Pain Flashcards

1
Q

What is fibromyalgia?

A

Fibromyalgia is a complex pain syndrome associated with widespread pain, sleep disturbances, fatigue, and depression

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2
Q

Diagnostic criteria for fibromyalgia:

A

1) Widespread pain index (WPI) ≥ 7 and symptom severity (SS) scale score ≥ 5
or WPI 3 - 6 and SS scale score ≥ 9.
2) Symptoms present for at least 3 months
3) No other disorder that would explain the pain

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3
Q

What is memantine?

A

Memantine is an NMDA antagonist that may be used in the treatment of CRPS.

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4
Q

What is CRPS? How does it present? Diagnosis? How can it be treated? Side effects of the treatment?

A

Complex regional pain syndrome is separated into types I and II according to the inciting event.
Type I s usually caused by a trivial injury, sprain, crush injury, or burn
Type 2: is caused by a traumatic injury to a MAJOR NERVE trunk such as significant orthopedic trauma, gunshot injuries, or knife wounds.
With either diagnosis, patients may develop burning pain and allodynia. Both syndromes are also characterized by autonomic dysfunction, which presents with localized temperature changes, cyanosis, and/or edema. If the disease progresses without treatment, the skin can become glossy, smooth, and hairless

Diagnostic criteria for CRPS I may include clinical signs and symptoms, in conjunction with a diagnostic sympathetic blockade. treatment goals include serial sympathetic blocks

Along with the risk of intravascular, epidural, and intrathecal injections, a fairly significant percentage of male patients undergoing bilateral blockade may develop ejaculatory problems. This is due to the sympathetic dependence of the ejaculatory mechanism

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5
Q

What is allodynia?

A

allodynia (pain to non-noxious stimuli)

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6
Q

what does chronic opioid use do to cortisol levels?
Sexual side effects of chronic opioids?
Body temp with chronic opioid use?
Addisonian symptoms?

A

It decreases them
these changes may lead to male/female infertility, reduced libido, galactorrhea, and menstrual changes.
A decrease in body temperature is commonly seen. Addisonian symptoms (e.g. orthostatic hypotension, muscle weakness, and hyperpigmentation) may also be observed due to reduced cortisol levels.

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7
Q

Phantom limb pain is what type of pain? Treatment:

A

Neuropathic (central). Legion of the somatosensory nervous system. Treatment: opioids, gabapentin, SC stimulators, antidepressants

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8
Q

Where is the celiac plexus located? Which nervous systems does it house? Possible complications of celiac plexus block?

A

Retroperitoneal T12-L1. House PS and SNS. Complications-diarrhea, orthostatic hypotension, retroperitoneal hemorrhage, hepatitis, aortic dissection and paraplegia. Why would anyone do this again?

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9
Q

TCA Side effects: And TCAs are good for-

A

Dry mouth, difficult urination and sedation

Good for neuropathic pain

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10
Q

What effects OPIOID spread on the epidural space?

A

Most affected by lipophilicity. Very lipophikic will att and the less lipophilic ones will spread (morphine)

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11
Q

Acidic drugs bind to:

A

ALbumin

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12
Q

Basic drugs bind to:

A

Acidic AAG

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13
Q

Protein binding signifies what with drugs:

A

Duration of action

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14
Q

What is Anesthesia dolorosa?

A

Numbness and pain in an area that lacks sensation-usually seem after a trigeminal nerve block

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15
Q

Discogenic pain is often described as _____. Pain can be relieved by:
Most references state that discogenic pain will increase with anything that

A

Decreased with standing, increased with bending/sitting
Pain relieved by: pain is often relieved by a lateral recumbent position.
discogenic pain will increase with: increases intradiscal pressure – sitting, flexion, sneezing, or coughing.

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16
Q

Jeopardy style: With this there is often a positive straight leg test and there may be associated weakness.

A

What is acute disc herniation?

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17
Q

Pain due to spinal stenosis:
What increases it?
Spinal stenosis pain-is it worse walking uphill or downhill?

A

aching with shooting pain or “pins and needles” sensation. They are increased with walking or anything that requires an incline and decreased with sitting. Although walking exacerbates spinal stenosis pain, patients may tolerate walking uphill more than walking downhill.

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18
Q

When you hear of people with morning back pain-who do you think of?

A

People with ankylosing spondylitis

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19
Q

Pt has a headache-when do you want to get imaging, and once you do-which type of imaging are you going to get?

A

In a patient presenting with headache and focal neurological symptoms, diagnostic imaging should be obtained. MRI is preferred over CT as it is able to diagnose posterior fossa and dural based abnormalities with higher sensitivity.
Those that have a recent change in headache pattern, a history of seizures, or focal neurologic findings might benefit from diagnostic testing.

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20
Q

What is paroxysmal hemicrania? How does it compare to migraine headaches and cluster headaches?

A

Paroxysmal hemicrania is a rare form of headache that has similar characteristics of pain and symptoms as cluster and migraine headaches. The difference between paroxysmal hemicrania, as opposed to cluster and migraine headaches, is that they are shorter in duration, occur more frequently, are more common in females, and they respond absolutely to indomethacin.

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21
Q

What are these symptoms of?

  • Severe, unilateral headache that is supraorbital or temporal in location and can last between 20-30 minutes in duration
  • Ipsilateral conjunctival injection and/or lacrimation
  • Ipsilateral nasal congestion and/or rhinorrhea
  • Ipsilateral eyelid edema
  • Ipsilateral forehead and facial sweating
  • Ipsilateral miosis and/or ptosis
A

Paroxysmal Hemicrania

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22
Q

What is myofascial pain syndrome?
Give an example of someone that would have it as far as their symptoms
Can it ever go dormant?

A

characterized by trigger points in skeletal muscles often secondary to repetitive use or trauma. The area of pain is localized but will cause radiation of pain in a characteristic non-dermatomal pattern upon palpation.

A 22-year-old male presents to the pain clinic with right upper back and neck pain. He is a collegiate basketball player and noted that the pain started after being struck in the head during a layup shot. This caused significant stretching of his neck to the left. The pain is described as dull and achy and gets worse with use. The pain is limiting his involvement in weight training and practice. On physical exam, you note tenderness in the lower right neck/upper back above the scapula with increased muscle tension.

Dormancy: Myofascial pain syndromes can become dormant with only tenderness to the site but reactivate with repeat trauma and stress.

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23
Q

Treatment for myofascial pain syndrome:

What’s seen in myofascial pain syndrome in trigger point injections

A

Treatment includes application of cold sprays such as ethyl chloride to relax the muscle and allow for implementation of stretching exercises and physical therapy. Soft tissue therapy such as massage and ultrasound is also of benefit. Interventional management can include dry needling and injections of local anesthetic. During trigger point injections, reproduction of pain radiation pattern or muscle twitch are seen.

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24
Q

Can you have autonomic dysfunction in myofascial pain syndrome? What about spontaneous EMG activity?
Dermatomal radiation of pain?

A

Yes-piloerection and vasoconstriction can occur with myofascial pain syndromes. spontaneous EMG activity can be seen in the affected region.
Characterized by a non-dermatomal radiation of pain.

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25
Q

Cardiac events and carbamazepine:

A

Cardiac events noted with carbamazepine toxicity include widening of the QRS complex (A), prolonged QT interval, ventricular arrhythmias, tachycardia, and hypotension (B) (from direct myocardial depression)

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26
Q

Neurologic symptoms and carbamazepine? myosis or mydriasis and why?

A

Neurologic changes include altered mental status, delirium, and a paradoxical reduction in seizure threshold (C). Nystagmus (D) and mydriasis are commonly noted.

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27
Q

Anticholinergic effects and carbamazepine:

A

Anticholinergic effects also include hyperthermia, flushing, dry mouth, and urinary retention.

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28
Q

symptoms of carbamazepine and calling a center vs side effects and calling a center:

A

The severity of symptoms at the time of initial contact with the poison control center correlates with outcome severity for children and adults. However, the amount of time between ingestion and poison control center contact does not appear to alter the correlation between initial severity of symptoms and final outcome severity.

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29
Q

Acute herpes zoster will initially present in which dermatome? Which dermatomes are more common after that?

A

Acute herpes zoster typically affects thoracic nerve roots, followed in descending order by: ophthalmic division of the trigeminal nerve (V1), maxillary division of the trigeminal nerve (V2), cervical spinal roots, and sacral spinal roots (least common)

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30
Q

Neuropathic pain: We don’t understand completely, but what are some components:

A

Peripheral-Inflammation, repair mechanisms, and adjacent tissue reactions can lead to hyper-excitability in afferent nociceptors (peripheral sensitization).
Central: This evokes central neurons that are innervated by the nociceptors to undergo functional changes (central sensitization).
Afferent pathway damage: Neuropathic pain states occur following injury to the afferent pathway.

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31
Q

What is post-herpetic neuralgia, and what are risk factors:

What decreases the incidence? What has nothing at all to do with it?

A

Postherpetic neuralgia is defined as pain persisting 30 days after the disappearance of the varicella/zoster rash and occurs with an overall incidence of 10-15%. Risk factors for the development of PHN include increased age (PHN incidence can be as high as 30-50% in elderly patients), female gender, increased pain or sensory abnormalities during the acute phase, a more severe skin lesion during the acute phase, and the presence of a prodrome.
VAccination decreases the incidence, and ethnicity has noting at all to do with it.

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32
Q

Why does upper extremity stuff never happen wiht celiac blocks?

A

Upper extremity injury does not occur because the approach to blocking the celiac plexus is approximately at the level of the first lumbar vertebra.

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33
Q

Side effects of celiac plexus block:

A

Celiac plexus neurolytic blocks are performed for chronic, intractable abdominal pain originating from most of the viscera. Adverse effects include hypotension, diarrhea, hiccups, pleurisy, retroperitoneal bleeding, abdominal aortic dissection, transient motor paralysis, and paraplegia.

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34
Q

The INR of 1.5 thing applies to which types of blocks?

A

Neuraxial, so if you were going to do a block in a compressible area (like intercostal) a higher INR wouldn’t really matter

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35
Q

What is a neurolytic block? What are the 5 criteria needed in order to reasonably do one of these?

A

A step further than a diagnostic block.
Five criteria for the use of neurolytic blocks are (all 5 needed):
1) The presence of severe pain
2) The failure of less invasive techniques to relieve the pain
3) The presence of well localized pain
4) The relief of pain with diagnostic local anesthetic blocks
5) The absence of adverse side effects after diagnostic blocks

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36
Q

Sympathetic blocks and Herpes Zoster vs Post-Herpetic neuralgia:
What is the treatment for PHN? Spinal cord stimulators?

A

Sympathetic blocks may be beneficial for acute herpes zoster infection but are NOT effective (C) for postherpetic neuralgia (PHN).
The treatment of PHN includes anticonvulsants, tricyclic antidepressants, lidocaine patches, topical capsaicin, opiates, and tramadol.
Spinal cord stimulators are also effective in PHN refractory to medical treatment.

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37
Q

What all does tramadol do?

A

ramadol has also proven effective in the treatment of PHN. It is a μ-opioid receptor agonist, NMDA antagonist, and norepinephrine and serotonin reuptake inhibitor. Tramadol also has a lower addiction profile relative to opioids which makes it attractive for providers to prescribe.

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38
Q

When are spinal cord stimulators contraindicated? Is this relative or absolute contraindication?
Absolute contraindications for spinal cord stimulators?

A

Spinal cord stimulators are relatively contraindicated in the setting of cognitive and psychological disability that interferes with proper usage and understanding of the device. (somatoform disorder)
Relative contraindications: Spinal cord stimulation is relatively contraindicated in the setting of major untreated psychological disease, substance abuse, and lack of social support.
Absolute contraindications for spinal stimulation include (but are not limited to): sepsis, coagulopathy, previous surgery or trauma obliterating the spinal canal, localized infection, and spinal bifida.

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39
Q

Where is the stellate ganglion located?
Possible complications of stellate ganglion block:
How would you think that there was an injection in the artery vs an injection intravenously? Bupi and this concept?

A

The stellate ganglion is located at the fusion of the inferior cervical and first thoracic ganglions at the level of the C7 transverse process. Subarachnoid injection, intraneural injection, pneumothorax, esophageal perforation, and chylothorax are other possible complications.
B/c with stellate ganglion block, a smaller amount is used, and the toxic dose for intrarterial injection (e.g. in the vertebral or carotid arteries) is lower due to a higher concentration of local anesthetic in the neurovascular tree.Injection of local anesthetic into the vertebral artery can result in CNS toxicity even at low doses due to the high local concentration. Bupivacaine, due to its potency and lipid-solubility, can cause CNS toxicity at lower doses than many other local anesthetics.

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40
Q

LAST and dosing of local anesthetics-lower doses=probs in which system vs higher doses?

A

Local anesthetic systemic toxicity occurs in a dose dependent fashion, with symptoms of lightheadedness, tinnitus, and numbness of the tongue occurring at lower doses followed by CNS toxicity and then progressing to CV toxicity at higher doses. Symptoms of CNS toxicity include seizures and unconsciousness.

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41
Q

Does fentanyl have active metabolites?
What is the deal with opioid induced neurotoxicity?
Who usually develops it, how long does it take to develop it?

A

No Opioids with active metabolites are more likely to cause symptoms and when development occurs the patient should stop the offending agent and be rotated to another agent.OIN can occur with any opioid, however those with active metabolites tend to be responsible more often - meperidine, codeine, morphine, and to a smaller extent hydromorphone. Neither fentanyl nor methadone has active metabolites and these opioids are least likely to cause neurotoxicity.

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42
Q

Which opioids do NOT have active metabolites?

A

Fentanyl and methadone

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43
Q

Does naloxone treat opioid induce neurotoxicity?

Would you add a benzo in OIN?

A

No.n addition, if the patient has severe neurologic symptoms and the clinician is concerned with development of seizures, they may start a trial of benzodiazepine to increase the seizure threshold. This may make the neurologic symptoms more pronounced in some patients thus needs to occur carefully and in selected patients.

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44
Q

How can someone go from having lower extremity regional complex pain syndrome to having failure of ejaculation? Why?

A

Lower extremity complex regional pain syndrome (CRPS) is treated with serial lumbar plexus sympathetic blocks which can be complicated by ejaculatory problems in males, particularly when bilateral blocks are performed.. This is due to the sympathetic dependance of the ejaculatory mechanism.

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45
Q

Complex regional pain syndrome types:

With either type, what symptoms can they have? What’ll happen if they progress w/out treatment?

A
Type I (formerly known as reflex sympathetic dystrophy or RSD) is usually caused by a TRIVIAL  injury, sprain, crush injury, or burn
Type II (formerly known as causalgia) is caused by a traumatic injury to a MAJOR NERVE TRUNK such as significant orthopedic trauma, gunshot injuries, or knife wounds. 
With either diagnosis, patients may develop burning pain and allodynia (pain to non-noxious stimuli).  Both syndromes are also characterized by autonomic dysfunction, which presents with localized temperature changes, cyanosis, and/or edema.  If the disease progresses without treatment, the skin can become glossy, smooth, and hairless
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46
Q

Diagnostic criteria for CRPS I:

A

signs, symptoms, and relief with a sympathetic block (upper or lower)

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47
Q

Treatment for CRPS:
Which medications do NOT work?
Any role for spinal cord stimulators?

A

Medications utilized in the treatment of CRPS, but with inconsistent success, include α-adrenergic blocking agents, calcium channel blockers, tricyclic antidepressants, and anticonvulsants. Surgical and neurolytic sympathectomies may also be performed for specific patients. Spinal cord stimulation has proven effective in the treatment of CRPS. Opioids are rarely effective or helpful in the management of CRPS.

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48
Q

methadone-Is it lipophilic? Metabolized by what? Excreted by what? Where does methadone work?

A

Because it is lipophilic, a considerable amount of tissue distribution occurs. Methadone undergoes hepatic metabolism and some renal excretion. Methadone works in the central nervous system on the mu, delta, and kappa receptors.

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49
Q

Methadone vs morphine-which one has the longer half life? Which one is easier to titrate?

A

Methadone, methadone is easier to titrate

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50
Q

What is TENS therapy? What theory is it based on?

A

Transcutaneous electrical nerve stimulation (TENS) uses low voltage electrical pulses to stimulate the nervous system and is used for a variety of pain syndromes. TENS can be used in a several different clinical settings: a physicians office, during physical therapy, and even for home use in selected patients. TENS therapy is based on the gate theory of pain where afferent input from large epicritic fibers competes with input from small pain fibers.

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51
Q

What is the GATE theory?

A

With the gate theory, it is proposed that second-order neurons at the level of the spinal cord dorsal horn act as a “gate” through which noxious stimuli must pass to reach higher centers in the brain and be perceived as pain. If these same neurons receive input from other sensory fibers entering through the same set of neurons in the spinal cord, the non-noxious input can effectively close the gate, preventing simultaneous transmission of noxious input. Thus, the light touch of rubbing an injured region or the pleasant electrical stimulation of TENS closes the gate to the noxious input of chronic pain.

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52
Q

When should TENS be used?

A

The device should only be used under medical supervision for adjunctive therapy and should not be intended for use as a substitute for pain medications and other pain management therapies”. Broader indications for TENS therapy include acute pain, musculoskeletal pain, neurologic pain, phantom limb pain, chronic pain and during the perioperative period

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53
Q

Contraindications for TENS:

A

Contraindications include patients with demand-type pacemakers, patients with known cardiac dysrhythmias, undiagnosed pain syndromes with unknown etiology, and mentally incompetent patients. There are differing thoughts on TENS therapy during pregnancy – some resources state it is safe following the first trimester while other sources consider it contraindicated throughout pregnancy due to the theoretical risk of premature labor. The FDA has not approved TENS use during pregnancy

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54
Q

Treatment for rib fractures:

Problems that can arise from rib fractures:

A

Treatment for rib fractures includes pain control and ventilatory supportThe ability to clear secretions also becomes impaired. This increases pulmonary complications and can lead to pneumonia. The elderly are at significant risk because of a decrease physiologic reserve. Patients older than 55 have nearly twice the mortality of younger patients with rib fractures.

55
Q

When would you use paravertebral blocks for rib fractures?

A

Paravertebral blocks have been shown to be similarly effective to epidural blockade when rib fractures are only on one side. Paravertebral blocks are associated with less hypotension when compared with epidural analgesia.

56
Q

What is the point of an epidural steroid injection, and what is the most common indication? Other indications:

A

Epidural steroid injections (ESI) are used to treat back pain, the most common indication for an ESI is radicular pain caused by a herniated disk.Additionally, indications for ESI include spinal stenosis with radicular symptoms and facet pain (difficulty turning)

57
Q

What is radicular pain and what does it indicate?

A

Radicular pain is pain that occurs along a nerve distribution. Radicular pain suggests compression and/or injury to the nerve root.

58
Q

Inability to void with back pain suggests _____. Will that respond favorably to ESI?

A

Cauda Equina Syndrome, and this will NOT respond favorably to epidural steroid injection

59
Q

Pain localized to the back-is it hard to treat? How does it respond to ESI? Paresthesias to S3-S5

A

Pain that is localized to the back is unlikely to respond favorably to ESI. Localized back pain is notoriously difficult to treat. Neither TENS nor ESI have demonstrated good response when treating localized back pain.
Paresthesia of the sacral dermatomes (S3-5)

60
Q

Non depolarizing neuromuscular blockers MOA:

A

competitive acetylcholine receptor inhibitors, effectively preventing the contraction of respiratory muscles.

61
Q

How does botulinium toxin work?

A

it blocks the release of acetylcholine at muscarinic and nicotinic receptors. It does this by inhibiting the intracellular fusion of acetylcholine containing vesicles to the nerve-terminal membrane (exocytosis) for release into the synaptic cleft.

62
Q

How do opioids work? Which type of receptors and second messenger system do they work with?

A

Opioids activate G-protein coupled inhibitory receptors both pre and postsynaptically to inhibit the release of excitatory neurotransmitters (presynaptic) and hyperpolarize postsynaptic neurons to inhibit neuronal transmission.

63
Q

Sweat glands ACh and NE thing

A

Okay

64
Q

Which opioid is lipophilic, and which one is hydrophilic and how does that work?
Delayed respiratory depression is a greater concern with which opioids?

A

Lipophilic opioids such as fentanyl work primarily at the dorsal horn of the spinal cord and through systemic absorption with passage to the brain, not by ascent in the CSF.
Ascent in the CSF to the brain (hydrophilic opioids such as morphine and hydromorphone)
Delayed respiratory depression is of greater concern with hydrophilic opioids like morphine and hydromorphone because they ascend in the CSF to reach the respiratory centers of the brainstem.

65
Q

How does carbamazepine work?

A

Carbamazepine inhibits sodium channels in neuronal cells inhibiting excitability and conduction.

66
Q

Most common complication of celiac plexus block:

A

Orthostatic hypotension

67
Q

When would you use a superior hypogastic block? what do those nerves supply? Where is that superior hypogastric plexus?

A

A superior hypogastric plexus block can provide pain relief for patients with PELVIC PAIN secondary to cancer or other nonmalignant conditions (post radiation inflammatory conditions, endometriosis, pelvic inflammatory disease, adhesions). The plexus lies in the retroperitoneum bilaterally from the lower third of L5 to the upper third of S1. The superior hypogastric plexus receives visceral afferents from the bladder (A), uterus (B), vagina, prostate, testes, urethra, descending colon, and rectum (E).

68
Q

When would you use a ganglion impar block?

A

a ganglion impar block may be indicated for chronic perineal pain.

69
Q

Does methadone have anything to do with serotonin?

A

NMDA antagonism and serotonin reuptake inhibition make methadone an effective choice for chronic neuropathic pain as well as modulation of some of the psychological concerns of patients living with chronic pain.

70
Q

T/F: Thoracic epidural analgesia and paravertebral blockade are considered the most effective methods of pain control in the management of post-thoracotomy pain.

A

Thoracic epidural analgesia and paravertebral blockade are considered the most effective methods of pain control in the management of post-thoracotomy pain.

71
Q

Again treatment of CRPS I and II

A

Treatment of CRPS I and II is the same and consists of physical therapy, sympathetic nerve blocks, oral gabapentin and memantine (an NMDA antagonist), and in refractory cases, spinal stimulators or intrathecal analgesic pumps.

72
Q

Pain chart over CRPS, myofascial pain syndrome and fibromyalgia:

A

Okay

73
Q

most common complication of celiac plexus blockade:

A

Orthostatic hypotension

74
Q

What is a major hurdle to determining optimal tx for phantom limb pain?

A

Phantom limb pain occurs in a significant number of amputee patients. No specific therapy has been shown through randomized controlled trials to be beneficial and the small sample sizes of patients in most of the studies makes it difficult to make solid recommendations. Pain management options are similar to those in other forms of chronic pain.

*Not enough RCT

75
Q

Methylprednisolone has what role in pain management? Not good for what?

A

Methylprednisolone, which may be beneficial during the acute phase of herpes zoster (another explanation said that it is not) is not effective for the treatment of chronic diabetic neuropathy. Better drug choices include methadone, tramadol, antiepileptics, TCAs, and SNRIs.

76
Q

How to treat neuropathic pain?

A

Better drug choices include methadone, tramadol, antiepileptics, TCAs, and SNRIs.

77
Q

Stepwise approach for cancer patients? And then look at photo:

A

Non-opioid analgesics (e.g., nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen) are first-line therapy for mild cancer-associated pain

78
Q

T/F: Neuroablation should be done immediately:

A

False.
Neuroablation, whether by thermal, chemical, or surgical techniques, should be avoided until life expectancy is short or unless one of the following conditions is present:
- Systemic therapy has failed
- Failure of neuraxial drug administration
- Selected focal lesions, such as pancreatic cancer
- Patient preference

79
Q

KIM that TCAs are good for ____ pain

A

neuropathic

80
Q

Fentanyl-is it more potent than morphine?

A

Yes-100x more potent

81
Q

How does a fentanyl patch work? How is fentanyl’s volume of distribution? How is transdermal fentanyl metabolized? Elimination after discontinuation?

A

When the patch is applied, there is a period of time where a depot is forming in the skin tissue which results in delayed analgesia. However, once this depot is formed there is a relatively constant delivery of fentanyl over the patch’s 72-hour application. This depot can take upwards of 12 to 24 hours to equilibrate out thus alternative forms of pain medication need to be provided during this time period. Fentanyl has a high volume of distribution and it is widely distributed in the lungs, kidneys, spleen, heart, brain, intestine, muscle, and adipose tissue. Transdermal fentanyl is mostly metabolized by the cytochrome P450 system in the liver. Fentanyl concentrations become clearance-limited after continuous administration compared with redistribution after a single dose of intravenous fentanyl. elimination after discontinuation of the transdermal patch is slow with an elimination half-life of approximately 17 hours.

82
Q

Transdermal fentanyl should be reserved for patients ___. Can you just give transdermal fentanyl out to all cancer patients?

A

over 12 years of age and those who weigh more than 50 kg.
No-in the U.S. it is indicated for more than just cancer pain. The manufacturers recommend that patients taking more than 45 mg of morphine equivalent a day be started on 25 mcg/hr transdermal patches.

83
Q

Transdermal fentanyl not indicated in:

A

Transdermal fentanyl is contraindicated for patients with acute pain or any pain state that requires rapid dose adjustments or any pain states that have states of pain-free intervals since the risk of respiratory depression is high.
No after surgery pain
No opioid maintenance program pain

84
Q

The most effective method for preventing postherpetic neuralgia (PHN) is

A

Prior vaccination

85
Q

Go through conversion of morphine all the way from intrathecal to PO

A

1 mg of intrathecal morphine = 10 mg of epidural morphine
1 mg of epidural morphine = 10 mg of IV morphine
1 mg of IV morphine = 3 mg of PO morphine

86
Q

Look at opioid conversion chart:

A

Okay

87
Q

Which pain meds lower the seizure thresholds?

A

tramadol and amitryptiline (TCAs)-especially in combo

88
Q

How would you know acetaminophen toxicity? Renal injury or hepatic injury first?

A

Typically patients will present with symptoms such as nausea, vomiting, abdominal pain, and/or malaise. Progressive hepatic injury may manifest as right upper quadrant pain and tenderness. Elevation in liver enzymes will typically start within 36 hours but may peak earlier, depending on the dosage. Maximal liver injury usually peaks between 3 and 5 days. Patients may develop jaundice, coagulopathy, and encephalopathy. The kidneys may be affected with resultant renal failure or oliguria. Renal injury lags behind hepatic injury.

89
Q

Treatment for acetaminophen toxicity:

Side effects of this toxicity

A

When administered early, NAC provides cysteine for the replenishment and maintenance of hepatic glutathione stores which enhances the elimination pathway and may reduce the hepatic toxicity of acetaminophen. NAC is most effective when administered within the first 8-10 hours after an overdose however it should be provided to patients outside this window according to the above nomogram or if toxicity is ever suspected. NAC has few side effects - nausea and vomiting being the most commonly reported. Minor anaphylactoid reactions do occur. More serious reactions are rare and more common with intravenous formulations.

90
Q

Is acetaminophen toxic?

A

Acetaminophen itself is not toxic; instead it results in enzyme induction that overwhelms the hepatic systems.

91
Q

Spinal cord stimulators and baclofen pumps in managing CRPS?

A
LAST RESORTS (try physical therapy, TCAs, and even a lumbar sympathetic block first) 
A spinal cord stimulator is a treatment of last resort in CRPS.  The other terminal treatment option is an intrathecal pump to deliver opioids or baclofen.
92
Q

Gabapentin has minimal ___ and ___ side effects.

A

Gabapentin has minimal cardiac and respiratory side effects

93
Q

What is gabapentin? How does it work? Uses? What are some side effects? Does it have abuse potential?

A

Gabapentin is an anticonvulsant originally approved for the treatment of partial seizure epilepsy and later for treatment of neuropathic pain. It binds and inhibits the alpha2-delta subunit of the voltage-gated calcium channel. This results in a decreased release of the excitatory neurotransmitter glutamate.
Gabapentin has multiple uses such as depression, anxiety, painful diabetic neuropathy, trigeminal neuralgia, and phantom-limb pain. Enhanced recovery after surgery (ERAS) protocols frequently incorporate gabapentin as part of a multimodal analgesia approach. Common side effects include nausea, sedation, dizziness, ataxia, nystagmus, peripheral edema, and weight gain.

94
Q

It is the primary neurotransmitter mediating afferent nociceptive transmission from the dorsal root ganglia to the spinal cord.

Response to this?

A

What is glutamate?

Response: Signal transmission triggers NMDA glutamate receptor activity.

95
Q

Efficacy of epidural steroid injections (ESIs) for lumbar radiculopathy is inversely correlated with

A

Duration of symptoms

96
Q

What is radiculopathy? Signs? Treatment?

A

Radiculopathy is one of the most common causes of lower back pain and is often due to intervertebral disc or spinal pathology. This includes herniated discs, facet syndrome, spinal or foraminal stenosis, or internal disc disruption. Symptoms of radiculopathy include pain described as sharp and shooting, paresthesias, and numbness in a dermatomal pattern. Signs include decreased reflexes, weakness, and positive straight-leg raise test.
SIs are a common treatment in those patients who do not respond to conservative measures such as physical therapy and pharmacologic treatment.

97
Q

Factors predicting decreased success of ESI include:

A

Factors predicting decreased success of ESI include: chronic symptoms, presence of psychopathology, and prior back surgery.

98
Q

Symptoms of spinal stenosis of worsened by _____. Spinal stenosis is made better by:

A

worsened by extension and improved with spinal flexion. Walking uphill or squatting causes lumbar flexion and improves symptoms.

99
Q

In spinal stenosis-sensory or motor nerves are damaged first? What is neurogenic claudication?

A

Sensory nerves are effected before motor nerves. Pain is often the first symptoms of spinal stenosis. Pain is followed by numbness and finally weakness. Neurogenic claudication is pain that worsens with exercise or activity.

100
Q

What is lateral recess stenosis, and how is its pain pattern?

A

Lateral recess stenosis causes radicular pain in the nerve above the spinal level. The lateral recess is very posterior in the spinal canal and impinges on nerves leaving the canal at the level above the corresponding vertebral level. For example, lateral recess stenosis of L3-4 will cause radicular pain of the L2 nerve.

101
Q

TENS is good when?

A

TENS is an effective modality in pain management of post-thoracotomy pain and can be especially useful in patients in whom neuraxial anesthesia is contraindicated. With regards to patients on antithrombotic agents, paravertebral blocks follow the same guidelines as neuraxial anesthesia.

102
Q

Refresh: contraindications to neuraxial anesthesia (not just spinals and epidurals for preggo, but paravertebral blocks andthoracic epidurals for other people)

A

contraindications to neuraxial anesthesia include hypovolemia, shock, increased intracranial pressure, coagulopathy or thrombocytopenia, sepsis, or infection at the puncture site.

103
Q

Tx of CRPS II:

A

Treatment of CRPS type II consists of physical therapy, tricyclic antidepressants, gabapentin, sympathetic blocks, somatic blocks, spinal cord stimulators, and intrathecal medications

104
Q

Can valproic acid ever be used for pain?

A

Valproic acid (E) has been effective in treating other neuropathic pain conditions, but has not been shown to provide effective pain relief in complex regional pain syndrome (CRPS) type II.

105
Q

Allodynia:

A

neuropathic pain that is not in any particular distribution and is elicited by stimuli that are not normally painful, which is characteristic of allodynia. Allodynia can be peripheral or central sensitization from inflammation or central dysregulation and results in pain from nonpainful stimuli

106
Q

What is anesthesia dolorosa:

A

Anesthesia dolorosa is when pain is invoked a region that is denervated and should not have sensation at all and is considered a pain referral phenomenon.

107
Q

What is hyperalgesia?

A

Hyperalgesia is an increased response to a stimulus which is normally painful

108
Q

Contraindications to trigger point injections (absolute and relative)

A

Absolute contraindications include a site that is not safely accessed by a needle and cellulitis or another conditions that cause a loss of skin integrity overlying the site of the TPI. There are several relative contraindications including severe fibromyalgia, numerous trigger points, poorly controlled systemic illness that may compromise healing or predispose to infection, bleeding disorder, anticoagulation use, history of keloid, and/or highly anxious needle-phobic patient.

109
Q

What is a trigger point?

A

n most cases, there is a defined and reproducible site of tenderness in the affected muscle that can be targeted for relief of pain and spasm. Trigger points are taut bands of skeletal muscle that produce a characteristic pattern of pain. There are two ‘types’ – active and latent. Active trigger points produce spontaneous pain and are painful on palpation where latent points produce pain only when palpated. Trigger points may result from prolonged use of muscle, overload or overuse injury, and/or trauma. Trigger point myofascial pain may have a referred pain pattern that will help allow distinction from tender points.

110
Q

Picture of lumbar dermatomes.

Inner thigh

A

Okay

L3

111
Q

Somatic pain: What is it caused by? How can you differentiate between it and neuropathic pain?

A

Somatic pain is caused by tissue injury and is sharp and well localized. This patient has no acute tissue injury, and her pain is burning and tingling, which is more characteristic of neuropathic pain.

112
Q

Myofascial pain is characterized by

A

the presence of loci of hypersensitivity within a tender, taut, palpable band of muscle called a trigger point. Trigger points are not a component of this patient’s pain.

113
Q

Define neuropathic pain:

A

Neuropathic pain is caused by abnormal signal processing in the peripheral or central nervous system and denotes nervous system damage or dysfunction. It is characterized by burning, tingling, or shooting sensations, which can happen with or without stimulus.
Often caused by a stimulus that would not usually cause pain.

114
Q

Inflammatory pain:

A

refers to pain following tissue injury but with no neural injury. It is characterized as a dull, aching, and poorly localized pain. This patient’s pain is burning, and tingling, which is more suggestive of neuropathic pain.

115
Q

In acute injury resulting in lumbosacral radiculopathy, conservative treatment such as______ should be the first line of therapy. Then,

A

acetaminophen and NSAIDs

Then you can go on to PT (2-4 weeks), ESI, Neuroablation, surgery, etc.

116
Q

When are sympathetic blocks useful?

A

vascular, neuropathic, and visceral pain. The theory is that the sympathetic block will improve circulation and relieve pain, especially in vaso-occlusive diseases. Vascular diseases such as arterial/venous occlusion, vasospasm, Raynaud syndrome, and thromboangiitis obliterans may benefit from a sympathetic block.

Visceral pain, such as those seen from various abdominal cancers, acute myocardial infarction, and refractory angina can be treated with sympathetic blocks. Neuropathic pain from diabetes, herpes zoster, and complex regional pain syndrome (CRPS) may see some improvement from these blocks.

117
Q

T/F:Chest pain from an acute infarction and angina that is refractory to treatment can be treated with a sympathetic block.

A

Apparently true (eye roll emoji) who blocks someone who literally just had a heart attack?

118
Q

Some common sympathetic ganglion blocks:

A

Stellate ganglion: Located between C6-7. Can be blocked for pain (vascular, neuropathic, or visceral) that is related to the upper extremities and thorax. Complications include Horner syndrome, tracheal/esophageal injury, pneumothorax, and recurrent laryngeal nerve injury.

Celiac plexus: Located beside the aorta and inferior vena cava at the level of L1. The block is frequently done with a posterior approach with the entry point just below the 12th rib. This block is done for pain relating to abdominal cancers. Complications include bleeding, retroperitoneal hematoma, chylothorax, perforation of nearby structures, and pneumothorax.

Lumbar sympathetic chain: Located anterior to L1-L5 and the block is done via a posterior approach. This block may benefit those with neuropathic pain in the lower limbs, phantom limb pain of the lower extremities, and visceral pain involving the intestinal/urinary system. Complications involve perforation of nearby structures, genitofemoral nerve injury, and bleeding.

119
Q

Sympathetic blocks from acute burn pain

A

No. only if they later go on to have neuropathic pain

120
Q

Nociceptive stimuli are mainly transmitted by

A

Nociceptive stimuli are mainly transmitted by smaller diameter, thinly myelinated, or unmyelinated Aδ and C fibers.

121
Q

How does a spinal cord stimulator work?

A

A spinal cord stimulator provides electrical stimulation to larger fibers, which have a lower threshold for recruitment by external electrical stimulation, and thereby closes the “gate” of the dorsal column. The closed “gate” prohibits transmission of the smaller, slower conducting fibers associated with chronic pain sensation. In other words, by triggering larger, faster transmitting Aα (conduction velocity 80-120 m/s) and Aβ fibers (30-70 m/s) within the same distribution as the slower Aδ (5-25 m/s) and C fibers (0.6-2 m/s) that are transmitting pain, a spinal cord stimulator effectively closes the “gate” in the dorsal horn, thereby reducing nociception.

122
Q

Is the anterior cingulate cortex involved in spinal cord stimulators?

A

The anterior cingulate cortex is involved in higher cortical processing of pain information and is not as directly affected by a spinal cord stimulator as is the substantia gelatinosa.

123
Q

Spinothalamic tract and spinal cord stimulators:

A

The spinothalamic tract contains second order neurons that cross to the contralateral side of the spinal cord via the anterior white commissure and ascend to the posterior complex of the thalamus. Since the tract is distal to the dorsal horn in the signal transmission sequence, a spinal stimulator will prohibit the noxious stimuli from making it to the spinothalamic tract.

124
Q

T/F: The rate of surgical intervention for management of intractable radicular symptoms is reduced with the use of cervical ESIs.

A

TRUE

125
Q

ESIs are used to treat what? Do they have a high success rate?

A

Epidural steroid injections (ESIs) are commonly used to provide short-term analgesia for acute radicular pain due to disk herniation/protrusion or spinal stenosis with nerve impingement
Epidural steroid injections have a high success rate for providing short-term analgesia for acute radicular pain due to disk herniation/protrusion or spinal stenosis with nerve impingement.

126
Q

Where are the lumbar sympathetic ganglia?

What muscle is located posteromedial to the ganglia? Does it have a risk of injection?

A

The lumbar sympathetic ganglia are located along the anterolateral surface of the second to fourth lumbar vertebral bodies, anteromedial to the psoas muscle.
The psoas major is located posteromedial to the ganglia, it can be injected into during a lumbar sympathetic block.

127
Q

Signs and symptoms of serotonin syndrome:

Treatment:

A

Signs and symptoms can include altered mental status, autonomic hyperactivity/instability (flushing, sweating, tachycardia, hyperthermia), metabolic acidosis, tremor, clonus, and muscle rigidity. The presence of muscle rigidity and hyperthermia are associated with life-threatening toxicity. Treatment primarily includes supportive care and withdrawal of offending drugs. Sedation with benzodiazepines may be needed. Cyproheptadine, an oral 5HT1A and 5HT2A antagonist, may also be administered for serious cases.

128
Q

Why are SSRIs and tramadol a bad idea?

A

First, the SSRI itself increases serotonin levels by inhibiting serotonin reuptake back into presynaptic cells. Second, SSRIs inhibit cytochrome CYP2D6. This enzyme is responsible for metabolism of tramadol.

129
Q

Buproprion and serotonin:

A

Bupropion is a selective norepinephrine reuptake inhibitor with only mild effects on serotonergic activity. It is much less likely to contribute to serotonin syndrome than an SSRI

130
Q

Tell me about cryoanalgesia:

Can ppl who get cryoanalgesia have weird nerve sensations afterwards?

A

Cryoanalgesia is a specialized type of nerve block that can be used as an adjunctive procedure to improve chronic or postoperative pain. Intercostal nerve cryoanalgesia for post-thoracotomy pain has been shown to decrease opioid use and improve postoperative pulmonary function. Nerve regeneration after cryoanalgesia occurs over the first 1-3 months following the procedure
Dysesthesia (tactile hallucination) can occur after cryoanalgesia, but this could not be differentiated from the patients who had persistent post-thoracotomy pain from surgical trauma.

131
Q

Trigeminal neuralgia: Best treated with what? Do opioids work?

A

The primary treatment for trigeminal neuralgia is an antiepileptic drug, such as carbamazepine. Opioid medications are not typically appropriate for neuropathic pain.

132
Q

How does Lyrica (Pregablin) work? Can it cause serotonin syndrome?

A

Pregabalin is a calcium channel ligand agent which results in a decreased release of glutamate, norepinephrine, and substance P (all chemicals that are considered pro-nociceptive). It can have major side effects such as sedation, dizziness, and peripheral edema.

133
Q

Serotonin syndrome vs malignant hyperthermia:

A

Often serotonin syndrome (SS) can present similar to malignant hyperthermia (MH), however MH is usually associated with a fever which continues to get worse. Furthermore, MH typically presents with severe muscle rigidity where SS may present with myoclonus.

134
Q

Visceral pain-5 things about it:

A

Visceral pain has five components:

  1. It is not evoked from all viscera. Some organs are not sensitive to pain.
  2. Visceral pain is not always linked to visceral injury. For example, cutting the intestine does not cause pain.
  3. Visceral pain is diffuse and poorly localized.
  4. Visceral pain can be referred to locations outside the one where injury is occurring.
  5. Visceral pain may be accompanied with motor and autonomic reflexes. An example is renal colic that can cause significant nausea, vomiting, and lower-back muscle spasms.