitory pathways. Effective pain management
requires an interdisciplinary approach using pharmacological, non-
pharmacological, psychological, and rehabilitative methods according to the
patient’s needs.
References
Porth & Matfin (2009) Pathophysiology – pain and somatosensory function.
IASP (2020) – revised definition of pain.
Melzack & Wall (1965) – Gate Control Theory of pain.
Basbaum et al. (2009) – cellular and molecular mechanisms of pain.
Woolf (2011) – central sensitization in chronic pain.
WHO (2019) – cancer pain management guidelines.
McCaffery & Pasero (1999) – clinical pain assessment and management.
Dhawan et al. (1996) – opioid receptor classification.
StatPearls (2023) – endogenous opioids overview.
TeachMePhysiology (2023) – pain pathways.