Week 3 Flashcards

Centrally acting nonopioid analgesics

1
Q

Spinal clonidine causes a 30% prolongation of ______________________ from local anesthetics

A
  • sensory and motor block

Stoelting’s, pg. 258

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2
Q

The FDA has issued a black box warning concerning the use of neuraxial clonidine in obstetric anesthesia because of _________________

A
  • maternal hemodynamic instability

hypotension and bradycardia

Stoelting’s, pg. 258

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3
Q

Dexmedetomidine has a ___________ affinity for a2 receptors than clonidine and is associated with ___________ hemodynamic and systemic side effects

A
  • higher
  • fewer/less

Stoelting’s, pg. 258

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4
Q

When used as an adjunct to intrathecal opioids, neostigmine reduced the ED50 of _____________ by approximately 25%

A
  • sufentanil

Stoelting’s, pg. 259

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5
Q

What adverse effects has made neostigmine an UNpopular choice for neuraxial adjuvant therapy?

A
  • GI - N/V
  • Bronchospasm

Stoelting’s, pg. 259

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6
Q

True or false:

Anesthetic and subanesthetic doses of ketamine have analgesic properties as a result of competetive antagonism of NMDA receptors

A
  • False - the action of ketamine is NONcompetetive antagonism

Stoelting’s, pg. 259

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7
Q

The primary analgesic effect of ketamine is mediated by antagonizing _____________ receptors located on _____________ neurons in the dorsal horn of the spinal cord

A
  • NMDA
  • secondary afferent

this prevents enhancement of excitatory neurotransmission

Stoelting’s, pg. 260

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8
Q

A ________ mg dose of epidural ketamine can produce excellent postoperative pain relief

A
  • 30

low doses (4, 6, 8 mg) were ineffective

Stoelting’s, pg. 260

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9
Q

Reported side effects of epidural ketamine include ____________, ______________, and ____________ with doses greater than 0.5 mg/kg

A
  • sedation
  • headache
  • transient burning back pain

Stoelting’s, pg. 260

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10
Q

The advantage of intrathecal ketamine is the lack of ___________ and ______________

A
  • cardiovascular effects
  • respiratory depression

Stoelting’s, pg. 261

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11
Q

Intrathecal midazolam produces analgesia by acting on ____________ receptors and reducing spinal cord excitability

A
  • GABA-A

also shown to act at opioid receptors

Stoelting’s, pg. 261

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12
Q

The addition of midazolam to epidural analgesia was associated with a significant reduction in the incidence of _______________

A
  • postoperative nausea and vomiting

Stoelting’s, pg. 261

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13
Q

True or false:

Intrathecal midazolam is more effective for treatment of somatic pain than visceral pain

A
  • True

Stoelting’s, pg. 262

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14
Q

Epidural droperidol is effective for reducing __________ and postoperative nause and vomiting

A
  • pruritus

direct actions on the brainstem CTZ

Stoelting’s, pg. 262

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15
Q

Intrathecal adenosine does not inhibit acute pain but is effective in treating ____________

A
  • allodynia
  • hyperalgesia
  • neuropathic pain

Stoelting’s, pg. 262

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16
Q

Adenosine shows antinociceptive activity at receptors located in the dorsal horn - another proposed mechanism is enhancement of spinal ______________ release

A
  • norepinephrine

Stoelting’s, pg. 262

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17
Q

__________ is the only FDA-approved, nonopioid approved for intrathecal administration for the treatment of neuropathic pain

hint - think snails

A
  • Ziconotide

marine snail venom derivative

Stoelting’s, pg. 263

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18
Q

___________ is a synthetic octapeptide of the somatostatin derivative of HGH, and causes analgesia when administered spinally

A
  • octreotide

Stoelting’s, pg. 263

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19
Q

Baclofen is an agonist of the ___________ receptor and has demonstrated efficacy in chronic pain syndromes (MS, CRPS), and the spasticiy/dystonia related to cerebral palsy

A
  • GABA-B

Stoelting’s, pg. 263

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20
Q

The intrathecal delivery of COX inhibitors such as __________ theoretically would reduce pain and central sensitization

A
  • ketorolac
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21
Q

The pharmacokinetics of ketorolac in CSF suggest ___________; therefore, continuous infusion may be more effective

A
  • rapid elimination

Stoelting’s, pg. 264

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22
Q

True or false:

Intrathecal ketorolac relieves chronic pain and extends anesthesia/analgesia from intrathecal bupivicaine administration

A
  • False - it does neither of these things and may have limited efficacy in humans

Stoelting’s, pg. 264

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23
Q

What is the mechanism of action for neuraxial magnesium?

A
  • regulates influx of calcium ions into cells
  • antagonism of central NMDA receptors

unclear neuraxial dosing

Stoelting’s, pg. 264

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24
Q

What are the differences in function of COX-1 and COX-2 isoenzymes?

A

COX-1→prostaglandins

  • renal function maintenance
  • GI mucosal protection
  • proaggretory A2 production

COX-2→prostaglandins

  • pain mediation
  • inflammation
  • fever

Stoelting’s, pg. 269

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25
Q

____________ is a poor inhibitor of COX-1 and COX-2 but evidence indicates that it may have action at central anti-nociceptive pathways

A
  • Acetaminophen

Stoelting’s, pg. 269, 274

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26
Q

COX-2 selective inhibitors have ____________ gastrointestinal toxicity than nonselective NSAIDS, and ________________ cardiovascular risk

A
  • less
  • more

Stoelting’s, pg. 269

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27
Q

Which drug is the only COX-2 selective inhibitor available for clinical use? Which patient population should it be used cautiously in?

A
  • Celecoxib
  • patients with underlying cardiovascular disease

Stoelting’s, pg. 269

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28
Q

Why has the use of nonspecific NSAIDs been limited in the perioperative setting?

A

Associated with:

  • platelet dysfunction
  • gastrointestinal toxicity

Stoelting’s, pg. 270

29
Q

True or false:

Because NSAIDs are primarily eliminated in bile, dose reduction is unnecessary in patients with impaired kidney function

A
  • False - primary elimination is renal AND biliary, and dose reduction is required

Stoelting’s, pg. 270

30
Q

The following is a list of nonselective NSAIDs - sort them into one of four groups (Acetic Acid Group, Oxicam Group, Propionic Acid Group, Salicylate)

  • Naproxen
  • Aspirin
  • Ketoprofen
  • Ketorolac
  • Fenoprofen
  • Meloxicam
  • Ibuprofen
A

Acetic Acid

  • Ketorolac

Oxicam

  • Meloxicam

Propionic Acid

  • Fenoprofen
  • Ibuprofen
  • Ketoprofen
  • Naproxen

Salicylate

  • Aspirin

Stoelting’s, pg. 271-272

31
Q

It is generally recommended that patients with gastrointestinal risk factors should be treated with ____________ or _____________

A
  • COX-2 selective agents
  • nonselective NSAIDs WITH gastrointestinal protective therapy

Stoelting’s, pg. 272

32
Q

NSAIDs are associated with an increased risk of cardiovascular adverse events such as ___________

A
  • MI
  • heart failure
  • hypertension

appears to be regardless of COX selectivity

Stoelting’s, pg. 272

33
Q

When NSAID therapy is required for patients at risk of cardiovacular complications, _____________ is recommended as the NSAID of choice

A
  • naproxen

AHA: use NSAIDs at lowest effective dose to reduce CV risks

Stoelting’s, pg. 273

34
Q

The effects of the NSAIDs on renal function are due to alterations in __________ and _____________

A
  • filtration rate
  • renal plasma flow

Stoelting’s, pg. 273

35
Q

Avoiding perioperative use of NSAIDs in patients with ___________ from any cause is an important means of minimizing renal injury

A
  • hypovolemia

Stoelting’s, pg. 273

36
Q

Renal side effects of NSAIDs occur more frequently in patients with __________ and ___________

A
  • congestive heart failure
  • established renal disease with altered intrarenal plasma flow (diabetes, hypertension, atherosclerosis)

Stoelting’s, pg. 273

37
Q

Patients with a history of ___________ and/or _________ are at an increased risk for anaphylaxis related to NSAIDs

A
  • nasal polyps
  • asthma

these patients should use COX-2 instead

Stoelting’s, pg. 273

38
Q

___________ is the leading cause of acute liver failure in the United States

A
  • Acetaminophen
39
Q

Nonselective NSAIDs may interact with the following drugs - describe the mechanism

  • antiplatelet agents
  • digoxin
  • anticonvulsant agents
A
  • antiplatelet agents via additive inhibition of platelet inhibition
  • digoxin via decreased renal clearance and increased plasma drug concentration
  • anticonvulsants via displacement from their protein binding sites

Stoelting’s, pg. 273-274

40
Q

Acetaminophen has little, if any, antiinflammatory action and debate exists about its primary site of action - what are 2 possible mechanisms of its analgesic effects?

A
  • central activation of descending serotonergic pathways
  • antagonizes neurotransmission of NMDA, substance P, nitric oxide pathways in the spinal cord

Stoelting’s, pg. 273

41
Q

Total daily doses of acetaminophen should not exceed _________ or __________ for chronic alcoholics

A
  • 4,000 mg
  • 2,000 mg

FDA advised maybe 2,600 has an alternative max daily dose

Stoelting’s, pg. 274

42
Q

____________ is administered as an antidote to acetaminophen toxicity - it acts as a precursor for ________ and neutralize __________ directly

A
  • acetylcysteine
  • glutathione
  • NAPQI

NAPQI is an active metabolite that depletes the antioxidant glutathione

Stoelting’s, pg. 274

43
Q

___________ irreversibly inactivates COX, leading to prolonged inhibition of platelet aggregation

A
  • aspirin

Stoelting’s, pg. 274

44
Q

__________ have the most powerful antiinflammatory characteristics of all the steroids

A
  • glucocorticoids

Stoelting’s, pg. 275

45
Q

Patients treated with which steroid experienced less postoperative pain and required less postoperative opioids?

A
  • Dexamethasone

Stoelting’s, pg. 277

46
Q

What type of steroid has a greater effect on water and electrolyte balance?

What is the main endogenous hormone with this effect?

A
  • mineralocorticoids
  • aldosterone

Stoelting’s, pg. 275

47
Q

True or false:

The use of dexamethsone and other glucocorticoids as an adjuvant in regional anesthesia is limited due to it’s neurotoxic effects

A
  • False - it has been found to prolong block duration and evidence supports its use in multimodal analgesia

Stoelting’s, pg. 277

48
Q

The only proven efficacy of epidural steroid injections is their ability to speed resolution of ____________

A
  • sciatica in patients with acute intervertebral disc herniation

Stoelting’s, pg. 277

49
Q

Local anesthetics that block _____________ channels have long been used to abolish pain temporarily

A
  • voltage gated sodium

these channels play a role in the control of neuron excitability

Stoelting’s, pg. 277

50
Q

Systemically administered local anesthetics such as ___________ are effective in a number of chronic pain conditions

A
  • IV lidocaine

Stoelting’s, pg. 277

51
Q

At low doses, initial CNS symptoms of local anesthetics include:

A
  • lightheadedness
  • dizziness
  • tinnitus
  • vertigo
  • blurred vision
  • altered taste

Stoelting’s, pg. 277

52
Q

At higher doses, local anesthetics may cause what serious CNS symptom

A
  • seizures

Stoelting’s, pg. 277

53
Q

Cardiovascular side effects of systemic local anesthetics include:

A
  • hypotension
  • bradycardia
  • cardiovascular collapse
  • cardiac arrest

Stoelting’s, pg. 277

54
Q

The topical application of __________ has been used in postherpetic neuralgia and after different surgical procedures

A
  • 5% lidocaine

Stoelting’s, pg. 277

55
Q

__________ is a transient receptor potential vanilloid (TRPV) channel agonist that can be used in conditions such as arthritis, myalgias, arthralgias, and neuralgias

A
  • capsaicin

Stoelting’s, pg. 278

56
Q

Ketamine, at low ____________ doses exerts a specific NMDA bloackade - this modulates ___________ induced by the incision/tissue damage

A
  • subanesthetic
  • central sensitization

Stoelting’s, pg. 278

57
Q

The clinical use of ketamine can be limited due to what adverse effects?

A
  • psychomimetic
  • dizziness
  • blurred vision
  • nausea/vomiting

Stoelting’s, pg. 278

58
Q

____________ is a highly selective, central alpha 2 agonist with sedative, proanesthetic, and proanalgesic effects

A
  • dexmedetomidine

Stoelting’s, pg. 278

59
Q

Which medications are approved as anticonvulsants, but have demonstrated some efficacy in treating pain by acting on voltage-dependent calcium channels at the dorsal horn of the spinal cord?

A
  • gabapentin
  • pregabalin

reduces release of glutamate

Stoelting’s, pg. 264

60
Q

How do peripherally acting analgesics work?

A

Peripheral analgesics act at the sensory input level by blocking transmission of the impulse to the brain

Their common feature was believed to be their site of action within the damaged tissues, and hence they were termed “peripheral analgesics”

61
Q

What are some inflammatory mediators that peripheral analgesics inhibit the release of?

A
  • Prostanoids
  • Bradykinin
  • Adenosine triphosphate
  • Histamine
  • Serotonin
62
Q

NSAIDS MOA?

A

NSAIDs inhibit the biosynthesis of prostaglandins by preventing the substrate arachidonic acid from binding to the cyclooxygenase (COX) enzyme active site

The COX enzyme exists as –>
* COX-1 isoenzyme
* COX-2 isoenzyme

63
Q

Oral dose of acetaminophen?

A
  • 325 to 650 mg every 4 to 6 hours
  • Not exceed 4,000 mg daily, most clinicians will not exceed 3,000 mg daily

IV preparation of acetaminophen is currently available for clinical use

64
Q

What are you likely to see with aspirin overdose?

A

The mechanism of NSAID toxicity in overdose is related to both their acidic nature and their inhibition of prostaglandin production

  • Nausea, vomiting, abdominal pain, tinnitus, hearing impairment, and central nervous system (CNS) depression
  • With higher dose aspirin ingestion –> Metabolic acidosis, renal failure, CNS changes (agitation, confusion, coma), and hyperventilation with respiratory alkalosis due to stimulation of the respiratory center occurs
65
Q

What is the primary corticosteroid in which all other corticosteroids are judged against?

A

The primary corticosteroid is hydrocortisone, which is the standard against which the pharmacologic properties of various synthetic corticosteroids are judged

66
Q

Ketolorac dosage in Adults and Peds?

A

Adult 15-30mg IV q6h

Pediatric 0.5mg/kg IV q6h

67
Q

Dexmedetomidines proanesthetic and proanalgesic dosage?

A

0.5 to 2mcg/kg given intravenously

68
Q

MOA of Ketamine?

A

Noncompetitive antagonism ofN-methyl-D-aspartate (NMDA) receptors