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Anesthesia MM/TL > Pain > Flashcards

Pain Flashcards

1
Q

What is the major hurdle for development of treatment for phantom limb pain?

A

Lack of randomized controlled trials to give treatment

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2
Q

What are the potential complications of a celiac plexus block?

A 
Diarrhea
Postural hypotension (most common)
PTX
Retroperitoneal hemorrhage
paraplegia (disruption of anterior spinal artery or subarachnoid injection)
hiccups
Pleurisy
Abdominal aortic dissection
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3
Q

What is the drug of choice for chronic neuropathic pain?

A

Methadone due to NMDA antagonism and SSRi

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4
Q

What is the mechanism of hyperalgesia?

A

Upregulation of NMDA receptors

Increased nitric oxide production

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5
Q

What is the Gaenslen test?

A

Significant hip flexion + posterior pressure on the sacrum

Indicates SI joint pain

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6
Q

What are the clinical manifestations of SI pain?

A

Pain at the site that is dull and constant
Worse with compression and distraction
Worse with standing or in one position for awhile
+ Gaenslen’s

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7
Q

What are the clinical manifestations of discogenic pain?

A

Worse with flexion and increased intraabdominal pressure (coughing/sneezing)

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8
Q

What are the clinical manifestations of facet joint pain?

A

Worse with facet loading
Not better or worse with flexion or extension
Non radiating

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9
Q

What is the treatment for facet joint pain?

A

Medial branch blocks

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10
Q

What are the clinical manifestations of spinal stenosis?

A

Radicular pain
Worse with extension
Better with flexion

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11
Q

How do you diagnose spinal stenosis?

A

MRI

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12
Q

What are the treatments for acute herpes zoster?

A

antivirals, corticosteroids, sympathetic blocks

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13
Q

What are the treatments for postherpetic neuralgia?

A 
TCAs
Anticonvulsants (lyrica, gabapentin)
Lidocaine patches (for allodynia)
Topical capsaicin
Opiates
Tramadol
Spinal cord stimulators
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14
Q

How does a spinal cord stimulator work?

A

Stimulates large nerve fibers in the substantial gelatinosa thereby decreasing excitatory signals and increasing inhibitory signals

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15
Q

What are the analgesic properties due to with low doses of ketamine?

A

NMDA receptors antagonism

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16
Q

What are the analgesic properties due to with high doses of ketamine?

A

Opioid receptors

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17
Q

What is the conversion of IT morphine to epidural?

A

1 mg to 10 mg of epidural

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18
Q

What is the conversion of epidural morphine to IV morphine?

A

1 mg to 10 mg of IV

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19
Q

What is the conversion of IT morphine to IV morphine?

A

1 mg to 100 mg

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20
Q

What is the conversion of IV morphine to po morphine?

A

1 mg to 3 mg

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21
Q

What is the conversion of IT hydromorphone to epidural?

A

1 mg to 100 mg

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22
Q

What is the conversion of IV hydromorphone to po hydromorphone?

A

1 mg to 3 mg

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23
Q

What is the conversion of epidural hydromorphone to IV?

A

1 mg to 10 mg

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24
Q

What is conversion of IT hydromorphone to IV?

A

1 mg to 1000

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25
Q

What do hydrophobic opioids do in the intrathecal/epidural space?

A

More likely to taken up in systemic system to act supra spinally and reach IV infusion levels (fentanyl) so have a smaller analgesic effect and respiratory depression effect.

Bind the white matter of the spinal cord in the intrathecal space

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26
Q

Where do hydrophilic opioids act in the intrathecal space?

A

The dorsal horn

Can cause respiratory depression via rostral spread

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27
Q

What is the rule when converting to different opioids to avoid cross-tolerance?

A

Do a 20% reduction

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28
Q

What is valproic acid used for?

A

Chronic neuropathic pain

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29
Q

What is CRPS II?

A

Caused by nerve damage - CAUSALGIA
Characterized by spontaneous pain, hyperalgesia, allodynia, vasomotor and sudomotor abnormalities, passive and active movement disorders, trophic problems

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30
Q

What is the first line treatment for CRPS II?

A

Physical therapy

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31
Q

What are the other treatment options for CRPS?

A

TCA, gabapentins, memantine
Spinal cord stimulators
IT pumps
Somatic and sympathetic nerve blocks

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32
Q

What is CRPS type I?

A

Autonomic dysfunction precipitated by non-nerve related injury or surgery
NO associated cause!

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33
Q

What are the symptoms of CRPS?

A

Sudden onset of pain
Sudomotor: increased sweating, erythema, edema
Vasomotor: temp changes
Motor: tremor, decreased ROM, weakness

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34
Q

What is fibromyalgia?

A

Widespread pain, sleep disturbances, fatigue, depression for over 3 months with no other explainable cause
WPI > 7, SS >5

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35
Q

What is myofascial pain syndrome?

A

Painful taut band and palpation of this produced same symptoms

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36
Q

What is the first line treatment for mild cancer pain?

A

APAP

NSAIDs

37
Q

What is the first line treatment for mild-moderate cancer pain?

A

Mild opioids: codeine

APAP, NSAIDs

38
Q

What is the treatment for nerve compression by a mass?

A

Corticosteroids

39
Q

What is the treatment for bone pain?

A

Bisphosphonates

Calcitonin

40
Q

What is the treatment for visceral pain?

A

Anticholinergics

41
Q

What is the treatment for neuropathic pain?

A

Anticonvulsants, antidepressants, TCAs, local anesthetics

42
Q

When should neuroablation be used in a cancer patient?

A

Only as a last resort, if the patient prefers or if there is a single focus to treat.

43
Q

What are the indications for spinal cord stimulator?

A 
Post-laminectomy syndrome
Postherpetic neuralgia
Phantom limb pain
Cauda equina syndrome
CRPS
CV angina
LE ischemic pain
Chronic cervical radiculopathy
Nerve root injury
44
Q

What are the contraindications to spinal cord stimulator placement?

A 
Sepsis
Coagulopathy
Local infection
Spina bifida
Somatoform disorder
Cognitive disability
Trauma obliterating spinal canal
Lack of social support
Substance abuse
Psych disorders
45
Q

What are the side effects of gabapentin?

A

Nausea, sedation, dizziness, nystagmus, ataxia, peripheral edema, urinary leakage, suicide

46
Q

Which chronic pain medication lower seizure threshold?

A

Tramadol, TCAs

47
Q

How are nociceptive signals transmitted?

A

Alpha delta and C fibers in the substantial gelatinous of the dorsal horn of the spinal cord via glutamate

48
Q

What is the “gate theory” of pain?

A

Large fibers in the substantial gelatinous open the gate to small afferent fibers that transmit the nociceptive signal

49
Q

Which nerves does a spinal cord stimulator affect?

A

Large A-alpha and A-beta fibers in substantia gelatinosa

50
Q

What structures transmit analgesic signals?

A

Periaqueductal gray and Rostroventromedial nucleus

51
Q

When does nerve regeneration occur after cryoanalgesia?

A

in 1-3 month following

52
Q

What is cryoanalgesia?

A

Intense cold to damaged select nerve that causes temporary conduction blocks

53
Q

What is cryoanalgesia used for?

A

Post-Thoracotomy pain for intercostal nerves

54
Q

What is dysesthesia?

A

Tactile hallucination

55
Q

What type of pain is phantom limb pain?

A

Neuropathic and central (due to mechanism)

56
Q

What is the pathophysiology of phantom limb pain

A

Misfiring in the somatosensory cortex

57
Q

What is allodynia?

A

Pain from a non painful stimulus

58
Q

What is nociceptive pain?

A

Pain caused by an actual or threatened damage to non neural tissue
Subtypes: mechanical (scrapes), thermal, chemical

59
Q

What is psychosomatic pain?

A

Caused by emotional, mental and behavioral factors

Most common: backache, headache, abdominal pain

60
Q

What is first line therapy for trigeminal neuralgia?

A

Carbamazepine

61
Q

What are the treatments for trigeminal neuralgia after failed medical therapy?

A

Radio frequency rhizotomy

Microvascular decompression

62
Q

What is transduction?

A

The conversion of a painful stimulus to an action potential. Happens at free nerve endings in the dorsal root ganglia

63
Q

What is transmission?

A

Done through 1st, 2nd, and 3rd order neurons through the dorsal root ganglia, dorsal horn and thalamus.

64
Q

What is the best treatment to prevent transmission of pain?

A

Local anesthetics

65
Q

What is modulation of pain?

A

Occurs at any site along the pathway but typically in the dorsal horn at NMDA sites, GABA, neurokinin, AMPA

66
Q

Which treatments are geared toward transduction?

A

NSAIDs, SSRIs, locals, antihistamines, opioids,

67
Q

What is perception of pain?

A

The final common pathway involves the somatosensory cortex and limbic system

68
Q

What alters perception of pain?

A

general anesthesia
opioids
alpha 2 agonists

69
Q

What are the most common to least common affect nerves from herpes zoster?

A

Thoracic > V1 > V2 > Cervical > Sacral

70
Q

How is carbamazepine metabolized?

A

By the liver

71
Q

What is the mechanism of action of carbamazepine?

A

Sodium channel blocker
Inhibits ectopic foci
Has larger volume of distribution and peak plasma concentration in 4-8 hours

72
Q

What does carbamazepine do in the liver?

A

Induces P450 – increases metabolism of other anti epileptic drugs: phenytoin

73
Q

What are the manifestations of carbamazepine toxicity?

A

Widened QRS, prolonged QT, ventricular arrhythmia, tachycardia, hypotension, mydriasis, dry mouth, flushing, reduction of seizure threshold, urinary retention, AMS, nystagmus, ataxia, hyperthermia

74
Q

Where is ganglion impar?

A

Retroperitoneum anterior to the sacrococcygeal junction

75
Q

What does a ganglion impar block do?

A

Pain relief for perineal malignancies: perineum, anus, distal rectum, distal urethra, distal third of vagina

76
Q

How does a TENS unit work?

A

Uses low voltage (10-30 mA) electrical pulses to stimulate the nervous system
Based on gate theory: large fibers compete for input from small fibers

77
Q

What are the contraindications for TENS unit?

A

Demand pacemakers, cardiac dysrhythmias, undiagnosed pain syndrome, mental incompetence, first trimester pregnancy

78
Q

What is anesthesia dolorosa?

A

Pain in an area that lacks sensation

Often in the face after rhizotomy for bigeminal neuralgia

79
Q

What is the treatment for anesthesia dolorosa?

A

Antidepressants, anticonvulsants, opiates, support

80
Q

What is stage I of CRPS?

A

1-3 months: pain, joint stiffness, muscle spasm, rapid hair growth, blood vessel changes leading to temp changes and discoloration

81
Q

What is stage II of CRPS?

A

3-6 months: intensified pain, hair loss, edema, bone weakness, weak muscles, joint stiffness,

82
Q

What is stage III of CRPS?

A

> 6 months: irreversible changes to bone and joint, muscle atrophy, involuntary spasms, contractures, distortion of limbs, pain involving the entire limb

83
Q

What does chronic opioid usage lead to?

A

Disruption of HPA axis: decreased cortisol levels, FH, LSH, estrogen and testosterone levels.
Increased prolactin
Addisonian like symptoms from decreased cortisol

84
Q

Where is the stellate ganglion?

A

Lies in close proximity to carotid sheath. Comprised of the inferior cervical and first thoracic sympathetic ganglia

85
Q

How are nociceptive cation (Na and Ca) channels opened?

A 
Via TRPV1 (transient receptor vanilloid OR
ATP purinergic P2X 3 receptor
86
Q

What does the thalamus do in pain?

A

Provides higher order neurons to the cingulate cortex (dull, poorly localized pain) and post central gyrus (sharp, localized pain)

87
Q

What does the dorsal raphe nucleus do?

A

Provides inhibitory signals via serotonergic pathways through serotonin excretion

88
Q

What does locus ceruleus do?

A

Provides inhibition of norepinephrine signals

Anesthesia MM/TL (36 decks)

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