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24 Principles of Anesthesia II > Acute Pain & Opioid-Free Analgesia (Exam II) > Flashcards

Acute Pain & Opioid-Free Analgesia (Exam II) Flashcards

1
Q

What types of somatic pain are there?

A
  • Superficial: skin, SQ, mucous membranes
  • Deep: muscles, bones, tendons
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2
Q

What types of visceral pain are there?

A
  • Parietal: sharp, localized organ pain.
  • Referred: Cutaneous pain from convergence of visceral and somatic afferent input.
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3
Q

Is chronic nociceptive pain or neuropathic pain more abnormal?

A

Neuropathic pain

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4
Q

What are some possible cardiac consequences of poorly managed pain?

A

↑ HR
↑ BP
↑ Cardiac workload

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5
Q

What are some possible respiratory consequences of poorly managed pain?

A
  • Splinting (resp muscle spasm)
  • ↓ VC
  • Atelectasis
  • Hypoxia
  • Pulmonary infection risk
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6
Q

What are some gastrointestinal consequences of poorly managed pain?

A

Ileus

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7
Q

What are some possible renal consequences of poorly managed pain?

A
  • Oliguria
  • Urine retention
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8
Q

What are some possible coagulative consequences of poorly managed pain?

A

↑ clot risk

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9
Q

What are some possible immunologic consequences of poorly managed pain?

A

Immunosuppression

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10
Q

What are some possible musculoskeletal consequences of poorly managed pain?

A
  • Fatigue & weakness
  • Limited mobility = clotting
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11
Q

What is the Specificity Theory?
Who came up with it?

A

Specific sensation w/ its own sensory system independent of touch and other senses - Descartes

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12
Q

What theory linked pain and emotion?

A

Intensity Theory (Plato)

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13
Q

Where is pain attenuated in the CNS according to gate theory?

A

Substantia Gelatinosa

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14
Q

What chemicals are released upon tissue injury that mediate pain?

A
  • Histamine
  • Bradykinin (peptide)
  • Prostaglandins (lipids)
  • Serotonin (neurotransmitter)
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15
Q

Give an example of first order neurons.

A

Aδ and C

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16
Q

Where do first order Aδ and C fibers synapse at?

A

Dorsal Root of the spinal cord

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17
Q

Where do second order neurons synapse at?

A

Thalamus

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18
Q

What is the name of the process by which noxious stimuli are converted to action potentials?

A

Transduction

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19
Q

What is the name of the process by which an action potential is conducted through the nervous system?

A

Transmission

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20
Q

What is the name of the process by which pain transmission is altered along its afferent pathway?

A

Modulation

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21
Q

What is the name of the process by which painful input is integrated in the somatosensory and limbic cortices of the brain?

A

Perception

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22
Q

Hyperalgesia is the process by which tissue trauma releases _____ _______ ______ that produced augmented sensitivity to stimuli.

A

local inflammatory mediators

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23
Q

What is primary hyperalgesia?

A

Augmented sensitivity to painful response.

or

Allodynia-style misinterpretation of non-painful stimuli.

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24
Q

What is secondary hyperalgesia?

A

Increased neuronal excitability due to glutamate activation of NMDA receptors.

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25
Q

What opioid will potentiate hyperalgesia?

A

Remifentanil

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26
Q

What is the treatment for hyperalgesia that was mentioned in lecture?

A

Ketamine

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27
Q

Differentiate Hyperalgesia and Allodynia.

In chart form.

A
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28
Q

What is the hallmark “negative” symptom of neuropathy?

A

numbness

Positive s/s can exist as well (pain, sensitivity, etc.

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29
Q

GI blood flow and motility increase as we age. T/F?

A

False.

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30
Q

Gastric acid secretion ______ as we age thus _______ gastric pH.

A

decreases; increasing

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31
Q

What effect does aging have on nutrient absorption in the GI tract?

A

Minimal

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32
Q

What occurs to muscle and fat mass as a patient ages?

A

Muscle decreases while fat increases

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33
Q

A decrease in _______ affects your protein-bound drugs in aging.

A

albumin

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34
Q

What occurs with hepatic function in the aging patient?

A
  • ↓ hepatic blood flow
  • ↓ liver mass and metabolic activity
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35
Q

What occurs with renal function due to aging?

A
  • ↓ GFR
  • ↓ kidney mass & functioning nephrons
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36
Q

Do opioids or non-opioid analgesics exhibit a ceiling effect?

A

Non-opioid analgesics

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37
Q

What opioid receptor is responsible for analgesia, respiratory depression, euphoria, and reduced GI motility?

A

μ receptor

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38
Q

What opioid receptor (when agonized) is responsible for analgesia, dysphoria, psychosis, miosis, and respiratory depression?

A

Κappa receptor

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39
Q

What opioid receptor causes analgesia alone when bound by an agonist?

A

Delta

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40
Q

What drug is described by the following organic structure:

Substitution of methyl group for hydroxyl group on #3 carbon of morphine molecule.

A

Codeine

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41
Q

______ is much more reliably absorbed orally than morphine.

A

Codeine

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42
Q

What drug exhibits side effects (without concurrent analgesia) in children?
Why is this?

A

Codeine

Children lack enzymatic maturity needed to properly break down codeine.

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43
Q

What CYPs metabolize codeine?

A

CYP2D6 → morphine
CYP3A4 → norcodeine

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44
Q

Codeine metabolism is variable due to more than ____ polymorphisms resulting in analgesic variability.

A

50

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45
Q

What is the adult dose and max of codeine?

A

15 - 60 mg q4

360mg max per day

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46
Q

What is the pediatric dose and max of codeine?

A

0.5 - 1 mg/kg/dose

60mg max per day

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47
Q

60mg of codeine (maximal dose) is equivalent to how much aspirin?

A

650mg

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48
Q

What drugs does codeine have interactions with?

A

Opioids, EtOH, and Anticholinergics

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49
Q

What drug is described by the following?

A

Tramadol

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50
Q

Where does the + enantiomer of tramadol have affinity and what does it do?

A

Centrally acting opioid agonist:
- μ → moderate affinity
- K & δ → weak affinity
- Opposes serotonin reuptake

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51
Q

What does the - entantiomer of tramadol do?

A
  • Inhibits NE reuptake
  • Stimulates α2 receptors
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52
Q

What is tramadol metabolized into and what is the relevance of its metabolite?

A

Tramadol → CYP3A4 & 2D6 → O-desmethyltramadol (2-4 times more potent)

53
Q

What is tramadol’s potency compared to morphine?

A

1/5 to 1/10

54
Q

What is the oral onset for tramadol?

A

1-2 hours

55
Q

What is the half life of tramadol?

A

6.3 hours

56
Q

When is tramadol contraindicated?

A
  • Seizure Disorders
  • PONV
57
Q

What are the benefits of tramadol vs other opioids?

A
  • Minimal respiratory depression
  • Minimal-none addiction
  • Minimal constipation
58
Q

Oral morphine dose is ____ times the IM or IV route.

A

3

59
Q

What receptors are primary affected by morphine?

A

μ-1 and μ-2

60
Q

What are the two principle active metabolites of morphine? (also list effects)

A
  • Morphine-6-glucuronide → analgesia
  • Morphine-3-glucuronide → neurotoxicity & hyperalgesia
61
Q

How is morphine metabolized?

A
  • Hepatic → conjugation w/ glucuronic acid
  • Kidneys
62
Q

What factors contribute to morphine’s minimal CNS absorption?

A
  • ↓ lipid solubility
  • ↑ protein binding
  • ↑ Ionization at normal bodily pH
63
Q

What is the IV/IM onset and peak of action for morphine?

A

Onset: 15-30 min
Peak: 45-90 min

64
Q

What differences does morphine exhibit in women vs men?

A

In women:
↑ potency
↓ speed of offset

65
Q

What is the protein binding of morphine?
What about the half-time?

A

35% protein binding
1.7 - 3.3 hours

66
Q

What is released from morphine administration?
What is the result?

A

Histamine → vasodilation and hypotension

67
Q

Morphine should be avoided in patients with ____ impairment as the metabolite morphine–6-glucuronide can accumulate and lead to _________ ________.

A

Renal impairment : respiratory depression

68
Q

What drug is a synthetic derivative of thebaine?

A

Oxycodone

69
Q

What are the metabolites of oxycodone?

A

Oxymorphone (active)
Noroxycodone (inactive)

Oxycodone is primary a prodrug.

70
Q

What is the site of action of oxycodone?

A

μ and κ receptors of the CNS

71
Q

What are the two types of PO oxycodone?

A

IR = Immediate release
CR = Controlled release

72
Q

What is the dose of oxycodone?

A

10 - 15mg (rough 1 to 1 equivalence with morphine)

73
Q

What is the onset of action of oxycodone?

A

< 1 hour

74
Q

Opioids (in general) exhibit an ____ effect with other drugs that are CNS depressants

A

additive

75
Q

Why is methadone used for opioid addiction maintenance?

A
  • 60-90% oral bioavailability
  • High potency
  • Long duration of action
76
Q

What should be known about methadone’s half life?

A

Very long and unpredictable (up to 36 hours)
Can accumulate w/ repeated doses

77
Q

What various receptors affinities does methadone have?

A
  • Weak noncompetitive NMDA antagonist
  • Serotonin reuptake inhibitor
  • Monoamine reuptake inhibitor
  • High μ receptor affinity
78
Q

What would occur with concurrent methadone and carbamazepine use?

A

Carbamazepine is a CYP450 inducer thus methadone will be metabolized faster.

79
Q

What agents can inhibit the metabolism of methadone?

A

CYP450 Inhibitors:

  • Antiretrovirals
  • Grapefruit juice
80
Q

How much is methadone clearance affected by hepatic and renal impairment?

A

Not much

81
Q

What is the dose of methadone?

A

2.5 - 10 mg PO/IM/SC q4-12 hours

82
Q

Why are standardized simple dosing guidelines unachievable for methadone?

A

High variable half life (8-80 hours)

83
Q

What is the worst med interaction associated with methadone?

A

MAOI’s

84
Q

What drugs are known to increase the concentration/effects of methadone?

A
  • Cipro
  • Diazepam
  • Acute EtOH
85
Q

What drugs are known to decrease concentration/effects of methadone?

A
  • Anti-retrovirals
  • Phenobarbital
  • Phenytoin
  • Rifampin
  • MAOI’s
86
Q

What cardiac complication can occur in rare cases with methadone usage?

A

Pause dependent dysrhythmia

87
Q

What drug is fentanyl structurally similar to?

A

Meperidine

88
Q

Fentanyl has ____ potency, ____ onset of action and _____ duration of action.

A

High potency
Rapid onset
Short duration

89
Q

What is the priniciple metabolite of fentanyl?

A

Norfentanyl

Detectable in urine up to 72 hours after single dose.

90
Q

Why is elimination of fentanyl slightly prolonged despite very short duration of action?

A

Lungs serve as large inactive reservoir (up to 75% of initial dose undergoes first pass pulmonary uptake).

91
Q

Why is fentanyl more potent and rapid than morphine?

A

Greater lipid solubility

92
Q

What is responsible for fentanyl’s short duration of action?

A

Rapid redistribution to fat and muscle

93
Q

What is the protein binding of fentanyl?

A

84%

94
Q

What is hydromorphone and how is it formed?

A

Hydrogenated ketone of morphine formed by N-demethylation of hydrocodone

95
Q

Hydromorphone is ______ times as potent as morphine when administered orally.

A

3 - 5 times

96
Q

Hydromorphone is ______ times as potent as morphine when administered parenterally.

A

8.5 times

97
Q

What is hydromorphone’s primary metabolite?

A

Hydromorphone-3-glucuronide

98
Q

What should be known about Hydromorphone-3-glucuronide?

A
  • Lacks analgesic effects
  • May potentiate neurotoxic effects (allodynia, myoclonus, seizures).
99
Q

When is Hydromorphone-3-glucuronide’s neurotoxic side effects an actual concern?

A

Patients with renal insufficiency

100
Q

What is the typical dose of parenteral Hydromorphone?

A

0.2 - 2 mg

101
Q

What is the typical oral dose of hydromorphone?

A

2 - 8 mg

102
Q

What is the duration of action of hydromorphone?

A

3 - 4 hours

103
Q

What is hydrocodone derived from?

A

Codeine

104
Q

How does the potency of hydrocodone and codeine compare?

A

Hydrocodone is 6 - 8 x more potent

105
Q

What are the two most abused opioids?

A

1st = Oxycodone
2ⁿᵈ = Hydrocodone

106
Q

What are the two metabolites of hydrocodone metabolism?

A
  • Hydromorphone (via CYP2D6)
  • Norhydrocodone (inactive) via CYP3A4
107
Q

What is the morphine equivalent of hydrocodone?

A

1 mg morphine = 3 mg hydrocodone

108
Q

What is typical hydrocodone dosing?

A

2.5 - 10mg w/ 300 - 750mg acetaminophen q4-6hours

109
Q

What receptors does buprenorphine have affinity to?

A

μ - partial agonist (strong)
κ - antagonist (strong)
δ - agonist (weak)

110
Q

What benefits does buprenorphine provide?

A
  • ↓ respiratory depression
  • ↓ immune suppression
  • ↓ constipation
  • No accumulation in renal patients
111
Q

What is the primary metabolite of buprenorphine?

A

Norbuprenorphine

112
Q

What should be known about norbuprenorphine?

A
  • 1/50th analgesic activity of buprenorphine
  • ↑↑↑ Respiratory depression
113
Q

What is the IV/IM buprenorphine dose equivalence for morphine?

A

0.3mg IM buprenorphine = 10mg morphine

114
Q

What is the half life of buprenorphine?

A

Long

20 - 73 hours

115
Q

Should buprenorphine be avoided in patients with renal impairment?

A

No. Hepatic elimination primarily

116
Q

What are the side effects and drug interactions of buprenorphine?

A
117
Q

What receptors do NSAIDs bind to?

A

Trick question. NSAIDs inhibition COX as their method of pain modulation.

118
Q

What is the recommended dose for celecoxib?

A

100mg daily

119
Q

What is the recommended dose for diclofenac?

A

50 mg BID

120
Q

How might antidepressants work as pain medication adjuvants?

A

Modulation of spinal cord transmission to reduce pain signaling

121
Q

Whats the IV dose of fentanyl for pain?

A

20 - 50 mcg

122
Q

What anticonvulsants are used as adjuvant medication to relieve pain?

A
  • Gabapentin (watch for sedation/ respiratory depression in older patients)
  • Phenytoin
  • Carbamazepine
  • Topiramate
123
Q

What skeletal muscle relaxants are used as adjuvant medication to relieve pain?

A
  • Baclofen (Lioresal®)
  • Carisoprodol (Soma®)
  • Cyclobenzaprine (Flexeril®)
  • Methocarbamol (Robaxin®)
  • Tizanidine (Zanaflex®)
124
Q

What is Opioid Free Anesthesia?

A
  • Technique where no intra-operative systemic, neuraxial, or intracavitary opioid is administered during the anesthetic.
125
Q

Opioids acting on the Mu receptor will produce these unwanted effects.

A
  • Respiratory depression
  • Decrease GI motility/ constipation
  • Urinary retention
  • Prurititis
  • Physical dependence
126
Q

Opioids acting on the Kappa receptor will produce these unwanted effects.

A
  • Respiratory depression
  • Dysphoria
127
Q

Opioids acting on the Delta receptor will produce these unwanted effects.

A
  • Respiratory depression
  • Urinary retention
  • Prurititis
  • Physical dependence
128
Q

What is opioid-induced hyperalgesia (OIH)?

A
  • State of nociceptive sensitization caused by exposure to opioids.
  • The condition is characterized by a paradoxical response whereby a patient receiving opioids for the treatment of pain might actually become more sensitive to certain painful stimuli.

24 Principles of Anesthesia II (23 decks)

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