Podcast
Questions and Answers
Which of the following is a characteristic of NSAIDs? (Select one)
COX II inhibitors, such as celecoxib, were developed primarily to:
Which of the following is TRUE regarding paracetamol (acetaminophen)? A) It is primarily an anti-inflammatory drug B) It is classified as an NSAID C) Its mechanism of action is not fully understood, but it may involve COX II selective inhibition D) It has significant gastrointestinal side effects like NSAIDs
Which of the following compounds is an opioid analgesic?
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Which of the following is a major inflammatory mediator that sensitizes pain fibers?
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What is the major difference between COX I and COX II inhibitors?
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Which of the following is NOT an opioid?
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Which of the following is a function of enkephalinase?
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Thiorphan is an active metabolite of which drug?
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Which of the following is a primary use of Thiorphan?
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Which opioid receptor type is NOT part of the classical five types?
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Which of the following opioid receptors is primarily associated with pain control?
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Opioid receptors are linked to which type of G-protein?
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Which of the following is a result of opioid receptor activation?
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Opioid receptors inhibit the opening of which channels to reduce neurotransmitter release?
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Which of the following opioid receptors does morphine primarily act on?
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Which of the following is a common side effect of morphine?
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Which opioid receptor is primarily responsible for euphoria in morphine use?
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Which of the following side effects of morphine can be alleviated with an anti-emetic (dopamine receptor antagonist)?
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What is the half-life (t1/2) of morphine?
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Which of the following is a typical route of administration for morphine?
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Which opioid-related effect is marked by constriction of the pupils and is useful in diagnosing overdose?
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Which of the following is a major mechanism by which morphine causes constipation?
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What is a characteristic feature of morphine administration in terms of its duration of action?
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Which of the following is a primary characteristic of pethidine (meperidine)?
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Codeine is primarily used for which of the following purposes?
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Which opioid agonist is 100 times more potent than morphine?
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Which of the following is true regarding codeine?
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Targin is a combination of which two drugs?
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Which opioid agonist is commonly prescribed alongside paracetamol for its added analgesic effect?
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Which opioid agonist is specifically mentioned for its use in cancer pain management?
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What is the main function of naloxone when combined with oxycodone in Targin?
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Which opioid agonist is primarily used for alleviating mild to moderate pain?
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Which of the following opioids is less likely to be abused due to its low efficacy and inability to be injected easily?
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What is the primary structure of novel opioid nitazines?
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Which of the following is 1000 times more potent than morphine?
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What is the main reason nitazines, such as etonitazene, are not clinically used?
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What class of substances are nitazines, such as etonitazene, also known as?
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Which of the following is true about naloxone? (Select all that apply)
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Why must naloxone be administered repeatedly in cases of opioid overdose?
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Which of the following is an approved use for naltrexone?
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What is a significant side effect of naltrexone?
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Which drug is specifically approved for opioid-induced constipation (OIC)?
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Which of the following statements is true about methylnaltrexone?
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What is the primary mechanism of action of naltrexone in treating opioid use disorder (OUD)?
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Which of the following is a characteristic of nalmefene compared to naloxone and naltrexone?
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What is the main difference between naloxone and naltrexone in terms of their clinical uses?
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Nalmefene acts as a μ (mu) receptor antagonist and a κ (kappa) receptor partial agonist. Which of the following is true about its use?
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Nalmefene is used to treat alcohol use disorder (AUD). What is its mechanism of action in this context?
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Which of the following is true about nalmefene compared to naltrexone? A) Nalmefene has a shorter half-life than naltrexone B) Nalmefene has a longer duration of action than naltrexone C) Nalmefene is used only for opioid overdose, while naltrexone is used for alcohol use disorder (AUD) D) Nalmefene is only available in injectable form, unlike naltrexone
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Which of the following opioid antagonists is a peripherally acting antagonist used to treat opioid-induced constipation?
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What is the main action of xylazine in the central nervous system?
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Xylazine was initially developed as a treatment for:
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Which of the following is a street name for xylazine when used as an additive in opioids like fentanyl?
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Xylazine enhances the effects of opioids. What makes treating overdose with xylazine challenging?
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Why is naloxone ineffective in reversing the effects of xylazine overdose?
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Which of the following is a characteristic of neuropathic pain?
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Gabapentinoids such as pregabalin and gabapentin primarily target which of the following?
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How do gabapentin and pregabalin differ from GABA in terms of their mechanism of action?
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What is the proposed mechanism by which gabapentinoids (pregabalin and gabapentin) relieve neuropathic pain?
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What is the primary mechanism of action of local anesthetics (LAs) in nerve blocks?
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Local anesthetics (LAs) preferentially bind to which state of the sodium channel?
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Which of the following is a common technique for performing a nerve block with local anesthetics?
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In addition to local anesthetics, which of the following can be included in a nerve block injection to enhance its effect?
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Which of the following is a potential adverse effect of nerve blocks with local anesthetics (LAs)?
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What was the main finding of the OPAL study regarding the use of opioids in managing low back/neck pain?
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What is the standard first-line therapy for chronic low back pain, which is an example of nociplastic pain?
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When managing nociplastic pain and if significant pain persists, which of the following therapies is recommended after exercise therapy?
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Which pharmacotherapy is recommended as a second-line treatment for nociplastic pain if exercise and mind-body interventions fail?
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When should NSAIDs be used in the treatment of chronic low back pain?
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What is the first choice of drug for patients with chronic low back pain who are non-responsive to NSAIDs?
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What type of drug is Duloxetine?
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Which of the following is a significant risk associated with Duloxetine, especially in young people?
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Tramadol is a racemic mixture of which two enantiomers?
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Which of the following actions does the (+) enantiomer of tramadol have?
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Which of the following is a potential risk of tramadol use?
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Amadol has a unique mechanism of action that involves which of the following?
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What is the risk associated with tramadol use in combination with other serotonergic drugs?
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What is the primary cause of neurogenic inflammation?
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Which neuropeptide is primarily involved in neurogenic inflammation?
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What is the classic example of a condition involving neurogenic inflammation?
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Which of the following describes the structure of the CGRP receptor complex?
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What is the function of the receptor coupling protein (RCP) in the CGRP receptor complex?
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Which of the following is a commonly used first-line treatment for acute migraine?
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Which class of drugs is used to treat acute migraine by acting as 5-HT1 agonists?
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Which of the following is NOT a triptan used for migraine treatment?
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Which of the following medications is a 5-HT1 agonist that is effective for treating acute migraine but should not be used in patients with coronary artery disease?
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Which of the following medications is a CGRP antagonist used in the acute treatment of migraines?
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Which of the following is a 5-HT1F receptor agonist used for acute migraine treatment?
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What is the primary role of anti-emetics in the treatment of acute migraines?
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Which of the following treatments is commonly used for the prophylaxis of frequent migraines?
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Which medication used in migraine prophylaxis is an antidepressant?
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Which medication is used in migraine prophylaxis but is specifically approved for chronic migraines?
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Which of the following is an anti-CGRP receptor antibody used in migraine prevention?
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What is the main mechanism of action of anti-CGRP antibodies in preventing migraines?
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Which of the following types of pain is caused by damage to the nervous system?
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Which of the following is an example of nociplastic pain?
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Which type of pain results from altered nociception without clear activation of peripheral nociceptors?
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Which of the following best describes mixed pain?
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Which of the following is a characteristic of acute pain?
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Chronic pain is typically defined as pain lasting for more than how long?
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Which of the following is an example of chronic secondary pain?
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Which of the following refers to an increased sensitivity to painful stimuli?
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Which of the following terms describes pain in response to a non-noxious stimulus?
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Which of the following factors can influence the subjective experience of pain?
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Which of the following is characterized by a 'burning' sensation in the skin?
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Which of the following best describes Aδ fibres?
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Which of the following is true about C fibres?
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Which pain fibres are responsible for transmitting dull, secondary pain and emotional responses?
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Where do Aδ fibres relay information after detecting noxious stimuli?
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Which pain fibres are involved in triggering an immediate withdrawal reflex?
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Which part of the brain is involved in processing the emotional response to pain transmitted by C fibres?
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C fibres are involved in transmitting pain signals to which of the following structures?
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Where do Aδ fibres synapse in the spinal cord?
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Where do C fibres synapse in the spinal cord?
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Which of the following accurately describes the pathway of primary afferent nociceptive neurons (Aδ and C fibers)?
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What happens after the second-order neurons in the spinal cord synapse with primary afferent neurons (Aδ and C fibres)?
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Which structure do third-order neurons in the spinothalamic tract project to?
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Where is the tract of Lissauer located, where primary afferent nociceptive neurons ascend or descend?
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Substance P primarily acts on which receptor to modulate pain transmission?
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Which of the following molecules is involved in pain modulation through endocannabinoid (eCB) pathways?
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According to the gate control theory of pain modulation, what role do large-diameter Aα and Aβ fibers play?
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In the gate control theory, what is the function of interneurons in the dorsal horn's substantia gelatinosa?
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Which neurotransmitters are released by stimulated interneurons in the substantia gelatinosa to modulate pain?
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Which of the following is the origin of descending pain-modulating pathways?
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What is the role of descending analgesic pathways in pain modulation?
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Which of the following neurotransmitters are involved in descending pain modulation pathways?
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How do endocannabinoids mediate their analgesic effect?
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Which cannabinoid receptors are involved in pain modulation via endocannabinoids?
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Where are CB1 receptors, involved in pain modulation, primarily expressed?
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CB2 receptors, involved in pain modulation, are predominantly expressed in:
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In the gate control theory, how do non-painful somatic signals inhibit pain transmission?
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What best describes the process of pain modulation?
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Which fibers are primarily responsible for inhibiting pain transmission according to Gate Control Theory?
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Which neurotransmitters are released by interneurons to inhibit pain transmission?
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Which key structure is involved in descending pain modulation?
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Which neurotransmitter is NOT typically involved in descending pain modulation pathways?
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How do endogenous opioids, like endorphins, exert their analgesic effect?
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Which receptors do endocannabinoids, like anandamide, bind to for pain modulation?
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What function do descending analgesic pathways primarily serve in pain modulation?
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What is the primary effect of the activation of CB1 receptors in pain modulation?
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Which statement is true regarding the role of Aα and Aβ fibers in the Gate Control Theory?
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How do endogenous opioids function in the context of pain modulation?
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Which area of the brain is responsible for initiating descending analgesic pathways?
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What is the function of endocannabinoids like anandamide in pain modulation?
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Which neurotransmitter plays a role in inhibiting pain signals in the descending pain modulation pathway?
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What is the primary function of the substantia gelatinosa in pain processing?
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Which pain fibers are primarily responsible for transmitting sharp, localized pain?
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What is a crucial action of descending analgesic pathways in the context of pain modulation?
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What is the primary mechanism by which CB1 receptor activation influences pain perception?
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Study Notes
Pain Modulation
- Pain modulation is the alteration of pain perception through various physiological mechanisms.
Gate Control Theory
- The Gate Control Theory suggests that pain transmission in the spinal cord can be modulated by the interaction of different types of nerve fibers.
- Aα and Aβ fibers, which transmit non-painful sensory input, can inhibit pain transmission by stimulating interneurons in the spinal cord.
- Interneurons release neurotransmitters, such as GABA and endogenous opioids, to inhibit pain transmission.
- C fibers, which carry primary pain signals, are inhibited by the activity of Aα and Aβ fibers.
Descending Pain Modulation
- The descending analgesic pathways originate in the brain, particularly in the peri-aqueductal gray (PAG).
- These pathways release neurotransmitters, such as serotonin, endorphins, and noradrenaline, to inhibit pain at the spinal cord level.
- These neurotransmitters work by activating opioid receptors on afferent pain fibers, inhibiting the release of pain-related neurotransmitters like substance P, and modulating the activity of interneurons in the spinal cord.
Role of Neurotransmitters in Pain Modulation
- Endorphins: Endogenous opioids that activate opioid receptors on afferent pain fibers, reducing pain transmission.
- GABA: Inhibitory neurotransmitter that reduces pain transmission by inhibiting the release of excitatory neurotransmitters.
- Serotonin: Neurotransmitter released by descending pain modulation pathways to inhibit pain transmission at the spinal cord level.
- Noradrenaline: Neurotransmitter involved in descending pain modulation pathways, contributing to pain reduction.
- Endocannabinoids: Neurotransmitters, such as anandamide, that bind to CB1 and CB2 receptors to modulate pain.
- Glutamate: Excitatory neurotransmitter involved in pain transmission, but not typically involved in descending pain modulation pathways.
- Substance P: Neurotransmitter involved in transmitting pain signals from the periphery to the spinal cord.
Key Structures Involved in Pain Modulation
- Thalamus: Relay center for sensory information, including pain, to the cerebral cortex.
- Spinal cord interneurons: Interneurons in the substantia gelatinosa modulate pain transmission between first and second-order neurons.
- Peri-aqueductal gray (PAG): Brain region responsible for initiating descending analgesic pathways.
- Substantia Gelatinosa: Region in the spinal cord where pain signals are modulated.
Pain Fibers
- Aα and Aβ fibers: Large, myelinated nerve fibers that transmit non-painful sensory information, playing a role in inhibiting pain transmission.
- Aδ fibers: Small, myelinated nerve fibers that transmit sharp, localized pain.
- C fibers: Small, unmyelinated nerve fibers that transmit dull, aching pain.
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Description
Test your knowledge on the key characteristics of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). This quiz will challenge you to select the correct traits that define these medications. Ideal for students in pharmacology or healthcare fields.