1.1.1 Flashcards

(85 cards)

1
Q

refers to reception of signals in the CNS evoked by the activation of specialized sensory receptors that provide information about tissue damage

A

nociception

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2
Q

receptors in this system are called _____ sensory neurons carrying then ____

A

nociceptors and nociceptive neurons

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3
Q

preventing the action of nociceptors or nociceptive neurons is called

A

antinociception

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4
Q

refers to the perception of an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in these terms

A

pain

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5
Q

preventing pain is called

A

analgesia

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6
Q

pain resulting from normally innocuous stimuli, even without sensory input

A

allodynia

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7
Q

exaggerated response to noxious stimuli, even without sensory input

A

hyperalgesia

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8
Q

noxious insult depolarizes sensory ending membrane to produce action potential

A

transduction

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9
Q

activated by extremes in temperature (<45 and <5 degrees C)

A

thermal

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10
Q

TRP

A

transient receptor potential (TRP) ion channels expressed selectively on nociceptive neurons

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11
Q

activated by ~45C temp and capsaicin

A

TRPV1

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12
Q

activated by cold (<20C) and menthol, may mediate cold sensitivity to chemotherapeutics

A

TRPM8

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13
Q

activated optimally by intense pressure

A

mechanical

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14
Q

activated by high intensity, mechanical, chemical, thermal (both hot AND cold) stimuli

A

polymodal

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15
Q

not normally activated by noxious stimuli, but inflammation and various chemical agents

what might it contribute to

A

silent

may contribute to the emergence to the emergence of hyperplasia and sensitization to pain, features of chronic pain

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16
Q

a voltage gated ion channel: encoded for by the SCN9A gene, not found in CNS. Has been found to be a key player in the perception of nociception by humans

A

Nav 1.7

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17
Q

loss of fxn can cause patient to be sensitive to pain, can also be hyperexcited and hypersensitive to pain

A

Nav 1.7

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18
Q

nociceptors transduce pain, but perception of pain in determine by

A

conducting nerves

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19
Q

small diameter, thinly myelinated, fast. small receptive field

what is the activation associated with

A

A-delta, fast, sharp, pricking pain

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20
Q

small -diameter, unmyelinated, slow, large receptive fields

A

c fibers

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21
Q

larger, faster, carry non-pain touch data

A

A alpha A beta

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22
Q

bradykinin released from

A

damaged tissues

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23
Q

histamine released from

A

immune mast cells

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24
Q

(I + V) relay sensory data to brain
neurons
high density in lamina 1 project directly up to the midbrain and thalamus
wide dynamic range neurons (may be difficult to treat)
lamina V project to brain stem and talamus projection neurons (visceral organ) heart attack, referred pain

A

projection neurons

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25
(lamina 2) relay data to projection neurons, enhancing nociceptive signaling
local excitatory interneurons
26
(lamina 2) regulate/suppress flow of nociceptive information to projection neurons - target of descending inhibitory pathway resulting pain
local inhibitory interneurons
27
activated by ATP released from peripheral cells after tissue damage
ionotropic purinergic receptor, PTX3
28
activated by peptide ligands, sensitize nociceptors
mas-related G protein-coupled receptor (Mrg) family
29
target of lidocaine
voltage-gated sodium ion channels (Nav 1.7)
30
tissue damage and reduced pH sensitize nociceptors, enhancing sensation of pain in response to stimuli by
-sensitizing nociceptors lowers threshold for action potential on nociceptor-bearing neurons -increasing frequency of action potentials, increasing magnitude of pain evoked by superthreshold stimuli -sensitization results from the release of chemical mediators that produce EPSPs
31
results from direct injury to nerves in the peripheral or central nervous system
neuropathic pain -can result from loss of inhibitory control (loss of impairment of interneurons; injured Abeta "sprouting" -may be exacerbated by activation of microglia and their release of inflammatory agents
32
primary sensory neurotransmitter, release triggers mild pain
glutamate
33
where does glutamate work
NMDA receptors
34
____ is stored in small clear vesicles and refilled quickly
glutamate
35
glutamate is used primarily by
both Adelta and C fibers for fast excitatory synaptic potentials
36
a tachykinin, activation of neuroinin receptors excites and prolong EPSPs
substance P
37
all neuropeptides are used ___ fibers for ___ synaptic potentials
C, slow
38
when released neuropeptides are released with glutamate, this triggers
a strong pain
39
local dorsal horn interneurons modulate nociception with
GABA and endorphins -GABA inhibition of projection neurons -endorphins act at all three opioid receptors
40
delta mu gaba
-enkephalin -B endorphin -dynorphin
41
endorphins reduce the perception of pain by
acting at opioid receptors to - decrease Ca, increase K influx -decrease duration of action potential -hyperpolarize dorsal horn neurons -decrease amplitude of evoke EPSP located at key points in the pain modulatory system
42
Gate theory
spinal cord areas that receive messages from pain receptors also receive input from other skin receptors and from axons descending from the brain. these outer inputs sometimes activate inhibitory interneurons, closing the "gates" for the pain messages by inhibiting projection neurons
43
PAG neuron activation releases endorphins, which ____ inhibitory GABA pathway interneurons
inhibits
44
both the ___ and ____ inhibit pain pathways in the spinal cord and brainstem
PAG and medulla
45
processes precise location of pain, relays to somatosensory cortex and consciousness as acute pain (lamina 1 and 5-7)
spinothalamic tract ( major ascending nociceptive pathway)
46
extensive collateral to mesencephalic reticular formation & periaqueductal gray matter, activating descending control (why pain stops) parabrachial neurons project to amygdala, controlling affect (emotion) (lamina 1 and 5)
spinoparabrachial tract (major ascending nociceptive pathway)
47
projection neurons of lamina 7 and 8 ascend with spinothalamic tract, terminating in both reticular formation and thalamus -- large bilateral receptive field: implicated in diffuse, unlocalized pain
spinoreticular tract (major ascending nociceptive pathway)
48
contains axons of projection neurons form lamina 1 5 and 7. projects to hypothalamic nuclei -- influences autonomic control, triggers, neuroendocrine, and cardiovascular response to pain
spinohyothalamic tract (major ascending nociceptive pathway)
49
lateral thalamus sends data to the medial thalamus and from there to the angular cingulate cortex to affect
cognition and mood, associated with the anticipation of pain
50
what are the key components in the descending inhibitory pathway regulating pain
serotonin norepinephrine GABA endorphins
51
descending inhibitory pathway starts in the ___
PAG
52
descending inhibitory pathway is an _____ pathway that synapses with the 5-HT neurons in the ______
excitatory, nucleus raphe magnus (medulla)
53
5-HT neurons project to the spinal cord (from nucleus raphe magnus), making _____connections with neurons in lamina ______ of the dorsal horn, including neurons of the ____ tract that carry noxious stimulation signals
inhibitory 1 2 and 5 spinothalamic
54
5-HT neurons project to the spinal cord (from nucleus raphe magnus), making _____connections with neurons in lamina ______ of the dorsal horn, including neurons of the spinothalamic tract that carry noxious stimulation signals
inhibitory
55
______ released from this pathway (descending inhibitory pathway) inhibits spinothalamic tract input, blocking pain
serotonin
56
_____ in the PAG, inhibits the excitatory pathway. they are constantly firing at a hihg rate and theyre used by the body to suppress that excitatory serotonergic pathway
GABA **THIS EFFECT IN ONLY IN PAG**
57
-initial response to tissue injury, usually preceded the immune response -cell damage associated with inflammation acts on cell membranes to cause the release of lysosomal enzymes, triggering cellular decay, arachidonic acid and eicosanoid synthesis -mediated by release of ______ which have specific overlapping effects
acute inflammation autocoids
58
-occurs when immunologically competent cells are activated in response to either foreign organisms or antigenic agents liberated during the acute or chronic response -outcome beneficial when invading organisms are neutralized -outcome deleterious if it leads to chronic inflammation without resolution of injury
immune inflammation
59
activity of _____ can also produce all the cardinal signs of inflammation (what are they)
peripheral nociceptors calor, rubor, swelling
60
______ and _______ released from c fibers at the site of injury provokes plasma extravasation and edema (__) and vasodilation (__)
substance P and CGRP SP CGRP
61
Spread of histamine and bradykinin to otherwise healthy nearby tissue contributes to secondary _____ and _________
hyperalgesia increased repetitive firing of C fibers
62
_____ acts of mast cells in the vicinity of sensory endings, evoking degranulation and the release of histamine _____ induced vasodilation leads to further inflammation that causes additional liberation of bradykinin
substance p gcrp
63
effect of substance p and cgrp induced hyperalgesia and increased firing of c fibers is to ______ what is this called?
enhance the sensitivity of dorsal horn neurons to nociceptor signals central sensitization
64
gradual enhancement of excitability or "wind up" of dorsal horn neurons thought to involve ___ long term potentiation causes prolonged ____
NMDA-R excitation
65
nerve growth factor and brain derived neurotrophic factor upregulated in inflamed peripheral tissues may also contribute to _____ (blocked by growth factor inhibitors)
persistent pain
66
nerve growth factor and brain-derived neurotrophic factor upregulated in inflamed peripheral tissues may also contribute to _____ (blocked by growth factor inhibitors)
persistent pain
67
sources and primary selective effects of interleukins (IL-1 through 17) GM-CSF
S: macrophages, t lymphocytes p: lymphocyte activation, prostaglandin production
68
sources and primary selective effects of TNF-alpha
s: macrophages p: prostaglandin production
69
sources and primary selective effects of interferons (IFN alpha and beta)
s: macrophages, endothelial cells, t lymphocytes p:many
70
sources and primary selective effects of PDGF
S: macrophages, endothelial cells, fibroblasts, platelets p: fibroblast chemotaxis, proliferation
71
chronic inflammation may produce severe__
disability, including systemic changes decreasing lifespan
72
chronic inflammation destroys bone, cartilage, produces severe pain, may be an autoimmune disease driven by excessive secretion of IL 1b and TNF alpha by t cells
rheumatoid arthritis
73
the interleukins, specifically 1 and TNF alpha both work to produce an increase in ____ production that can produce an acceleration in the _____ and ___responses
prostaglandins inflammatory pain
74
TNF alpha IL 1beta and IL 8liberate prostaglandins and bradykinin to induce _____
hyperalgesia -this is pain
75
tnf alpha IL 1beta and IL6 increase PGE, levels thereby causing the hypothalamus to elevate body temperature through increased heat generation and decreased heat loss
fever
76
increased sleepiness is thought to be IL beta acting through ___ release
prostaglandin
77
____ is thought to be a principal mediator of the response to infection and endotoxins
IL 1
78
______are increasingly important mediators in immunopharmacology with many applications: some may have antiproliferative, antimicrobial, and antitumor effects
cytokines
79
cytokines operate in ___, many different cytokines working sequentially or simultaneously
cascades
80
cytokines mediate their effects via ___ on relevant target cells
cell surface receptors
81
the condition where nerves in the somatosensory, PNS or CNS are diseased or damaged
neuropathy
82
results from this nerve injury, although results vary based on the specific nerves damaged,
neuropathic pain
83
tingling, pricking senation
paresthesia
84
numbness, impairment of senses, especially touch
dyesthesia
85
burning pain
causalgia