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54 Cards in this Set
- Front
- Back
What results from a combination of genetic, biologic,environmental, psychological, andsocial factors, often requiring comprehensive approaches to prevention andmanagement?
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pain
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What factors can lead to persistent pain conditions/amplification?
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genetic polymorphisms combined with environmental factors and psychological stress
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What is the difference in the sensation of pain and chronic clinical pain?
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-sensation of pain = nociception
-chronic clinical pain = 1) pain thatpersists for >3-6months, 2) is oftenprogressive, 3) andthe cause can be difficult to determine |
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What do nociceptors sense?
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potential tissue damage
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What are free-nerve endings in skin or other tissues that actas sensors of noxious physical stimuli interpreted as painsensation?
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nociceptors
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What are specialized heat and cold sensors called?
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thermosensors
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What is nociception?
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-Transductionof Noxious Stimuli by Nociceptors
-conversionof physical energy imposed by noxious stimuli into neuronal action potentials |
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mechanoreceptors
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transduce mechanicalpressure for transmission by primarily by A-delta fibers
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thermoreceptors
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transduce heat andcold for transmission, primarily byC- and A-delta fibers, respectively
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polymodal nociceptors
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combined mechanicaland thermal information is transmitted primarily by C-fibers
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chemoreceptors
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respond to H+ andother noxious chemicals for transmission by C- and A-delta fibers
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pain transduction occurs at...
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free nerve endings
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pain transmission occurs via...
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c and a-delta axons
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pain transduction and transmission process
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-peripheral activation
-receptor potential (merge to become...) -generator potential (long enough duration and great enough strength becomes...) -action potential -central activation -synaptic potential |
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difference in conduction velocity (and myelination) of nociceptive afferent nerve fibers
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-A alpha and A beta pretty rapid
-much slower = C fibers and a-delta fibers -C fibers = unmyelinated -A delta fibers = lightly myelinated |
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What is an area on the skinsurface where adequate stimulus activating the terminal endings of a particularneuron will fire an action potential?
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receptor field?
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What happens when you apply a stimulus outside the receptor field?
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will NOT generate an action potential
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example of two point discrimination
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< 5 mm on the finger tips = great sensitivity
vs. 40 mm on the thigh = lowsensitivity |
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smaller receptive field =
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increased discrimination
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increased receptor density =
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increased sensitivity
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Receptive fields should not be confused with what?
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dermatomes
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Where do nociceptor afferents terminate?
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in the dorsal horn onto spinothalamic tract neurons
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lamina I spinothalamic tract
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-myelinated nociceptors (A-delta fiber)
-unmyelinated (C-fiber)nociceptors |
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lamina V spinothalamic tract
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-polymodal (wide dynamic range) type
-nociceptive afferents(A-delta and C fibers) -low-threshold input fromlarge-diameter myelinated fibers (A-beta) of mechanoreceptorswhen sensitized |
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What is the result of sensory fiber release of substance P?
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-activates and internalizes NK1 receptors on spinothalamic and trigeminothalamic tract cells
-leads to release of glutamate |
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main differences in somatosensation/fine touch pathway and pain/temp pathway (spinothalamic)
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-somatosensation/fine touch:
•1stsynapse and cross in medulla •ascends in dorsalcolumn -pain/temp: •1stsynapse and cross in spinal cord •ascends in ventrolateral white matter |
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somatic and visceral pain pathway
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spinothalamic (anterolateral) tract
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fine, discriminative touch and post synaptic visceral pain pathways
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dorsal column, medial lemniscal system
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Where are collaterals dropped off on the way into the brain, and what is the significance of that?
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reticular formation - for sensitization
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Where does neural processing of sensory input occur?
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at specialized locations in the brain with point to point codingthroughout the pain signaling pathway
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What is the purpose/concept behind a somatotopic map?
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somatosensoryareas in the cortex of the brain are anatomically organized in relation to thesource of information, with larger areas dedicated to parts of the body withgreater discrimination and sensitivity
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What is the result of tissue damage in terms of peripheral sensitization?
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-releaseof ATP, H+,and oxidation product
-draws in mast cells releasing bradykinin (BK),serotonin, andprostaglandins (PG) -which activate and sensitize nociceptors |
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In peripheral sensitization, neuronal release of what producesdilationof peripheral blood vessels and protein/plasma extravasation, resulting in rednessand edema?
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CGRP & Substance P
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2 "steps" of spinal cord central sensitization
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-Activatedprimary afferent endings release glutamate, substance P, and other peptidescentrally
-Glialactivation near the central terminals releasescytokines and oxidants |
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What is the net effect of spinal cord central sensitization?
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Overactivation of theCentral Nerve Endings, Postsynaptic Neurons and Glia
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What is the overall role of dorsal root reflexes in neurogenic inflammation?
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ActionPotentials Generated Both InwardAND Outward (orthodromic& antidromic)
-net effect: MORE PAIN |
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What 3 specific things does neurogenic inflammation increase?
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1) peripheral& central release of transmitters
2) depolarizationof the central and peripheral nerveendings 3) peripheral& central sensitization |
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What generally happens in pre-synaptic inhibition?
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1) Pre-synaptic inhibitory synaptic input
2) Hyperpolarizationof terminal 3) Decreasedsynaptic neurotransmitter release 4) Diminishedsynaptic transmission |
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What 2 specific things happen in pre-synaptic inhibition?
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-Less Ascending Transmission of Pain Signaling
-Less Synaptic Transmission of C and AδFiber Signaling (less info going to thalamus than normal) |
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pre-synaptic excitation
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*More ascending transmission of pain signaling after K+/Cl- Co-Transporters (KCC2, NKCC1) Promote Switch toGABA Excitatory Activation!*
Persistent nociceptor firingincreases GABA, [Cl-]i & outward drive; Cl- reversal potential = Post-synapticDepolarization |
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What may account for referred pain?
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convergence of visceral and somaticafferents on the same spinal neurons
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What is a scenario in which areas of deep and referred pain may occur?
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myocardial infarction and angina
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In the visceral pain system, pain is...
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-Typically silent orfelt as dull ache that is hard to localize.
-But, signals from visceral nociceptorscan be felt as painelsewhere in the body. -The source of the pain can be readily predicted from thesite of referred pain. |
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Visceral and Somatic Sensory Information Convergence Centrally in the Spinal Cord Results in
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specific regional patterns
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What does "the placebo effect" or "endogenous pain control" refer to?
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descending inhibition and action of endogenous opiates
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Generally speaking, how do descending axons from neurons in the brainstem modulate pain?
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byactivating opiate-containing interneurons within the brainstem and dorsal hornof the spinal cord
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What do these“naturalopioid”neuropeptides act to inhibit?
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activation of the spinothalamic tract and other sites
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Opiates reduce what to diminish pain?
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synaptic transmission
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In descending inhibition, brainstem neurons release serotonin, norepinephrine and opioids, activating local inhibitory interneurons & suppressing activity of spinothalamic tract neurons by at least 3mechanisms. What are they?
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Action of Endogenous Opioids & Opiates
1) Opioidsdecreasethe duration of the sensory neuron action potentials by decreasing Ca2+ influx and neurotransmitter release 2) Monoamines and opioids decreasethe postsynapticpotential amplitude 3) Opiates hyperpolarize the membrane of dorsal horn neurons by activating a K+ conductance |
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individual differences in pain perception are due to...
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cognitivesupra spinalfocus, evident as increased cortical activation (ACC, PFC, and insula)
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"pain network"
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CORTICAL AND SUBCORTICAL AREAS ARE INVOLVED IN PAIN PERCEPTION AND PAIN AFFECT
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6 examples of pain as a disease
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1) inflammatory pain - ex) arthritis
2) neuropathic pain - ex) diabetic neurpathy 3) cancer pain - ex) pancreatic cancer 4) orofacial pain - ex) burning mouth 5) headache/migraine 6) central pain |
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inflammatory pain
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1) back pain
2) arthritis -rheumatoid -osteoarthritis 3) vasculitis 4) hypoxia -sickle cell anemia |
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chronic pain conditions
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-neuropathic pain
1) diabetic neuropathy 2) post-herpetic neuralgia 3) phantom pain 4) trigeminal neuralgia -complex regional pain syndrome |