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Pain > Acute pain > Flashcards

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
Q

Glutamate receptors

A

NMDA, AMPA, kainite, mGluRs

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26
Q

Inhibitory Neurotransmitters

A

Glycine, GABA, Enkephalin, Serotonin, Norepinephrine

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27
Q

Glycine receptors

A

Chloride linked (GlyR)

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28
Q

GABA receptors

A

GABA-A, B, C

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29
Q

Enkephalin receptors

A

Mu & delta

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30
Q

Serotonin receptors

A

5-HT (1-3)

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31
Q

Norepinephrine receptors

A

Alpha-2 adrenergic

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32
Q

Peripheral tissues different approach to peripheral pain transduction

A

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

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33
Q

Substance P

A

Peptide found & released from peripheral afferent nociceptor C-fibers = slow & chronic pain

Acts via g-linked protein neurokinin-1 receptor

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34
Q

Neurokinin-1 receptor activation

A

Vasodilation, extravasation of plasma proteins, degranulation of mast cells, sensitization of the stimulated sensory nerve

35
Q

Glutamate

A

Major excitatory NT released in CNS from = A-delta & C-primary afferent nerve fibers

36
Q

Bradykinin

A

Released during inflammatory process
-Increased sensitivity = algesic
-Direct stimulating effects on peripheral nociceptors B1 & B2 bradykinin receptors

37
Q

Histamine

A

-Released from mast cell granules, basophils, and PLTs
-Substance P causes this release
-Potentiates bradykinin induced pain

38
Q

5-hydroxytryptamine (Serotonin)

A

-Stored & released from PLTs after tissue injury
-Algesic (increased sensitivity) effects on peripheral nociceptors
-Potentiates bradykinin induced pain

39
Q

Prostaglandin (PGs) thromboxanes & leukotrienes

A

-Synthesized from COX 1 & 2
-Metabolite of arachidonic acid
-Chronic pain
-Hyperalgesia

40
Q

Cytokines

A

-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
Q

Calcitonin gene-related peptide (CGRP)

A

-Released from peripheral afferent nociceptor C-fibers
-Local cutaneous vasodilation

42
Q

Which drugs work at Transduction

A

-Local anesthetics in spinals & epidurals
-NSAIDs
-Steroids
-Opioids

43
Q

Which drugs work at Transmission

A

-Local anesthetics in PNBs, TCAs, steroids

44
Q

Which drugs work at Modulation

A

-NMDA antagonists
-Opioids
-Alpha 2 agonists
-NSAIDs
-SNRIs
-TCAs

45
Q

Which drugs work at Perception

A

-General anesthetics
-Opioids
-NMDA antagonists
-Alpha 2 agonists
-SNRIs
-TCAs

46
Q

Acute pain increases what?

A

Neuroendocrine responses primarily by the SNS which increases release of catecholamines from SNS & Adrenal glands w/ cortisol

Increases myocardial demand & myocardial O2 consumption

47
Q

NSAIDs

A

Inhibit COX & prevent the conversion of arachidonic acid to PG where PGs respond to peripheral & central nociceptors in the inflammatory process

48
Q

Acetaminophen

A

-Reduces PG synthesis (unknown how)
-Inhibits COX activity but only in the CNS

49
Q

Opioids

A

-Bind & activate g-protein coupled opioid receptors both peripherally & in the CNS
-Mu, Delta, Kappa

50
Q

Kappa positive effects of receptor

A

Spinal analgesia

51
Q

Mu positive effects of receptor

A

Analgesia & euphoria

52
Q

Delta positive effects of receptor

A

Dopamine release

53
Q

Which opioid receptor causes pruritis

A

Mu

54
Q

Which opioid receptor causes dysphoria & dependence

A

Kappa

55
Q

Which opioid receptor has psychomimetic effects & dysphoria

A

Delta

56
Q

What opioid receptor(s) does morphine work on

A

Mu & Delta

57
Q

What opioid receptor(s) does hydromorphone work on

A

Primarily Mu agonist but had significant kappa activity (spinal analgesia)

58
Q

What opioid receptor does oxycodone significantly agonize?

A

Kappa = highly addictive

59
Q

What opioid receptors do oxymorphone agonize

A

Mu&raquo_space;> delta&raquo_space; Kappa

60
Q

What opioid receptors do hydrocodone agonize

A

Mu w/ some delta

61
Q

What opioid receptor(s) does methadone agonize

A

Mu agonist with NMDA antagonist activity

62
Q

What do alpha-2 adrenergic agonists exhibit?

A

Sedative, anxiolytic, analgesic, sympatholytic, vagomimetic effects

63
Q

What receptors do Clonidine (Catapress) work on and their ratio

A

-Central acting, Alpha 2 & Alpha 1
-400:1
-Sedation, bradycardia, hypotension

64
Q

Precedex receptors & ratio

A

Highly selective Alpha-2 (1600:1)

65
Q

What is important about the pediatric pain pathways and why?

A

Maturation of the descending pathway comes before the ascending neural pathway = pain perception & stress response may be more exaggerated

66
Q

Acute pain with chronic pain affects receptors how

A

Various degrees of tolerance & receptor downregulation intraoperatively

67
Q

3 Subdivisions of Painful Stimulation

A

Progressively gets worse to the end result of nerve damage.
-Painful stimulation WITHOUT tissue damage
-Tissue damage WITHOUT nerve damage
-Nerve damage

68
Q

Evolution of Chronic Pain (Wind-up)

A

-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
Q

Wind-up process

A

-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
Q

3 Anatomical regions that are associated with every pain response

A

-Peripheral, Spinal, Cerebral Areas

71
Q

Peripheral Chronic Pain Pathway Changes

A

-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
Q

Spinal Chronic Pain Pathway Changes

A

Galanin (neuropeptide) may be involved with chronic pain issues

73
Q

All pain experiences have a ________ Component

A

Psychological component

74
Q

Inflammatory chronic pain

A

-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
Q

Neuropathic Chronic Pain

A

-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
Q

Painful diabetic peripheral neuropathy pain

A

Caused by damage to small unmyelinated nerve fibers
-Directly r/t glycemic control
-Tx = TCAs, SNRIs, anticonvulsants

77
Q

Chronic Postsurgical Pain (CPSP)

A

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
Q

Postherpetic Neuralgia (PHN)

A

-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
Q

Complex Regional Pain Syndrome (CRPS)

A

-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
Q

Type 1 CRPS

A

No distinct nerve lesions (reflex sympathetic dystrophy)

81
Q

Type 2 CRPS

A

Distinct nerve lesions present (causalgia)

82
Q

CRPS treatment

A

Bisphosphonates, sympathetic nerve blocks, spinal cord stimulator
-Multidisciplinary approach w/ medical management, PT, & psychologist = most effective

83
Q

Myofascial Pain Syndrome (MPS)

A

-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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