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

Week 11 - Acute and Chronic Pain Flashcards

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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
What type of fibers are cutaneous nociceptors?
Nerve endings of A-delta and C fibers - polymodal - activated by mechanical, heat, cold - incision stimulates cutaneous nociceptors but not visceral nociceptors
26
What type of fibers are muscle and joint nociceptors?
Groups II, III (thin myelin), and IV (unmyelinated) - joint activated by stretching or pressure applied to capsule - muscle activated by pressure and ischemia
27
What type of fibers are visceral nociceptors?
A-Delta and C fibers - polymodal (mechanical, heat, chemical) - activated by distension (68% low intensity, 32% high intensity)
28
What are silent nociceptors?
Silent but activated after tissue injury and then respond to normally noxious stimulus
29
Why might a patient with a complete peripheral block still feel pain?
keratinocytes in the epithelial cells can transmit pain and are not blocked in peripheral block because they are not neural cells
30
What is the TRPV1 receptor? Where is it expressed?
A thermal, osmotic receptor that is activated by capsaicin, protons, endocannabinoids, and diphenyl compounds Expressed on C fibers, A-delta fibers and keratinocytes
31
How is nociceptive and non-nociceptive sensory information for the head, neck and dura transmitted?
Via the trigeminal nerve -innervates the dorsal horn of the spinal trigeminal nucleus in the caudal medulla
32
How does peripheral sensitization occur?
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
How does central spinal cord sensitization occur?
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
What is the Spinothalamic Tract of pain transmission?
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
What is the Spinobulbar Pathway of pain transmission?
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
What are the excitatory pain modulating neurotransmitters?
``` Glutamate Substance P Aspartate Vasoactive intestinal polypeptide Cholecystokinin Gastrin releasing peptide Angiotensin ```
37
What are the inhibitory pain modulating neurotransmitters?
``` Enkephalins Endorphins Somatostatin Glycine GABA Serotonin Norepinephrine ```
38
What is the definition of chronic pain?
- 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
What is the Visceral Pain Pathway?
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
What does lack of acute pain control lead to?
- 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
What are independent predictors for development of persistent postsurgical pain?
- 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
What is multimodal analgesia?
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
Preemptive Analgesia vs Preventive Analgesia
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
What is the chronic pain pathophysiology?
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
How does acute pain transition to chronic pain?
* 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
What is neuropathic pain?
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
How do you treat chronic neuropathic pain?
Tricyclic antidepressants Anticonvulsants Topical medications Opioids
48
What is Fibromyalgia? What pain mediators are increased in these patients?
- 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
How do you treat fibromyalgia?
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
What is Complex Regional Pain Syndrome?
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
How do you treat Complex Regional Pain Syndrome?
- 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
What causes phantom pain?
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
How do you treat phantom pain?
- Epidural, LAs, and/or clonidine - Peripheral nerve blocks - Opioids, gabapentin, and NMDA antagonists - Some use of antidepressants - TENS units - Spinal cord stimulators - Biofeedback
54
What are the types of Cancer Pain?
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
What is the AANA guidelines goal of chronic pain management?
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
What is opioid induced hyperalgesia?
Worsening pain to high escalating dosages of opioids Treatment with non-opioid analgesics
57
How do Antidepressants (Tricyclics) treat pain?
- 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
How Antidepressants (SNRIs) treat pain?
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
How do anticonvulsants treat pain?
- 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
How do steroids treat pain?
- 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
How do you prevent chronic pain?
- 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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