p.8
Mechanism of Stimulation of Pain Receptors
What are the sensitizers that decrease the threshold of pain receptors?
Prostaglandin E2 and Substance P.
p.7
Release of Pain Producing Compounds (PPS)
What compounds are classified as 1st class pain-producing substances?
K ions, histamine, serotonin, and bradykinin.
p.4
Types of Pain Receptors
What type of damage do chemical pain receptors respond to?
Tissue damage produced by chemical agents, such as concentrated sulphuric acid (H2SO4) or high concentration of HCL in the esophagus in cases of reflux esophagitis.
p.5
Types of Pain Receptors
Where are pain receptors most abundant?
Skin, periosteum, vascular walls, joints, and dura of falx & tentorium.
p.7
Types of Pain Receptors
What temperature ranges are considered thermal stimuli that can directly stimulate pain receptors?
Temperatures greater than 45°C and less than 10°C.
p.13
Types of Pain Receptors
What are the three main sources (types) of pain?
Cutaneous Pain, Deep Pain, Visceral Pain.
p.4
Types of Pain Receptors
What type of stimuli do polymodal pain receptors respond to?
Tissue damage produced by a wide variety of painful stimuli.
p.7
Types of Pain Receptors
What are the three types of stimuli that can directly stimulate pain receptors?
Chemical stimuli, mechanical stimuli, and thermal stimuli.
p.7
Release of Pain Producing Compounds (PPS)
What is the role of 1st class pain-producing substances?
They directly stimulate pain receptors.
p.17
Emotional and Autonomic Reactions to Pain
What are some examples of emotional and psychogenic reactions to pain?
Anxiety and fear, crying, depression, and feeling of hurt.
p.10
Neuropathic Pain Characteristics
What is neuropathic pain?
A chronic type of pain caused by damage to or pathological changes in the nerve fibers either in the peripheral or central nervous system.
p.8
Mechanism of Stimulation of Pain Receptors
What compounds are released due to tissue damage?
Pain producing compounds.
p.8
Mechanism of Stimulation of Pain Receptors
Which substances are involved in the sensitization of pain receptors?
Prostaglandin E2 and Substance P.
p.12
Neuropathic Pain Characteristics
How is neuropathic pain typically described?
As tingling, numbness, burning, or shooting pain.
p.12
Neuropathic Pain Characteristics
What syndrome is neuropathic pain usually associated with?
Reflex sympathetic dystrophy.
p.17
Emotional and Autonomic Reactions to Pain
What changes occur in the body during a parasympathetic (depressor) reaction to pain?
Decreased blood pressure (B.P.) and decreased heart rate (H.R.).
p.21
Hyperalgesia and Sensitization
What is the local axon reflex?
Collaterals (antidromic) nerve fibers arise from the afferents carrying pain impulses from the primary site of injury.
p.21
Hyperalgesia and Sensitization
In which direction do the collaterals pass in the local axon reflex?
In the opposite direction to the skin area surrounding the primary site of injury.
p.2
Physiological Significance of Pain
What is one physiological significance of pain sensation?
Warning signal of tissue damage.
p.10
Neuropathic Pain Characteristics
What is an example of central neuropathic pain?
Central pain such as thalamic infarct.
p.12
Neuropathic Pain Characteristics
What type of medication may neuropathic pain respond to?
Tricyclic antidepressants.
p.17
Emotional and Autonomic Reactions to Pain
What changes occur in the body during a sympathetic (pressor) reaction to pain?
Increased blood pressure (B.P.) and increased heart rate (H.R.).
p.19
Hyperalgesia and Sensitization
What are the types of hyperalgesia?
Primary and secondary hyperalgesia.
p.18
Chronic vs Acute Pain
Is chronic pain considered to be masked depression?
No, chronic pain is not masked depression.
p.18
Chronic vs Acute Pain
Is depression more likely to be a cause or a consequence of chronic pain?
Depression is more likely to be a consequence of pain rather than a cause of pain.
p.10
Neuropathic Pain Characteristics
What are some examples of peripheral neuropathic pain?
Nerve compression such as Sciatica, Trigeminal neuralgia, neuralgias (diabetic neuropathy), and neuropathy.
p.7
Release of Pain Producing Compounds (PPS)
What is the result of tissue damage in the context of pain receptor stimulation?
Release of pain-producing compounds (PPS).
p.12
Neuropathic Pain Characteristics
What conditions usually accompany neuropathic pain?
Hyperalgesia and allodynia.
p.18
Chronic vs Acute Pain
Is there evidence supporting the theory of a 'pain-prone personality'?
No, there is no evidence for the theory of 'pain-prone personality'.
p.20
Hyperalgesia and Sensitization
What is the definition of cutaneous hyperalgesia?
Increased skin sensitivity to pain.
p.2
Physiological Significance of Pain
What is another physiological significance of pain sensation?
Evokes protective reactions.
p.4
Types of Pain Receptors
What type of stimuli do mechanical pain receptors respond to?
Mechanical trauma, such as heavy pressure.
p.3
Types of Pain Receptors
What classification is used for pain receptor subtypes?
Functional classification.
p.6
Types of Pain Receptors
Why are certain tissues considered pain-insensitive?
These tissues have no pain receptors.
p.9
Nociceptive Pain Classification
What are examples of nociceptive pain in the classification of chronic non-malignant pain?
Osteoarthritis, Rheumatoid Arthritis, Colitis, Myositis, Migraine
p.7
Types of Pain Receptors
What are examples of chemical stimuli that can directly stimulate pain receptors?
Strong acids or alkalies.
p.8
Mechanism of Stimulation of Pain Receptors
What are the direct stimulators of pain receptors?
Potassium ions, serotonin, histamine, and bradykinin.
p.1
Definition of Pain Sensation
What is the definition of pain sensation?
It is an unpleasant, uncomfortable sensation due to tissue damage associated with somatic, autonomic, and emotional reactions.
p.3
Types of Pain Receptors
To what may the specificity of pain receptors be related?
The nature of the injurious agents.
p.8
Mechanism of Stimulation of Pain Receptors
What initiates the stimulation of pain receptors?
Noxious stimuli and tissue damage.
p.10
Neuropathic Pain Characteristics
What are some examples of mixed neuropathic pain?
Post herpetic (Herpes zoster) neuralgia and Phantom limb.
p.11
Nociceptive Pain Classification
What is the primary difference between nociceptive pain and neuropathic pain?
Nociceptive pain is caused by a noxious stimulus activating nociceptors, while neuropathic pain occurs without an external stimulus, often due to nerve damage.
p.16
Chronic vs Acute Pain
When does chronic slow (delayed) pain onset?
Shortly after application.
p.7
Release of Pain Producing Compounds (PPS)
What compounds are classified as 2nd class pain-producing substances?
PGE2, leukotrienes, and substance P.
p.8
Mechanism of Stimulation of Pain Receptors
What role does ATP play in the stimulation of pain receptors?
ATP is released during tissue injury and contributes to the activation of pain receptors.
p.20
Hyperalgesia and Sensitization
When does primary hyperalgesia develop?
30-60 minutes after injury.
p.4
Types of Pain Receptors
What type of stimuli do thermal pain receptors respond to?
Tissue damage produced by thermal stimuli, such as temperatures above 45°C or below 10°C.
p.6
Types of Pain Receptors
Which tissues are considered pain-insensitive?
Brain tissue, liver parenchymal tissue, renal parenchymal tissue, and lung parenchymal tissue.
p.9
Neuropathic Pain Characteristics
What are examples of neuropathic pain in the classification of chronic non-malignant pain?
Amputations, Nerve injuries, HIV neuropathy
p.7
Release of Pain Producing Compounds (PPS)
What is the role of 2nd class pain-producing substances?
They sensitize the pain receptors by lowering their threshold to stimuli.
p.8
Mechanism of Stimulation of Pain Receptors
How does histamine contribute to pain sensation?
Histamine acts as a direct stimulator of pain receptors.
p.11
Neuropathic Pain Characteristics
What happens to the nerve in neuropathic pain?
The nerve is damaged, leading to pain sensation without an external stimulus.
p.15
Hyperalgesia and Sensitization
What is cutaneous hyperalgesia?
Increased sensitivity to pain if noxious stimulus causes injury.
p.19
Hyperalgesia and Sensitization
What is the significance of hypersensitivity to pain?
Hypersensitivity to pain helps healing by minimizing contact with the injured tissue until repair is complete.
p.15
Types of Pain Receptors
What stimuli can evoke cutaneous pain?
Noxious stimuli such as mechanical, thermal, and chemical.
p.17
Emotional and Autonomic Reactions to Pain
What are the two types of autonomic reactions to pain?
Sympathetic (pressor) reaction and parasympathetic (depressor) reaction.
p.18
Chronic vs Acute Pain
Do personality disorders and maladaptive coping styles have a higher prevalence in chronic pain populations compared to the general population?
No, they do not have a higher prevalence in chronic pain populations than in the general population.
p.20
Hyperalgesia and Sensitization
What are the two types of cutaneous hyperalgesia?
Primary hyperalgesia and secondary hyperalgesia.
p.22
Hyperalgesia and Sensitization
What is the convergence facilitation theory?
The theory states that fibers from both the primary site of injury and the area of secondary hyperalgesia converge on the same neuron in the dorsal horn and thalamic neurons, which are already facilitated by impulses from the primary site of injury. This makes the response to mild painful stimuli from or applied to the healthy skin more than normal, a phenomenon known as central sensitization.
p.5
Types of Pain Receptors
Where are pain receptors less abundant?
Most viscera and many deep tissues.
p.10
Neuropathic Pain Characteristics
What are the two main systems where nerve fibers can be damaged to cause neuropathic pain?
The peripheral nervous system and the central nervous system.
p.8
Mechanism of Stimulation of Pain Receptors
What is the effect of bradykinin on pain receptors?
Bradykinin acts as a direct stimulator of pain receptors.
p.14
Definition of Pain Sensation
What is the definition of cutaneous pain?
It is an unpleasant uncomfortable sensation due to tissue damage associated with somatic, autonomic, and emotional reactions originating from the skin.
p.12
Neuropathic Pain Characteristics
How easy is it to treat neuropathic pain?
It is hardly to be treated.
p.17
Emotional and Autonomic Reactions to Pain
What are the three main types of reactions to pain?
Somatic Motor Reactions, Autonomic Reactions, and Emotional & Psychogenic Reactions.
p.21
Hyperalgesia and Sensitization
What effect do the chemical transmitters released in the local axon reflex have on pain receptors?
They decrease the threshold of pain receptors.
p.12
Neuropathic Pain Characteristics
How does neuropathic pain respond to opioid therapy?
It is partially responsive to opioid therapy.
p.17
Emotional and Autonomic Reactions to Pain
How do emotional and psychogenic reactions to pain vary?
They vary according to circumstances and from person to person.
p.16
Chronic vs Acute Pain
When does acute fast (immediate) pain onset?
During application of the stimulus.
p.20
Hyperalgesia and Sensitization
What is the mechanism behind primary hyperalgesia?
Decreased pain threshold due to local axon reflex releasing substance P.
p.24
Hyperalgesia and Sensitization
What is hyperalgesia and how is it related to deep pain?
Hyperalgesia is an increased sensitivity to pain, and it may be associated with the skin area overlying the site of injury in deep pain.
p.27
Visceral Pain Characteristics
What reactions are associated with visceral pain?
Somatic, autonomic, and emotional reactions.
p.26
Mechanisms of Ischaemic Pain
What happens to pain-producing substances in muscles with normal blood supply?
They are washed away rapidly.
p.17
Emotional and Autonomic Reactions to Pain
What are the components of somatic motor reactions to pain?
Withdrawal reflexes, increased neuromuscular excitability, and reflex spasm of nearby muscles.
p.16
Chronic vs Acute Pain
What are the significances of acute fast (immediate) pain?
Determine site & severity, initiate withdrawal reflexes.
p.23
Definition of Pain Sensation
What are the sources of deep pain?
Muscles, tendons, ligaments, joints, periosteum, fascia, and vascular walls.
p.23
Hyperalgesia and Sensitization
What are the effects of deep pain?
Reflex spasm of nearby muscles, hyperalgesia of deep tissues, and depressor reaction.
p.22
Hyperalgesia and Sensitization
What is central sensitization?
Central sensitization is a condition where the response to mild painful stimuli from or applied to the healthy skin is more than normal due to the facilitation of neurons by impulses from the primary site of injury.
p.25
Definition of Pain Sensation
What is the definition of ischaemic pain?
It is an unpleasant, uncomfortable sensation due to tissue damage associated with somatic, autonomic, and emotional reactions originating from a decrease in the blood supply or flow to an active organ, such as skeletal muscles, smooth muscles, and cardiac muscles.
p.18
Chronic vs Acute Pain
What may depression predict in relation to chronic pain?
Depression may predict pain severity, pain behavior, disability, and treatment seeking/compliance.
p.20
Hyperalgesia and Sensitization
Where does secondary hyperalgesia occur?
In healthy skin surrounding the red area.
p.23
Mechanisms of Ischaemic Pain
What are the causes of deep pain?
Injury, inflammation, and ischemia.
p.24
Emotional and Autonomic Reactions to Pain
What autonomic reactions are associated with deep pain?
Parasympathetic manifestations such as nausea, vomiting, decreased heart rate, decreased arterial blood pressure (ABP), and fainting.
p.27
Visceral Pain Characteristics
What is the definition of visceral pain?
It is an unpleasant, uncomfortable sensation due to tissue damage associated with somatic, autonomic, and emotional reactions originating from stimulation of pain receptors in viscera.
p.23
Definition of Pain Sensation
What are the characteristics of deep pain?
Diffuse, deep, and dull aching.
p.26
Mechanisms of Ischaemic Pain
What occurs in muscles during ischaemia?
Pain-producing substances accumulate and stimulate pain receptors.
p.16
Chronic vs Acute Pain
What are the significances of chronic slow (delayed) pain?
Associated with arousal, autonomic & emotional reactions.
p.20
Hyperalgesia and Sensitization
What theory explains central sensitization in secondary hyperalgesia?
Convergence-facilitation theory.
p.24
Types of Pain Receptors
Which type of nerve fibers primarily transmit deep pain?
C – non-myelinated nerve fibers.
p.25
Mechanisms of Ischaemic Pain
What are some clinical examples of ischaemic pain?
Angina pectoris due to decreased blood flow in coronary arteries, intermittent claudications due to decreased blood flow in lower limb vessels, and muscle spasm due to decreased blood flow and metabolism.
p.26
Mechanisms of Ischaemic Pain
When does cardiac pain (angina pectoris) typically develop and how is it relieved?
It develops during physical exertion and is relieved by rest.
p.24
Emotional and Autonomic Reactions to Pain
What somatic reactions are associated with deep pain?
Reflex spasm of the nearby or surrounding muscles, limiting or immobilizing the injured part to minimize tissue damage and pain sensation.
p.25
Mechanisms of Ischaemic Pain
What mechanisms are involved in ischaemic pain?
Decreased oxygen supply and the release of pain-producing chemicals (PPCs) such as bradykinin and lactic acid stimulate ischaemic pain receptors.
p.26
Mechanisms of Ischaemic Pain
What happens during a muscle spasm that leads to ischaemic pain?
Compression on blood vessels causes muscle ischaemia, increasing metabolism and producing more pain-producing compounds (PPCs).
p.20
Hyperalgesia and Sensitization
What happens to non-painful stimuli in primary hyperalgesia?
Non-painful stimuli (such as touch) become painful.
p.20
Hyperalgesia and Sensitization
How long does secondary hyperalgesia last compared to primary hyperalgesia?
It has a shorter duration than primary hyperalgesia.
p.25
Mechanisms of Ischaemic Pain
What causes ischaemic pain?
A marked decrease in blood supply to tissues, especially muscular tissue.
p.26
Mechanisms of Ischaemic Pain
In which patients does intermittent claudication usually occur?
Old patients with severe arteriosclerosis.
p.29
Visceral Pain Characteristics
What are the common characteristics of visceral pain?
Colicky, burning, or dull aching pain.
p.29
Hyperalgesia and Sensitization
What is hyperalgesia and how is it related to visceral pain?
Hyperalgesia is an increased sensitivity to pain, often associated with the skin area related to the affected viscus.
p.20
Hyperalgesia and Sensitization
When does secondary hyperalgesia develop?
Later than primary hyperalgesia.
p.22
Hyperalgesia and Sensitization
Where do the fibers from the primary site of injury and the area of secondary hyperalgesia converge according to the convergence facilitation theory?
They converge on the same neuron in the dorsal horn and thalamic neurons.
p.29
Visceral Pain Characteristics
Is visceral pain usually referred?
Yes, visceral pain is usually referred.
p.23
Definition of Pain Sensation
What is the definition of deep pain?
It is an unpleasant uncomfortable sensation due to tissue damage associated with somatic, autonomic, and emotional reactions originating from deeper structures such as muscles, tendons, ligaments, joints, periosteum, fascia, and vascular walls.
p.24
Visceral Pain Characteristics
What are the common sensations associated with deep pain?
Dull aching, burning, or throbbing in nature.
p.27
Visceral Pain Characteristics
What type of sensation is visceral pain described as?
Unpleasant and uncomfortable.
p.26
Mechanisms of Ischaemic Pain
What is intermittent claudication?
Severe colicky pain in the calf muscles that appears on walking and is relieved by rest.
p.29
Visceral Pain Characteristics
What somatic reaction is usually associated with visceral pain?
Contraction of overlying muscles, known as the guarding response.
p.29
Visceral Pain Characteristics
How is the neural pathway of visceral pain different from other types of pain?
The afferent pain fibers from the viscera reach the central nervous system (CNS) by two separate routes.
p.20
Hyperalgesia and Sensitization
How is pain perceived in secondary hyperalgesia?
Pain is felt more severe than normal.
p.28
Visceral Pain Characteristics
How does ischemia of viscera contribute to visceral pain?
Ischemia of viscera is a cause of visceral pain.
p.28
Visceral Pain Characteristics
How does inflammation affect pain threshold in viscera?
Inflammation decreases pain threshold, leading to hyperalgesia in viscera.
p.22
Hyperalgesia and Sensitization
How does the convergence facilitation theory explain the increased response to mild painful stimuli?
The theory explains that the increased response is due to the convergence of fibers from both the primary site of injury and the area of secondary hyperalgesia on the same neuron, which is already facilitated by impulses from the primary site of injury, leading to central sensitization.
p.26
Mechanisms of Ischaemic Pain
What causes cardiac pain (angina pectoris)?
Decrease of blood supply to cardiac muscle due to atherosclerosis.
p.28
Visceral Pain Characteristics
Which fibers mediate Parietal Visceral Pain?
A-delta & C pain fibers that join the somatic spinal nerves
p.28
Visceral Pain Characteristics
What is a cause of visceral pain due to overdistension?
Overdistension of a hollow viscous
p.29
Emotional and Autonomic Reactions to Pain
What autonomic reactions are commonly associated with visceral pain?
Parasympathetic manifestations such as decreased heart rate (HR), decreased arterial blood pressure (ABP), nausea, vomiting, and miosis.
p.28
Visceral Pain Characteristics
What type of irritation can cause visceral pain?
Chemical irritation, such as heartburns due to hyperacidity of gastric juice
