Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Nurs 575 Anesthesia Pharmacology > Week 3 > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A
  • sufentanil

Stoelting’s, pg. 259

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A
  • GI - N/V
  • Bronchospasm

Stoelting’s, pg. 259

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A
  • cardiovascular effects
  • respiratory depression

Stoelting’s, pg. 261

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

True or false:

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

A
  • True

Stoelting’s, pg. 262

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A
  • allodynia
  • hyperalgesia
  • neuropathic pain

Stoelting’s, pg. 262

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A
  • octreotide

Stoelting’s, pg. 263

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A
  • ketorolac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A
  • rapid elimination

Stoelting’s, pg. 264

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
____________ is a poor inhibitor of COX-1 and COX-2 but evidence indicates that it may have action at central anti-nociceptive pathways
* Acetaminophen ## Footnote Stoelting's, pg. 269, 274
26
COX-2 selective inhibitors have ____________ gastrointestinal toxicity than nonselective NSAIDS, and ________________ cardiovascular risk
* less * more ## Footnote Stoelting's, pg. 269
27
Which drug is the only COX-2 selective inhibitor available for clinical use? Which patient population should it be used cautiously in?
* Celecoxib * patients with underlying cardiovascular disease ## Footnote Stoelting's, pg. 269
28
Why has the use of nonspecific NSAIDs been limited in the perioperative setting?
Associated with: * platelet dysfunction * gastrointestinal toxicity ## Footnote Stoelting's, pg. 270
29
# True or false: Because NSAIDs are primarily eliminated in bile, dose reduction is unnecessary in patients with impaired kidney function
* False - primary elimination is renal AND biliary, and dose reduction is required ## Footnote Stoelting's, pg. 270
30
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
**Acetic Acid** * Ketorolac **Oxicam** * Meloxicam **Propionic Acid** * Fenoprofen * Ibuprofen * Ketoprofen * Naproxen **Salicylate** * Aspirin ## Footnote Stoelting's, pg. 271-272
31
It is generally recommended that patients with gastrointestinal risk factors should be treated with ____________ or _____________
* COX-2 selective agents * nonselective NSAIDs WITH gastrointestinal protective therapy ## Footnote Stoelting's, pg. 272
32
NSAIDs are associated with an increased risk of cardiovascular adverse events such as ___________
* MI * heart failure * hypertension | appears to be regardless of COX selectivity ## Footnote Stoelting's, pg. 272
33
When NSAID therapy is required for patients at risk of cardiovacular complications, _____________ is recommended as the NSAID of choice
* naproxen | AHA: use NSAIDs at lowest effective dose to reduce CV risks ## Footnote Stoelting's, pg. 273
34
The effects of the NSAIDs on renal function are due to alterations in __________ and _____________
* filtration rate * renal plasma flow ## Footnote Stoelting's, pg. 273
35
Avoiding perioperative use of NSAIDs in patients with ___________ from any cause is an important means of minimizing renal injury
* hypovolemia ## Footnote Stoelting's, pg. 273
36
Renal side effects of NSAIDs occur more frequently in patients with __________ and ___________
* congestive heart failure * established renal disease with altered intrarenal plasma flow (diabetes, hypertension, atherosclerosis) ## Footnote Stoelting's, pg. 273
37
Patients with a history of ___________ and/or _________ are at an increased risk for anaphylaxis related to NSAIDs
* nasal polyps * asthma | these patients should use COX-2 instead ## Footnote Stoelting's, pg. 273
38
___________ is the leading cause of acute liver failure in the United States
* Acetaminophen
39
Nonselective NSAIDs may interact with the following drugs - describe the mechanism * antiplatelet agents * digoxin * anticonvulsant agents
* 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 ## Footnote Stoelting's, pg. 273-274
40
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?
* central activation of descending serotonergic pathways * antagonizes neurotransmission of NMDA, substance P, nitric oxide pathways in the spinal cord ## Footnote Stoelting's, pg. 273
41
Total daily doses of acetaminophen should not exceed _________ or __________ for chronic alcoholics
* 4,000 mg * 2,000 mg | FDA advised maybe 2,600 has an alternative max daily dose ## Footnote Stoelting's, pg. 274
42
____________ is administered as an antidote to acetaminophen toxicity - it acts as a precursor for ________ and neutralize __________ directly
* acetylcysteine * glutathione * NAPQI | NAPQI is an active metabolite that depletes the antioxidant glutathione ## Footnote Stoelting's, pg. 274
43
___________ irreversibly inactivates COX, leading to prolonged inhibition of platelet aggregation
* aspirin ## Footnote Stoelting's, pg. 274
44
__________ have the most powerful antiinflammatory characteristics of all the steroids
* glucocorticoids ## Footnote Stoelting's, pg. 275
45
Patients treated with which steroid experienced less postoperative pain and required less postoperative opioids?
* Dexamethasone ## Footnote Stoelting's, pg. 277
46
What type of steroid has a greater effect on water and electrolyte balance? What is the main endogenous hormone with this effect?
* mineralocorticoids * aldosterone ## Footnote Stoelting's, pg. 275
47
# True or false: The use of dexamethsone and other glucocorticoids as an adjuvant in regional anesthesia is limited due to it's neurotoxic effects
* False - it has been found to prolong block duration and evidence supports its use in multimodal analgesia ## Footnote Stoelting's, pg. 277
48
The only proven efficacy of epidural steroid injections is their ability to speed resolution of ____________
* sciatica in patients with acute intervertebral disc herniation ## Footnote Stoelting's, pg. 277
49
Local anesthetics that block _____________ channels have long been used to abolish pain temporarily
* voltage gated sodium | these channels play a role in the control of neuron excitability ## Footnote Stoelting's, pg. 277
50
Systemically administered local anesthetics such as ___________ are effective in a number of chronic pain conditions
* IV lidocaine ## Footnote Stoelting's, pg. 277
51
At low doses, initial CNS symptoms of local anesthetics include:
* lightheadedness * dizziness * tinnitus * vertigo * blurred vision * altered taste ## Footnote Stoelting's, pg. 277
52
At higher doses, local anesthetics may cause what serious CNS symptom
* seizures ## Footnote Stoelting's, pg. 277
53
Cardiovascular side effects of systemic local anesthetics include:
* hypotension * bradycardia * cardiovascular collapse * cardiac arrest ## Footnote Stoelting's, pg. 277
54
The topical application of __________ has been used in postherpetic neuralgia and after different surgical procedures
* 5% lidocaine ## Footnote Stoelting's, pg. 277
55
__________ is a transient receptor potential vanilloid (TRPV) channel agonist that can be used in conditions such as arthritis, myalgias, arthralgias, and neuralgias
* capsaicin ## Footnote Stoelting's, pg. 278
56
Ketamine, at low ____________ doses exerts a specific NMDA bloackade - this modulates ___________ induced by the incision/tissue damage
* subanesthetic * central sensitization ## Footnote Stoelting's, pg. 278
57
The clinical use of ketamine can be limited due to what adverse effects?
* psychomimetic * dizziness * blurred vision * nausea/vomiting ## Footnote Stoelting's, pg. 278
58
____________ is a highly selective, central alpha 2 agonist with sedative, proanesthetic, and proanalgesic effects
* dexmedetomidine ## Footnote Stoelting's, pg. 278
59
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?
* gabapentin * pregabalin | reduces release of glutamate ## Footnote Stoelting's, pg. 264
60
How do peripherally acting analgesics work?
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
What are some inflammatory mediators that peripheral analgesics inhibit the release of?
* Prostanoids * Bradykinin * Adenosine triphosphate * Histamine * Serotonin
62
NSAIDS MOA?
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
Oral dose of acetaminophen?
* 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
What are you likely to see with aspirin overdose?
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
What is the primary corticosteroid in which all other corticosteroids are judged against?
The primary corticosteroid is **hydrocortisone**, which is the standard against which the pharmacologic properties of various synthetic corticosteroids are judged
66
Ketolorac dosage in Adults and Peds?
Adult 15-30mg IV q6h Pediatric 0.5mg/kg IV q6h
67
Dexmedetomidines proanesthetic and proanalgesic dosage?
0.5 to 2mcg/kg given intravenously
68
MOA of Ketamine?
Noncompetitive antagonism of N-methyl-D-aspartate (NMDA) receptors

Nurs 575 Anesthesia Pharmacology (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions