This document discusses inflammation and pain, describing them as physiological processes. It outlines the body's inflammatory response, involving substances like arachidonic acid, prostaglandins, cytokines, and interleukins. Interleukins like IL-1α and IL-1β are identified as primary triggers of inflammation. Conventional anti-inflammatory drugs work by inhibiting enzymes involved in these processes, but often have side effects. Physiological Regulating Medicine provides low-dose formulations of substances like anti-interleukins and β-endorphin that can control inflammation and pain without strong side effects by respecting the body's physiological processes.
NSAIDs are a chemically diverse group of drugs that are grouped together because they have common analgesic, antipyretic, and anti-inflammatory effects. They work by inhibiting cyclooxygenase (COX) enzymes and reducing the production of prostaglandins. NSAIDs are generally weaker analgesics than opioids except for inflammatory pain conditions. Common adverse effects include gastrointestinal irritation and potential kidney toxicity. Newer selective COX-2 inhibitors were developed to reduce gastrointestinal side effects.
1. The document discusses the pathophysiology of pain, which involves transduction, transmission, perception, and modulation of pain signals in the body.
2. Pain signals are transmitted from nociceptors via the peripheral nervous system to the spinal cord and brain. Various neurotransmitters are involved at different stages of transmission.
3. Pain perception is influenced by both physical and psychological factors and can be modulated in the brain using various pharmacological and non-pharmacological treatments.
This document discusses NSAIDs (non-steroidal anti-inflammatory drugs). It provides a brief history of NSAIDs including the isolation of salicylic acid in 1836 and the development of aspirin in 1899. It also covers the common characteristics, mechanisms of action, and therapeutic uses of NSAIDs for treating pain, inflammation, and fever by inhibiting prostaglandin synthesis. The document further explains the pathophysiology of these conditions and how NSAIDs work to reduce symptoms.
This document discusses pain pathways and pharmacotherapy for pain management. It describes how pain is transmitted through three pathways - neospinothalamic, paleospinothalamic, and archispinothalamic tracts. It also outlines different types of pain including nociceptive, neuropathic, inflammatory, acute, chronic, and referred pain. The document further discusses inflammatory processes and mediators involved in pain signaling like eicosanoids, cytokines, and biological oxidants. It concludes by covering recommendations for pharmacotherapy of acute and chronic pain.
NSAIDs are the chemically diverse class of drugs that have anti-inflammatory, analgesic & antipyretic properties.
They are also called as Non Narcotic, Non Opioid, Aspirin like analgesics.
They are among the widely used therapeutic agents world wide and often taken without prescription for minor aches and pain.
They are used to suppress the symptoms of inflammation associated with rheumatic disease.
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.
Peripheral and central sensitization can cause pain hypersensitivity. Peripheral sensitization occurs when tissue damage and inflammation reduce the threshold and increase responsiveness of peripheral nerve endings, causing them to fire in response to normally non-painful stimuli. Central sensitization manifests as hyperalgesia and allodynia due to changes in the dorsal horn neurons of the spinal cord that cause non-painful stimuli to be interpreted as painful. Repetitive firing of C fibers can cause wind up, where increasing amounts of glutamate are released with each stimulus, further depolarizing dorsal horn neurons. Together, peripheral and central sensitization are responsible for hypersensitivity states like hyperalgesia and allodynia.
Physiology of Pain, Characteristic of pain, Basic consideration of nervous system, Pain receptor, Mechanism of pain causation, Theories of pain, Pathways of pain, Pain Receptors
NSAIDs are a chemically diverse group of drugs that are grouped together because they have common analgesic, antipyretic, and anti-inflammatory effects. They work by inhibiting cyclooxygenase (COX) enzymes and reducing the production of prostaglandins. NSAIDs are generally weaker analgesics than opioids except for inflammatory pain conditions. Common adverse effects include gastrointestinal irritation and potential kidney toxicity. Newer selective COX-2 inhibitors were developed to reduce gastrointestinal side effects.
1. The document discusses the pathophysiology of pain, which involves transduction, transmission, perception, and modulation of pain signals in the body.
2. Pain signals are transmitted from nociceptors via the peripheral nervous system to the spinal cord and brain. Various neurotransmitters are involved at different stages of transmission.
3. Pain perception is influenced by both physical and psychological factors and can be modulated in the brain using various pharmacological and non-pharmacological treatments.
This document discusses NSAIDs (non-steroidal anti-inflammatory drugs). It provides a brief history of NSAIDs including the isolation of salicylic acid in 1836 and the development of aspirin in 1899. It also covers the common characteristics, mechanisms of action, and therapeutic uses of NSAIDs for treating pain, inflammation, and fever by inhibiting prostaglandin synthesis. The document further explains the pathophysiology of these conditions and how NSAIDs work to reduce symptoms.
This document discusses pain pathways and pharmacotherapy for pain management. It describes how pain is transmitted through three pathways - neospinothalamic, paleospinothalamic, and archispinothalamic tracts. It also outlines different types of pain including nociceptive, neuropathic, inflammatory, acute, chronic, and referred pain. The document further discusses inflammatory processes and mediators involved in pain signaling like eicosanoids, cytokines, and biological oxidants. It concludes by covering recommendations for pharmacotherapy of acute and chronic pain.
NSAIDs are the chemically diverse class of drugs that have anti-inflammatory, analgesic & antipyretic properties.
They are also called as Non Narcotic, Non Opioid, Aspirin like analgesics.
They are among the widely used therapeutic agents world wide and often taken without prescription for minor aches and pain.
They are used to suppress the symptoms of inflammation associated with rheumatic disease.
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.
Peripheral and central sensitization can cause pain hypersensitivity. Peripheral sensitization occurs when tissue damage and inflammation reduce the threshold and increase responsiveness of peripheral nerve endings, causing them to fire in response to normally non-painful stimuli. Central sensitization manifests as hyperalgesia and allodynia due to changes in the dorsal horn neurons of the spinal cord that cause non-painful stimuli to be interpreted as painful. Repetitive firing of C fibers can cause wind up, where increasing amounts of glutamate are released with each stimulus, further depolarizing dorsal horn neurons. Together, peripheral and central sensitization are responsible for hypersensitivity states like hyperalgesia and allodynia.
Physiology of Pain, Characteristic of pain, Basic consideration of nervous system, Pain receptor, Mechanism of pain causation, Theories of pain, Pathways of pain, Pain Receptors
The document summarizes the physiology of pain. It discusses how pain is a complex experience involving nociception and pain behaviors. It defines acute and chronic pain and describes the different pain fiber types and receptors. The gate control theory of pain is also summarized, which proposes that large diameter fibers can inhibit pain transmission while small fibers facilitate it through a "gate" in the spinal cord.
This document discusses neuropathic pain, including its causes, evaluation, and treatment approaches. Some key points covered include:
- Neuropathic pain can originate from the central or peripheral nervous systems and have various etiologies such as metabolic issues, trauma, compression, autoimmune conditions, or genetics.
- Evaluation involves taking a pain history including characteristics of the pain and examining for sensory and motor dysfunction, as well as potentially ordering imaging or lab tests.
- Treatment approaches include interventional procedures like spinal cord stimulation as well as pharmacologic options like anticonvulsants, benzodiazepines, antidepressants, antiarrhythmics, corticosteroids, baclofen, and capsaicin
Pain is the common symptom in many chronic conditions such as cancers, neuropathies, and chronic disease. It is also experienced in trauma varying from mild to severe based on the location and degree of trauma. This presentation is a brief outline on types of pain, classification of pain, pain pathways and management of pain
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.
This document discusses the pathway, physiology, and perception of pain. It begins with an introduction to pain and its significance as a warning signal. It then covers the history of theories about pain. The document defines pain and discusses its characteristics such as threshold, intensity, and localization. It classifies pain into acute and chronic types and looks at the components involved in pain perception including receptors, neural pathways, and sensory neurons. The document examines peripheral mechanisms of injury-induced pain and theories of pain such as the gate control theory. It also discusses visceral pain, referred pain, and tooth pain pathways.
This document provides an overview of the pathophysiology of pain. It discusses the definition of pain, pain receptors and pathways in the peripheral and central nervous systems. It describes the gate control theory of pain modulation in the spinal cord and descending pain inhibitory pathways in the brain. The document also covers physiological and psychological effects of pain, classifications of pain including nociceptive and neuropathic pain, and assessments used to evaluate pain.
This document discusses pain classification, perception, and evaluation. It describes acute and chronic pain, including mechanisms and systemic responses. Specific pain syndromes are reviewed like neuropathic pain, fibromyalgia, low back pain, headaches, and cancer pain. Acute pain is usually nociceptive and self-limited, while chronic pain persists over 3 months and involves psychological factors. Pain is classified by etiology and location. Evaluation includes scales, imaging, and psychological assessments.
The document discusses pain pathways and mechanisms. It defines pain and describes the different types of pain receptors and fibers that detect pain. The dual nature of pain as both a sensory and emotional experience is explained. Several theories of pain mechanisms are presented, including the specificity theory, pattern theory, and gate control theory. The gate control theory proposes that activity in large nerve fibers inhibits transmission of pain signals while activity in small fibers facilitates transmission. Neurotransmitters and chemical mediators involved in pain signaling are also discussed.
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.
This document discusses drugs used to treat pain and inflammation. It defines acute and chronic pain, as well as neuropathic and inflammatory pain. Nociceptors detect painful stimuli. NSAIDs like aspirin and ibuprofen work by inhibiting prostaglandin synthesis to reduce pain and inflammation. Steroidal anti-inflammatory drugs also reduce inflammation. NSAIDs can cause side effects like ulcers, bleeding, and kidney damage, so should be used carefully.
This document provides an overview of pain and pain pathways. It defines pain, discusses its history and characteristics. It describes the classification and receptors of pain, as well as the chemical mediators and neural pathways involved in pain transmission and modulation. Specifically, it outlines the three orders of sensory neurons - first order neurons transmit signals from receptors to the spinal cord, second order neurons relay signals within the spinal cord, and third order neurons transmit signals from the spinal cord to the brain. It also briefly discusses theories of pain transmission and modulation.
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.
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
This document provides an outline and overview of the neurophysiology of pain. It begins with definitions of pain and discusses the dual nature of pain perception and reaction. It describes the types of pain receptors and the chemical mediators involved in pain signaling. The theories of pain perception including specificity theory, central summation theory, and the gate control theory are summarized. The physiology of pain processing from transduction to transmission and modulation is explained. Assessment scales for pain are also mentioned. The document provides references for further reading on the topic.
This document provides an overview of pain, including its definition, classification, transmission pathways, and management. It begins with defining pain and discussing its incidence and epidemiology. Pain is then classified based on its source, duration, and transmission. The pathways of pain transmission from nociceptors to the central nervous system are explained. Finally, the document discusses pain assessment, management guidelines, and concludes with references.
This document discusses classifications of pain. It defines pain according to several organizations and researchers. It notes the historical understanding of pain from Greek, Latin, and early philosophers' perspectives. It then describes types of pain based on speed of onset and duration, including experimental, transient, acute, and chronic pain. It also discusses types based on stimulation level, including somatic and visceral pain. The document outlines specific pains such as headaches, toothaches, and trigeminal neuralgia. It concludes by defining abnormal pains including hyperalgesia, allodynia, hyperpathia, and phantom limb pain.
This document provides information on the nervous system and pain pathways. It discusses how pain signals travel through the nervous system, from nociceptors through the spinal cord and brain. It outlines the roles of different nerve fibers and neurotransmitters in pain signaling and modulation. The document also differentiates between acute and chronic pain, covering signs, symptoms, classifications, and treatment approaches including medications and physical therapies.
The document provides an overview of pain, including its definition, classification, theories, pathways, and assessment tools. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is classified based on duration (acute, chronic), pathophysiological mechanisms (nociceptive, neuropathic), and clinical context. Theories of pain discussed include specificity theory, intensity theory, pattern theory, and gate control theory. Pain pathways involve nociception in the peripheral nervous system and transmission/perception in the central nervous system. Common pain assessment tools are also mentioned.
The document discusses pain pathways and pain control methods. It defines pain as an unpleasant sensation associated with actual or potential tissue damage that serves as a defensive mechanism. Pain consists of pain perception and pain reaction. Pain perception is the physiological process of receiving and transmitting pain from tissues to the central nervous system, while pain reaction is the patient's manifestation and differs between individuals. The most accepted pain pathway theory involves three neurons - the first receives touch or pain and transmits signals to the second neuron which crosses and terminates in the thalamus, and the third carries impulses from the thalamus to the cortex where sensation is felt. Methods to control pain include removing the cause, blocking pathways with local anesthesia, preventing pain reaction through
Physiological Regulating Medicine (PRM) is the latest integration between Conventional Medicine and Homeopathic Medicine. PRM integrates classic Homeopathy with a new therapeutic concept - the restoration of physiological conditions through molecules such as hormones, neuropeptides, interleukins and growth factors in homeopathic dilutions corresponding to physiological concentrations. The method includes current knowledge on Homeopathy, Homotoxicology, the Psycho-Neuro-Endocrine-Immune axis, and nutrition. PRM offers injectable formulations for the control of nociceptive, neuropathic and mixed pain that can be injected into acupuncture points with excellent therapeutic results and no side effects.
This document summarizes information about pain, inflammation, and fever. It defines pain and classifies pain based on duration, location, intensity, and etiology. It also discusses the management of pain through pharmacological and non-pharmacological interventions. Inflammation is described as the body's response to harmful stimuli and signs of inflammation include heat, redness, swelling, pain, and loss of function. Both acute and chronic inflammation are summarized. Common inflammatory mediators are also listed. Fever is defined as an elevated body temperature regulated by the hypothalamus in response to infection or other stimuli. Management of fever includes conservative measures as well as medications like NSAIDs.
The document summarizes the physiology of pain. It discusses how pain is a complex experience involving nociception and pain behaviors. It defines acute and chronic pain and describes the different pain fiber types and receptors. The gate control theory of pain is also summarized, which proposes that large diameter fibers can inhibit pain transmission while small fibers facilitate it through a "gate" in the spinal cord.
This document discusses neuropathic pain, including its causes, evaluation, and treatment approaches. Some key points covered include:
- Neuropathic pain can originate from the central or peripheral nervous systems and have various etiologies such as metabolic issues, trauma, compression, autoimmune conditions, or genetics.
- Evaluation involves taking a pain history including characteristics of the pain and examining for sensory and motor dysfunction, as well as potentially ordering imaging or lab tests.
- Treatment approaches include interventional procedures like spinal cord stimulation as well as pharmacologic options like anticonvulsants, benzodiazepines, antidepressants, antiarrhythmics, corticosteroids, baclofen, and capsaicin
Pain is the common symptom in many chronic conditions such as cancers, neuropathies, and chronic disease. It is also experienced in trauma varying from mild to severe based on the location and degree of trauma. This presentation is a brief outline on types of pain, classification of pain, pain pathways and management of pain
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.
This document discusses the pathway, physiology, and perception of pain. It begins with an introduction to pain and its significance as a warning signal. It then covers the history of theories about pain. The document defines pain and discusses its characteristics such as threshold, intensity, and localization. It classifies pain into acute and chronic types and looks at the components involved in pain perception including receptors, neural pathways, and sensory neurons. The document examines peripheral mechanisms of injury-induced pain and theories of pain such as the gate control theory. It also discusses visceral pain, referred pain, and tooth pain pathways.
This document provides an overview of the pathophysiology of pain. It discusses the definition of pain, pain receptors and pathways in the peripheral and central nervous systems. It describes the gate control theory of pain modulation in the spinal cord and descending pain inhibitory pathways in the brain. The document also covers physiological and psychological effects of pain, classifications of pain including nociceptive and neuropathic pain, and assessments used to evaluate pain.
This document discusses pain classification, perception, and evaluation. It describes acute and chronic pain, including mechanisms and systemic responses. Specific pain syndromes are reviewed like neuropathic pain, fibromyalgia, low back pain, headaches, and cancer pain. Acute pain is usually nociceptive and self-limited, while chronic pain persists over 3 months and involves psychological factors. Pain is classified by etiology and location. Evaluation includes scales, imaging, and psychological assessments.
The document discusses pain pathways and mechanisms. It defines pain and describes the different types of pain receptors and fibers that detect pain. The dual nature of pain as both a sensory and emotional experience is explained. Several theories of pain mechanisms are presented, including the specificity theory, pattern theory, and gate control theory. The gate control theory proposes that activity in large nerve fibers inhibits transmission of pain signals while activity in small fibers facilitates transmission. Neurotransmitters and chemical mediators involved in pain signaling are also discussed.
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.
This document discusses drugs used to treat pain and inflammation. It defines acute and chronic pain, as well as neuropathic and inflammatory pain. Nociceptors detect painful stimuli. NSAIDs like aspirin and ibuprofen work by inhibiting prostaglandin synthesis to reduce pain and inflammation. Steroidal anti-inflammatory drugs also reduce inflammation. NSAIDs can cause side effects like ulcers, bleeding, and kidney damage, so should be used carefully.
This document provides an overview of pain and pain pathways. It defines pain, discusses its history and characteristics. It describes the classification and receptors of pain, as well as the chemical mediators and neural pathways involved in pain transmission and modulation. Specifically, it outlines the three orders of sensory neurons - first order neurons transmit signals from receptors to the spinal cord, second order neurons relay signals within the spinal cord, and third order neurons transmit signals from the spinal cord to the brain. It also briefly discusses theories of pain transmission and modulation.
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.
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
Pain is one of the most commonly experienced symptom . It is often spoken of as a protective mechanism since it is usually manifested when an environmental change occurs that causes injury to responsive tissue
This document provides an outline and overview of the neurophysiology of pain. It begins with definitions of pain and discusses the dual nature of pain perception and reaction. It describes the types of pain receptors and the chemical mediators involved in pain signaling. The theories of pain perception including specificity theory, central summation theory, and the gate control theory are summarized. The physiology of pain processing from transduction to transmission and modulation is explained. Assessment scales for pain are also mentioned. The document provides references for further reading on the topic.
This document provides an overview of pain, including its definition, classification, transmission pathways, and management. It begins with defining pain and discussing its incidence and epidemiology. Pain is then classified based on its source, duration, and transmission. The pathways of pain transmission from nociceptors to the central nervous system are explained. Finally, the document discusses pain assessment, management guidelines, and concludes with references.
This document discusses classifications of pain. It defines pain according to several organizations and researchers. It notes the historical understanding of pain from Greek, Latin, and early philosophers' perspectives. It then describes types of pain based on speed of onset and duration, including experimental, transient, acute, and chronic pain. It also discusses types based on stimulation level, including somatic and visceral pain. The document outlines specific pains such as headaches, toothaches, and trigeminal neuralgia. It concludes by defining abnormal pains including hyperalgesia, allodynia, hyperpathia, and phantom limb pain.
This document provides information on the nervous system and pain pathways. It discusses how pain signals travel through the nervous system, from nociceptors through the spinal cord and brain. It outlines the roles of different nerve fibers and neurotransmitters in pain signaling and modulation. The document also differentiates between acute and chronic pain, covering signs, symptoms, classifications, and treatment approaches including medications and physical therapies.
The document provides an overview of pain, including its definition, classification, theories, pathways, and assessment tools. It defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is classified based on duration (acute, chronic), pathophysiological mechanisms (nociceptive, neuropathic), and clinical context. Theories of pain discussed include specificity theory, intensity theory, pattern theory, and gate control theory. Pain pathways involve nociception in the peripheral nervous system and transmission/perception in the central nervous system. Common pain assessment tools are also mentioned.
The document discusses pain pathways and pain control methods. It defines pain as an unpleasant sensation associated with actual or potential tissue damage that serves as a defensive mechanism. Pain consists of pain perception and pain reaction. Pain perception is the physiological process of receiving and transmitting pain from tissues to the central nervous system, while pain reaction is the patient's manifestation and differs between individuals. The most accepted pain pathway theory involves three neurons - the first receives touch or pain and transmits signals to the second neuron which crosses and terminates in the thalamus, and the third carries impulses from the thalamus to the cortex where sensation is felt. Methods to control pain include removing the cause, blocking pathways with local anesthesia, preventing pain reaction through
Physiological Regulating Medicine (PRM) is the latest integration between Conventional Medicine and Homeopathic Medicine. PRM integrates classic Homeopathy with a new therapeutic concept - the restoration of physiological conditions through molecules such as hormones, neuropeptides, interleukins and growth factors in homeopathic dilutions corresponding to physiological concentrations. The method includes current knowledge on Homeopathy, Homotoxicology, the Psycho-Neuro-Endocrine-Immune axis, and nutrition. PRM offers injectable formulations for the control of nociceptive, neuropathic and mixed pain that can be injected into acupuncture points with excellent therapeutic results and no side effects.
This document summarizes information about pain, inflammation, and fever. It defines pain and classifies pain based on duration, location, intensity, and etiology. It also discusses the management of pain through pharmacological and non-pharmacological interventions. Inflammation is described as the body's response to harmful stimuli and signs of inflammation include heat, redness, swelling, pain, and loss of function. Both acute and chronic inflammation are summarized. Common inflammatory mediators are also listed. Fever is defined as an elevated body temperature regulated by the hypothalamus in response to infection or other stimuli. Management of fever includes conservative measures as well as medications like NSAIDs.
This document summarizes information about NSAIDs (non-steroidal anti-inflammatory drugs) and COX-2 inhibitors for pain management. It defines pain and classifications of pain such as acute vs chronic pain. It describes the mechanisms of COX-1 and COX-2 enzymes and how different NSAIDs and COX-2 inhibitors work. It discusses the use of NSAIDs and COX-2 inhibitors for various types of pain and their potential adverse effects.
This document discusses analgesics used in dentistry, focusing on NSAIDs. It defines NSAIDs and explains their mechanism of action as inhibiting the cyclooxygenase enzymes, thereby reducing the formation of prostaglandins. The document classifies NSAIDs chemically and by mechanism of action. It outlines the indications of NSAIDs in dentistry and discusses commonly used NSAIDs, their pharmacokinetics, pharmacodynamics, adverse effects, and interactions. The document also briefly discusses opioids and their uses, mechanisms of action, and considerations.
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 document provides information on non-steroidal anti-inflammatory drugs (NSAIDs) including their classification, mechanisms of action, and major effects. NSAIDs are chemically diverse drugs that reduce pain, fever, and inflammation by inhibiting cyclooxygenase (COX) enzymes and subsequent prostaglandin synthesis. They are classified based on their selectivity for COX-1 versus COX-2 isoenzymes. The major effects of inhibiting prostaglandin synthesis include analgesia, antipyresis, anti-inflammatory action, antiplatelet aggregation, and closure of the ductus arteriosus in newborns. NSAIDs produce gastric mucosal damage by inhibiting protective prostaglandins in
COX inhibitors like NSAIDs work as nonopioid analgesics and anti-inflammatory drugs. They function by inhibiting the COX enzymes and thereby decreasing the production of prostaglandins and other inflammatory mediators derived from arachidonic acid. This leads to their analgesic, antipyretic, and anti-inflammatory effects but also side effects involving the gastrointestinal tract and kidney function. Aspirin is a prototypical NSAID that was first isolated from willow bark and introduced in 1899, demonstrating the clinical usefulness of this class of drugs.
Dr. Manish Chandila presented on analgesics. He began by defining pain and discussing the gate control theory of pain. He then classified analgesics into three main categories - non-opioids, opioids, and adjuvants. Under non-opioids, he discussed NSAIDs like ibuprofen and aspirin. He provided details on various opioid analgesics like morphine, codeine, and tramadol. Adjuvants discussed included Cox-2 inhibitors and ketorolac. He concluded with a discussion on management of acute morphine poisoning.
This document discusses the treatment of muscle pain and disorders. It covers the mechanisms and uses of skeletal muscle relaxants, NSAIDs, and local injection therapies like corticosteroids and anesthetics. It compares the mechanisms of action, uses, and side effects of selective and non-selective NSAIDs. The key resources listed provide information on controlling muscle pain using NSAIDs, muscle relaxants, and local therapies for muscle disorders.
Overview of Discussion
Introduction
Which are the features of inflammation…?
Functional importance of eicosanoids and other chemical mediators
Pharmacological/physiological effects of inflammatory mediators
How PGs produce PAIN?
How PGs produces FEVER?
How PGs produces INFLAMMATION?
About NSAIDs...
Classification of NSAIDs
Mechanism of Action: NSAIDs
Pharmacology of Individual Class of NSAIDs
Choice of NSAIDs
Analgesic combinations
Analgesics are medicines that selectively relieve pain without altering consciousness. They act in the central nervous system or on peripheral pain mechanisms. Analgesics are classified as narcotic analgesics/opioids, non-narcotic analgesics, or nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes, which produce prostaglandins that sensitize nerve endings and cause hyperalgesia during inflammation.
The document discusses inflammation and the mechanisms by which nonsteroidal anti-inflammatory drugs (NSAIDs) work to reduce inflammation. It describes how NSAIDs inhibit the cyclooxygenase (COX) enzymes that produce prostaglandins, leading to their analgesic, antipyretic, and anti-inflammatory effects. However, it also notes that NSAID inhibition of prostaglandin production can cause gastric mucosal damage and bleeding risks as side effects. The document provides details on the classification and mechanisms of different types of NSAIDs including selective and non-selective COX inhibitors.
Psychoneuroimmunology examines the relationship between mental processes, the nervous system, and the immune system. Stress can negatively impact immune function through pathways like the hypothalamic-pituitary-adrenal axis and proinflammatory cytokine production. Chronic stress is associated with increased risk of diseases like cancer, autoimmune disorders, and infections. Exercise and relaxation techniques may help mitigate stress's immune effects by modulating cytokine levels. Psychoneuroimmunology research underscores the interaction between psychological, neurological, and immunological factors in health and disease.
Dr. Kumar presented on acute pain management. He discussed how acute pain is initiated by nociceptors and transmitted through three neurons to the brain. Poorly managed acute pain can lead to central sensitization and chronic pain. He described the anatomy and pathways of acute pain transmission, including modulation by descending pathways. Drugs like opioids, NSAIDs, ketamine, alpha-2 agonists, and gabapentinoids were discussed as treatment options, as well as patient-controlled analgesia and regional anesthesia techniques.
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.
This document provides information on analgesics and anti-inflammatory drugs. It begins by defining analgesics as drugs that relieve pain without altering consciousness, and anaesthesia as loss of sensation. It then classifies analgesics into two main groups - opioid analgesics like morphine and non-opioid analgesics like NSAIDs. The document goes on to describe various opioid and non-opioid analgesics in detail, their mechanisms of action, uses, and adverse effects. It focuses on the role of prostaglandins in pain and inflammation, and how different NSAIDs work by inhibiting prostaglandin synthesis.
This document summarizes different types of anti-inflammatory medications and treatments. It discusses steroidal anti-inflammatories like glucocorticoids. It also discusses non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin, ibuprofen, and naproxen which work by inhibiting the COX enzyme and preventing prostaglandin synthesis. The document also introduces a new class of anti-inflammatory peptides called Immune Selective Anti-Inflammatory Derivatives (ImSAIDs) which were discovered from studies of the submandibular gland. Herbs, diet, ice treatment, and certain cannabinoids are also mentioned as having potential anti-inflammatory effects.
This document summarizes different types of anti-inflammatory medications and treatments. It discusses steroidal anti-inflammatories like glucocorticoids. It also discusses non-steroidal anti-inflammatory drugs (NSAIDs) like aspirin, ibuprofen, and naproxen which work by inhibiting the COX enzyme and preventing prostaglandin synthesis. The document also mentions immune selective anti-inflammatory derivatives (ImSAIDs) which are peptides that alter immune cell activation and migration to reduce inflammation. Foods and herbs with potential anti-inflammatory properties are also outlined.
El documento describe la composición de CELLFOOD, un suplemento nutricional. Contiene una amplia variedad de minerales, aminoácidos, enzimas y electrolitos que proporcionan nutrientes esenciales para el cuerpo. Al tomar CELLFOOD, algunas personas pueden experimentar una "crisis de curación" en la que el cuerpo elimina toxinas acumuladas, lo que puede causar síntomas temporales de desintoxicación. Esto es un signo positivo de que el cuerpo se está limpiando a profundidad. Siguiendo las
I. Un estudio prospectivo evaluó el efecto de Rowatinex® en 50 pacientes tratados con litotripsia para cálculos renales o ureterales.
II. A los 14 días, el 60% de pacientes estaban libres de cálculos y el 82% a los 28 días.
III. Los resultados para el alivio de dolor también fueron excelentes, con un 82% libres de dolor a los 14 días y un 94% a los 28 días.
La dispepsia o indigestión se define como un síntoma que incluye náuseas, ardor de estómago y dolor abdominal superior. Rowachol contiene seis terpenos purificados que mejoran la bilis, son coleréticos, antiespasmódicos, estimulan la secreción pancreática y tienen efectos carminativos, lo que alivia los síntomas de la dispepsia. Varios estudios con animales y humanos han demostrado que Rowachol mejora la función del sistema digestivo y la composición de la bilis.
This document is a medication guide for non-steroidal anti-inflammatory drugs (NSAIDs) that outlines important safety information. It states that NSAIDs can increase the risk of heart attack, stroke, ulcers and bleeding in the stomach and intestines. It lists common side effects like stomach pain and serious side effects like kidney problems. The guide provides information on who should not take NSAIDs and cautions to stop use and seek medical help if concerning symptoms arise. It also lists examples of prescription NSAID medicines.
Este documento describe un estudio clínico sobre el tratamiento de la celulitis mediante mesoterapia homeopática y fitoterapia. El estudio incluyó 1,564 pacientes tratados entre 1991 y 1994 con una mezcla homeopática llamada Lipodistrofin inyectada mediante mesoterapia, complementada con tratamientos dietéticos, de ejercicio y aplicaciones tópicas. Los resultados mostraron mejoras en la pérdida de peso, disminución del diámetro de la cintura y síntomas relacionados con la celulitis, sin efectos
This study evaluated the effectiveness of Osteobios and Guna-Fem supplements for treating early postmenopausal osteoporosis compared to calcium and vitamin D supplements. 70 postmenopausal women with osteoporosis were divided into two groups. The group treated with Osteobios and Guna-Fem showed greater reductions in pain levels, improvements in quality of life, and decreases in bone resorption markers compared to the calcium/vitamin D group. The results suggest Osteobios and Guna-Fem may be effective treatments for reducing symptoms of early postmenopausal osteoporosis.
This document discusses using cytokines and homeopathic dilutions therapeutically. It argues that cytokines, which are protein molecules that regulate the immune system, can be used in homeopathic form to help defend the body against illness. The document states that homeopathy uses extremely diluted stimuli that are able to precisely target ultrafine body structures. It asserts that this approach can help restore balance to the complex fractal dynamics of various biological systems interacting in the body. Overall, the document proposes that cytokines can be applied homeopathically to provide a balanced, non-toxic stimulation that supports the body's natural healing responses.
The document summarizes a study on the use of Osteobios to treat calcium metabolism disorders in patients with chronic kidney disease stages II-III. 20 patients received Osteobios drops daily for a month in addition to other treatments, while a control group of 20 similar patients received no such treatment. Testing showed improvements in calcium, phosphorus, parathyroid hormone, and pain levels in the treatment group compared to baseline and the control group. The study concluded that Osteobios safely improves calcium metabolism in patients with chronic kidney disease without the need for additional medications.
Este documento presenta los resultados de un estudio multicéntrico sobre el uso de la mesoterapia homeopática con Condrotrofín R para tratar la patología articular. El estudio evaluó 200 pacientes durante 5 semanas y encontró una mejoría significativa de los síntomas en el 40% de los pacientes después de la primera semana de tratamiento. El tratamiento con Condrotrofín R redujo la necesidad de medicamentos convencionales y fue bien aceptado por los pacientes.
1. The extracellular matrix (ECM) represents the basic system of living organisms, where nourishment, control, and management of cells takes place through mutual information exchange.
2. The ECM is composed of proteoglycans and glycosaminoglycans which help maintain homeostasis. It also contains collagen, elastin, and other glycoproteins.
3. Over a lifetime, catabolites can accumulate in the ECM, making energy exchange between cells more difficult and contributing to the aging process. Physiological Regulating Medicine aims to cleanse and restore the ECM, such as through the product GUNA-MATRIX.
This study aimed to determine the safety and efficacy of three popular mesotherapy cocktails in treating localized fat deposits in Filipino women. Sixty subjects received injections of one of three cocktails - phosphatidylcholine and organic silicium (PC-OS), phaphatidylcholine, tiratricol and L-carnitine (PC+L), or the homeopathic formula Omeoformula 1. Measurements and blood tests showed PC-OS and Omeoformula 1 were comparable in reducing arm circumference and had fewer adverse effects than PC+L. Overall, mesotherapy was deemed safe and effective for reducing localized fat deposits with some benefit to HDL and LDL cholesterol levels.
Este estudio experimental evaluó los efectos de un preparado homeopático llamado Musclebig en parámetros antropométricos y dinamométricos de 32 culturistas masculinos. Los participantes fueron asignados aleatoriamente a un grupo tratado con inyecciones de Musclebig o a un grupo control. Tras 12 semanas, el grupo tratado mostró aumentos estadísticamente significativos en su índice de masa corporal, masa magra y fuerza de resistencia, así como una disminución en la grasa corporal, en comparación con el
The document describes a clinical study on 681 patients that evaluated the efficacy of the homeopathic remedy MADE® in treating wrinkles and skin slackening. The study found MADE® to be an effective alternative to conventional pharmacological treatments, showing good results in preventing and treating wrinkles and skin slackening, especially in patients aged 30-40 and 40-50.
1. The study investigated the effectiveness of antihomotoxic preparations Traumeel S and Osteobios in combination treatment of degenerative spinal diseases. Patients receiving these preparations in addition to traditional therapy saw greater improvements in pain, mobility, and bone healing markers than the control group receiving only traditional therapy.
2. Specifically, those receiving Traumeel S injections and ointment experienced greater reductions in pain levels and muscle spasms after 4 days compared to the control group. They also had faster wound healing after surgery.
3. The group also receiving Osteobios showed higher blood alkaline phosphatase levels upon discharge, indicating increased bone formation compared to the control group. This supported Osteobios' role
This document discusses inflammation and cytokines. It notes that cytokines are proteins secreted by immune cells in response to antigens that induce inflammation. Cytokines influence each other in cascades and have pleiotropic, redundant, synergistic and antagonistic effects. Their secretion is brief and self-limiting, requiring multiple cytokines in relay to achieve a targeted biological response. Physiological regulating medicine uses homeopathic cytokines and other remedies to reset and coordinate the immune system.
The document discusses the transition from homeopathy to physiological regulating medicine (PRM). While homeopathy is based on the principle of treating "like with like" using highly diluted substances, PRM was developed by an Italian research group inspired by homeopathy but aiming to have a more scientifically valid treatment approach based on the latest immunology and neuroendocrinology discoveries. Key aspects of homeopathy discussed include the principle of similarity in symptom matching, and the use of potentized dilutions, which some research has found can induce physical changes in water and potentially have physiological effects.
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2) 28 elderly patients with difficult CBD stones underwent biliary stenting and were given UDCA and terpene preparation daily for 6 months on average.
3) After treatment, CBD stone size and CBD diameter decreased significantly. Complete stone removal was achieved in 26 of 28 patients (92.8%) with an average of 1.7 additional ERCP sessions.
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Inflamación: nuevas evaluaciones
1. PHYSIOLOGICAL REGULATING MEDICINE 2011
INFLAMMATION
- NEW TRENDS IN ASSESSMENT
AND CONTROL AT
THE PHYSIOLOGICAL LEVEL
SUMMARY
L. A. Urgelles
INTRODUCTION
The word inflammation derives from
Latin “inflammare” (to light a fire).
It is a process where the body fights
against an “irritant agent” at the level
of receptors (nociceptors), and it essen-
tially characterized by: pain, swelling,
heat, redness, and loss of functions.
Nociceptors are sensitive receptors to
damage; they act as transducers and
conduct nerve impulses to the Central
Nervous System (CNS) through small
A- delta fibers (myelinated, fast) for
acute pain, and c fibers (slow,
unmyelinated) for chronic pain.
When a tissue is damaged, its cells
release various substances that cause
blood vessels dilatation, and therefore
greater blood supply to the triggered area.
Furthermore, in the affected tissues, the
inflammatory exudate increases capil-
lary permeability, leukocyte migration,
the presence of cytokines and other
local processes that excite and “irri-
tate” the nerve endings, making the
physiological functioning of the area
blocked.
– All this, within the so-called arachi-
donic acid cascade.
The inflammatory response occurs
with a defending goal in order to iso-
late and destroy the damaging agent,
as well as repairing the tissue of the
damaged tissue/organ; when the
inflammation is chronic it occurs a
local tissue destruction, and therefore
it is difficult to restore the lost func-
tions.
Inflammation can be short term in
association with physiological pain,
but when kept beyond expectations
should be considered chronic, and it is
the result of a longer neuron irritation
at the receptors level, with periods of
greater or less intensity.
– In this situation, it is higly recom-
mended an effective treatment, avoid-
ing side effects.
– This paper discusses the importance
of clinical control of inflammation with
specific low dose formulations (S.K.A.)
and for different anatomical areas, for-
mulated with the intention to restore
optimal physiological states avoiding
undesirable side effects, according to
the Principles of the Physiological
Regulating Medicine (PRM).
PAIN
We have previously pointed out that
pain is a complex process; it can be
classified into four categories, namely:
1) Physiological pain, related to the
preservation of life, associated with a
short-term inflammation level.
Pain is a complex process and can be
classified into four categories namely:
1) Physiological pain, related to the
preservation of life, associated with a
short-term inflammation level.
2) Nociceptive pain, related to the long-
lasting inflammation; it is usually
chronic.
3) Neuropathic pain, usually chronic,
results from damage, compression or
dysfunction of the peripheral nerves or
neural loops in the CNS.
Inflammation is usually associated with
pain, but it can be pain without inflam-
mation, such as the neuropathic pain.
4) Mixed pain in which various factors
are involved. The best example is the
pain associated with cancer, which is
chronic, permanent and difficult to con-
trol for which the use of analgesics is
frequently combined with opioids.
Interleukins are the primary means of in-
tercellular communication against an
aggression starting the inflammatory re-
sponse.
Physiological Regulating Medicine has
really filled a gap and allowed to settle
two main problems controlling the in-
flammation and pain, despite the exis-
tence of NSAIDs for more than a centu-
ry, with a biological approach, respect-
ing the physiological processes without
the risk of unwanted strong side effects
associated with the conventional medi-
cines already known.
The 11 products are: Guna®
-Neck, Gu-
na®
-Thoracic, Guna®
-Lumbar, Guna®
-
Shoulder (shoulder and elbow), Guna®
-
Hip, Guna®
-Knee, Guna®
-HandFoot, Gu-
na®
-Ischial, Guna®
-Polyarthritis, Guna®
-
Muscle, and Guna®
-Neural, of which 10
contain β-endorphin 4C [equivalent to
nanograms (ng)].
Nine products of these contain Anti IL-
1 α and β 4 C [equivalent to nanograms
(ng)], which ascribe an analgesic and an-
ti-inflammatory effect at the physiolog-
ical level without the side effects of
medications known.
Excellent results are obteined for: bur-
sitis, epicondylitis, fibromyalgia, os-
teoarthritis of the hip and knee, sacroili-
itis, cervical pain, thoracic pain, low
back pain, trigeminal neuralgia, etc.
PHYSIOLOGICAL
REGULATING MEDICINE, PAIN,
INFLAMMATION, NERVE IRRITATION,
CYCLOOXYGENASES, INTERLEUKINS,
β-ENDORPHIN, INJECTABLE AMPOULES
KEY WORDS
37
CLINICAL
Urgelles-A:Art. Del Giudice 15/12/11 09.27 Pagina 37
2. 38
PHYSIOLOGICAL REGULATING MEDICINE 2011
2) Nociceptive pain, related to the
long-lasting inflammation; it is usually
chronic.
3) Neuropathic pain, usually chronic,
resulting from damage, compression or
dysfunction of the peripheral nerves or
neuronal loops in the CNS.
Inflammation is usually associated with
pain, but can be pain without inflamma-
tion, such as the neuropathic pain.
4) Mixed pain in which various factors
are involved.
The best example is the pain associat-
ed with cancer, which is chronic, per-
manent and difficult to control for
which the use of analgesics is fre-
quently combined with opioids (1-7).
In this work we will discuss matters
related to inflammation.
CYTOKINES IN INFLAMMATION
Cytokines are polypeptides mainly pro-
duced by activated lymphocytes and
macrophages, but can also be produced
by elements of the connective tissue.
According to the cells that produce
them, they take their name: lym-
phokines, monokines, interleukins.
Interleukins are cytokines; the name
comes from Greek language leukós
(white) and kinè (movement).
– Interleukins act as chemical messen-
gers within short distance.
Their main functions is to regulate the
events concerning within the Immune
System functions and the mechanism of
inflammation.
Interleukins are the primary means of
intercellular communication against an
aggression, starting the inflammatory re-
sponse.
There are pro-inflammatory cytokines
and anti-inflammatory cytokines.
At least 33 interleukins are now known.
– Th1 lymphocytes produce pro-in-
flammatory interleukins IL-1α, IL-1β,
IL-2, IL-6, etc.
– Th2 lymphocytes produce anti-in-
flammatory interleukins IL-4, IL-10, etc.
The complex process of inflammation
is regulated partly by the balance be-
tween Th1/Th2 lymphocytes (8-11).
Inflammation is a physiological process
in response to tissue aggression.
The injury causes the release of phos-
pholipids (PL) of the cellular membrane;
PL are transformed by the action of the
enzyme phospholipase A2 into arachi-
donic acid (AA).
The AA, in the presence of the enzymes
cyclooxygenases (COXs), produces
prostaglandins (PGs).
The PGs excite the nerve endings (no-
ciceptors) triggering the sensation of
pain and starting the inflammatory
process where at the site of injury oth-
er mediators are released, such as
bradykinin, histamine, nitric oxide,
interleukins, etc.
– So far it has been demostrated differ-
ent ways starting from the transforma-
tion of the AA:
1 - The way of the 5-lipoxygenase to the
leukotrienes (LT), which are ex-
tremely smooth muscle constrictors
and participate in the processes of
the chronic inflammation, increas-
ing vascular permeability and favor-
ing the edema of the, affected area.
– Low dose aspirin is a specific in-
hibitor of this pathway, while avoid-
ing the action of thromboxanes.
2 - The way of COX-1 (present in the tis-
sues) to PGs E2, with the result of
stimulating pain receptors.
Must be noted that there exists cy-
toprotective PGs mainly preserving
the stomach and kidney functions.
– Here the NSAIDs, are inhibitors of
this way at pharmachological doses,
but do not inhibit the lipoxygenase
pathway and therefore do not elim-
inate, the formation of leukotrienes.
3- The way of COX-2 to PGs (does not
exist in physiological conditions),
mainly related to inflammation.
– Here the conventional NSAIDs are
inhibitors of this pathway when us-
ing high doses or if we use the se-
lective COX-2 inhibitors such as
nimesulide, celecoxib at pharma-
chological doses, which are low
compared to other NSAIDs (12,13).
4 - The way of COX-3 (present only in
the brain and in the heart) involved
with PGs related with fever.
– Here paracetamol has shown spe-
cific inhibition of this pathway
(14,15) (FIG. 1).
5 - There is the inhibition of PGs start-
ing from blocking the phospholi-
pase.
– Here steroids have shown thera-
peutic effectiveness.
6 - Interleukins besides activating COX 2,
stimulate nitric oxide (NO) synthase
enzyme (FIG. 2), increasing the NO
levels starting from the L-arginine
acting as a free radical, as a pro-
inflammatory element of short-term
and local action.
COX-1 COX-2 COX-3
TISSUES
AA
ARACHIDONIC
ACID
BRAIN
HEART
FIG. 1
COX-2 PGs-E2 NO
ACTIVATE
IL-1α,β
FIG. 2
Urgelles-A:Art. Del Giudice 15/12/11 09.27 Pagina 38
3. 39
PHYSIOLOGICAL REGULATING MEDICINE 2011
– Here salicylates reduce the NO lev-
els.
In all these cases we cannot fail to men-
tion the side effects of the convention-
al medicines listed above.
We note the following: IL-1α, IL-1β are
the main factors triggering the inflam-
mation by activating COX-2, PGsE2,
and NO, which are responsable for pro-
voking irritation of nociceptors.
– An anti-inflammatory effect from the
physiological point of view is induced
by the use of Anti-interleukins with oth-
er elements that sinergically achieve ex-
cellent results in the control of inflam-
mation (FIG. 3).
On the other hand, a decrease in β-en-
dorphin is one of the factors that main-
tain neuropathic pain for a prolonged
period in a chronic form.
Finally we can define that when there
is a neuronal irritation at the nocicep-
tor level, the clinical expression is In-
flammation. Pro inflammatory inter-
leukins here are the most important fac-
tors in their evolution, instead of a neu-
ronal irritation in CNS; the disturbance
is at the synaptic level, and is modulat-
ed largerly by the levels of glutamate,
excitatory neurotransmitter, and by β-
endorphin with high analgesic power
where the latter plays an important role
in its control.
In this case the clinical manifestation
is pain (neuropathic).
– Lastly irritation at the cortical level re-
sults clinically as convulsions.
The clinical expression is different, de-
pending on the location in the CNS
where the neural irritation occurs (FIG. 4).
USE OF LOW DOSES FROM THE
ORIGINAL SUBSTANCE
One of the Principles of Physiological
Regulating Medicine (PRM) is to provide
low-dose formulations, intended to avoid
the unwanted side effects usually pro-
duced by the conventional drugs.
Low dose medicine (PRM) are created
mainly with substances from plant,
animal and/or mineral origin and can be
prepared in two main dilutions: Decimal
(X) and Centesimal (C).
The first, when a part of the MotherTinc-
ture (TM) is diluted in 9 parts (total 10
parts); on the other hand in the second
one when a part of the Mother Tincture
is diluted in 99 parts (total 100 parts), re-
peating the procedure until the desired
dilution is obtained, 1X, 2X…or 1C, 2C,
3C, 4C…..and are classified as: Low Di-
lution, between 2X – 8X (10-2
-10-8
) or 1C
PROSTAGLANDINS
Cell membrane
Pain
Inflammation
+ PHOSPHOLIPASE A2
- STEROIDS
INFLAMMATORY
STIMULATION
COX-1
Costitutive
Stomach
Kidney
Gastric mucosal
protection
Calor
Rubor
Tumor
CITOKINES
ANTI INTERLEUKIN 1
NO
Nitric oxide
synthase
-
-
+ Activation
Nerve
ending
Nerve
ending
Blood
capillars
COX-2
Inducible
Physiological
undetectable
conditions
NSAIDs
(Coxib)
NSAIDs Ararachidonic Acid
FIG. 3
FIG. 4
Urgelles-A:Art. Del Giudice 15/12/11 09.27 Pagina 39
4. 40
PHYSIOLOGICAL REGULATING MEDICINE 2011
– 4C, Intermediate Dilution between 9X
– 23X (10-9
-10-23
) or 5C -11C, and High
Dilution above 24X or 12C (>10-24
).
In the first two dilutions (low and inter-
mediate) active molecules are present,
on the contrary in the high dilution
there are no active molecules, for ex-
ceeding the Number of Avogadro.
– Ultimately to be therapeutically effec-
tive dilutions must be complemented
with a dynamic process (SKA = Sequen-
tial Kinetic Activation), consisting in vig-
orous shaking and giving special charac-
teristic to these formulations (16,17).
As regards PGsE2, thromboxanes and
leukotrienes are considered as an “hor-
monal” group more, as such they act lo-
cally, but sometimes act on distant tis-
sues, all of them are involved in many
physiological processes, such as the in-
flammation at concentrations correspon-
ding between 10-9
– 10-12
g (9X-12X or
C4-C6) respectively, which are the dilu-
tions most used in Physiological Regulat-
ing Medicine formulations.
Other studies have shown that low dos-
es interact at the cell nucleus level, while
the effect of high concentrations is most-
ly at the cytoplasmatic level (18).
CONCLUSION AND
RECOMMENDATIONS
Physiological Regulating Medicine has
really filled a gap and allowed to settle
two main problems controlling the in-
flammation and pain, despite the exis-
tence of NSAIDs for more than a cen-
tury, with a biological approach, re-
specting the physiological processes
without the risk of unwanted strong side
effects associated with the conventional
medicines.
It is well known that the release of me-
diators direct of hyperalgesia is second-
ary to the release of interleukins in the
process of inflammation, particularly IL-
1α, IL-1β, responsible for the nocicep-
tors “irritation” through PGs.
Likewise, bradykinin may contribute to
further release of cytokines (inter-
leukins) apparently mediated by TNFα.
NSAIDs have the intention either of
blocking the enzyme cyclooxygenase
(COX-1) or selectively (COX 2), such as
celecoxib; on the other hand nimesulide
inhibits the release of TNFα.
In all cases the anti-inflammatory effect
is achieved by reduction of PGs (12, 13).
Corticosteroids reduce PGs by stimula-
tion of lipocortin. Lipocortin blocks the
activity of phospholipase A2 inhibiting
the release of PGs by decreasing of the
enzyme cyclooxygenase.
On the other hand, salycilates decrease
levels of cytokines by inhibiting the en-
zyme NO synthase, with which lowers
the levels of NO starting from L-argi-
nine.
Additionally, the proposed drugs for
neuropathic pain have tendencially
been tipped for the use of antiepilectic
drugs, antidepressant and others with
the intention of relieving pain by acting
on the CNS at the synaptic level, espe-
cially associated with diabetic neuropa-
thy and fibromyalgia (19, 20). This type
of pain is modulated largely by the lev-
els of neurotransmitters glutamate (exci-
tatory) and β-endorphin (inhibitory),
which own a high analgesic power.
As noted above, we can achieve an an-
ti-inflammatory effect starting from the
utilization of Anti-Interleukins pro-in-
flammatory (Anti-IL-1 and y β), in phys-
iological doses, with the intention of de-
creasing COX-2 levels without the ad-
verse effects of NSAIDs.
With this background we can better un-
derstand the objectives of Physiological
Regulating Medicine, with 11 injectable
ampoules and others oral, to control in-
flammation and pain.
The formulations contain also: Anti-in-
terleukin 1 (Anti IL-1 α and β) and β-
endorphin, with the intention to act at
the physiological level and in the com-
plex process of inflammation and pain.
The 11 PRM injectable products are:
Guna®
-Neck, Guna®
-Thoracic, Guna®
-
Lumbar, Guna®
-Shoulder (Shoulder
and elbow), Guna®
-Hip, Guna®
-Knee,
Guna®
-HandFoot, Guna®
-Ischial, Gu-
na®
-Polyarthritis, Guna®
-Muscle, and
Guna®
-Neural, of which 10 contain β-
endorphin 4C [equivalent to nanograms
(ng)]. Nine products of these contain
Anti IL-1 α and β 4 C [equivalent to
nanograms (ng)], which ascribe an anal-
gesic and anti-inflammatory effect at the
physiological level without the side ef-
fects of medications known (FIG. 5) (21).
Excellent results are obtained in:
bursitis, epicondylitis, fibromyalgia, os-
teoarthritis of the hip and knee, sacroili-
itis, cervical pain, thoracic pain, low
back pain, trigeminal neuralgia, etc.
(22,23,24).
The powerful anti-inflammatory effect
of these products is namely due to sev-
eral factors.
The Anti Il-1α and β low dose inhibit
COX-2, PGs and nitric oxide (NO), ob-
taining the same result of NSAIDs,
steroids and salicylate, respectively, with-
out contraindications or side effects (8).
For over a century medicine doctors
have fought for the noble task of reliev-
ing pain; in this work doctors set out the
worthy results of a Group of scientists
and researchers who have come to-
gether in Italy and brouhgt new ideas
in the control of pain and inflammation,
resulting in an innovative concept
(Physiological Regulating Medicine),
with the same objective to contribute in
the hope of every person to be free of
pain without unwanted side effects.
THE 11 PRM INJECTABLE LOW DOSE
PRODUCTS FOR THE PAIN CONTROL
10 out of 11 contain
β endorphin
9 out of 11 contain
Anti-IL 1α, and Anti-IL 1β
FIG. 5
Urgelles-A:Art. Del Giudice 15/12/11 09.27 Pagina 40
5. 41
PHYSIOLOGICAL REGULATING MEDICINE 2011
– We hope, this is an encouraging start
for the medical community to have
a new method in the relentless battle
against the evil that is inflammation and
pain. í
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