Pain Pathophysiology Overview
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Pain Pathophysiology Overview - Peripheral Sensitization - Central Sensitization - Gate Control Theory of Pain
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Physiology and pharmacology of pain
This document discusses physiology and pharmacology of pain. It defines pain and describes nociceptors, types of pain pathways, and opioid analgesics. It focuses on the mechanism of action, efficacy, and adverse effects of morphine, the prototypical opioid analgesic. It summarizes morphine's pharmacological actions including analgesia, tolerance, dependence, and interactions with other drugs.
Neuropathic Pain
The document discusses neuropathic pain, including its pathophysiology, symptoms, causes, assessment, and treatment approaches. It provides details on pharmacological and non-pharmacological treatment options for peripheral and central neuropathic pain, including guidelines on first-line therapies such as antidepressants, anticonvulsants, and topical lidocaine. Emerging treatments currently under investigation are also mentioned.
Pain pathway physiology- Dr. Anil babu Swarna
Data from Guyton and Hall 13th edition, Stoelting Physio Pharma, Clinical Anesthesiology by Paul G. Barash
Acute pain management
Acute pain management involves classifying pain and identifying its underlying cause. Treatment options include nonopioid medications like acetaminophen and NSAIDs, opioids, and adjuvant analgesics. Opioids are effective for moderate to severe acute pain but can cause adverse effects like respiratory depression, nausea, and constipation. Adjuvant analgesics like gabapentin, pregabalin, and ketamine may enhance opioid analgesia and reduce opioid requirements and side effects. Close monitoring is important when using opioids to manage acute pain.
Current Concepts and Strategies in Pain Management
Current strategies in pain management focus on a multimodal approach using both pharmacological and interventional techniques. While opioids remain an important treatment, their use requires prudent prescribing strategies to reduce risk of abuse and overdose. Non-opioid medications and interventional procedures such as spinal cord stimulation provide alternatives for chronic pain. The goal of treatment is reducing pain while avoiding undertreatment and toxicity through a multidisciplinary, multimodal approach.
Recent advances in Pain treatment
This document discusses mechanisms of pain transmission and modulation as well as recent advances in pharmacological pain therapy. It begins by outlining various mechanisms including transduction, sensitization, and descending pain pathways. It then summarizes common analgesic classes like opioids, NSAIDs, acetaminophen, gabapentinoids, local anesthetics, antidepressants and their mechanisms of action. The document concludes by mentioning new modalities like patient-controlled analgesia that provide better pain relief than conventional methods.
Neuropathic pain management
The document discusses neuropathic pain management and treatment options. It defines neuropathic pain and differentiates it from acute pain. It describes the pathophysiology and possible descriptions of neuropathic pain. The goals of clinical assessment are to achieve diagnosis, identify underlying causes, evaluate comorbidities, and develop a targeted treatment plan. Treatment options discussed include nonpharmacological approaches, topical medications, systemic medications like anticonvulsants, antidepressants, and opioids. New treatments and applications of existing treatments are improving management of neuropathic pain conditions.
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Physiology and pharmacology of pain
This document discusses physiology and pharmacology of pain. It defines pain and describes nociceptors, types of pain pathways, and opioid analgesics. It focuses on the mechanism of action, efficacy, and adverse effects of morphine, the prototypical opioid analgesic. It summarizes morphine's pharmacological actions including analgesia, tolerance, dependence, and interactions with other drugs.
Neuropathic Pain
The document discusses neuropathic pain, including its pathophysiology, symptoms, causes, assessment, and treatment approaches. It provides details on pharmacological and non-pharmacological treatment options for peripheral and central neuropathic pain, including guidelines on first-line therapies such as antidepressants, anticonvulsants, and topical lidocaine. Emerging treatments currently under investigation are also mentioned.
Pain pathway physiology- Dr. Anil babu Swarna
Data from Guyton and Hall 13th edition, Stoelting Physio Pharma, Clinical Anesthesiology by Paul G. Barash
Acute pain management
Acute pain management involves classifying pain and identifying its underlying cause. Treatment options include nonopioid medications like acetaminophen and NSAIDs, opioids, and adjuvant analgesics. Opioids are effective for moderate to severe acute pain but can cause adverse effects like respiratory depression, nausea, and constipation. Adjuvant analgesics like gabapentin, pregabalin, and ketamine may enhance opioid analgesia and reduce opioid requirements and side effects. Close monitoring is important when using opioids to manage acute pain.
Current Concepts and Strategies in Pain Management
Current strategies in pain management focus on a multimodal approach using both pharmacological and interventional techniques. While opioids remain an important treatment, their use requires prudent prescribing strategies to reduce risk of abuse and overdose. Non-opioid medications and interventional procedures such as spinal cord stimulation provide alternatives for chronic pain. The goal of treatment is reducing pain while avoiding undertreatment and toxicity through a multidisciplinary, multimodal approach.
Recent advances in Pain treatment
This document discusses mechanisms of pain transmission and modulation as well as recent advances in pharmacological pain therapy. It begins by outlining various mechanisms including transduction, sensitization, and descending pain pathways. It then summarizes common analgesic classes like opioids, NSAIDs, acetaminophen, gabapentinoids, local anesthetics, antidepressants and their mechanisms of action. The document concludes by mentioning new modalities like patient-controlled analgesia that provide better pain relief than conventional methods.
Neuropathic pain management
The document discusses neuropathic pain management and treatment options. It defines neuropathic pain and differentiates it from acute pain. It describes the pathophysiology and possible descriptions of neuropathic pain. The goals of clinical assessment are to achieve diagnosis, identify underlying causes, evaluate comorbidities, and develop a targeted treatment plan. Treatment options discussed include nonpharmacological approaches, topical medications, systemic medications like anticonvulsants, antidepressants, and opioids. New treatments and applications of existing treatments are improving management of neuropathic pain conditions.
Management of Neuropathic Pain
Presented by Dr.Perry Fine at Pain Management for the Elderly Course, 2010.
Scribe medical events Egypt. www.scribeofegypt.org
Chronic pain Managment
Trauma or injury causes the release of chemicals that stimulate nerve fibers, leading to pain signals being sent to the brain. The integration of these pain signals with cognitive, emotional, and environmental factors results in the perception of pain. When this balance is disturbed, chronic pain can develop. Chronic pain is defined as pain lasting beyond normal tissue healing time, typically three months. A multidisciplinary approach is often needed to treat chronic pain through non-pharmacological and pharmacological methods.
Autonomic system and Autonomic Pharmacology
Autonomic Nervous System & Autonomic Pharmacology
Sympathetic: ADRENERGIC
Central: EPINEPHRINE
Peripheral: NOREPINEPHRINE
Parasympathetic: CHOLINERGIC
Acetylcholine
Local anesthetics and counter irritants
Local anesthetics work by reversibly blocking nerve impulse conduction, providing transient loss of sensation to perform minor surgery without loss of consciousness. Cocaine was the first local anesthetic discovered in the 1860s. Local anesthetics are classified as amide or ester types and work by decreasing sodium ion entry during nerve action potentials. They are administered via various routes including topical application, infiltration, nerve blocks, and regional techniques to block sensation in restricted body areas. Common adverse effects involve the central nervous, cardiovascular, and allergic systems. Counterirritants like essential oils, mustard, and capsaicin work by stimulating cutaneous nerves to obscure deeper pain sensations.
Skeletal muscle relaxants (or) Neuromuscular blockers
Skeletal muscle relaxants (or) Neuromuscular blockers
Classification and Mechanism of action of drugs.
Interventional Pain Management
This document discusses interventional pain management (IPM) as a specialty focused on diagnosing and treating pain through minimally invasive procedures. It provides an overview of common IPM procedures like diagnostic nerve blocks, radiofrequency ablation, vertebroplasty, and percutaneous discectomy. The document also presents four case studies where IPM procedures like epidurolysis, percutaneous discectomy, vertebroplasty, and radiofrequency rhizotomy successfully treated chronic pain when other options had failed. It concludes that contrary to common beliefs, over 85% of spinal pain causes can be accurately diagnosed through IPM procedures and that IPM can provide long-term relief when pharmacologic treatments and surgery are not suitable options.
Acute pain management
مشروع إعداد طبيب حكيم ناجح- المعهد العربي للتنمية المهنية المستدامة دورة الطوارئ و التخدير و الرعاية 8-4-2014
Chronic pain assessment & management
Dr. Shekhar Anand presented on methods of chronic pain management to the Department of Anesthesiology. He discussed that chronic pain is defined as pain lasting longer than 3-6 months and can be nociceptive, neuropathic, or mixed in nature. Chronic pain is best managed using a multidisciplinary approach including pharmacological interventions like opioids, antidepressants, anticonvulsants, as well as non-pharmacological therapies like cognitive behavioral therapy, physical therapy, and interventional procedures. The goals of chronic pain management are to improve function and quality of life, rather than to cure the underlying cause of pain.
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This document discusses treatments for rheumatoid arthritis and gout. It outlines that for rheumatoid arthritis, first line treatments include NSAIDs and disease-modifying drugs like methotrexate. Methotrexate is often the disease-modifying drug of choice as it has potent anti-inflammatory and immunosuppressive effects through inhibiting T-cell proliferation and cytokine production. For acute gout attacks, first line treatments include NSAIDs, colchicine, and corticosteroids. Colchicine works by depolymerizing microtubules in granulocytes to reduce inflammation. Chronic gout is treated with uricosuric drugs like probenecid to promote uric acid excretion or allopur
1.pain pathophysiology and mechanisms
In this ppt I mentioned all the imp point related to pain pathway and pain pathophysiology. refrence: essentials of interventional techniques in managing chronic pain (laxmaiah manchikanti)
Neuropathic pain
this presentation discusses pain pathways, definition and glossary of pain symptoms, classification of pain, pathogenesis, causes, diagnosis , types and treatment of neuropathic pain
illustrated with figures
Muscle pain mechanism
Muscle pain occurs through the activation of muscle nociceptors by mechanical and chemical stimuli. During ischemia or low pH conditions, chemicals like ATP and protons are released activating nociceptors. Muscle spasms can develop through ischemia reducing blood flow, releasing pain-causing substances, and sensitizing nociceptors. Chronic work-related myalgia may occur through energy depletion in small muscle fibers and impaired blood flow due to sympathetic activation during exertion.
Ans pharmacology
The autonomic nervous system (ANS) regulates involuntary functions and has two divisions: the parasympathetic nervous system (PNS) and sympathetic nervous system (SNS). Both use two neurons - a preganglionic neuron that synapses in an autonomic ganglion and a postganglionic neuron that innervates the target organ. In the PNS, acetylcholine is released at both synapses to activate nicotinic then muscarinic receptors. In the SNS, acetylcholine is released at the ganglion, while norepinephrine is released at the organ to activate adrenergic receptors. The PNS activates "rest and digest" functions, while the SNS activates "fight
Chronic pain management
This document discusses chronic pain management. It defines chronic pain as pain lasting over 3 months. It describes different types of pain such as somatic, visceral and neuropathic pain. It discusses various chronic pain conditions like fibromyalgia, complex regional pain syndrome, postherpetic neuralgia and diabetic neuropathy. It covers evaluation of chronic pain, pathophysiology of chronic pain, brain regions involved, and the multidimensional nature of chronic pain including physical, psychological and social factors. Finally, it discusses various management approaches for chronic pain including pharmacological, physical, psychological and invasive techniques.
Opioid Pharmacology
This document summarizes the pharmacology of various opioid analgesics. It discusses classical opioid effects like analgesia, sedation, respiratory depression. It then profiles specific opioids like fentanyl, sufentanil, morphine, hydromorphone, remifentanil and others. It also discusses evidence for different mu opioid receptor subtypes and the potential for mu-1 selective agonists.
Chronic pain management
This document discusses chronic pain management. It defines chronic pain as pain that lasts months or years in any part of the body and can lead to depression, anxiety, and sleep issues. Chronic pain differs from acute pain in that it continues long after an injury heals. The document describes three types of chronic pain - neuropathic, somatic, and visceral - and their characteristics. It discusses evaluating and measuring pain, as well as pharmacological, physical, psychological, and invasive treatment methods for managing chronic pain. The goal of chronic pain treatment is to improve daily functioning and quality of life by decreasing pain and suffering through a multidisciplinary approach.
Opioid Analgesics
This document discusses different types of pain medications, including opioids. It describes various opioid drugs like morphine, codeine, heroin, methadone, fentanyl, and others. It explains how opioids work by binding to mu, delta, and kappa receptors in the central nervous system and periphery. Tolerance and dependence are noted as issues with long-term opioid use. Guidelines are provided for using different opioids to treat mild, moderate, and severe acute and chronic pain according to the World Health Organization.
Opioid Agonists And Antagonists
This document summarizes various opioid agonists and antagonists. It discusses natural and synthetic opioids like morphine, codeine, heroin, hydromorphone, fentanyl, meperidine, methadone, and diphenoxylate. It also covers opioid receptors, endogenous opioid peptides, pharmacokinetics, effects, tolerance, toxicity, and antagonists like naloxone and naltrexone. Non-steroidal anti-inflammatory drugs are also briefly mentioned.
Lecture 2 Electrotherapy- pain physiology
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.
Neurophysiology of pain
1) The document discusses the neurophysiology of pain, including what pain is, types of pain receptors and fibers, pathways in the spinal cord, and modulation of pain.
2) It describes fast pain and slow pain fibers, nociceptors that respond to noxious stimuli, and receptors like vanilloid receptor-1 and VRL-1 that detect harmful temperatures.
3) Pathways like the spinothalamic tract and paleospinothalamic tract transmit signals from nociceptors to the brain.
dr priyJc ppt
The document discusses neuropathic pain, specifically trigeminal neuralgia. It defines trigeminal neuralgia as paroxysmal attacks of intense, sharp, superficial pain affecting one or more divisions of the trigeminal nerve. The pain is often triggered by innocuous stimuli like tooth brushing or talking. Trigeminal neuralgia is mostly idiopathic, but can occasionally be caused by underlying conditions like multiple sclerosis or tumors. The most widely accepted theory is that trigeminal neuralgia is caused by vascular compression of the trigeminal nerve root, which results in demyelination and hyperexcitability of nerve fibers.
NERVE COMPESSION SYNDROMES. FINAL.pdf
This document provides an overview of nerve compression syndromes, including their pathophysiology, clinical presentation, assessment, and management. It discusses how nerve compression can lead to neuropathic pain through mechanisms like ischemia, inflammation, and central nervous system changes. Common compression neuropathies like carpal tunnel syndrome and sciatica are mentioned. The document emphasizes that entrapment neuropathies have complex presentations that do not always clearly fit the grading criteria for neuropathic pain. A thorough clinical assessment including history, exam, and provocation tests is important for diagnosis.
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Management of Neuropathic Pain
Presented by Dr.Perry Fine at Pain Management for the Elderly Course, 2010.
Scribe medical events Egypt. www.scribeofegypt.org
Chronic pain Managment
Trauma or injury causes the release of chemicals that stimulate nerve fibers, leading to pain signals being sent to the brain. The integration of these pain signals with cognitive, emotional, and environmental factors results in the perception of pain. When this balance is disturbed, chronic pain can develop. Chronic pain is defined as pain lasting beyond normal tissue healing time, typically three months. A multidisciplinary approach is often needed to treat chronic pain through non-pharmacological and pharmacological methods.
Autonomic system and Autonomic Pharmacology
Autonomic Nervous System & Autonomic Pharmacology
Sympathetic: ADRENERGIC
Central: EPINEPHRINE
Peripheral: NOREPINEPHRINE
Parasympathetic: CHOLINERGIC
Acetylcholine
Local anesthetics and counter irritants
Local anesthetics work by reversibly blocking nerve impulse conduction, providing transient loss of sensation to perform minor surgery without loss of consciousness. Cocaine was the first local anesthetic discovered in the 1860s. Local anesthetics are classified as amide or ester types and work by decreasing sodium ion entry during nerve action potentials. They are administered via various routes including topical application, infiltration, nerve blocks, and regional techniques to block sensation in restricted body areas. Common adverse effects involve the central nervous, cardiovascular, and allergic systems. Counterirritants like essential oils, mustard, and capsaicin work by stimulating cutaneous nerves to obscure deeper pain sensations.
Skeletal muscle relaxants (or) Neuromuscular blockers
Skeletal muscle relaxants (or) Neuromuscular blockers
Classification and Mechanism of action of drugs.
Interventional Pain Management
This document discusses interventional pain management (IPM) as a specialty focused on diagnosing and treating pain through minimally invasive procedures. It provides an overview of common IPM procedures like diagnostic nerve blocks, radiofrequency ablation, vertebroplasty, and percutaneous discectomy. The document also presents four case studies where IPM procedures like epidurolysis, percutaneous discectomy, vertebroplasty, and radiofrequency rhizotomy successfully treated chronic pain when other options had failed. It concludes that contrary to common beliefs, over 85% of spinal pain causes can be accurately diagnosed through IPM procedures and that IPM can provide long-term relief when pharmacologic treatments and surgery are not suitable options.
Acute pain management
مشروع إعداد طبيب حكيم ناجح- المعهد العربي للتنمية المهنية المستدامة دورة الطوارئ و التخدير و الرعاية 8-4-2014
Chronic pain assessment & management
Dr. Shekhar Anand presented on methods of chronic pain management to the Department of Anesthesiology. He discussed that chronic pain is defined as pain lasting longer than 3-6 months and can be nociceptive, neuropathic, or mixed in nature. Chronic pain is best managed using a multidisciplinary approach including pharmacological interventions like opioids, antidepressants, anticonvulsants, as well as non-pharmacological therapies like cognitive behavioral therapy, physical therapy, and interventional procedures. The goals of chronic pain management are to improve function and quality of life, rather than to cure the underlying cause of pain.
12.drugs used in rheumatoid arthritis and gout
This document discusses treatments for rheumatoid arthritis and gout. It outlines that for rheumatoid arthritis, first line treatments include NSAIDs and disease-modifying drugs like methotrexate. Methotrexate is often the disease-modifying drug of choice as it has potent anti-inflammatory and immunosuppressive effects through inhibiting T-cell proliferation and cytokine production. For acute gout attacks, first line treatments include NSAIDs, colchicine, and corticosteroids. Colchicine works by depolymerizing microtubules in granulocytes to reduce inflammation. Chronic gout is treated with uricosuric drugs like probenecid to promote uric acid excretion or allopur
1.pain pathophysiology and mechanisms
In this ppt I mentioned all the imp point related to pain pathway and pain pathophysiology. refrence: essentials of interventional techniques in managing chronic pain (laxmaiah manchikanti)
Neuropathic pain
this presentation discusses pain pathways, definition and glossary of pain symptoms, classification of pain, pathogenesis, causes, diagnosis , types and treatment of neuropathic pain
illustrated with figures
Muscle pain mechanism
Muscle pain occurs through the activation of muscle nociceptors by mechanical and chemical stimuli. During ischemia or low pH conditions, chemicals like ATP and protons are released activating nociceptors. Muscle spasms can develop through ischemia reducing blood flow, releasing pain-causing substances, and sensitizing nociceptors. Chronic work-related myalgia may occur through energy depletion in small muscle fibers and impaired blood flow due to sympathetic activation during exertion.
Ans pharmacology
The autonomic nervous system (ANS) regulates involuntary functions and has two divisions: the parasympathetic nervous system (PNS) and sympathetic nervous system (SNS). Both use two neurons - a preganglionic neuron that synapses in an autonomic ganglion and a postganglionic neuron that innervates the target organ. In the PNS, acetylcholine is released at both synapses to activate nicotinic then muscarinic receptors. In the SNS, acetylcholine is released at the ganglion, while norepinephrine is released at the organ to activate adrenergic receptors. The PNS activates "rest and digest" functions, while the SNS activates "fight
Chronic pain management
This document discusses chronic pain management. It defines chronic pain as pain lasting over 3 months. It describes different types of pain such as somatic, visceral and neuropathic pain. It discusses various chronic pain conditions like fibromyalgia, complex regional pain syndrome, postherpetic neuralgia and diabetic neuropathy. It covers evaluation of chronic pain, pathophysiology of chronic pain, brain regions involved, and the multidimensional nature of chronic pain including physical, psychological and social factors. Finally, it discusses various management approaches for chronic pain including pharmacological, physical, psychological and invasive techniques.
Opioid Pharmacology
This document summarizes the pharmacology of various opioid analgesics. It discusses classical opioid effects like analgesia, sedation, respiratory depression. It then profiles specific opioids like fentanyl, sufentanil, morphine, hydromorphone, remifentanil and others. It also discusses evidence for different mu opioid receptor subtypes and the potential for mu-1 selective agonists.
Chronic pain management
This document discusses chronic pain management. It defines chronic pain as pain that lasts months or years in any part of the body and can lead to depression, anxiety, and sleep issues. Chronic pain differs from acute pain in that it continues long after an injury heals. The document describes three types of chronic pain - neuropathic, somatic, and visceral - and their characteristics. It discusses evaluating and measuring pain, as well as pharmacological, physical, psychological, and invasive treatment methods for managing chronic pain. The goal of chronic pain treatment is to improve daily functioning and quality of life by decreasing pain and suffering through a multidisciplinary approach.
Opioid Analgesics
This document discusses different types of pain medications, including opioids. It describes various opioid drugs like morphine, codeine, heroin, methadone, fentanyl, and others. It explains how opioids work by binding to mu, delta, and kappa receptors in the central nervous system and periphery. Tolerance and dependence are noted as issues with long-term opioid use. Guidelines are provided for using different opioids to treat mild, moderate, and severe acute and chronic pain according to the World Health Organization.
Opioid Agonists And Antagonists
This document summarizes various opioid agonists and antagonists. It discusses natural and synthetic opioids like morphine, codeine, heroin, hydromorphone, fentanyl, meperidine, methadone, and diphenoxylate. It also covers opioid receptors, endogenous opioid peptides, pharmacokinetics, effects, tolerance, toxicity, and antagonists like naloxone and naltrexone. Non-steroidal anti-inflammatory drugs are also briefly mentioned.
Lecture 2 Electrotherapy- pain physiology
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.
Neurophysiology of pain
1) The document discusses the neurophysiology of pain, including what pain is, types of pain receptors and fibers, pathways in the spinal cord, and modulation of pain.
2) It describes fast pain and slow pain fibers, nociceptors that respond to noxious stimuli, and receptors like vanilloid receptor-1 and VRL-1 that detect harmful temperatures.
3) Pathways like the spinothalamic tract and paleospinothalamic tract transmit signals from nociceptors to the brain.
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The document discusses neuropathic pain, specifically trigeminal neuralgia. It defines trigeminal neuralgia as paroxysmal attacks of intense, sharp, superficial pain affecting one or more divisions of the trigeminal nerve. The pain is often triggered by innocuous stimuli like tooth brushing or talking. Trigeminal neuralgia is mostly idiopathic, but can occasionally be caused by underlying conditions like multiple sclerosis or tumors. The most widely accepted theory is that trigeminal neuralgia is caused by vascular compression of the trigeminal nerve root, which results in demyelination and hyperexcitability of nerve fibers.
NERVE COMPESSION SYNDROMES. FINAL.pdf
This document provides an overview of nerve compression syndromes, including their pathophysiology, clinical presentation, assessment, and management. It discusses how nerve compression can lead to neuropathic pain through mechanisms like ischemia, inflammation, and central nervous system changes. Common compression neuropathies like carpal tunnel syndrome and sciatica are mentioned. The document emphasizes that entrapment neuropathies have complex presentations that do not always clearly fit the grading criteria for neuropathic pain. A thorough clinical assessment including history, exam, and provocation tests is important for diagnosis.
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pain physiology , pathology, types , assessment, management , recent advances
1. Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It is mediated through peripheral sensory nerves and transmitted through the spinal cord and brain.
2. Pain can be classified based on its underlying mechanism as nociceptive, neuropathic, or mixed. Neuropathic pain occurs as a direct result of damage or dysfunction of the nervous system.
3. Pain is also classified based on duration as either acute pain, which resolves with healing, or chronic pain, which persists longer than 3 months and is associated with disability and mood changes. Chronic pain often requires a multidisciplinary treatment approach.
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This document provides an overview of neurophysiology and pharmacology concepts related to pain management. It discusses the basic pain pathways including transduction, transmission, modulation and perception. It then examines various pharmacological interventions for pain including combination analgesics, acetaminophen, diclofenac, capsaicin, local anesthetics, antiepileptic drugs, opioids like methadone, and the roles of descending pathways and endocannabinoids. Non-pharmacological approaches like menthol are also addressed. The document aims to match neurophysiology concepts with appropriate pharmacological treatments for both acute and chronic pain.
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Pain Pathophysiology - The Role of Neurotrophic Interactions
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The document discusses acupuncture pain management and its mechanisms. It covers several theories of acupuncture including the gate control theory of pain, neurohumoral theory, and endorphin theory. It also discusses clinical applications for treating various pain conditions like headaches, arthritis, lower back pain, and more. Key acupuncture points are provided for different types of pain.
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Neuropathic pain is caused by damage or dysfunction in the nervous system. It is initiated or caused by a primary lesion or dysfunction in either the peripheral or central nervous system. Common causes include diabetes, shingles, spinal cord injury, stroke, alcoholism and medications. This document discusses various types of neuropathic pain such as peripheral nerve damage and peripheral neuropathies. It also covers symptoms, diagnosis, examination tests and management options. The management of neuropathic pain focuses on treating underlying causes, reducing pain, improving function and quality of life. Pregabalin and gabapentin are considered first-line treatments and one study found that pregabalin was as effective as gabapentin for neuropathic pain associated with spinal cord injury.
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This document discusses acute pain management and pre-emptive analgesia. It defines acute pain as pain caused by actual or potential tissue damage that is usually nociceptive in nature. Acute pain management primarily deals with patients recovering from surgery or acute medical conditions. Pre-emptive analgesia aims to prevent central neural sensitization by administering analgesics before a painful stimulus occurs, which can reduce both acute postoperative pain and the risk of chronic postsurgical pain. The document outlines various treatment approaches for acute pain management, including opioids, non-opioid analgesics, regional anesthetic techniques, and multimodal analgesia.
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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.
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1) The document describes the administration of the drug Bupivacaine Hydrochloride to a 46-year-old male patient diagnosed with diabetes mellitus and a foot wound.
2) Bupivacaine Hydrochloride is administered epidurally to provide local or regional anesthesia and analgesia by inhibiting the transmission of pain signals. Common adverse reactions include decreased blood pressure, dizziness, and respiratory depression.
3) Nurses are responsible for closely monitoring the patient's vital signs, assessing for signs of local anesthetic toxicity, and notifying the physician of any unwanted motor or sensory deficits resulting from the epidural administration.
PAIN PHYSIOLOGY.ppt
This document discusses the pathophysiology of pain. It begins with an introduction that defines pain and discusses pain perception. It then covers the pathophysiology of pain perception including transduction, transmission, modulation, and the physiological effects of pain. The document classifies pain into nociceptive, neuropathic, and referred pain, and by duration as acute or chronic. It concludes with a discussion of pain assessment methods.
The role of the central nervous system in the generation and maintenance of c...
The role of the central nervous system in the generation and maintenance of chronic pain in rheumatoid arthritis, osteoarthritis and fibromyalgia
P147
Peripheral nerve injury in the upper extremity is common and can result from repetitive strain, direct trauma, or compression. The most common site of injury is the carpal tunnel. A thorough history and physical exam is important to determine the location and nature of symptoms in order to establish a differential diagnosis. While imaging and electrodiagnostic testing may be warranted for persistent or worsening symptoms, most nerve injuries are initially treated conservatively with splinting, injections, or activity modification. Recovery depends on the severity of injury, with mild injuries having better prognosis.
Neuropathic pain
Neuropathic pain is chronic, severe pain that occurs as a result of damage or dysfunction in the nervous system. It is characterized by allodynia (pain from normally non-painful stimuli) and hyperalgesia (exaggerated pain response). Neuropathic pain can be caused by mechanical nerve injury, metabolic diseases like diabetes, viral infections, inflammation, ischemia, or multiple neurotransmitter system dysfunctions. The mechanisms of neuropathic pain involve peripheral and central sensitization, uncontrolled neuronal firing, glial cell activation, loss of endogenous inhibitory pathways, and neuroplastic changes in the brain.
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Pain Pathophysiology - The Role of Neurotrophic Interactions
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Dolore pelvico cronico: epidemiologia ed eziopatogenesi
bupivacaine compress. and deliberation of terminology
bupivacaine compress. and deliberation of terminology
The role of the central nervous system in the generation and maintenance of c...
The role of the central nervous system in the generation and maintenance of c...
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Flail Arm Syndrome: An Atypical Variant of Motor Neuron Disease
Flail Arm Syndrome (FAS) is an atypical form of Motor Neuron Disease characterized by predominantly proximal, progressive and symmetric wasting and paresis of the upper limb muscles, while lower limbs and bulbar muscles are spared. Diagnosis is made clinically and supported by electrodiagnostic studies and genetic testing. There is no cure, so treatment is supportive and symptomatic. Prognosis is generally better than ALS, with prolonged survival.
Dentatorubral Pallidoluysian Atrophy.pptx
Dentatorubral pallidoluysian atrophy (DRPLA) is a progressive, autosomal dominant disorder caused by an abnormal CAG repeat, characterized by symptoms such as ataxia, myoclonus, epilepsy, and progressive cognitive and motor deterioration. It typically has an adult onset and poor prognosis, with death often occurring within 15 years of symptom onset. Diagnostic evaluation includes genetic testing, EEG, and brain MRI showing nonspecific atrophy. Treatment is supportive and multidisciplinary to address symptoms.
Anti-MAG Neuropathy.pptx
This document summarizes myelin-associated glycoprotein (MAG) neuropathy. It presents as a chronic, slowly progressive large-fiber sensory-motor polyneuropathy, usually affecting the lower extremities initially. Diagnosis involves detecting anti-MAG antibodies and demonstrating demyelination on electrophysiology. While the condition progresses slowly over decades, it can ultimately cause significant muscle weakness, wasting, and ataxia. Current treatments focus on B cell depleting therapies like rituximab, while future therapies may involve antigen-specific immunotherapy.
Trigeminal Trophic Syndrome.pptx
Trigeminal trophic syndrome (TTS) is a rare condition characterized by cutaneous ulceration in the distribution of the trigeminal nerve, most commonly the infraorbital nerve, due to self-inflicted trauma from facial dysesthesia. It results from damage to the trigeminal nerve pathway from various etiologies like iatrogenic nerve injury, cerebrovascular disease, or malignancy. Clinically, patients present with trigeminal anesthesia, facial paresthesia, and crescent-shaped nasal ulcers. Treatment is multidisciplinary and includes behavioral modification, neurologic evaluation, pain management, and various medical therapies.
Acute Exacerbation of Trigeminal Neuralgia.pptx
Trigeminal neuralgia is a painful condition of the trigeminal nerve that causes sudden, severe facial pain. It can be primary due to blood vessel compression or secondary from tumors or multiple sclerosis. While treatments aim to reduce long-term symptoms, there is limited evidence on interventions for acute exacerbations that provide pain relief within 24 hours. Most rescue options provide less than 24 hours of relief, so a more comprehensive care plan is needed. Future studies on potential acute rescue analgesics like lidocaine, sumatriptan, and magnesium sulfate are still needed.
Management of Motor Fluctuations in Parkinson Disease.pptx
- Motor fluctuations are a common complication of Parkinson's disease that occur in approximately one-third of patients after 2 years of levodopa therapy. They involve unpredictable switching between "on" periods where symptoms are relieved and "off" periods where symptoms return.
- Management of motor fluctuations involves both non-pharmacological and pharmacological approaches. Non-pharmacologically, diet, exercise, and treating constipation may help. Pharmacologically, increasing levodopa doses, adding COMT inhibitors, dopamine agonists, or MAO-B inhibitors can help reduce off periods.
- There is no single best treatment, as the appropriate treatment depends on each individual patient's fluctuation patterns, symptoms, risk factors, and other considerations
Role of Clopidogrel in Minor Stroke and Transient Ischaemic Attack.pptx
This document discusses the role of clopidogrel in treating transient ischemic attack (TIA) and minor stroke. It defines TIA and stroke, and explains that clopidogrel works by inhibiting platelet activation and aggregation. It reviews several clinical trials that evaluated the efficacy of clopidogrel combined with aspirin in secondary stroke prevention. The recommendations from health organizations like AHA/ASA and ESO are that clopidogrel can be used for secondary stroke prevention in ischemic stroke. For high-risk TIA or minor stroke patients who are not at high bleeding risk, the recommendation is dual antiplatelet therapy with clopidogrel and aspirin for 21 days, followed by single antiplatelet therapy thereafter.
Transient Epileptic Amnesia.pptx
Transient epileptic amnesia (TEA) is a form of focal epilepsy characterized by recurrent episodes of retrograde or anterograde amnesia. During episodes, patients exhibit repetitive questioning and confusion but otherwise intact neurological function. Diagnosis requires witnessed amnesic episodes, intact cognition otherwise during episodes, and evidence of epilepsy from EEG, seizures, or response to anti-seizure medication. TEA can be differentiated from conditions like transient global amnesia and is frequently underdiagnosed in older adults.
Management of Benzodiazepine Misuse and Dependence.pptx
The document discusses the management of benzodiazepine misuse and dependence. It notes that long-term benzodiazepine use has been associated with increased risks, harms, and mortality. The management of benzodiazepine dependence involves preventing misuse through short prescriptions, substituting to longer-acting benzodiazepines or other drugs, gradually tapering doses to avoid withdrawal symptoms, and using psychotherapy or other pharmacological interventions during tapering. Abrupt discontinuation can cause seizures, so slow tapering is generally recommended.
Mild Malformation of Cortical Development with Oligodendroglial Hyperplasia a...
This document discusses MOGHE (Mild Malformation of Cortical Development with Oligodendroglial Hyperplasia and Epilepsy), a recently recognized and highly epileptogenic histopathological entity involving the frontal lobes that causes drug-resistant epilepsy. MOGHE is characterized by blurred gray-white matter boundaries, heterotopic neurons in white matter, and an increased number of oligodendroglial cells. It represents an emerging histopathological entity associated with frontal lobe epilepsy that can be difficult to treat surgically.
Cerebral Superficial Siderosis.pptx
Cerebral superficial siderosis is characterized by linear hemosiderin deposits in the leptomeninges and superficial layers of the cerebral and cerebellar cortices, brainstem, and spinal cord. It can present as either classical infratentorial or cortical superficial siderosis. Potential etiologies include cerebral amyloid angiopathy, vascular malformations, head trauma, and other conditions. Diagnosis is made through MRI brain imaging. Treatment depends on the underlying cause and may involve surgery to repair vascular abnormalities.
Frontotemporal Brain Sagging Syndrome.pptx
This document discusses frontotemporal brain sagging syndrome, a potentially treatable disorder characterized by apathy, behavioral changes, cognitive dysfunction, and orthostatic headache. Imaging shows sagging of the brain similar to spontaneous intracranial hypotension. Symptoms can mimic frontotemporal dementia. The syndrome is caused by mechanical forces on the frontal and temporal lobes from spontaneous intracranial hypotension. Early diagnosis and treatment are important as it is a reversible condition.
Epidural Blood Patch.pptx
An epidural blood patch involves injecting the patient's own blood into the epidural space to treat a post-dural puncture headache that has not responded to conservative treatments like bed rest. It has an 85% success rate initially and up to 90% with repeated patches. The procedure involves identifying the epidural space and slowly injecting 5-25mL of blood drawn from the patient over 30-60 seconds. Complications can include worsening headaches from additional dural rents, back pain, or infection at the injection site.
Spontaneous Intracranial Hypotension.pptx
Spontaneous intracranial hypotension is a medical condition caused by loss of cerebrospinal fluid from the spinal canal, resulting in headaches and neurological symptoms. It most commonly presents with orthostatic headaches that are less apparent over time. Brain MRI and spine MRI are used to diagnose and locate CSF leaks. Treatment involves conservative measures, percutaneous patching of leaks, or surgical closure. Spontaneous intracranial hypotension can lead to complications like subdural hematomas if not properly diagnosed and treated.
Clinical Evaluation and Management of Facial Nerve Trauma
This document summarizes the clinical evaluation and management of facial nerve trauma. It discusses that facial palsy occurs in 20 per 100,000 people, with 16% being traumatic from temporal bone fractures. The duration, mechanism, and location of the injury provide important clues for evaluation and prognosis. Diagnostic tests include CT, MRI, and electrodiagnostic testing. Management options include conservative treatment with steroids and physical therapy or surgical decompression of the facial nerve, with earlier surgical intervention found to have better outcomes.
Argyrophilic Grain Disease.pptx
Argyrophilic grain disease (AGD) is a progressive neurodegenerative condition characterized by argyrophilic grains in neuronal processes. It is the second most common neurodegenerative disease after Alzheimer's disease. AGD prevalence increases with age to over 30% in centenarians. Clinically, AGD typically presents as a slowly progressive mild cognitive impairment, often with early emotional or personality changes. Diagnosis of AGD can only be made post-mortem by brain biopsy.
Anti-IgLON5 Disease.pptx
Anti-IgLON5 disease is a rare autoimmune neurological disorder characterized by tau deposits in the hypothalamus and brainstem. It is caused by autoantibodies against the IgLON5 protein. Clinical features include sleep disorders, bulbar dysfunction, cognitive impairment, and gait instability. Diagnosis involves detecting IgLON5 antibodies in serum or cerebrospinal fluid along with clinical signs. Neuroimaging shows brain atrophy and white matter changes. Treatment involves long-term immunotherapy but prognosis is generally poor with high mortality.
Globular Glial Tauopathies.pptx
The document discusses globular glial tauopathies (GGTs), a group of neurodegenerative diseases characterized by cytoplasmic tau protein inclusions. GGTs include progressive supranuclear palsy, corticobasal degeneration, and argyrophilic grain disease. They are defined by inclusions predominantly composed of tau isoforms with four microtubule-binding domains. GGTs are characterized neuropathologically by tau-positive globular oligodendroglial inclusions and granular astrocytic inclusions, which are mostly Gallyas-negative. These features help distinguish GGTs from other four-repeat tauopathies, particularly progressive supranuclear palsy.
The Tauopathies.pptx
This document discusses tauopathies, which are neurodegenerative diseases characterized by abnormal tau aggregates in neurons and glial cells. Tau is a microtubule-associated protein that promotes cytoskeleton structure and axonal transport in the nervous system. In tauopathies, tau becomes pathological and forms inclusions like paired helical filaments. Tauopathies show heterogeneity in clinical presentations depending on the type and location of tau aggregates. Classification is based on the tau isoforms involved, with 4-repeat tauopathies including progressive supranuclear palsy and corticobasal degeneration. Understanding tau aggregation mechanisms and their role in toxicity is important for developing targeted therapies for these diseases.
Primary Progressive Aphasia.pptx
Primary progressive aphasia (PPA) is a neurodegenerative syndrome characterized by a gradual deterioration of language abilities over time due to left-hemisphere brain atrophy. It is classified into three main variants - logopenic, nonfluent agrammatic, and semantic - based on distinct language profiles and brain regions affected. Diagnosing PPA and differentiating between variants can be challenging due to overlapping language impairments, clinical variability, and disease progression over time. Management involves a multidisciplinary approach, though treatment options are limited as there is no cure currently.
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The Electrocardiogram - Physiologic Principles
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Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
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12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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- Link to NephroTube website: www.NephroTube.com
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Pain Pathophysiology Overview
- 1. PAIN PATHOPHYSIOLOGY AN OVERVIEW Ade Wijaya, MD – December 2019
- 2. IASP Definition of Pain ◦ Pain An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
- 5. Peripheral Sensitization Peripheral sensitization indicates increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation, which usually occurs after peripheral tissue injury and inflammation Si-Qi Wei, Zhuo-Ying Tao, Yang Xue and Dong-Yuan Cao (December 4th 2019). Peripheral Sensitization [Online First], IntechOpen
- 6. Peripheral sensitization Tissue irritation Release inflammatory mediators Nociceptor threshold Allodinia Hyperalgeusia Recruitment of so-called silent nociceptors, which are not usually sensitive to painful stimuli or inflammatory substrates such as prostaglandins or bradykinin.
- 7. Mechanism ◦ (1) early post-translational changes in the peripheral terminals of nociceptors, for example, the phosphorylation of the ion channels prolongs depolarization and enhances response by lowering the open threshold or prolonging the open time of channels; ◦ (2) altered gene expression, changing transcription or translation of certain protein. For instance, deletion or silencing of calcitonin gene-related peptide alpha (αCGRP) gene expression drastically reduces TRPV1 potentiation in peptidergic nociceptors by abrogating its Ca2+-dependent exocytotic recruitment. Si-Qi Wei, Zhuo-Ying Tao, Yang Xue and Dong-Yuan Cao (December 4th 2019). Peripheral Sensitization [Online First], IntechOpen
- 9. Central Sensitization A condition of the nervous system that is associated with the development and maintenance of chronic pain A change in functional state of neurons and nociceptive pathways throughout the neuraxis, caused by increased membrane excitability and synaptic efficiency or by decreased inhibition on this system Woolf CJ. Evidence for a central component of post-injury pain hypersensitivity. Nature. 1983;306(5944):686-8.
- 10. Mechanism ◦ NEURONAL SENSITIZATION ◦ REDUCTION IN INHIBITORY INTERNEURON ACTIVITY ◦ MODULATION BY DESCENDING PATHWAYS
- 12. ◦ Intense electrical or noxious stimulation of C fibers can promote wide-dynamic-range (WDR) neuron hyperexcitability in the dorsal horn ◦ Molecular mechanism of WDR: excitatory amino acids, tachykinins, and calcitonin gene–related peptide (CGRP) ◦ These transmitters and neuromodulators affect dorsal horn neuron activity by directly increasing cation fluxes, impinging on intracellular transduction mechanisms, and modulating receptor and transmitter gene transcription. ◦ Synaptic transmission augmentation at NMDA receptors is the final common pathway
- 18. THANK YOU