1. Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It is subjective and based on expectations, past experience, and emotional factors.
2. Pain is transmitted via nociceptors that detect extreme mechanical, thermal, or chemical stimuli and transmit signals along nerve fibers to the spinal cord and brain.
3. Chronic pain lasts longer than 6 months and is more complex, often involving altered anatomy and neural pathways. It is a lasting condition compared to acute pain which subsides with healing.
This document defines pain and describes the physiology of pain. It states that pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is transmitted via nociceptors and travels along afferent nerve fibers to the spinal cord. The gate control theory proposes that pain transmission can be modulated by interactions between pain fibers and touch fibers at the spinal cord. Chronic pain may involve different nerve fibers and neurotransmitters than acute pain. Various brain regions are also involved in pain perception and modulation.
Pain is a complex physiological process involving nociceptors, nerve fibers that transmit signals to the spinal cord and brain. The perception of pain involves multiple areas of the brain and its experience is influenced by both physiological and psychological factors. Pain signals travel through the neospinothalamic and paleospinothalamic pathways and are modulated by descending inhibitory pathways from the brain. The gate control theory explains how non-painful stimuli can reduce pain perception.
This document discusses pain mechanisms and pathophysiology. It begins by outlining the objectives of understanding acute pain mechanisms, phases of pain, modes of analgesia, types of pain, and how pain can potentially kill patients if not properly treated. It then discusses various topics related to pain including acute versus chronic pain, major categories of pain classified by pathophysiology, the generation and perception of pain involving multiple body systems, phases of nociceptive pain, gate control theory, types of pain fibers, centrally acting analgesics like opiates, and harmful effects pain can have on the cardiovascular and respiratory systems. The document aims to dispel common myths regarding pain management.
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The document discusses the physiology of pain. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It describes the dual nature of fast and slow pain mediated by different nerve fiber types. Stimuli that can cause pain and the receptors involved are discussed. The pathways that carry pain signals from receptors to the brain through the spinal cord and thalamus are summarized. Finally, it outlines the gate control theory of pain modulation by interactions between pain and touch fibers at the spinal cord.
This document discusses the physiology of pain, including:
- Types of pain receptors and the pathways for fast and slow pain transmission.
- Pain is transmitted via A-delta fibers for fast pain and C fibers for slow pain to the spinal cord.
- From the spinal cord, pain travels via the spinothalamic tracts to the thalamus and brain for perception. Modulatory pathways can inhibit pain transmission.
The document discusses pain management. It defines pain and describes its components and types. It outlines the physiology of pain through four phases: transduction, transmission, perception, and modulation. It also discusses nursing assessments of pain, common nursing diagnoses for patients in pain, and approaches to pain management, including pharmacological and non-pharmacological interventions as well as health teaching.
This document defines pain and describes the physiology of pain. It states that pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is transmitted via nociceptors and travels along afferent nerve fibers to the spinal cord. The gate control theory proposes that pain transmission can be modulated by interactions between pain fibers and touch fibers at the spinal cord. Chronic pain may involve different nerve fibers and neurotransmitters than acute pain. Various brain regions are also involved in pain perception and modulation.
Pain is a complex physiological process involving nociceptors, nerve fibers that transmit signals to the spinal cord and brain. The perception of pain involves multiple areas of the brain and its experience is influenced by both physiological and psychological factors. Pain signals travel through the neospinothalamic and paleospinothalamic pathways and are modulated by descending inhibitory pathways from the brain. The gate control theory explains how non-painful stimuli can reduce pain perception.
This document discusses pain mechanisms and pathophysiology. It begins by outlining the objectives of understanding acute pain mechanisms, phases of pain, modes of analgesia, types of pain, and how pain can potentially kill patients if not properly treated. It then discusses various topics related to pain including acute versus chronic pain, major categories of pain classified by pathophysiology, the generation and perception of pain involving multiple body systems, phases of nociceptive pain, gate control theory, types of pain fibers, centrally acting analgesics like opiates, and harmful effects pain can have on the cardiovascular and respiratory systems. The document aims to dispel common myths regarding pain management.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The document discusses the physiology of pain. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It describes the dual nature of fast and slow pain mediated by different nerve fiber types. Stimuli that can cause pain and the receptors involved are discussed. The pathways that carry pain signals from receptors to the brain through the spinal cord and thalamus are summarized. Finally, it outlines the gate control theory of pain modulation by interactions between pain and touch fibers at the spinal cord.
This document discusses the physiology of pain, including:
- Types of pain receptors and the pathways for fast and slow pain transmission.
- Pain is transmitted via A-delta fibers for fast pain and C fibers for slow pain to the spinal cord.
- From the spinal cord, pain travels via the spinothalamic tracts to the thalamus and brain for perception. Modulatory pathways can inhibit pain transmission.
The document discusses pain management. It defines pain and describes its components and types. It outlines the physiology of pain through four phases: transduction, transmission, perception, and modulation. It also discusses nursing assessments of pain, common nursing diagnoses for patients in pain, and approaches to pain management, including pharmacological and non-pharmacological interventions as well as health teaching.
The document discusses the pathophysiology of pain. It defines pain and describes the three systems - sensory, motivational, and cognitive - that interact to produce the experience of pain. It categorizes pain into somatogenic, psychogenic, acute, and chronic types and discusses their characteristics. It also describes age-related differences in pain perception and the neuroanatomy of pain processing, including the roles of the afferent and efferent pathways and different areas of the central nervous system.
Somatic pain comes from skin and deep tissues, while visceral pain comes from internal organs. Both types of pain are detected by nociceptors and felt differently. Somatic pain is usually easier to locate and more intense, described as musculoskeletal pain. Visceral pain feels dull, vague, and hard to pinpoint, described as constant or crampy. The gate control theory proposes that stimulation of large diameter fibers can inhibit pain transmission through the substantia gelatinosa in the spinal cord. Various pain modulation techniques like TENS work through this mechanism.
This document provides an overview of pain, including its definition, types, and pathway in the human body. It discusses how pain is sensed by nociceptors and transmitted through the nervous system to be perceived in the brain. Acute and chronic pain are compared, and the mechanisms of nociceptive and neuropathic pain explained. Somatic, visceral, referred, somatogenic, and psychogenic pain are defined. The neuroanatomy and physiology of pain processing through transduction, transmission, modulation, and perception are outlined in detail.
1) The document discusses pain physiology including types of pain, pain pathways, and the brain's analgesic system.
2) It describes how pain is carried via different nerve fibers and pathways to the dorsal horn, thalamus, and sensory cortex.
3) It explains referred pain and how visceral pain can be felt in distant areas of the body according to dermatomal rules due to convergence in the central nervous system.
1) The document summarizes the history of theories of pain pathways and receptors, including Descartes' specificity theory, Goldscheider's summation theory, and Melzack and Wall's gate control theory.
2) It describes the molecular basis of nociceptor activation by noxious stimuli like heat, mechanical stimuli, and chemicals. Peripheral and central sensitization mechanisms are also summarized.
3) The roles of voltage-gated sodium and calcium channels, opioids, and neuroplasticity in pain transmission and modulation are highlighted.
Pain is defined as an unpleasant sensory and emotional experience caused by actual or potential tissue damage. It is subjective and based on past experiences. Pain is transmitted through nociceptors and nerve fibers to the spinal cord and brain. It can be acute or chronic. Various factors like emotions, beliefs, and expectations can influence one's pain experience. The brain modulates pain transmission through descending pain pathways that release neurotransmitters like endorphins and serotonin.
This document provides an overview of pain, including definitions, mechanisms, and assessment. It discusses the levels of pain processing from transduction to perception. The functional neuroanatomy and pathways of pain are described, including nociceptors, nerve fibers, spinal cord tracts, and brain regions involved. Modulation of pain within the central nervous system is explained through theories like the gate control theory. Methods of pain assessment and various types of pain are also summarized.
The document discusses pain pathways and mechanisms of pain control. It defines pain and describes different types of pain such as acute vs chronic, nociceptive vs neuropathic, somatic vs visceral, referred vs non-referred, and somatogenic vs psychogenic pain. It then explains the neuroanatomy of pain transmission from nociceptors to the central nervous system and perception in the brain. Finally, it discusses current analgesic options and the WHO analgesic ladder for treating mild to severe pain.
This document provides an overview of the physiology of pain. It discusses:
1. The definition of pain according to the International Association for the Study of Pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
2. The dual nature of pain as either fast, acute pain transmitted by thin myelinated nerve fibers or slow, chronic pain transmitted by unmyelinated nerve fibers.
3. The pathways that carry pain signals from nociceptors to the brain, including nerve fibers entering the spinal cord and traveling via the lateral spinothalamic tract to the thalamus and sensory cortex.
4. Descending pain modulatory pathways from the brainstem that can inhibit pain
Nociceptors the sensors of the pain pathway Asmae LGUENSAT
Nociceptors are sensory neurons that detect potentially damaging stimuli and mediate the pain response. The document discusses the anatomy and physiology of nociception, including:
1) Nociceptors express receptors that detect noxious heat, cold, and mechanical stimuli.
2) Nociceptor activation leads to action potentials that are conducted to the spinal cord and brain.
3) Central modulation and sensitization can lower pain thresholds and lead to hyperalgesia and allodynia.
4) While specific nociceptor populations respond to different stimuli, their roles in transmitting specific pain modalities require further study.
This document discusses the physiology of pain. It covers topics such as the definition of pain, the dual nature of fast and slow pain, pain stimuli and the nerve pathways that carry pain signals to the brain. It also discusses the brain areas involved in pain perception, pain modulatory pathways, and the neurochemicals involved in pain pathways. The gate control theory of pain and theories on referred pain are also summarized.
Knowledge of pain physiology is very important in understanding of electrotherapy prescription. So, this slide may be useful in understanding the background of the pain processes.
This document summarizes the pathophysiology of pain. It describes how pain is detected by nociceptors in the periphery and transmitted through the spinal cord and brain. Pain serves an important protective function but can also become chronic through peripheral and central sensitization. Psychological factors and brain circuits can also modulate pain perception. Damage to the peripheral or central nervous system can cause neuropathic pain, which is often severe and resistant to treatment.
- Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It can be acute or chronic.
- Acute pain is sharp and short-lived, while chronic pain is intermittent or constant and lasts longer. Chronic pain is more difficult to treat.
- Pain has protective benefits like warning of injury and preventing further damage, but also has negative impacts. The physiology of pain involves receptors, pathways in the peripheral and central nervous systems, and neurotransmitters like glutamate and substance P. The gate control theory proposes mechanisms of pain modulation in the spinal cord and brain.
This document provides an overview of pain pathways and mechanisms. It defines pain and discusses the different types of pain receptors and fibers that detect and transmit nociceptive signals. It describes the dual pain pathway and outlines the pathways from peripheral receptors to the central nervous system. It also discusses theories of pain and the three systems (sensory-discriminative, motivational-affective, cognitive-evaluative) that interact to produce the pain experience. Finally, it provides details on the nerve supply and innervation of maxillary and mandibular teeth.
This document provides an overview of pain, including its definitions, classifications, mechanisms and management. It defines pain as an unpleasant sensory experience associated with actual or potential tissue damage. Pain is classified as acute, chronic, neuropathic, musculoskeletal and others, based on duration and source. The pathways involve nociceptors detecting pain, first order neurons in the dorsal root ganglion, second order neurons in the spinal cord projecting to the thalamus, and third order neurons projecting to the brain. Managing pain involves understanding its types, causes, receptors and pathways.
This document discusses pain anatomy and physiology. It defines pain as an unpleasant sensory and emotional experience associated with tissue damage. Nociception is the process by which nociceptors detect and transmit signals of potential tissue damage to the brain. There are different types of nociceptors and pain fibers that detect fast, sharp pain or slow, dull pain. The ascending pain pathway involves three neurons that transmit nociceptive signals from receptors to the spinal cord and thalamus. The gate control theory proposes that non-painful input can close the "gates" and inhibit pain transmission.
This document summarizes the pain pathway in the human body. It begins with an introduction to pain and its characteristics. It then discusses the different types of pain sensations conducted by different nerve fibers. It explains Gate Control Theory and the differences between somatic and visceral sensory function. It provides details on pain receptors, the pathway of sensory impulses from receptors to the brain, and examples of tooth pulp pain and referred pain. It concludes with management strategies for pain.
This document defines pain and discusses its pathophysiology. It notes that pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Two major classes of pain are described: normal/nociceptive pain and abnormal/pathophysiologic pain. Nociception involves a complex series of physiological events between tissue damage and pain perception. Nociceptors are activated by mechanical, thermal, and chemical stimuli. The receptors that mediate pain are called nociceptors, which come in two types: Aδ myelinated nerve fibers and C unmyelinated nerve fibers. The neuroanatomy of pain processing involves afferent pathways, the central nervous system, and efferent pathways.
This document provides information on pain management. It begins with the history and theories of pain. It then discusses the neurophysiology of pain including nociception, transmission, modulation and perception. Gate control theory is explained in detail. Non-pharmacological approaches like rest, distraction, electrotherapy and exercise are covered. The WHO analgesic ladder is introduced and different classes of pharmacological pain medications like non-opioids, opioids, antidepressants and antiepileptics are summarized.
The document discusses the pathophysiology of pain. It defines pain and describes the three systems - sensory, motivational, and cognitive - that interact to produce the experience of pain. It categorizes pain into somatogenic, psychogenic, acute, and chronic types and discusses their characteristics. It also describes age-related differences in pain perception and the neuroanatomy of pain processing, including the roles of the afferent and efferent pathways and different areas of the central nervous system.
Somatic pain comes from skin and deep tissues, while visceral pain comes from internal organs. Both types of pain are detected by nociceptors and felt differently. Somatic pain is usually easier to locate and more intense, described as musculoskeletal pain. Visceral pain feels dull, vague, and hard to pinpoint, described as constant or crampy. The gate control theory proposes that stimulation of large diameter fibers can inhibit pain transmission through the substantia gelatinosa in the spinal cord. Various pain modulation techniques like TENS work through this mechanism.
This document provides an overview of pain, including its definition, types, and pathway in the human body. It discusses how pain is sensed by nociceptors and transmitted through the nervous system to be perceived in the brain. Acute and chronic pain are compared, and the mechanisms of nociceptive and neuropathic pain explained. Somatic, visceral, referred, somatogenic, and psychogenic pain are defined. The neuroanatomy and physiology of pain processing through transduction, transmission, modulation, and perception are outlined in detail.
1) The document discusses pain physiology including types of pain, pain pathways, and the brain's analgesic system.
2) It describes how pain is carried via different nerve fibers and pathways to the dorsal horn, thalamus, and sensory cortex.
3) It explains referred pain and how visceral pain can be felt in distant areas of the body according to dermatomal rules due to convergence in the central nervous system.
1) The document summarizes the history of theories of pain pathways and receptors, including Descartes' specificity theory, Goldscheider's summation theory, and Melzack and Wall's gate control theory.
2) It describes the molecular basis of nociceptor activation by noxious stimuli like heat, mechanical stimuli, and chemicals. Peripheral and central sensitization mechanisms are also summarized.
3) The roles of voltage-gated sodium and calcium channels, opioids, and neuroplasticity in pain transmission and modulation are highlighted.
Pain is defined as an unpleasant sensory and emotional experience caused by actual or potential tissue damage. It is subjective and based on past experiences. Pain is transmitted through nociceptors and nerve fibers to the spinal cord and brain. It can be acute or chronic. Various factors like emotions, beliefs, and expectations can influence one's pain experience. The brain modulates pain transmission through descending pain pathways that release neurotransmitters like endorphins and serotonin.
This document provides an overview of pain, including definitions, mechanisms, and assessment. It discusses the levels of pain processing from transduction to perception. The functional neuroanatomy and pathways of pain are described, including nociceptors, nerve fibers, spinal cord tracts, and brain regions involved. Modulation of pain within the central nervous system is explained through theories like the gate control theory. Methods of pain assessment and various types of pain are also summarized.
The document discusses pain pathways and mechanisms of pain control. It defines pain and describes different types of pain such as acute vs chronic, nociceptive vs neuropathic, somatic vs visceral, referred vs non-referred, and somatogenic vs psychogenic pain. It then explains the neuroanatomy of pain transmission from nociceptors to the central nervous system and perception in the brain. Finally, it discusses current analgesic options and the WHO analgesic ladder for treating mild to severe pain.
This document provides an overview of the physiology of pain. It discusses:
1. The definition of pain according to the International Association for the Study of Pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
2. The dual nature of pain as either fast, acute pain transmitted by thin myelinated nerve fibers or slow, chronic pain transmitted by unmyelinated nerve fibers.
3. The pathways that carry pain signals from nociceptors to the brain, including nerve fibers entering the spinal cord and traveling via the lateral spinothalamic tract to the thalamus and sensory cortex.
4. Descending pain modulatory pathways from the brainstem that can inhibit pain
Nociceptors the sensors of the pain pathway Asmae LGUENSAT
Nociceptors are sensory neurons that detect potentially damaging stimuli and mediate the pain response. The document discusses the anatomy and physiology of nociception, including:
1) Nociceptors express receptors that detect noxious heat, cold, and mechanical stimuli.
2) Nociceptor activation leads to action potentials that are conducted to the spinal cord and brain.
3) Central modulation and sensitization can lower pain thresholds and lead to hyperalgesia and allodynia.
4) While specific nociceptor populations respond to different stimuli, their roles in transmitting specific pain modalities require further study.
This document discusses the physiology of pain. It covers topics such as the definition of pain, the dual nature of fast and slow pain, pain stimuli and the nerve pathways that carry pain signals to the brain. It also discusses the brain areas involved in pain perception, pain modulatory pathways, and the neurochemicals involved in pain pathways. The gate control theory of pain and theories on referred pain are also summarized.
Knowledge of pain physiology is very important in understanding of electrotherapy prescription. So, this slide may be useful in understanding the background of the pain processes.
This document summarizes the pathophysiology of pain. It describes how pain is detected by nociceptors in the periphery and transmitted through the spinal cord and brain. Pain serves an important protective function but can also become chronic through peripheral and central sensitization. Psychological factors and brain circuits can also modulate pain perception. Damage to the peripheral or central nervous system can cause neuropathic pain, which is often severe and resistant to treatment.
- Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It can be acute or chronic.
- Acute pain is sharp and short-lived, while chronic pain is intermittent or constant and lasts longer. Chronic pain is more difficult to treat.
- Pain has protective benefits like warning of injury and preventing further damage, but also has negative impacts. The physiology of pain involves receptors, pathways in the peripheral and central nervous systems, and neurotransmitters like glutamate and substance P. The gate control theory proposes mechanisms of pain modulation in the spinal cord and brain.
This document provides an overview of pain pathways and mechanisms. It defines pain and discusses the different types of pain receptors and fibers that detect and transmit nociceptive signals. It describes the dual pain pathway and outlines the pathways from peripheral receptors to the central nervous system. It also discusses theories of pain and the three systems (sensory-discriminative, motivational-affective, cognitive-evaluative) that interact to produce the pain experience. Finally, it provides details on the nerve supply and innervation of maxillary and mandibular teeth.
This document provides an overview of pain, including its definitions, classifications, mechanisms and management. It defines pain as an unpleasant sensory experience associated with actual or potential tissue damage. Pain is classified as acute, chronic, neuropathic, musculoskeletal and others, based on duration and source. The pathways involve nociceptors detecting pain, first order neurons in the dorsal root ganglion, second order neurons in the spinal cord projecting to the thalamus, and third order neurons projecting to the brain. Managing pain involves understanding its types, causes, receptors and pathways.
This document discusses pain anatomy and physiology. It defines pain as an unpleasant sensory and emotional experience associated with tissue damage. Nociception is the process by which nociceptors detect and transmit signals of potential tissue damage to the brain. There are different types of nociceptors and pain fibers that detect fast, sharp pain or slow, dull pain. The ascending pain pathway involves three neurons that transmit nociceptive signals from receptors to the spinal cord and thalamus. The gate control theory proposes that non-painful input can close the "gates" and inhibit pain transmission.
This document summarizes the pain pathway in the human body. It begins with an introduction to pain and its characteristics. It then discusses the different types of pain sensations conducted by different nerve fibers. It explains Gate Control Theory and the differences between somatic and visceral sensory function. It provides details on pain receptors, the pathway of sensory impulses from receptors to the brain, and examples of tooth pulp pain and referred pain. It concludes with management strategies for pain.
This document defines pain and discusses its pathophysiology. It notes that pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Two major classes of pain are described: normal/nociceptive pain and abnormal/pathophysiologic pain. Nociception involves a complex series of physiological events between tissue damage and pain perception. Nociceptors are activated by mechanical, thermal, and chemical stimuli. The receptors that mediate pain are called nociceptors, which come in two types: Aδ myelinated nerve fibers and C unmyelinated nerve fibers. The neuroanatomy of pain processing involves afferent pathways, the central nervous system, and efferent pathways.
This document provides information on pain management. It begins with the history and theories of pain. It then discusses the neurophysiology of pain including nociception, transmission, modulation and perception. Gate control theory is explained in detail. Non-pharmacological approaches like rest, distraction, electrotherapy and exercise are covered. The WHO analgesic ladder is introduced and different classes of pharmacological pain medications like non-opioids, opioids, antidepressants and antiepileptics are summarized.
The document discusses pain and its pathways in the human body. It defines pain and describes its characteristics and theories. It discusses the neurochemistry and types of pain receptors. The main pain pathway described is the lateral spinothalamic tract, which carries pain and temperature sensations from the periphery to the thalamus and somatosensory cortex via the dorsal horn and spinal cord. It relays information via three orders of neurons and can be modulated in the substantia gelatinosa of the spinal cord.
1. Pain is transmitted by two types of nerve fibers: fast pain via A-delta fibers and slow pain via C fibers. Fast pain is sharp and localized while slow pain is dull and poorly localized.
2. Pain receptors are free nerve endings that respond to mechanical, thermal, and chemical stimuli. They are present mainly in the skin, joints, and blood vessels.
3. Pain pathways involve the transmission of pain stimuli from receptors to the spinal cord and then to the brain. This involves both neospinothalamic and paleospinothalamic tracts.
This document discusses the pathophysiology of pain. It covers topics such as the definition of pain, categories of pain (somatogenic, psychogenic, acute, chronic), the neuroanatomy and neurophysiology of pain processing, and different types of neuropathic pain. The gate control theory of pain is also explained, which proposes that stimulation of large nerve fibers can close the "gate" in the spinal cord and decrease pain transmission.
I. Pain pathways involve nociceptors detecting damaging stimuli and transmitting signals along primary afferent neurons to the dorsal horn. Signals then project up the spinal cord and through ascending tracts to various brain regions for processing. Descending pathways from the brain modulate pain transmission.
II. The document outlines the history of pain theories, definitions of pain terminology, embryological development of pain pathways, types of pain, and components of the pain pathway including nociceptors, neurons, and brain regions involved in perception.
III. Key aspects of acute and chronic pain are distinguished. The gate control theory proposes that non-painful stimuli can inhibit pain transmission at the dorsal horn. Overall the document provides a comprehensive overview of
This document provides an overview of the anatomy and physiology of pain. It begins by outlining the learning objectives which are to gain insight into the anatomy and physiology of pain, recognize terminology, identify the body's physiological response to pain, recognize the effects of pain on different body systems, and apply knowledge to assess and treat pain. It then discusses the types of pain including acute, chronic, nociceptive, neuropathic, and nociplastic pain. It describes the pain pathway from peripheral nerves to the central nervous system. It outlines the processes of transduction, transmission, modulation, and perception of pain. It discusses the functional effects of pain on different body systems and the psychological effects of pain. It concludes by emphasizing the complexity
New product dedisions provide a dear path to the business. New product development
astep by step process. A Complete idea is required behind new product.
1 1deal Generation: The development of a product starts with the concept and idea.
The remaining process is depending on that idea.
2 Screening of Idea: This step is cruial to ensure that unsuitable ideas, for whatever
reason, are rejected as soon as possible. Ideas need to be considered objectively,
ideally by a group or committee.
3. Concept Development and Testing: After having an idea, next is the sreening
stage. The idea should now convert into concept. It has depth information which can
be visualizing by the consumer.
4. Anaysis of business: After finalization of concept, a business case needs to be kept
algTStogether to consider whether the new service /product will be gainful.
2665.Product Development If the nev product is approved, it will be approved to the
2marketing and technical development step.
6. Test Marketing: Market testing (test marketing or) is different to consumer testing.
in that it introduces the product that follows proposed plan of marketing.
od7. Commercialization: When the concept has been tested and developed, final
0decisions are required to move the product to its introduction into the market.
8. Launch: A detailed plan of launch is required for this step. This is the important
stage for success of a product
New Drug Development
So In present business atmosphere, it is more important to take smart decisions for
business. Innovative approaches and new products can put an organization on proper
pathway and to make a big success if appropriately analyzed and executed. Make it simpler
(Fig.2.1).0
Following parameters should keep in mind for a better decision:
Analyzing existing service and product portfolio frequently.
Knowing the position of functions of business, projects of departments and
initiatives.
Understanding the distribution of funds and assessing efficiency.
Having understanding of market for new opportunities and possible competition.
2.B PRODUCT BRANDING, PACKAGING AND LABELLING DECİSIONs
2.8.1 Branding
Branding has its existence from ancient era. According to Nilson (2000), the first example
of branding is found in the oil lamps' manufacture on the Greek islands thousands of years
back. Brand elements are name, sign, term, symbol, design or distinguishing characteristics.
Brand is not only a graphical design or a logo; it is the unique identity of the product.
By American Marketing Association, Brand can be defined as name, term, sign, symbol
or design, or a combination of them intended to identijy the goods and services of one seller or
group of sellers and to diferentiate them from those of other sellersa54
Branding is a process, where a company generates loyalty among consumers in the
market. Brands are designed with a motive to communicate customers the reason for the
existence of their product. Brand should have a strong connection with customers;
This document provides an overview of the physiology of pain. It discusses the definition of pain, the dual nature of fast and slow pain pathways, pain stimuli and receptors, the nerve pathways that carry pain signals to the brain, brain areas involved in pain perception, descending pain modulatory pathways, and neurochemicals involved in pain transmission. Key topics covered include the gate control theory of pain, referred pain, capsaicin and vanilloid receptors, the endocannabinoid system, and excitatory and inhibitory neurotransmitters in pain pathways in the central nervous system.
Physiology of pain involves nociceptors that detect actual or potential tissue damage and transmit signals along afferent nerve fibers. Nociceptive signals synapse in the dorsal horn and ascend via the spinothalamic tract. The brain perceives pain based on these signals. Pain is modulated by descending pathways that release inhibitory neurotransmitters like opioids. The gate control theory proposes that activity in large diameter fibers can inhibit pain transmission. Various methods aim to reduce pain transmission or enhance descending inhibition including NSAIDs, local anesthetics, TENS, opioids, and psychotherapy.
This document discusses pain and the pain pathway. It defines pain and describes the three hierarchical levels that interact to produce the pain experience. It then categorizes different types of pain such as nociceptive, neuropathic, inflammatory, acute, chronic, psychogenic, referred, and phantom pain. It explains the neuroanatomy of pain including the afferent pathways that transmit pain signals to the central nervous system and efferent pathways that modulate pain. Finally, it outlines the stages of the pain pathway including transduction, conduction, transmission, modulation, and perception of pain signals.
Physiology of pain was discussed covering several key topics:
1. Pain was defined by the IASP as an unpleasant sensory and emotional experience associated with actual or potential tissue damage.
2. Pain pathways involve nociceptors transmitting signals via Aδ and C fibers to the spinal cord and brain areas involved in perception.
3. Descending pain modulatory pathways originate in the brainstem and midbrain and can inhibit pain transmission via neurotransmitters like enkephalins.
4. The gate control theory proposes that activity in large diameter fibers can close the "gate" and inhibit pain transmission in the spinal cord. Modifications to this theory incorporate concepts like wide dynamic range neurons and endogenous opioids.
This document provides an overview of the physiology of pain. It discusses the definition of pain, the dual nature of fast and slow pain, pain stimuli and receptors, nerve pathways carrying pain signals to the brain, brain areas involved in pain perception, descending pain modulatory pathways, and neurochemicals involved in pain pathways. It summarizes different types of pain such as neuropathic pain and nociceptive pain. The gate control theory of pain and modifications to this theory are also briefly described.
This document provides an overview of the physiology of pain. It discusses:
1. Definitions of pain and terms used to describe pain.
2. Nociceptors, the receptors that detect potentially damaging stimuli and transduce them as pain signals.
3. The ascending pain pathway from nociceptors to the brain through the spinal cord and thalamus.
4. Descending pain modulatory systems from the brain that can inhibit pain transmission through pathways using neurotransmitters like endogenous opioids.
5. Theories of pain transmission and modulation including the gate control theory.
The document discusses the sensory system and pain pathways. It defines key terms like nociception, nociceptors, transduction, and different types of pain. The ascending pain pathways involve C fibers synapsing in the substantia gelatinosa and traveling via the spinothalamic tract to the thalamus and somatosensory cortex. Descending pathways from the brain modulate pain perception. Nociceptors are activated by various physical and chemical stimuli. Endogenous opioid peptides in these pathways help reduce pain transmission.
Pain definition, pathway,analgesic pathway, types of painekta dwivedi
This document provides an overview of pain physiology, including definitions of pain, pain receptors and pathways, and theories of pain modulation. It discusses fast and slow pain fibers, pain transmission through the spinal cord and brain, and endogenous analgesic pathways. The gate control theory of pain is explained in detail. Different types of pain and assessment methods are outlined. Both pharmacological and non-pharmacological pain management approaches are summarized.
The document discusses the physiology of pain and local anesthesia. It defines different types of pain including somatic, visceral, neuropathic, acute and chronic pain. It describes theories of pain transmission including the specific theory, pattern theory, and gate control theory. It discusses pain receptors, fibers, stimuli, and the four processes of pain - transduction, transmission, modulation and perception.
This document discusses various types of orthoses used to stabilize, immobilize, or assist body parts. It defines an orthosis as any device added to the body to serve these purposes. It then describes different types of orthoses for the upper limbs, lower limbs, spine, and their indications, designs, materials, and examples. Common orthotic devices discussed include ankle-foot orthoses, knee-ankle-foot orthoses, cervical collars, and scoliosis braces. The document provides details on orthotic selection and use for various musculoskeletal conditions and injuries.
1. The document discusses osteoporosis and provides information on its definition, diagnosis, risk factors, treatment, and management.
2. Key points covered include WHO definitions of osteoporosis, fracture risk assessment tools like FRAX, FDA-approved medications for treatment, importance of calcium and vitamin D supplementation, and lifestyle factors like exercise and nutrition.
3. New and emerging treatments for osteoporosis are discussed, such as denosumab, romosozumab, and abaloparatide, which aim to reduce bone resorption or increase bone formation.
This document provides information about mesotherapy, including its history, indications, contraindications, drugs used, and complications. Some key points:
- Mesotherapy involves injecting small doses of medications into the mesoderm layer of skin to treat dermatological or internal lesions.
- It was first suggested by Dr. Michel Pistor in 1958 as a treatment between allopathic and homeopathic therapies.
- Common indications include aesthetic treatments like lipolysis and cellulite reduction, as well as pain management.
- Phosphatidylcholine is often used for its lipolytic effects, working to dissolve fat cells for elimination.
- Potential complications include vasovagal reactions
NSAIDs are a class of drugs that relieve pain, fever, and inflammation by inhibiting cyclooxygenase enzymes. There are various types of NSAIDs classified by their chemical structure. All NSAIDs work by blocking prostaglandin production, but they differ in their selectivity for COX-1 vs COX-2 enzymes. Common adverse effects include gastrointestinal irritation and bleeding, as well as renal impairment. NSAIDs are commonly used to treat pain, fever, and inflammatory conditions like arthritis.
The document provides an overview of foot and ankle anatomy, including the 26 bones and 30 joints of the ankle and foot complex. It describes the three arches of the foot - transverse, medial longitudinal, and lateral longitudinal. Key ankle and foot joints are identified along with their range of motion. Common movements like plantarflexion, dorsiflexion, inversion, and eversion are defined. Physical examination techniques for the foot and ankle are outlined, including inspection, palpation, range of motion testing, and special tests. Common injuries and conditions like shin splints are also mentioned.
This document discusses range of motion (ROM) exercises, including passive, active, and active-assistive ROM. It describes the goals and techniques for each type of exercise, as well as precautions. The principles of ROM techniques involve examination, patient preparation, and application of movements within a patient's pain-free range.
- 10-40% of stroke survivors experience moderate to severe impairments requiring special care or long-term facilities, while 15% die shortly after the stroke.
- Stroke rehabilitation aims to restore lost abilities, prevent complications, and improve quality of life through therapies targeting mobility, activities of daily living, communication, swallowing, orthotics, and cognitive/emotional issues.
- Early rehabilitation beginning within 24-48 hours, a systematic assessment, careful therapy planning, gradual progression, and family involvement promote successful recovery from stroke.
This document provides an overview of orthotics, including their goals and common types. It defines an orthosis as any device added to the body to stabilize, immobilize, prevent deformity, protect from injury, or assist with function. The document then describes common lower extremity orthoses like foot orthosis, ankle foot orthosis, knee orthosis, knee ankle foot orthosis, and hip orthosis, providing examples and uses for each. It also lists objectives for understanding orthotic terminology, goals, types, and selecting the appropriate orthosis for different scenarios.
The document discusses the immune system. It describes that innate immunity provides immediate protection from birth through nonspecific responses like physical barriers and phagocytes. Acquired immunity develops after exposure through specific responses by B cells and T cells. B cells produce antibodies targeted to extracellular pathogens. T cells help activate other immune cells and cytotoxic T cells destroy infected cells. The adaptive immune response involves clonal selection of lymphocytes and generation of memory cells that provide faster responses. Antibodies function by agglutination, opsonization, neutralization, complement activation, and antibody-dependent cell-mediated cytotoxicity to eliminate pathogens.
This document provides information on corticosteroid injection therapy for treating inflammatory arthritis and other musculoskeletal conditions. It discusses the history of local corticosteroid injections, their reported medical benefits, and conditions often treated. Details are given on common corticosteroid preparations used, their potencies and dosages. Contraindications, materials needed, injection techniques for various joints, and potential complications are outlined. Other injection therapies like hyaluronic acid, autologous blood, and prolotherapy are also mentioned.
Osteoporosis is a systemic bone disease characterized by low bone mass and deterioration of bone structure, leading to increased bone fragility and risk of fracture. It is most commonly seen in postmenopausal women and the elderly. Key risk factors include aging, female sex, family history, small body frame, cigarette smoking, excessive alcohol, low calcium/vitamin D intake, and certain medications. Diagnosis is made through bone mineral density testing and x-rays. Treatment focuses on lifestyle modifications like exercise and fall prevention as well as pharmacologic therapies like bisphosphonates, parathyroid hormone, and estrogen to preserve bone mass.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
2. What is Pain?
• “An unpleasant sensory & emotional experience
associated with actual or potential tissue damage,
or described in terms of such damage” –
The International Association for the Study of Pain
• Subjective sensation
• Pain Perceptions – based on expectations, past
experience, anxiety, suggestions
– Affective – one’s emotional factors that can
affect pain experience
– Behavioral – how one expresses or controls pain
– Cognitive – one’s beliefs (attitudes) about pain
3. What is Pain
• Physiological response produced by activation of
specific types of nerve fibers
• Experienced because of nociceptors being sensitive to
extreme mechanical, thermal, & chemical energy.
• Composed of a variety of discomforts
• One of the body’s defense mechanism (warns the brain
that tissues may be in jeopardy)
• Acute vs. Chronic –
– The total person must be considered. It may be
worse at night when the person is alone. They are
more aware of the pain because of no external
diversions.
4. Where Does Pain Come From?
• Cutaneous Pain – sharp, bright, burning; can have
a fast or slow onset
• Deep Somatic Pain – stems from tendons,
muscles, joints, periosteum, & b. vessels
• Visceral Pain – originates from internal organs;
diffused @ 1st
& later may be localized (i.e.
appendicitis)
• Psychogenic Pain – individual feels pain but
cause is emotional rather than physical
5. Pain Sources
• Fast vs. Slow Pain –
– Fast – localized; carried through A-delta axons in
skin
– Slow – aching, throbbing, burning; carried by C
fibers
– Nociceptive neuron transmits pain information to
spinal cord via unmyelinated C fibers & myelinated
A-delta fibers.
• The smaller C fibers carry impulses : rate 0.5 to 2.0
m/sec.
• The larger A-delta fibers carry impulses : of 5 to 30
m/sec.
9. Most Common Chronic Pain
Syndromes
• Low Back
• Headaches
• Neck
• Facial
• Arthritides
• Fibromyalgia
• Cancer
10. What is Referred Pain?
• Occurs away from pain site
• Examples: McBurney’s point
• Types of referred pain:
– Myofascial Pain – trigger points, small
hyperirritable areas within a m. in which n.
impulses bombard CNS & are expressed at
referred pain
– Sclerotomic & Dermatomic Pain – deep pain; may
originate from sclerotomic, myotomic, or
dermatomic n. irritation/injury
• Sclerotome: area of bone/fascia that is supplied by a
single n. root
11. Terminology
• Noxious – harmful,
injurious
– Noxious stimuli –
stimuli that activate
nociceptors (pressure,
cold/heat extremes,
chemicals)
• Nociceptor – nerve
receptors that
transmits pain
impulses
• Pain Threshold – level
of noxious stimulus
required to alert an
individual of a
potential threat to
tissue
• Hyperesthesia – abnormal
acuteness of sensitivity to
touch, pain, or other sensory
stimuli
• Paresthesia – abnormal
sensation, such as burning,
pricking, tingling
• Inhibition – depression or
arrest of a function
– Inhibitor – an agent that
restrains/retards
physiologic, chemical, or
enzymatic action
• Analgesic – a neurologic or
pharmacologic state in
which painful stimuli are no
longer painful
12. • Dysesthesia – An unpleasant abnormal sensation,
whether spontaneous or evoked.
• Allodynia – Pain due to a stimulus which does not
normally provoke pain, such as pain caused by light
touch to the skin
• Hyperalgesia – An increased response to
a stimulus which is normally painful
• Hyperesthesia - Increased sensitivity to
stimulation, excluding the special senses.
Hyperesthesia includes both allodynia and
hyperalgesia, but the more specific terms should
be used wherever they are applicable.
13. Nerve Endings
• “A nerve ending is the termination of a nerve
fiber in a peripheral structure.” (Prentice, p.
37)
• Nerve endings may be sensory (receptor) or
motor (effector).
• Nerve endings may be:
– Respond to phasic activity - produce an impulse
when the stimulus is ↓ or ↑, but not during
sustained stimulus; adapt to a constant stimulus
(Meissner’s corpuscles & Pacinian corpuscles)
– Respond to tonic receptors produce impulses as
long as the stimulus is present. (muscle spindles,
free n. endings, Krause’s end bulbs)
15. Types of Nerves
• Afferent (Ascending) – transmit
impulses from the periphery to the brain
– First Order neuron
– Second Order neuron
– Third Order neuron
• Efferent (Descending) – transmit
impulses from the brain to the periphery
16. Peripheral and Central Pathways for Pain
Ascending TractsAscending Tracts Descending TractsDescending Tracts
Cortex
Midbrain
Medulla
Spinal Cord
Thalamus
Pons
17. First Order Neurons
• Stimulated by sensory receptors
• End in the dorsal horn of the spinal cord
• Types
– A-alpha – non-pain impulses
– A-beta – non-pain impulses
• Large, myelinated
• Low threshold mechanoreceptor; respond to light
touch & low-intensity mechanical info
– A-delta – pain impulses due to mechanical
pressure
• Large diameter, thinly myelinated
• Short duration, sharp, fast, bright, localized sensation
(prickling, stinging, burning)
– C – pain impulses due to chemicals or
mechanical
18. Second Order Neurons
• Receive impulses from the FON in the dorsal
horn
– Lamina II, Substantia Gelatinosa (SG) -
determines the input sent to T cells from
peripheral nerve
• T Cells (transmission cells): transmission cell that
connects sensory n. to CNS; neurons that organize
stimulus input & transmit stimulus to the brain
– Travel along the spinothalmic tract
– Pass through Reticular Formation
• Types
– Wide range specific
• Receive impulses from A-beta, A-delta, & C
19. Third Order Neurons
• Begins in thalamus
• Ends in specific brain centers (cerebral
cortex)
– Perceive location, quality, intensity
– Allows to feel pain, integrate past
experiences & emotions and determine
reaction to stimulus
20. Descending Neurons
• Descending Pain Modulation (Descending
Pain Control Mechanism)
• Transmit impulses from the brain
(corticospinal tract in the cortex) to the
spinal cord (lamina)
– Periaquaductal Gray Area (PGA) – release
enkephalins
– Nucleus Raphe Magnus (NRM) – release
serotonin
– The release of these neurotransmitters inhibit
ascending neurons
• Stimulation of the PGA in the midbrain &
NRM in the pons & medulla causes
21. Pain Process
The neural mechanisms by which pain is
perceived involves a process that has
four major steps:
–Transduction
–Transmission
–Modulation
–Perception
28. Acetaminophen (paramol)
• Analgesic, antipyretic
• Inhibits prostaglandin synthetase in the
CNS, weak peripheral anti-inflammatory
activity
• Serotonergic effect at descending
pathway
• Used to treat osteoarthritis
29. Acetaminophen (Tylenol)
• American Pain Society: Maximum dose
4,000 mg/day,
• American Liver Foundation: 3,000
mg/day
• Risk of hepatotoxicity with higher doses
• Antidote – acetylcysteine (Mucomyst,
Acetadote)
30. Major Categories of Pain
Classified by inferred pathophysiology:
1. Nociceptive pain (stimuli from somatic
and visceral structures)
2. Neuropathic pain (stimuli abnormally
processed by the nervous system)
31. Mixed Type
Caused by a
combination of both
primary injury or
secondary effects
Nociceptive vs Neuropathic Pain
Nociceptive
Pain
Caused by activity in
neural pathways in
response to potentially
tissue-damaging stimuli
Neuropathic
Pain
Initiated or caused by
primary lesion or
dysfunction in the
nervous system
Postoperative
pain
Mechanical
low back pain
Sickle cell
crisis
Arthritis
Postherpetic
neuralgia
Neuropathic
low back pain
CRPS*
Sports/exercise
injuries
*Complex regional pain syndrome
Central post-
stroke pain
Trigeminal
neuralgia
Distal
polyneuropathy
(eg, diabetic, HIV)
32. COMPONENT DESCRIPTORS EXAMPLES
Steady,
Dysesthetic
• Burning, Tingling
• Constant, Aching
• Squeezing, Itching
• Allodynia
• Hypersthesia
• Diabetic neuropathy
• Post-herpetic neuropathy
Paroxysmal,
Neuralgic
• Stabbing
• Shock-like, electric
• Shooting
• Lancinating
• trigeminal neuralgia
• may be a component of any
neuropathic pain
FEATURES OF NEUROPATHIC PAIN
34. Local Anesthetics
Blocks conduction of nerve impulses
by decreasing or preventing an
increase in the permeability of
excitable membranes to Na+.
Inhibits depolarization of nerve
Blocks neuronal firing
39. Methyl Salicylate Toxicity
• Salicylic acid derivative
• Lipid solubility increases toxicity
–More toxic than aspirin
–1 teaspoon (5ml) wintergreen oil
contains 4,000 mg salicylate
–30ml wintergreen oil is a fatal dose in
adults
• Risk of toxicity reduced with use for acute
pain, limited to a small area of dermal
application
40. Anticonvulsants
1)Inhibit sustained high-frequency
neuronal firing by blocking Na+ channels
after an action potential, reducing
excitability in sensitized C-nociceptors.
2)Blockade of Na+ channels and increase
in synthesis and activity of GABA, in
inhibitory neurotransmitter, in the brain.
3)Modulates Ca+ channel current and
increases synthesis of GABA.
41. Antiepileptic Agents
• Broad clinical
actions in the CNS:
– Reduce seizures
– Neuropathic pain
– Bipolar disorder
– Anxiety
– Schizophrenia
– Agitation
• Impulse
dyscontrol
• Dementia
• Delirium
• Three proposed
mechanisms of action:
– Blockade of voltage
gated sodium channels
(↓ glutamate
release)
– Blockade of voltage
gated calcium channels
– alpha 2 delta subunits
(reduces excessive
neurotransmitter
release)
– Enhancement of GABA
actions
46. Transmission
• The presynaptic terminal is the
axon terminal of the
presynaptic neuron
• Here that the presynaptic
neuron releases
neurotransmitters which are
found in vesicles
47.
48.
49. Neurotransmitters
Chemical substances that allow nerve impulses to
move from one neuron to another Found in
synapses
– Substance P - thought to be responsible for the
transmission of pain-producing impulses
– Acetylcholine – responsible for transmitting
motor nerve impulses
– Enkephalins – reduces pain perception by
bonding to pain receptor sites
– Norepinephrine – causes vasoconstriction
– Endorphins - morphine-like neurohormone;
thought to ↑ pain threshold by binding to
receptor sites
– Serotonin - substance that causes local
vasodilation & ↑ permeability of capillaries
50.
51. Capsaicin
• Hot peppers
• May deplete & prevent
re-accumulation of
substance P in primary
afferent neurons
responsible for
transmitting painful
impulses from peripheral
sites to the CNS.
• Absorption, distribution,
metabolism & excretion,
half life – unknown
• May produce transient
burning with application,
usually disappears in 2-4
days, but may persist for
several weeks.
52.
53. Transmission
• The synaptic cleft is the narrow
intercellular space between neurons.
• Neurotransmitters cross the synaptic
cleft and bind to specific receptors
on the postsynaptic neurons
• This will excite or inhibit the
postsynaptic neurons.
54.
55.
56. Questions to Ask about Pain
• P-Q-R-S-T format
• Provocation – How the injury occurred & what activities ↓ ↑
the pain
• Quality - characteristics of pain – Aching (impingement),
Burning (n. irritation), Sharp (acute injury), Radiating within
dermatome (pressure on n.)?
• Referral/Radiation –
– Referred – site distant to damaged tissue that does not
follow the course of a peripheral n.
– Radiating – follows peripheral n.; diffuse
• Severity – How bad is it? Pain scale
• Timing – When does it occur? p.m., a.m., before, during, after
activity, all the time
Pattern: onset & duration
Area: location
Intensity: level
Nature: description
The physiology of normal pain transmission involves some basic concepts that are necessary to understand the pathophysiology of abnormal or nonphysiologic pain. These include the concept of transduction of the first-order afferent neuron nociceptors. The nociceptor neurons have specific receptors that respond to specific stimuli if a specific degree of amplitude of the stimulus is applied to the receptor in the periphery. If sufficient stimulation of the receptor occurs, then there is a depolarization of the nociceptor neuron.
The nociceptive axon carries this impulse from the periphery into the dorsal horn of the spinal cord to make connections directly, and indirectly, through spinal interneurons, with second-order afferent neurons in the spinal cord.
The second-order neurons can transmit these impulses from the spinal cord to the brain. Second-order neurons ascend mostly via the spinothalamic tract up the spinal cord and terminate in higher neural structures, including the thalamus of the brain.
Third-order neurons originate from the thalamus and transmit their signals to the cerebral cortex.
Evidence exists that numerous supraspinal control areas—including the reticular formation, midbrain, thalamus, hypothalamus, the limbic system of the amygdala and the cingulate cortex, basal ganglia, and cerebral cortex—modulate pain. Neurons originating from these cerebral areas synapse with the neuronal cells of the descending spinal pathways, which terminate in the dorsal horn of the spinal cord.
Reference: Polomano, R.C. (2010). Neurophysiology of Pain. In B. St. Marie (Ed.) Core Curriculum for Pain Management Nursing. Lenexa, KA: American Society for Pain Management Nursing, p. 68.
Nociceptive, or inflammatory, pain is pain resulting from activity in neural pathways caused by potentially tissue-damaging stimuli.1 Examples include postoperative pain, arthritis, mechanical low back pain, sickle cell crisis, and sports or exercise injuries.
Neuropathic pain is pain caused by a primary lesion or dysfunction in the peripheral and/or central nervous systems.2 Examples of peripheral neuropathic pain syndromes include HIV sensory neuropathy, postherpetic neuralgia (PHN), and diabetic neuropathy. Examples of central neuropathic pain include central poststroke pain, spinal cord injury pain, trigeminal neuralgia, and multiple sclerosis pain.
As indicated by the “mixed type” area on the slide, chronic pain can be of mixed etiology with both nociceptive and neuropathic characteristics.
Two types of neuropathic pain—PHN and diabetic neuropathy—will be emphasized within this module. These types of pain are being stressed because the great majority of randomized controlled trials of treatments for neuropathic pain have examined these two disorders, and because our understanding of the mechanisms of neuropathic pain is largely derived from those studies.
1.Portenoy RK, Kanner RM. Definition and Assessment of Pain. In: Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, Pa: FA Davis Company; 1996:4.
2.Galer BS, Dworkin RH. A Clinical Guide to Neuropathic Pain. Minneapolis, Minn: The McGraw-Hill Companies Inc; 2000:8-9.
Addressing analgesia, the first of the “Four A’s of Pain,” requires an assessment of pain intensity to determine whether existing treatment is providing adequate relief. This slide depicts four of the pain scales that are used to assess a patient’s pain. The scales are considered simple for patients to use as well as being validated methods for measuring the severity of pain.1-3 These scales can be used at the patient’s bedside, and patients can be asked to respond to either a spoken or written a question. The 0-10 numeric scale can be administered over the phone.
With some scales, especially the visual analog scale, the patient marks the line at the point that best indicates the pain’s intensity. Older patients may have difficulty using visual analog scales and it might be more appropriate to use a 0-10 numeric pain intensity scale.4
The Wong-Baker FACES Pain Rating Scale is validated and recommended for patients aged 3 years or older. On this scale, Face 0 indicates no pain at all, Face 1 feels mild pain, Face 2 feels moderate pain, Face 3 feels severe pain, Face 4 feels very severe pain, and Face 5 feels the worst possible pain. The original appears above, and can be used as is or with the brief word descriptions under each number. In a study of 148 children aged 4 to 5 years, there were no differences in pain scores when children used the original or brief word instructions.2
People with cognitive impairments and limited ability to communicate (eg, stroke patients) may have difficulty with the use of any self-report pain assessment scales. For these patients it will be necessary for the physician to rely on behavioral observation of patients' facial expressions, movement patterns (eg, bracing, guarding, distorted postures, avoidance of activity), and nonverbal sounds (eg, moans, winces) and reports of significant others (eg, partner, spouse, child) to make judgment of pain intensity.5
However, remember that patient pain is multidimensional and involves more than just assessment of pain intensity.
1.Portenoy RK, Kanner RM. Definition and Assessment of Pain. In: Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, Pa: FA Davis Company; 1996:8-10.
2. Wong DL. Waley and Wong’s Essentials of Pediatric Nursing. 5th ed. St. Louis, Missouri: Mosby, Inc.; 1997:1215-1216.
3. McCaffery M, Pasero C. Pain: Clinical Manual. St. Louis, Missouri: Mosby, Inc.;1999:16.
4. Jensen MP, Karoly P, Braver S. The measurement of Clinical pain intensity: a comparison of six methods. Pain. 1986;27:117-126.
5. Hadjistavropoulos T, von Baeyer C, Craig KD. Pain assessment in persons with limited ability to communicate. In: Turk DC, Melzack R, eds. Handbook of Pain Assessment. 2nd ed. New York, New York: Guilford; 2001:134-152.