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Basics of Anesthesia > Week 11 - Acute and Chronic Pain > Flashcards

Week 11 - Acute and Chronic Pain Flashcards

1
Q

What are pulmonary system adverse effects of postop pain?

A
  • Atelectasis
  • Ventilation to perfusion mismatching
  • Arterial hypoxemia
  • Hypercapnia
  • Pneumonia

*Due to decreased lung volumes

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2
Q

What are CV system adverse effects of postop pain?

A
  • Systemic HTN
  • Tachycardia
  • MI
  • Cardiac dysrhythmias

*Due to sympathetic nervous system stimulation

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3
Q

What are endocrine system adverse effects of postop pain?

A
  • Hyperglycemia
  • Sodium and water retention
  • Protein catabolism
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4
Q

What are immune system adverse effects of postop pain?

A

Decreased immune function

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5
Q

What are coagulation system adverse effects of postop pain?

A
  • Increased platelet adhesiveness
  • Decreased fibrinolysis
  • Hypercoagulation
  • DVT
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6
Q

What are GI/GU system adverse effects of postop pain?

A

Ileus

Urinary retention

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7
Q

Fast Pain vs Slow Pain

A

Fast Pain = short, well localized, sharp, stabbing sensation, duration matched to a stimulus (Myelinated A-delta fibers)

Slow Pain = throbbing, burning, aching, diffuse, poorly localized and less related to the stimulus (unmyelinated C-fibers)

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8
Q

Define eudynia, maldynia, and allodynia

A

Eudynia: symptomatic or “normal” pain

Maldynia: pathophysiologic disease of the nervous system - “abnormal” pain

Allodynia: pain from a stimulus that doesn’t normally produce pain

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9
Q

Define Hyperalgesia, Hypoalgesia, Dysesthesia

A

Hyperalgesia: an increased response to a stimulus that is normally painful

Hypoalgesia: diminished pain in response to a normally painful procedure

Dysesthesia: unpleasant abnormal sensation, whether spontaneous or evoked

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10
Q

Neurogenic Pain vs Neuropathic Pain

A

Neurogenic: pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the PNS or CNS

Neuropathic: pain initiated or caused by a primary lesion or dysfunction of the nervous system

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11
Q

What is pain sensitization?

A

Increased responsiveness of neurons to their normal input or recruitment of a response to normally subthreshold inputs

  • Peripheral Sensitization: increased responsiveness and reduced threshold of nociceptors to stimulation of their receptive fields
  • Central Sensitization: increased responsiveness of nociceptive neurons in the CNS to their normal or subthreshold afferent input
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12
Q

What are the three dimensions of pain?

A

Sensory-Discriminative: sensation, location, quality (burning, dull, sharp)

Motivational-Effective: unpleasantness and bother to the pt (nauseating, sickening)

Cognitive-Evaluative: past experiences and the probability of outcomes and can modify the other two dimensions
*based on pt beliefs, cultural background, and past experience

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13
Q

What is the basic pathway of pain?

A

Activation of the PNS –> Transmission –> Activation of CNS at spinal cord –> Input –> Transmission of the pain signal to the brain –> Perception –> Modulation (descending inhibition or central sensitization) –> Activation of CNS at spinal cord

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14
Q

What is the Gate Control Theory of Pain?

A

“Gated” or modulated response varies with bodies needs:

  • during fight or flight the incoming nociceptive signals are dampened by descending control allowing of flight or fight
  • if withdrawal and heeling is required, descending pathways enhance the signals and produce sensitization and nociception
  • balance between inhibited and facilitated responses is dynamic and changes over the course of acute and chronic injuries

Application of light peripheral mechanical stimuli resulting in excitation of A-beta fibers can activate the inhibitory interneurons in the dorsal horn and thus close the “gate” to the simultaneous incoming pain signals carried by A-delta and C fibers

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15
Q

How does Substance P mediate pain?

A

Peptide released from C fibers

  • slow, chronic pain
  • acts via the G-protein-linked neurokinin-1 receptor resulting in vasodilation, extravasation of plasma proteins, degranulation of mast cells, and sensitization of the stimulated sensory nerve.

*Arthritic pain

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16
Q

How does Glutamate mediate pain?

A

Released from A-delta and C primary afferent nerve fibers
-effects are instantaneous,
producing initial, fast, sharp pain
-upregulated in joints after inflammation
-injection of glutamate cause hyperalgesia
-blockade of Glutamate receptors reduces pain and hyperalgesia

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17
Q

How does Calcitonin gene-related peptide (CGRP) mediate pain?

A

Peptide released from the C fibers
-produces local cutaneous vasodilation, plasma
extravasation (inflammatory mediators), and sensitization of the stimulated sensory nerve

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18
Q

How do Ion Channels mediate pain?

A

Acid sensing: low pH in inflamed tissues

Vanilloid receptor activated by capsaicin and mediates hyperalgsia

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19
Q

How does Bradykinin mediate pain?

A

Peptide released during the inflammation process and is notably algesic
-it has a direct stimulating effect on peripheral nociceptors via specific bradykinin receptors (B1/B2)

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20
Q

How does Histamine mediate pain?

A

Released from mast cell granules, basophils, and platelets vis substance P

-reacts with various histamine receptors to produce edema and vasodilation

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21
Q

How does Serotonin mediate pain?

A

Amine stored and released from platelets after tissue injury

  • reacts with multiple receptor subtypes and exhibits algesic effects on peripheral nociceptors
  • like histamine, serotonin can potentiate bradykinin-induced pain
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22
Q

How do Prostaglandins (PGs), Thromboxanes, and Leukotrienes mediate pain?

A

Metabolite of arachidonic acid (PGs specifically are synthesized form COX-1 and COX-2)

  • associated with chronic pain
  • PGs sensitize peripheral nociceptors, causing hyperalgesia
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23
Q

How do Cytokines mediate pain?

A

Released due to tissue injury by a variety of immune and nonimmune cells via the inflammatory response
-interleukin-1beta, IL-6, and TNF alpha can lead to the increased production of prostaglandins, exiting and sensitizing nociceptive fibers

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24
Q

What are the three components of the Peripheral (Somatic) pain pathway?

A

First Order Neuron: transmits pain from a peripheral receptor to the 2nd order neuron

Second Order Neuron: in the dorsal horn of the spinal cord (rexed lamina), where the axon crosses the midline to ascend in the spinothalamic tract to the thalamus

Third Order Neuron: in the brain, projects to the post central gyrus of cerebral cortex

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25
Q

What type of fibers are cutaneous nociceptors?

A

Nerve endings of A-delta and C fibers

  • polymodal
  • activated by mechanical, heat, cold
  • incision stimulates cutaneous nociceptors but not visceral nociceptors
26
Q

What type of fibers are muscle and joint nociceptors?

A

Groups II, III (thin myelin), and IV (unmyelinated)

  • joint activated by stretching or pressure applied to capsule
  • muscle activated by pressure and ischemia
27
Q

What type of fibers are visceral nociceptors?

A

A-Delta and C fibers

  • polymodal (mechanical, heat, chemical)
  • activated by distension (68% low intensity, 32% high intensity)
28
Q

What are silent nociceptors?

A

Silent but activated after tissue injury and then respond to normally noxious stimulus

29
Q

Why might a patient with a complete peripheral block still feel pain?

A

keratinocytes in the epithelial cells can transmit pain and are not blocked in peripheral block because they are not neural cells

30
Q

What is the TRPV1 receptor? Where is it expressed?

A

A thermal, osmotic receptor that is activated by capsaicin, protons, endocannabinoids, and diphenyl compounds

Expressed on C fibers, A-delta fibers and keratinocytes

31
Q

How is nociceptive and non-nociceptive sensory information for the head, neck and dura transmitted?

A

Via the trigeminal nerve

-innervates the dorsal horn of the spinal trigeminal nucleus in the caudal medulla

32
Q

How does peripheral sensitization occur?

A

Innocuous stimuli may excite peripheral nociceptors following repeated or injury or inflammation leading to allodynia or hyperalgesia

Occurs via several inflammatory mediators including bradykinin, prostaglandins, serotonin, and histamine

33
Q

How does central spinal cord sensitization occur?

A

Persistent C fiber activation of lamina I and lamina V – enhances the response to subsequent stimulation and increases the size of the receptive field of the respective dorsal horn neuron

Axons also begin to spread forming neuromas which have up-regulated Na channels or a down regulation of K+ channels – leads to neuronal excitability and increased nociception

34
Q

What is the Spinothalamic Tract of pain transmission?

A

Carries pain signals from the trunk and extremities and terminates in the ventral posterior thalamus
-thalamus allows for localization of pain

*Spinohypothalmic and Spinoamygdalar pathways mediate autonomic responses such as increased HR and BP and provocation of fear

35
Q

What is the Spinobulbar Pathway of pain transmission?

A

Some ascending axons terminate in the brainstem at the reticular formation of the ventrolateral medulla

  • contains neurons that are activated by catecholamines and serotonin
  • modulate pain transmission in spinal cord resulting in descending inhibitory input

*Descending Inhibitory Pain Pathway (involves the locus coreruleus and raphe nucleus)

36
Q

What are the excitatory pain modulating neurotransmitters?

A 
Glutamate
Substance P
Aspartate
Vasoactive intestinal polypeptide
Cholecystokinin
Gastrin releasing peptide
Angiotensin
37
Q

What are the inhibitory pain modulating neurotransmitters?

A 
Enkephalins
Endorphins
Somatostatin
Glycine
GABA
Serotonin
Norepinephrine
38
Q

What is the definition of chronic pain?

A
  • Persists beyond “normal time” for acute pain /disease process (1-6 months or longer)
  • Starts around 6 weeks to 3 months
  • Nociceptive, neuropathic, cancer, unknown etiology
  • Not Protective and No Biological Purpose
  • not a symptom… it is a disease process
39
Q

What is the Visceral Pain Pathway?

A

A-delta and C fibers innervating the viscera project to the CNS through the SNS and PNS nerves

Terminate in lamina I and V in the spinal cord converging with somatic fibers which leads to referred pain

40
Q

What does lack of acute pain control lead to?

A
  • Cardiac arrhythmias, tachycardia, ischemia
  • Hyperglycemia, depressed immune function
  • Decreased tidal volumes and FRC d/t increased abdominal and intercostal muscle tone
  • Impaired cognitive function
  • Decreased GI motility and gastric ileus
41
Q

What are independent predictors for development of persistent postsurgical pain?

A
  • Preop pain levels
  • Age (younger is worse)
  • Type of surgery
  • Preop anxiety (increase anxiety = increased pain)
  • Severity of immediate postop pain
  • Size of incision
  • Gender (female are worse w/ outpatient)
  • Need for information

*BMI, duration of surgery, and type of anesthesia have no predictable effects

42
Q

What is multimodal analgesia?

A

Using a combination of interventional analgesic techniques and a combination of systemic pharmacologic therapies

  • Signal Transduction: LAs, NSAIDs, Steroids, Opioids
  • Transmission: LAs, TCAs, Steroids
  • Modulation: NMDA antagonists, TCAs, SNRIs, Opioids, Alpha-2 agonists, NSAIDs
  • Perception: TCAs, SNRIs, Opioids, Alpha-2 agonists, General anesthesia, NMDA antagonists
43
Q

Preemptive Analgesia vs Preventive Analgesia

A

Preemptive Analgesia: an
analgesic intervention initiated BEFORE the
noxious stimulus develops in order to block peripheral and central pain transmission

Preventive Analgesia: an attempt to block pain
transmission PRIOR to the injury (incision),
DURING the noxious insult (surgery itself), and AFTER the injury and throughout the recovery period

44
Q

What is the chronic pain pathophysiology?

A

Windup phenomenon is a chronic discharge of neurons that leads to overwhelming of the inhibitory systems of neuropathways:

Chronic repetitive stimulation –> Increased cellular calcium –> Release of inflammatory substances –> COX production –> Synthesis of prostaglandins (responsible for reduction in inhibition) –> Increased neurologic pathway excitability –> Formation of hyperalgesia –> Back to beginning

45
Q

How does acute pain transition to chronic pain?

A
  • Neuromas altered sensitivity to humoral factors
  • TNF-alpha = decreased K+ conductance = increased neuronal excitability
  • Prostaglandins enhance Na+ channel opening
  • Nerve growth factor released from glial & inflammatory cells – sprouting of postganglionic efferents
  • TRPV1 sensitized by protease activated receptors = sensitive to thrombin = hematoma pain
  • Upregulation of adrenergic receptors demonstrated after nerve damage = increased release of catecholamines
  • Phenotypic-switch: explains allodynia. AB fibers do not express substance P, after peripheral injury somatic AB fibers express substance P (blocking AB fibers decreases light touch allodynia)
46
Q

What is neuropathic pain?

A

Damage or disease to the somatosensory system (thermoreceptors, photoreceptors, mechanoreceptors, and chemoreceptors)

  • intermittent or chronic
  • burning, sharp, pins/needles
  • abnormal sensations (dysesthesia) or pain with non-painful stimuli (allodynia) or exaggerated response to mildly noxious stimuli (hyperalgesia)

Ex: peripheral neuropathy, nerve injury, status post chemo/radiation

47
Q

How do you treat chronic neuropathic pain?

A

Tricyclic antidepressants
Anticonvulsants
Topical medications
Opioids

48
Q

What is Fibromyalgia? What pain mediators are increased in these patients?

A
  • History of widespread pain for at least 3 months, evidence of allodynia at certain trigger points, and/or presence of fatigue, sleep disturbance, and cognitive dysfunction
  • 18 tender points (need 5 to be diagnosed)

Higher concentrations of substance P and glutamate in CSF (evidence of sensitization)

49
Q

How do you treat fibromyalgia?

A

Physical activity is best

Increased endogenous endorphins: opioids are ineffective, drugs that raise serotonin or NE levels are more effective along with gabapentin (ex: Duoloxetine, Milnacipran)

50
Q

What is Complex Regional Pain Syndrome?

A

Malfunction of the peripheral and central nervous system characterized by:
-hyperesthesia, temperature or skin color changes, sweating abnormalities or edema, muscle weakness, or tremor, allodynia or hyperalgesia

CRPS-I: reflex sympathetic dystrophy syndrome – no known or confirmed injury
CRPS-II: causalgia – known injury or known trauma to limb

51
Q

How do you treat Complex Regional Pain Syndrome?

A
  • Early intervention to prevent chronic CRPS (focus on maintenance and restoration thru aggressive PT)
  • Sympathetic blockade
  • Spinal cord stimulator
  • Gabapentin (poor evidence meds help, includes TCA, carbamazepine)
  • NMDA blockers (memantine)
  • Ketamine Infusion
52
Q

What causes phantom pain?

A

Caused by peripheral and central factors:

  • neuromas, increased C fiber activity, increased sodium channel activation
  • development of new synaptic connections in the cerebral cortex
53
Q

How do you treat phantom pain?

A
  • Epidural, LAs, and/or clonidine
  • Peripheral nerve blocks
  • Opioids, gabapentin, and NMDA antagonists
  • Some use of antidepressants
  • TENS units
  • Spinal cord stimulators
  • Biofeedback
54
Q

What are the types of Cancer Pain?

A

Somatic pain: due to soft tissue inflammation or bone metastasis)
-well localized, sharp in nature – responds to NSAIDS, opioids, Cox-2 inhibitors and neuronal blockade

Visceral pain: due to tumor infiltration, stretching, distension or ischemia of organs)
-poorly localized, ill defined – responds to sympathetic blocks

Neuropathic Pain: due to nerve injury by the effects of tx or tumor invasion
-burning or electrical in nature – responsive to anticonvulsants, tricyclic depressants, 5ht/NE reuptake inhibitors, opioids or combination

55
Q

What is the AANA guidelines goal of chronic pain management?

A

To use a PATIENT-CENTERED approach to treat the patient’s pain and improve the patient’s well-being, functionality, and quality of life

-reduce pain, improve function, return to work, resolve medication issues, reduce healthcare utilization

56
Q

What is opioid induced hyperalgesia?

A

Worsening pain to high escalating dosages of opioids

Treatment with non-opioid analgesics

57
Q

How do Antidepressants (Tricyclics) treat pain?

A
  • Effects at serotonin reuptake and binding
  • Interacts with alpha receptors
  • Opioid like effects
  • NMDA blockade
  • Inhibition of uptake of adenosine
  • Blockade of Na and Ca channels
  • Anti-inflammatory
  • Many side effects

*Nortriptyline and amitriptyline have been shown to be effective in post herpetic neuralgia and other neuropathic pain syndromes.

58
Q

How Antidepressants (SNRIs) treat pain?

A

Have an antinociceptive effect

  • recommended for first line treatment in diabetic peripheral neuropathy
  • has been shown to be effective in fibromyalgia
  • better side effect profile than the tricyclics.

Side effects of of antidepressants include cholinergic effects: dry mouth, sedation, urinary retention

59
Q

How do anticonvulsants treat pain?

A
  • Block sodium channels – effective in neuropathic pain syndromes
  • Some act on ion channel systems including GABA
  • Some block T-type calcium channels and alpha2 subunits
  • RTCs demonstrate efficacy in several neuropathic pain syndromes
60
Q

How do steroids treat pain?

A
  • Anti-inflammatory by preventing the release of arachidonic acid and decreasing inflammatory cytokines and prostaglandins
  • Block C fiber transmission in the spinal cord
  • Suppress excessive firing of nociceptors in the presence of nerve injury
  • Have many systemic side effects
61
Q

How do you prevent chronic pain?

A
  • Return to physical activity
  • Control weight
  • Avoid injury
  • Receive appropriate pre and post surgical pain management
  • Pt personality traits such as resilience and positive affect
  • Adequate treatment of acute pain

Basics of Anesthesia (35 decks)

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