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Acute pain Flashcards

1
Q

Algesia

A

increased sensitivity to pain (more sensitive to pain)

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2
Q

Algogenic

A

Pain producing

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3
Q

Allodynia

A

A normally non-harmful stimulus is perceived as painful

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4
Q

Analgesia

A

Absence of pain in the presence of a normally painful stimulus

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5
Q

Dysesthesia

A

Unpleasant painful abnormal sensation, whether evoked or spontaneous

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6
Q

Hyperalgesia

A

Hightened response to a normally painful stimulus

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7
Q

Neuralgia

A

Pain in the distribution of peripheral nerves

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8
Q

Neuropathy

A

Abnormal disturbance in the function of a nerve

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9
Q

Paresthesia

A

Abnormal SENSATION whether spontaneous or evoked

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10
Q

Opioid-induced hyperalgesia

A

Paradoxical increase in patient’s pain severity & decrease in pain tolerance demonstrated by patients who received intraoperative opioid infusion

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11
Q

Nociceptive pain

A

Specific nociceptors are stimulated that can be somatic or visceral

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12
Q

Nonnociceptive “Neuropathic Pain”

A

caused by damage to peripheral or central neural structures that result in abnormal processing of painful stimulus. CNS dysfunction that allows for spontaneous excitation in a chronic pain state

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13
Q

Inflammatory Pain

A

Sensitization of nociceptive pathways from multiple mediators being released at the site of tissue inflammation but there is NO Neural Injury

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14
Q

4 Processes of Somatic Nociceptive Pain

A

Transduction, Transmission, Perception, Modulation

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15
Q

Transduction

A

Transformation of a noxious stimulus (chemical, mechanical, thermal) into an action potential.

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16
Q

What are the peripheral nociceptors that conduct noxious stimuli to the dorsal horn of the spinal cord during the Transduction process

A

A-delta & C-fibers

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17
Q

Transmission

A

Process where an action potential is conducted from the periphery (site of pain) to the CNS where multiple pathways carry the noxious stimuli to the brain

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18
Q

Spinothalamic tract

A

Afferent neurons, Terminate in Rexed Laminae 1, 2, 5

DRG of SC, Ascend & Descend several spinal segments via the Tract of Lissauer.

Grey Matter of dorsal horn

Synapse w/ 2nd order neurons & cross midline through the anterior commissure

Ascend in anterolateral pathway of spinothalamic tract to thalamus

Synapse w/ 3rd order neurons sending projections to the cerebral cortex

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19
Q

2nd order neurons

A

Nociceptive neurons that receive input only from primary A-delta & C-fibers

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20
Q

Wide-dynamic range (WDR) neurons

A

Type of 2nd order neurons that receives input from BOTH nociceptive & nonnociceptive (A-beta & A-alpha) primary afferents

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21
Q

Perception

A

occurs once the signal is recognized by various areas of the brain (4 place) = amygdala, somatosensory areas of the cortex, hypothalamus, anterior cingulate cortex

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22
Q

Modulation

A

alters neural afferent activity along the pain pathway and can suppress or enhance pain signals

-Occurs through inhibitory interneurons & descending efferent pathways via the dorsolateral funiculus (DLF) = synapse & suppress pain transmission to the brain stem & spinal cord dorsal horn

Descending dorsolateral efferent pathway is activated by noxious stimulus

Actional potential arrives at substantia gelatinosa via DLF = activate Enkephalin-releasing neurons

-Enkephalin binds to opiate receptors on pre-synaptic 1st order or post-synaptic 2nd order afferent fibers = decrease substance P release

Decreasing substance P release = suppresses ascending pain transmission

-The descending efferent modulation pathways from the brain are considered the body’s analgesia system or pain control system

-Many pain-modulating neurotransmitters come into play here

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23
Q

Excitatory Neurotransmitters

A

Substance P & Glutamate

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24
Q

Substance P receptors

A

Neurokinin 1 & neurokinin 2

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25
Glutamate receptors
NMDA, AMPA, kainite, mGluRs
26
Inhibitory Neurotransmitters
Glycine, GABA, Enkephalin, Serotonin, Norepinephrine
27
Glycine receptors
Chloride linked (GlyR)
28
GABA receptors
GABA-A, B, C
29
Enkephalin receptors
Mu & delta
30
Serotonin receptors
5-HT (1-3)
31
Norepinephrine receptors
Alpha-2 adrenergic
32
Peripheral tissues different approach to peripheral pain transduction
Release of chemical mediators from inflammatory response & release of neurotransmitters from nociceptive nerve endings Stimulate peripheral nociceptors which cause an influx of Na ions for depolarization and the subsequent efflux of K ions for repolarizations = action potential generated which then generates a pain impulse
33
Substance P
Peptide found & released from peripheral afferent nociceptor C-fibers = slow & chronic pain Acts via g-linked protein neurokinin-1 receptor
34
Neurokinin-1 receptor activation
Vasodilation, extravasation of plasma proteins, degranulation of mast cells, sensitization of the stimulated sensory nerve
35
Glutamate
Major excitatory NT released in CNS from = A-delta & C-primary afferent nerve fibers
36
Bradykinin
Released during inflammatory process -Increased sensitivity = algesic -Direct stimulating effects on peripheral nociceptors B1 & B2 bradykinin receptors
37
Histamine
-Released from mast cell granules, basophils, and PLTs -Substance P causes this release -Potentiates bradykinin induced pain
38
5-hydroxytryptamine (Serotonin)
-Stored & released from PLTs after tissue injury -Algesic (increased sensitivity) effects on peripheral nociceptors -Potentiates bradykinin induced pain
39
Prostaglandin (PGs) thromboxanes & leukotrienes
-Synthesized from COX 1 & 2 -Metabolite of arachidonic acid -Chronic pain -Hyperalgesia
40
Cytokines
-Released d/t tissue injury from immune & nonimmune cells from the inflammatory response -Interleukin-1 Beta, IL-6, TNF-Alpha -Can increase PGs which would excite & sensitize nociceptive fibers
41
Calcitonin gene-related peptide (CGRP)
-Released from peripheral afferent nociceptor C-fibers -Local cutaneous vasodilation
42
Which drugs work at Transduction
-Local anesthetics in spinals & epidurals -NSAIDs -Steroids -Opioids
43
Which drugs work at Transmission
-Local anesthetics in PNBs, TCAs, steroids
44
Which drugs work at Modulation
-NMDA antagonists -Opioids -Alpha 2 agonists -NSAIDs -SNRIs -TCAs
45
Which drugs work at Perception
-General anesthetics -Opioids -NMDA antagonists -Alpha 2 agonists -SNRIs -TCAs
46
Acute pain increases what?
Neuroendocrine responses primarily by the SNS which increases release of catecholamines from SNS & Adrenal glands w/ cortisol Increases myocardial demand & myocardial O2 consumption
47
NSAIDs
Inhibit COX & prevent the conversion of arachidonic acid to PG where PGs respond to peripheral & central nociceptors in the inflammatory process
48
Acetaminophen
-Reduces PG synthesis (unknown how) -Inhibits COX activity but only in the CNS
49
Opioids
-Bind & activate g-protein coupled opioid receptors both peripherally & in the CNS -Mu, Delta, Kappa
50
Kappa positive effects of receptor
Spinal analgesia
51
Mu positive effects of receptor
Analgesia & euphoria
52
Delta positive effects of receptor
Dopamine release
53
Which opioid receptor causes pruritis
Mu
54
Which opioid receptor causes dysphoria & dependence
Kappa
55
Which opioid receptor has psychomimetic effects & dysphoria
Delta
56
What opioid receptor(s) does morphine work on
Mu & Delta
57
What opioid receptor(s) does hydromorphone work on
Primarily Mu agonist but had significant kappa activity (spinal analgesia)
58
What opioid receptor does oxycodone significantly agonize?
Kappa = highly addictive
59
What opioid receptors do oxymorphone agonize
Mu >>> delta >> Kappa
60
What opioid receptors do hydrocodone agonize
Mu w/ some delta
61
What opioid receptor(s) does methadone agonize
Mu agonist with NMDA antagonist activity
62
What do alpha-2 adrenergic agonists exhibit?
Sedative, anxiolytic, analgesic, sympatholytic, vagomimetic effects
63
What receptors do Clonidine (Catapress) work on and their ratio
-Central acting, Alpha 2 & Alpha 1 -400:1 -Sedation, bradycardia, hypotension
64
Precedex receptors & ratio
Highly selective Alpha-2 (1600:1)
65
What is important about the pediatric pain pathways and why?
Maturation of the descending pathway comes before the ascending neural pathway = pain perception & stress response may be more exaggerated
66
Acute pain with chronic pain affects receptors how
Various degrees of tolerance & receptor downregulation intraoperatively
67
3 Subdivisions of Painful Stimulation
Progressively gets worse to the end result of nerve damage. -Painful stimulation WITHOUT tissue damage -Tissue damage WITHOUT nerve damage -Nerve damage
68
Evolution of Chronic Pain (Wind-up)
-Cyclical response that leads to an abnormal pain response & chronic pain sensation -Chronic discharge of neurons = overwhelms the inhibitory system neuropathways -Preventing wind up is critical to preventing chronic pain -Treat underlying cause of pain & not ignore the pain symptoms
69
Wind-up process
-Chronic repetitive stimulation -Increased cellular calcium (Ca2+) -Release of inflammatory substance -Cyclooxygenase production -Synthesis of prostaglandins (responsible for reduction of inhibition -Increased neurologic pathways excitability - Hyperalgesia = leads back to #1
70
3 Anatomical regions that are associated with every pain response
-Peripheral, Spinal, Cerebral Areas
71
Peripheral Chronic Pain Pathway Changes
-Magnesium is displaced so running a magnesium sulfate infusion helps this problem -NMDA receptors are activated & greatly contribute to the peripheral pathway -Calcium enters the cell -Exaggerated release of Substance P & excitatory amino acids -
72
Spinal Chronic Pain Pathway Changes
Galanin (neuropeptide) may be involved with chronic pain issues
73
All pain experiences have a ________ Component
Psychological component
74
Inflammatory chronic pain
-Tissue damage causes neurochemical responses -Both local & sensory (PNS + CNS) systems -Substance P specifically associated w/ inflammatory pain -Histamine + bradykinin + substance P -Inflammatory mediators create an action potential
75
Neuropathic Chronic Pain
-Nerves injured & pain radiates along a dermatome supplied by that nerve -Hyperalgesia + Allodynia -Persistent pain -NOT adequately managed w/ NSAIDs = use gabapentin or lyrica (pregabalin) -A & C fibers are dysfunctional
76
Painful diabetic peripheral neuropathy pain
Caused by damage to small unmyelinated nerve fibers -Directly r/t glycemic control -Tx = TCAs, SNRIs, anticonvulsants
77
Chronic Postsurgical Pain (CPSP)
Peristent pain state, >2 mo postoperatively, cannot be explained by other causes -Most common from= thorocatomy, thoracic penetration, amputations, inguinal hernias -Preventative preoperative methods to reduce central sensitization = Regional, preop anti-inflammatories, ketamine
78
Postherpetic Neuralgia (PHN)
-Virus lies dormant in DRG -Vesicular rash typically limited to 1 or 2 dermatomes on one side of body -Leads to damage of small unmyelinated nerve fibers = severe persistent pain -Severe stabbing pain & allodynia -TCAs & anticonvulsants 1st treatment
79
Complex Regional Pain Syndrome (CRPS)
-Localized pain disorder within 4-6 weeks after trauma to an extremity -Characteristics of neuropathic pain w/ S&S of dysfunctional SNS = swelling, edema, erythema, bluish discoloration, temperature asymmetry when compared to contralateral limb -Focus on aggressive PT/OT -Must have at least 1 symptom in the 3/4 categories = sensory, vasomotor, sudomotor/edema. motortrophic -Must have at least 1 symptom in the 2/4 categories at time of evaluation
80
Type 1 CRPS
No distinct nerve lesions (reflex sympathetic dystrophy)
81
Type 2 CRPS
Distinct nerve lesions present (causalgia)
82
CRPS treatment
Bisphosphonates, sympathetic nerve blocks, spinal cord stimulator -Multidisciplinary approach w/ medical management, PT, & psychologist = most effective
83
Myofascial Pain Syndrome (MPS)
-Regional presence of spots of tenderness & hyperirritability in muscles or fascia w/ referred pain -Tx w/ trigger point injections & PT for treatment

Pain (1 decks)

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