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Anesthesia Pharmacology > NonOpioid Analgesia > Flashcards

NonOpioid Analgesia Flashcards

1
Q

Describe the major mechanism of action of NSAIDS

A

Inhibit the biosynthesis of prostaglandins by preventing the substrate arachidonic acid from binding to the cyclooxygenase enzyme active site.

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2
Q

According to Dr. C’s PowerPoint, which nonopioids are centrally acting?

A

Clonidine
Dex
Ketamine
Magnesium

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3
Q

What forms does the COX enzyme exist in?

A

COX-1 isoenzyme
COX-2 isoenzyme

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4
Q

Name three functions of COX-1 Isoenzyme?

A

-Maintenance of normal renal function in the kidneys
-Mucosal protection in the GI tract
-Production of proaggregatory thromboxane A2 in the platelets

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5
Q

What is the only COX-2 selective inhibitor available?

A

Celecoxib (Celebrex)

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6
Q

COX-2 expression can be induced by? Leading to?

A

Inflammatory mediators in many tissues, therefore, plays a role in the mediation of pain, inflammation, and fever.

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7
Q

What are the benefits of coxibs (cox-2 selective inhibitors)?

A

Improved quality of analgesia
Reduced incidence of GI side effects
No platelet inhibition

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8
Q

All NSAIDs are weakly basic or weakly acidic?

A

Weakly acidic

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9
Q

How long does GI absorption of NSAIDS take

A

within 15-30 minutes

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10
Q

What organ metabolizes most NSAIDs?

A

Liver

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11
Q

How are NSAIDs excreted?

A

into urine or bile

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12
Q

How does reduced renal function affect NSAIDs?

A

Prolongs half-life, the dose should be lowered proportionally in patients with impaired kidney function

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13
Q

Moderate to severe liver disease impairs NSAID metabolism, increasing the potential for?

A

Toxicity

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14
Q

Is the volume of distribution of NSAIDs high or low?

A

Low. 0.1-0.3L/kg, suggesting minimal tissue binding.

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15
Q

Why does Celecoxib (Celebrex) not impact platelet function?

A

Celecoxib is a COX-2 Selective inhibitor. There is no COX-2 isoenzyme in platelets.

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16
Q

What patient population is contraindicated to give nonselective NSAIDs to?

A

GI Gastric Sleeve, Roux-N-Y surgeries due to the risk of ulcers, perforation, and bleeding.

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17
Q

It’s generally recommended that patients with GI risk factors should be treated with COX-2–selective agents or non-selective NSAIDs with GI protective co-therapy.
Risk factors for NSAID-associated GI complications include:

A

High NSAID dose, older age, H. Pylori infection, anticoagulants, corticosteroids, concomitant low-dose aspirin use

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18
Q

Why do COX-2 inhibitors have a higher risk of cardiac side effects?

A

Imbalance Between Prostacyclin (PGI₂) and Thromboxane A₂ (TXA₂). COX-2 inhibits prostacylin, leaving procoag thromboxane a2 predominating.

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19
Q

List some possible cardiac side effects of NSAIDS

A

hypertension, prothrombotic effect (more likely with coxibs)

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20
Q

List some possible respiratory side effects of NSAIDs

A

Nasal Polyps, Dyspnea, bronchospasm, and angioedema, may exacerbate asthma

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21
Q

Are hypersensitivities to NSAIDs rare or common? What patient population experiences reactions more?

A

Rare.
If they occur, they are more common in people with nasal polyps or asthma

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22
Q

More than ____% of NSAIDs are bound to albumin after absorption.

A

90%!
(Influencing their distribution and drug-drug interaction.)

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23
Q

List 2 possible renal side effects of NSAIDs

A

Renal insufficiency
Sodium/Fluid Retention

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24
Q

Describe the MOA of Alpha 2 Agonists

A

Stimulates alpha 2 receptors in brainstem. Reducing catecholamine release therefore a reduction in sympathetic outflow.

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25
Q

What are some adverse reactions associated with alpha 2 agonists

A

Dex: Bradycardia - common
- Hypotension - common

Clonidine: Dry mouth
-Sedation
-Bradycardia
-Sexual dysfunction
-Withdrawal syndrome and potentially life threatening rebound hypertension
-Prolonged sedation (especially in the elderly)

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26
Q

Describe the MOA of gabapentinoids

A

reduction of the axon excitability

Gabapentin interacts with cortical neurons at delta subunits of calcium channels

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27
Q

Where do peripheral analgesics act at?

A

The sensory input level by blocking the impulse to the brain

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28
Q

Why can peripherally administered medications lead to lower systemic levels and fewer adverse systemic effects?

A

Peripherally administered drugs can potentially optimize drug concentrations at the site of pain origin

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29
Q

Nociceptive, inflammatory, and neuropathic pain depend to some degree on peripheral activation of?

A

Primary sensory afferent neurons

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30
Q

Name five inflammatory mediators that analgesics try to target

A

Prostanoids
Bradykinin
Adenosine Triphosphate
Histamine
Serotonin

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31
Q

True or False: Combinations of agents that act via different mechanisms may be particularly useful.

A

True

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32
Q

NSAIDs have 3 shared properties. What are they?

A

Analgesia, Anti-Inflammatory, and Antipyretic

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33
Q

What does NSAIDs stand for?

A

Nonsteroidal anti-inflammatory drugs

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34
Q

Ketorolac (Toradol) is dosed at?

A

15-30mg IV or IM q6 hours
(some literature, there is no increase in the efficacy of 30mg)

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35
Q

Pediatric dosing of Ketorolac (Toradol)

A

0.5mg/kg up to 15mg q6 hours

36
Q

What is the elimination half-life of Ketorolac (Toradol)?

A

2.5-8.5 hours

37
Q

What doses are available for Celecoxib (Celebrex)?

A

100-200mg

38
Q

What is the elimination half-life of Celecoxib (Celebrex)

A

11-16 hours

39
Q

What is the leading cause of acute liver failure in the US?

A

Acetaminophen
About half are due to unintentional overdoses

40
Q

How does acetaminophen damage the liver?

A

Results from one of the acetaminophen metabolites, N-acetyl-p-benzoquinone imine (NAPQI). NAPQI depletes liver antioxidant glutathione and directly damages liver cells.

41
Q

What is the treatment/antidote to acetaminophen toxicity?

A

Acetylcysteine. It acts as a precursor for glutathione and can neutralize NAPQI directly.
Activated charcoal - can decrease absorption if administered shortly after ingestion of overdose.

42
Q

Conventional dosing of acetaminophen is?

A

325-650mg every 4-6 hours.

43
Q

The total daily dose of acetaminophen should not exceed?

A

Most now say 3,000mg daily. (used to be 4,000)

44
Q

How is the oral bioavailability of acetaminophen? Poor or Good?

A

excellent

45
Q

What drug is included in IV Tylenol (OFIRMEV)?

A

Mannitol
3,850mgs, almost 4 grams, in each 100mL bottle.

46
Q

Dosing of IV Tylenol (OFIRMEV) for patients <50kg?

A

15mg/kg

47
Q

Which steroids have the most powerful anti-inflammatory characteristics?

A

Glucocorticoids

48
Q

What are Mineralcorticoids?

A

Adrenal cortical steroid hormones that have a greater effect on water and electrolyte imbalance.

49
Q

The main endogenous hormone is?

A

Aldosterone

50
Q

Corticosteroids are a subgroup of compounds known as?

A

Adrenocorticoids that are naturally secreted from the adrenal gland

51
Q

How does use of corticosteroids influence opioid use?

A

There is evidence supporting their use for post-op recovery, minimizing opioid doses and, therefore, side effects

52
Q

What is the effect of adding dexamethasone to anesthetic blocks?

A

Has been found to prolong local anesthetic block duration

53
Q

What is the dosing for Dexamethasone (Decadron) for PONV prophylaxis?

A

4-8mg

54
Q

What is the dosing for Dexamethasone (Decadron) for pain management?

A

0.1-0.2mg/kg

Some cap dose at 10mg to minimize side effects, others cap at 20mg.

55
Q

How much more potent is Dexamethasone (Decadron) compared to natural human cortisol?

A

~25-26 more potent
(~6 times more potent than prednisone)

56
Q

Duration of action of Dexamethasone (Decadron)?

A

36-54 hours

57
Q

The half-life of Dexamethasone (Decadron)?

A

3.5-5 hours

58
Q

What are a few potential side effects of corticosteroids?

A

Hyperglycemia
Delayed wound healing
osteoporosis
(remember short term verse long term SEs)

59
Q

How do systemic local anesthetics, such as Lidocaine, work?

A

Produces analgesia by suppressing sodium channels in neurons that respond to noxious stimuli, thereby preventing nerve conduction and pain transmission.

60
Q

What effect does systemic lidocaine have on MAC of volatile anesthetics?

A

Decrease in MAC

61
Q

What is the dosing of IV Lidocaine for bolus and continuous infusion for pain management?

A

Bolus: 100mg or 1-2mg/kg
Infusion: 0.5-2mg/kg/hour

62
Q

What is the onset of IV Lidocaine?

A

45-90 seconds

63
Q

What is the half-life of IV lidocaine?

A

Initial (Distribution) 7-30 minutes
(why Dr. C says to turn drip off 30 min before end of case)

Terminal (Elimination): 1.5-2 hours

64
Q

What are the two Gabapentinoids we commonly see?

A

Gabapentin (Neurontin)
Pregabalin (Lyrica)

65
Q

Both Gabapentin (Neurontin) and Pregabalin (Lyrica) bind to?

A

Alpha 2 delta subunits of the voltage-gated calcium channels in the CNS

66
Q

Gabapentin (Neurontin) is an effective analgesic particularly for what kind of pain?

A

Diabetic neuropathy, post-herpetic neuralgia, and neuropathic pain

67
Q

What is the dosing of Gabapentin that can reduce opioid administration?

A

300-900mg PO (commonly administered in preop)
smaller doses in the elderly - can be very sedating

68
Q

How does Pregabalin (Lyrica) provide analgesia

A

reduces hyper-excitability of dorsal horn neurons

69
Q

What is the dose of Pregabalin (Lyrica) for analgesia

A

150-600mg/day in 2-3 doses

70
Q

Dosing for Clonidine epidural administration

A

75-150mcg

71
Q

Dosing for Clonidine intrathecal administration

A

30-65mcg

72
Q

What is Clonidine’s MOA?

A

Selective partial Alpha-2 Receptor Agonist
(Ultimately limits Norepi release, decreasing overall sympathetic outflow)

73
Q

Neuraxially administered opioids and alpha 2 agonists exhibit?

A

Synergism

74
Q

The addition of clonidine to opioids for postoperative analgesia as a continuous epidural infusion reduces opioid requirements by what %?

A

20-60%

75
Q

Neuraxial clonidine is indicated for the treatment of intractable pain in ______ patients unresponsive to max opioid doses.

A

Cancer patients

76
Q

How will Dexmedetomidine (Precedex) effect MAC levels?

A

Will reduce MAC requirements

77
Q

A dose of ____ mcg of intrathecal Precedex is equipotent to _____ mcg of clonidine

A

3mcg precedex =
30mcg clonidine intrathetcal

78
Q

Epidural Dexmedetomidine (Precedex) exhibits:

A

-Synergism with local anesthetics
-Increasing the density of a motor block
-Prolonging the duration of both sensory and motor block
-Improves postop analgesia

79
Q

What is the IV bolus dosing and continuous infusion dosing for Dexmedetomidine (Precedex)?

A

Bolus: 4-10mcg/mL

Infusion: 0.2-0.8mcg/kg/hr

80
Q

What is the bolus and infusion doses of IV Ketamine?

A

Bolus: small incremental boluses. 0.1-0.5 mg/kg. Up to 0.5mg/kg.

Infusion: 10-25mg/hr

81
Q

Time onset for IV Ketamine

A

30-60 seconds

82
Q

Time to onset for IM Ketamine

A

2-4 minutes

83
Q

Mechanism of action of Ketamine (Ketalar)

A

noncompetitive antagonism of N- methyl-D-aspartate (NMDA) receptors. Blocks influx of calcium, resulting in a decrease in glutamate release.

84
Q

Magnesium works best in conjunction with which medication to produce analgesia?

A

Ketamine

85
Q

What is Magnesium’s MOA for analgesia?

A

NMDA antagonist.

86
Q

What is the bolus and continuous infusion dosing for Magnesium?

A

Bolus/Loading: 30-50mg/kg (usually give 1-2g IVPB) for adults

Infusion: 6-20mg/kg/h

87
Q

Side effects of Magnesium Sulfate

A

Hypotension
Diarrhea

Anesthesia Pharmacology (5 decks)

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