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
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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 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?
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.
