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Priniclpes Of Anesthesia > Exam 3 - acute pain > Flashcards

Exam 3 - acute pain Flashcards

1
Q

Definition of pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

a physiological, emotional and behavioral experience

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2
Q

algesia

A

Increased sensitivity to pain

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3
Q

algogenic

A

pain producing

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4
Q

allodynia

A

a normally nonharmful stimuli is perceived as painful

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5
Q

analgesia

A

absence of pain in presence of normally painful stimuli

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6
Q

dysesthesia

A

unpleasant painful abnormal sensation, whether evoked or spontaneous

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7
Q

hyperalgesia

A

a heightened response to a normally painful stimulus

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8
Q

Neuralgia

A

pain in distribution of a peripheral nerve

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9
Q

Neuropathy

A

Abnormal disturbance in the function of nerves

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10
Q

Paresthesia

A

abnormal sensation whether spontaneous or evoked

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11
Q

fibromyalgia has

A

allodynia

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12
Q

herpes zoster has

A

neuralgia

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13
Q

surgical incision has

A

algogenic

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14
Q

Nociceptive is

A

tissue injury

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15
Q

non nociceptive neuropathic is

A

nerve injury

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16
Q

nociceptors detect

A

acute pain to tissue injury and chronic pain from swelling or injury

temp, pressure, stretch

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17
Q

Nociceptive pain can be (3)

A
  1. somatic
  2. visceral
  3. radicular
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18
Q

Somatic pain

A

identifiable location as a result of tissue causing release of chemicals from injured cells

localized, sharp in nature

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19
Q

Visceral pain definition and associations

A

diffuse, can be referred

dull cramping/squeezing or vague

associated with autonomic reflexes (nausea, vomiting, diarrhea)

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20
Q

Radicular pain description and cause

A

irritation of the nerve root

numbness, weakness, tingling, pins and needles

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21
Q

Neuropathic pain description and cause

A

caused by damage to peripheral or central neural structures

burning, tingling or shocl like

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22
Q

Non-nociceptive pain

A

Chronic - neuropathic or idopathic

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23
Q

Idiopathic pain description

A

Psychogenic pain associated with chronic pain

No apparent cause

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24
Q

Phases of Nociceptive pain (4)

A
  1. Transduction
  2. transmission
  3. Perception
  4. Modulation
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25
Q

transduction

A

Transmission of noxious stimuli into action potential

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26
Q

transmission

A

Pain message moves to spine and on to brain (signal enters brainstem or thalmus and extends to cerebral cortex)

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27
Q

A-delta and C fibers are

A

noxious stimulus pathways to the brain

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28
Q

A-gamma and C fiber are (afferent or efferent)

A

afferent

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29
Q

A-delta and C fiber pathway:

A

found in dorsal root ganglion –> dorsal cord –>divide and ascend in the tract of Lissauer

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30
Q

A-delta and C fibers decend:

A

1-3segmetns of tract of Lissauer

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31
Q

Perception includes (3)

A
  1. attention
  2. expectation
  3. interpretation
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32
Q

Modulation roles (4)

A
  1. Brain interacts with nerves to modulate or alter pain experience
  2. adjust the intensity and duration
  3. involves release of chemicals (i.e. endorphins and serotonin
  4. decrease transmission of pain signals
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33
Q

Modulation stages

A
  1. Periphery
    2.Dorsal horn
  2. Descending inhibitory pathway
  3. Cortical
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34
Q

Periphery stage of modulation

A

descending dorsolateral efferent pathway is activated

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35
Q

Primary afferent fibers:

A

A-delta and C fibers

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36
Q

A delta fiber pathway: Speed, characteristics and pain type

A

fast-sharp,peircing pain
large myelinated

(fast bunny)

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37
Q

A delta fibers terminate in

A

Rexed’s lamina I, V

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38
Q

C fibers pathway: speed, characteristics, pain type

A

Dull, chronic pain. Dull, aching, burning
small unmyelinated

slow turtle

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39
Q

C fibers terminate in

A

lamina II and III

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40
Q

Dorsal horn modulation stage

A

nural impulses modulated in spinal cord (dorsal horn) by “gatelike” process before traveling to CNS

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41
Q

Gate theory

A

APs are transmitted that inhibit inhibitory neuron

projection neuron is activated opening the gate

*think of pressure before IV stick

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42
Q

Modulation stage 3: Descending inhibitory pathway controls the

A

ascending pathway

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43
Q

Modulation stage 3: Descending inhibitory pathway releases _____ and inhibits ____

A

releases serotonin and noradrenergic neuron and inhibits substance P

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44
Q

Inhibitory nerotransmitters in descending pathway:

A

-enkephalin
-glycine
-norepinephrine
-serotonin
-GABA

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45
Q

Enkephalin

A

binds to opiate receptors on pre-synaptic first order neurons and post-synaptic second order afferent fibers

=decrease substance P release = suppress ascending pain transmission

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46
Q

Stage 4 modulation: Cortical
role

A

Pain learning and memory

remembers “that hurt”

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47
Q

central sensitization

A

neural plasticity that occurs in CNS

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48
Q

central sensitization occurs by

A

Repetitive stimulation of injury and repetitive firing in dorsal horn nociceptorsce

49
Q

central sensitization can cause

A

activation of lower non-nociceptive mechanoreceptors to trigger a pain response - chronic pain

50
Q

Two major ascending pain pathways:

A
  1. Direct lateral spinothalmic
  2. Indirect medial spinoreticulothalmic
51
Q

Indirect medial spinoreticulothalamic pathway pain

A

deep somatic and visceral (dull)

52
Q

Lateral spinothalmic pathway pain

A

sharp

53
Q

Second order neuron location

A

dorsal horn - cross midline of spinal cord –>thalmus

54
Q

Third order neuron location

A

Thalmus –>specific area of somatosensory cortex

55
Q

mediators are

A

released from inflammatory cells/injured tissue

56
Q

Mediator categories:

A
  1. vasoactive amines
  2. peptides
  3. Eicosanoids
57
Q

Vasoactive amiens:

A
  1. HIstamine
  2. Serotonin
58
Q

Peptide amines:

A
  1. bradykinen
59
Q

Eicosanoids:

A
  1. Thromboxane
  2. Leukotrienes
  3. Prostaglandins
60
Q

Bradykinen role and cause

A

stimulates peripheral nociceptors

causes algesia (increased sensitivity to pain)

61
Q

Histamine role and cause

A

maintain acute-phase response

vasodilation and edama

62
Q

Arachidonic acid role and examples

A

important substrate in synthesis of active mediators of inflammation (such as cox 1 and 2)

ex: prostiglandins and thromboxanes

63
Q

Cyclooxygenase (aka cox 1) is secreted in

A

vascular endothelium, stomach, forbrain, uterine epithelium, kidney

64
Q

cox two is stimulated at

A

site of inflammation
primary periphery

64
Q

Cox 2 is responsible for

A

pain and fever

64
Q

IP receptor biological effects

A

Vasodilator
antiaggregant

64
Q

Endorphins (peptide NTs) role and example

A

attatches to endorphin (opiate) receptors of axon terminals of pain afferents –> inhibits release of substance P –>limits sensation of pain
(mediated by descending projections)

ex. enkephalin

65
Q

TP receptor biological effects

A

Vasoconstrictor
Proaggregant

66
Q

EP receptor biological effects

A

Vasodilator
Neuroprotective
Neurodestructive

67
Q

DP receptor biological effects

A

Vasodilator
antiinflammatory
proapoptotic

68
Q

FP receptor biological effects

A

vasodilator
antiaggregant

69
Q

Substance P is a _____ released from _______

A

Neurotransmitter released from afferent nociceptor C fibers

70
Q

Substance P is involved with

A

slow chronic pain, systemic

71
Q

Substance P action

A
  1. vasodilation
  2. extravasation of plasma proteins (edema)
  3. degranulation of mast cells
  4. sensitization of stimulated sensory nerve
72
Q

Glutamate

A

major excitatory neurotransmitter

73
Q

glutamate is released in

A
  1. CNS
  2. A-delta afferent nerve fibers
  3. C primary afferent nerve fibers
74
Q

glutamate is involved with what type of pain?

A

fast and sharp

75
Q

Serotonin location and release

A

descending pathway, released from platelets after tissue injury

76
Q

Serotonin role

A

algesic effect of peripheral nociceptors

77
Q

Prostaglandins (PGs) are synthesized from

A

cox 1 and cox 2

78
Q

Prostaglandins role

A

sensitize peripheral nociceptors, cause hyperalgesia

Prolonged pain, keeps going

79
Q

Cytokines: what are they and what to they cause

A

released in response to tissue injury

Increasein PGs –>cause excitation and sensitization of nociceptive fibers

80
Q

CGRP released from _____ and cause ____ effects
(calcitonin gene related peptide)

A

released from peripheral C fibers and cause LOCAL vasodilation, plasma extravasation, sensitization of sensory nerve

81
Q

Major neurotransmitter released from A-delta fibers is

A

glutamate

82
Q

glutamate binds to

A

AMPA and NMDA receptors on postsynaptic membrane

83
Q

Major neurotransmitter that is released from C fibers

A

Substance P

84
Q

substance P binds to

A

NK-1 neurokinen-1 receptors on postsynaptic membrane

85
Q

Endorphine MOA and result

A

binds to pre-synaptic neuron (from descending pathway) to prevent substance P secretion

Substance P does not bind to norciceptive neuron

86
Q

How does acute pain activate SNS?

A

Increases released catecholamines and adrenal glands, increased cortisol release

87
Q

Pain effects on respiratory system (3)

A
  • decreased vital capacity (VC)
    -decreased inspiratory capacity (IC)
    -decreased functional residual capacity (FRC)
88
Q

decreased VS can cause

A

V/Q mismatch

89
Q

NSAID MOA

A

inhibits cox-2 = prevents PG formation = less substance P and glutamate

90
Q

Ketorolac MOA

A

nonselective COX inhibitor

91
Q

Ketorlac contraindication

A

GI bleeding, renal impairment, asthma, possible impairment in bone healing

92
Q

Celbrex class and MOA

A

NSAID inhibitor of Cox-2

93
Q

Fentanyl vs morphine

A

fentanyl is 80-100 x more potent than morphine

94
Q

Fentanyl onset and duration

A

short
2-5 min onset
30 min duration

95
Q

most widely used narcotic for acute and chronic pain

A

morphine

96
Q

Hydromorphone vs morphine

A

Hydromorphone 7-8 times more potent

97
Q

Dependence can be

A

physiologic or psychologic

98
Q

physiologic dependence

A

Withdrawal

99
Q

psychological dependence

A

need for a specific substance either for positive effect or avoidance of negative

100
Q

Addiction

A

cravings, obsessive thinking, impaired behavior control, compulsive drug taking, inability to recognize problem

101
Q

Pseudoaddiction

A

origin in inadequate analgesia - actually have a pain problem. Not drug seeking

NOT psychological dependence

102
Q

Opioid tolerance

A

repeated exposure to a drug = need higher dose for analgesia

103
Q

opioid tolerance mechanisms (4)

A
  1. enzyme induction or down regulation of opioid receptors

2.drug-receptor interaction

  1. cellular alteration
  2. long term adaptations in gene expression
104
Q

If opioid tolerance is suspected:

A

opioid rotation

105
Q

Opioid-induced hyperalgesia

A

worsening pain/spreading pain/pain in different location

hard to differentiate from tolerance

106
Q

Ketamine MOA

A

NMDA antagonist

107
Q

Clonidine MOA

A

Centrally acting selective partial alpha-2 agonist (and some alpha 1)

108
Q

Acute pain adjucts

A
  1. ketamine
  2. clonidine
  3. dexmedetomidine
  4. local anesthestics
  5. PCA
  6. Epidural
  7. Spinal
109
Q

Dexmedetomidine MOA

A

highly selective alpha-2 agonist

110
Q

activation of alpha 2 receptor results in

A

inhibition of adenylate cyclase and decreased cAMP levels = reduced neurotransmitter release

111
Q

Local anesthetics MOA

A

inhibit conduction of action potentials in ascending pathway

112
Q

common PCA drugs (3)

A
  1. morphine
  2. hydromophone
  3. fentanyl
113
Q

Epidurals are a combination of

A

local anesthetic and narcotic (synergy)

114
Q

Spinal MOA

A

Hydrophillic opioids surround spinal cord and bind to specific pre and post synaptic receptors within the dorsal horn

115
Q

McLott mix is for _____ and includes _____ (4)

A

opioid free anestheisla

  1. lidocaine
  2. ketamine
  3. magnesium
  4. dex

Priniclpes Of Anesthesia (19 decks)

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