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Pharmacology of Chronic Pain Management > Pharmacology of Chronic Pain Management > Flashcards

Pharmacology of Chronic Pain Management Flashcards

1
Q

Hydrocodone MAO

A

Full opioid agonists

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2
Q

Hydrocodone Indications

A

Relief of moderate pain. As an antitussive when used
in combination with other Nrespiratory agents
(expectants/decongestants/ antihistamines)

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3
Q

Hydrocodone Dosage

A

Equianalgesic Dose: (PO): 30

5-10mg every 4-6h

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4
Q

Hydrocodone Duration and Half life

A

Duration: 4-8h

Half-life: 3.3- 4.5h

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5
Q

Hydrocodone formulation

A

Weak opioid only available in combination with nonopioid analgesic (acetaminophen or ibuprofen)

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6
Q

Hydrocodone compared to Hydromorphone

A

Hydrocodone is the methyl ether of hydromorphone, but is much weaker an analgesic than hydromorphone.

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7
Q

Hydrocodone Metabolism

A

Undergoes-O-demethylation to dihydromorphine and its
major metabolites excreted into urine are dihydrocodeine
and nordihydrocodeine

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8
Q

Hydromorphone MOA

(Dilaudid)

A

Full opioid agonists

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9
Q

Hydromorphone Indications

(Dilaudid)

A

Immediate – release: relief of moderate to severe pain due to conditions such as biliary/renal, colic burns,
cancer, myocardial infarction, surgery, and trauma
Long-acting: relief of moderate to severe pain in
patients requiring continuous, around the clock analgesia

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10
Q

Hydromorphone Dosage

(Dilaudid)

A

Equianalgesic Dose
Hydromorphone (IV/IM/SC): 1.5
Hydromorphone (PO): 7.5
Immediate Release: 2-4mg q 4-6h (tablets), 2.5- 10mg q3-6h (solution)
Titrated by response; higher doses may be needed for severe pain
SR preparation (exalgo)
For breakthrough pain: 5-15% of total daily dose may be given every 2h prn
Dosing interval for long acting formulation: 24h

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11
Q

Hydromorphone Duration and Half Life

(Dilaudid)

A

Duration: 4-5h

Half-life: 2-3h

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12
Q

Hydromorphone Metabolism and Excretion

(Dilaudid)

A

Hydromorphone is preferred over morphine in patients
with renal dysfunction due to less accumulation of active
metabolites compared to morphine
Renal excretion

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13
Q

Meperidine (Demerol) MAO

A

Meperidine binds to opioid receptors, particularly
μ receptors. It also binds well to κ receptors

Meperidine cab block voltage dependent sodium channels.
Meperidine also has agonist activity at the alpha 2B adrenoreceptor subtype.
Inhibit serotonin and norepinephrine reuptake

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14
Q

Meperidine (Demerol) Indications

A

Not used for chronic pain because of short duration of
action and toxicities associated with chronic use
The use of meperidine should be limited to 1 to 2
days for acute pain and should be avoided in chronic
pain management
Relief of moderate to severe pain

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15
Q

Meperidine (Demerol) Side Effects

A

Seizures and central nervous system effects have been
associated with high doses or prolonged use because of
accumulation of the metabolite Normeperidine. Especially in elderly and pts with renal dysfunction not affected by naloxone
Meperidine similar to Atropine may elevate the heart rate
interactions of Meperidine and MAOIs are combined,
severe respiratory depression or excitation, arrhythmias,
delusions, hyperpyrexia, seizures and coma can be seen.
Meperidine has cardiac (hypotension and myocardial
depression), local anesthetic, and anticholinergic
properties

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16
Q

Meperidine (Demerol) Dosage

A

Meperidine (IV/IM/SC): 75
Meperidine (PO): 300
50-150mg q 3-4 prn

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17
Q

Meperidine (Demerol) Duration and Half Life

A

Duration: 2-4h

Half-life: 3-4h

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18
Q

Morphine (Roxanol, Contin, Oramorph, Kadian, Avinza) MAO

A

Morphine acts at κ receptors in laminae I and II of
the dorsal horn of the spinal cord, and it
decreases the release of substance P, which
modulates pain perception

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19
Q

Morphine Indications

A

Immediate- release: relief of moderate to severe pain
Long-acting: relief of moderate to severe pain in
patients requiring continuous around the clock analgesia
Morphine has greater potency but slower speed of
onset and offset in women

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20
Q

Morphine Side Effects

A

Morphine and other opioids produce seizures at HIGH doses due to inhibition of release of GABA at synaptic levels.
Therapeutic doses of morphine decrease
Minute Ventilation by decreasing Respiratory Rate (as oppose to tidal volume).
Opioids acting in μ- and κ- receptors constrict
the pupil by exciting the Edinger Westphal nucleus (parasympathetic)
Long-term opioid use can produce tolerance to miotic effects of opioids

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21
Q

Morphine dosing

A 
Morphine (IV/IM/SC): 10 
Morphine (acute PO): 60 
Morphine (chronic PO): 30 
Immediate Release formulation: 5- 30mg every 4h, titrated by  response 
Dosing intervals for long acting 
formulations: 8-12h for MS Contin 
and Oramorph SR, 12h for Kadian, 
24h for Avinza
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22
Q

Morphine Metabolism and Excretion

A

Hepatic metabolism, renal excretion
Morphine is metabolized by the liver to morphine-6-glucuronide which is more potent than morphine itself
and has a longer half-life, resulting in additional analgesia. Morphine is also metabolized to morphine-3-
glucuronide which causes adverse effects and is inactive according to others.
Renal dysfunction can produce accumulation of morphine-6- glucuronide, with subsequent opioid effects, including respiratory depression, so morphine should be used with care in renal dysfunction.
Patients with liver failure can tolerate morphine (even in hepatic precoma), because glucuronidation is rarely impaired

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23
Q

Morphine and Respiratory Depression

A

Delayed respiratory depression is likely to occur with
larger dose of epidural opioids, particularly morphine that
is hydrophilic and therefore subject to spread in the CSF,
reaching the respiratory center in the brainstem. Morphine in the epidural space produces a biphasic respiratory depression pattern. One portion
of the initial bolus is absorbed systemically, accounting for the initial phase, which usually occurs within 2 hours of the bolus dose. The second phase occurs 6 to 12 hours later owing to the slow rostral spread of the remaining drug as it reaches the brainstem. Pts should be monitored 24hrs after administration epidurally.
Intrathecal doses of morphine produce only a uniphasic
pattern of respiratory depression.
Neurotoxic metabolites cause hyperalgesia, myoclonus,
and seizures

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24
Q

Morphine Duration, Half-life, Bioavailability

A

Duration: 3-7 h
Half-life: 1.5- 2h
Oral Bioavailability: 25-35%

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25
Q 
Oxycodone MOA
(OxyContin)
A

.

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26
Q

Oxycodone Indication

A

Immediate- release: relief of moderate to severe pain
Long-acting: relief of moderate to severe pain in
patients requiring continuous around the clock analgesia

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27
Q

Oxycodone Dosage

A

Oxycodone (PO): 20
Oxycodone has been typically used in combination with nonopioids (acetaminophen, aspirin)
Immediate release: 10-30mg q4h, titrated by response
5mg capsules and oral concentrate 5mg q6h, titrated by response Dosing intervals for long acting formulations: 12h

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28
Q

Oxycodone Duration and Half Life

Bioavailability

A

Duration: 4-6h
Half-life: N/A
Higher bioavailability than that of morphine (approximately 60%).

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29
Q

Oxycodone Metabolism and Excretion

A

Metabolite via 3-0 demethylation is Oxymorphone. Must
be converted to oxymorphone by CYP2D6 to be effective
Renal excretion

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30
Q

Oxymorphone MOA

Opana

A

.

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31
Q

Oxymorphone Indications

Opana

A

Immediate- release: relief of moderate to severe acute
pain
Long-acting: relief of moderate to severe pain in
patients requiring continuous around the clock analgesia

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32
Q

Oxymorphone Dosage

A

Oxymorphone (IV/IM/SC): 1.0
Oxymorphone (PO): 10
Immediate- release formulation: 10- 20mg q4-6h; titrated by response
Dosing intervals for long acting formulations: 12h

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33
Q

Oxymorphone Duration and Half-life

A

Duration: 3-6h

Half-life: N/A

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34
Q

Oxymorphone metabolism

A

Active metabolite of oxycodone

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35
Q

Fentanyl (Actiq, Duragesic, Fentora, Onsoild) MOA

A

Full opioid agonists
Fentanyl is a potent mu agonist, with high lipid
solubility, low molecular weight and high potency,
making it an ideal drug for transdermal and
transmucosal administration 92% of fentanyl delivered transdermally reaches the circulation as unchanged fentanyl.
Transmucosal route at the buccal and sublingual
mucosa skips the first pass effect and overall
bioavailability is 50%.
For opioid rotation when tolerance to opioid
develops. Do not reduce the dose but maintain
the equianalgesic dose.

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36
Q

Fentanyl Indications

A

Transdermal patches: relief of moderate to severe
chronic pain in patients requiring continuous around
the clock analgesia when other analgesia have failed
Oral formulations (sublingual, lozenges, buccal
tablets/films): management of breakthrough cancer pain
in patients on or tolerant to opioid therapy

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37
Q

Fentanyl Side Effects

A

Causes less constipation than sustained-release morphine

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38
Q

Fentanyl Dosage

A

Equianalgesic Dose: Fentanyl is 80
times as potent as morphine
Fentanyl (IM/IV): 0.1
Fentanyl (Transdermal): 0.2

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39
Q

Fentanyl (Transdermal)

A

92% of fentanyl delivered transdermally reaches systemic circulation as unchanged fentanyl
Peak plasma concentration after application is 12 to 24 hours and a residual depot remains in subcutaneous tissues for about 24 hours after removal of the patc

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40
Q

Advantages of Fentanyl Patch

A

Low MW, High Lipid Solubility; this allows it to be administered by the transdermal route. It interacts
primarily with mu receptors, 80X more potent than morphine, and low abuse potential which is a
property of the delivery system not opioid itself.

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41
Q

Fentanyl Duration and Half Life

A

Duration: 1-2h
Half-life: 1.5-6 h
Time of onset of IM: 7-15 mins

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42
Q

Fentanyl Characteristics

A

Fentanyl is both lipophilic and highly protein bound.
Fentanyl
also distributes to fat tissue and redistributes slowly from
there into the systemic circulation

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43
Q

Fentanyl Metabolism

A

Fentanyl is metabolized to inactive metabolites by the
CYP450 3A4 system mainly in the Liver and minor extent
in CNS, Kidneys, lung, placenta
Best given in patient with Chronic Kidney Disease and
Liver Disease

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44
Q

Oral transmucosal fentanyl citrate (OTFC)

A

Applied against the buccal mucosa. 25% of total dose is absorbed from GI tract but escapes hepatic and intestinal first pass elimination. Total apparent bioavailability: 50%

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45
Q

Actiq lollipop

A

25% absorbed transmucosally, 75% GI, 2/3
of which is inactivated. Net = ½ the dose is available for
analgesia

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46
Q

Codeine MOA

A

Full opioid agonists
Metabolized to Morphine
The analgesic actions of codeine derive from its
conversion to morphine by the CYP450 2D6
enzyme system

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47
Q

Codeine Indications

A

Relief of mild-mod pain.
As an antitussive when used in combination with other
respiratory agents (expectants/decongestants/
antihistamines)

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48
Q

Codeine Side Effects

A

avoid in renal insufficiency

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49
Q

Codeine Dosage

A

Equianalgesic Dose:
Codeine (IM/IV): 120
Codeine (PO): 200
15-60mg every 4-6h

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50
Q

Codeine Duration and Half life

A

Duration: 4-6h
Half-life: 3h
Weak opioid only available in combination with nonopioid
analgesic (acetaminophen or Ibuprofen)

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51
Q

Codeine in Caucasians

A

10% ineffective as an analgesic in the Caucasian with
genetic polymorphisms in CYP2D6 (enzyme necessary to
O methylate codeine to morphine)

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52
Q

Methadone (Dolophine) MOA

A

Mediated by μ- agonist (pure) and agonist, NMDA
inhibitor, inhibitor of serotonin and norepinephrine
reuptake
In addition, methadone is an antagonist of NMDA receptor, which is useful in the treatment of neurogenic pain.
Addition of an NMDA antagonist is a strategy
available for opioid rotation when tolerance to
opioid develops. Reduce the dose by 75-90%

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53
Q

Methadone Indications

A

Methadone is used as an analgesic in nociceptive and
neurogenic pain as well as in the controlled withdrawal of dependent abusers from heroin and morphine
because withdrawal symptoms tend to be less severe than morphine’s, this and its long duration of action, good oral bioavailability, and high potency

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54
Q

Methadone Dosage

A

Methadone (acute IV): 5.0
Methadone (acute PO): 10
2.5-10mg every 8-12h, slowly
titrated by response

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55
Q

Methadone Titration

A

Rapid titration is not possible, making this drug more useful for stable type of pain

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56
Q

Methadone Formulation

A

Methadone is the only opioid with prolonged activity not achieved by controlled release formulation.
Can be used in a intrathecal pump

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57
Q

Methadone Excretion

A

Excreted exclusively in the feces and can be given in patient with renal dysfunction

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58
Q

Methadone Duration and Half-life

A

Duration: 4-6h

Half-life: 15- 30h

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59
Q

Methadone Metabolism

A

Methadone unlike morphine is metabolized through N-demethylation by the liver cytochrome P-450 enzyme (CYP1A2) caution in patients receiving multiple medications
Safe in liver and renal disease

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60
Q

Methadone Elimination

A

Methadone has biphasic elimination. β-elimination phase (ranges from 30 to 60 hours) producing sedation and respiratory depression can outlast the analgesic action which equates the α-elimination phase (6-8 hours).

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61
Q

Levorphanol MOA

A

Full opioid agonists

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62
Q

Levorphanol Indications

A

Relief of moderate to severe
pain
As a preoperative medication

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63
Q

Levorphanol Dose

A

Equianalgesic Dose
Levorphanol (acute PO): 4.0
Levorphanol (chronic PO): 1.0
2mg every 6-8h

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64
Q

Levorphanol Duration and Half Life

A

Duration: 6-8h
Half-life: 12-16h
Long half life may lead to accumulation with chronic use

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65
Q

Buprenorphine (Buprenex, Subutex) MOA

A

A partial agonist at the μ-receptor and very little
activity at the κ- and δ-receptors. It has high
affinity but low intrinsic activity at the μ-receptor
and has a pharmacologic ceiling owing to its
partial agonist activity.
It acts like morphine in naive patients, but it can
also precipitate withdrawal in morphine users

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66
Q

Buprenorphine Indications

A

A partial agonist at the μ-receptor and very little
activity at the κ- and δ-receptors. It has high
affinity but low intrinsic activity at the μ-receptor
and has a pharmacologic ceiling owing to its
partial agonist activity.
It acts like morphine in naive patients, but it can
also precipitate withdrawal in morphine users.
The tablets are indicated for the treatment of opioid
dependence and are available in buprenorphine alone
(Subutex) and also in a combination product containing
buprenorphine and naloxone (Suboxone). Naloxone was
added to buprenorphine to prevent the abuse of
buprenorphine via IV administration

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67
Q

Buprenorphine Dosage

A

Equianalgesic Dose: (IM/IV): 0.4
Opioid Naïve patients: 5mcg/h transdermal patch initially, titrated at intervals of 72h up to maximum of 20mcg/h transdermal patch
Nonopioid naïve patients: Taper current opioid dose for up to 7 days to no more than morphine 30mg/d; patients originally requiring < 30mg/d of morphine (or equivalent)
can be started on a 5mcg /h patch.
Patients originally requiring 30-80mg/d of morphine (or equivalent) can be started on a 10mcg /h patch

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68
Q

Buprenorphine Transdermal

A

Each transdermal patch should be worn for 7 days
Transdermal patch: relief of moderate to severe chronic
pain in patients requiring continuous, around the clock
analgesia

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69
Q

Buprenorphine Sublingual

A

Sublingual: treatment of opioid dependence

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70
Q

Butorphanol (Stadol) MOA

A

Mixed Opioid agonists/ antagonist

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71
Q

Butorphanol (Stadol) Dosage

A

Equianalgesic Dose: (IM/IV): 2.0
1-2mg intranasally; may be repeated in 3-4h, if needed
If a 1mg dose is used initially, a 2nd 1 mg dose may be
given 60-90min later if pain relief is not adequate

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72
Q

Nalbuphine (Nubain)

A

.

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73
Q

Pentazocine (Talwin) MOA

A

Mixed Opioid agonists/ antagonist
Acts as an agonist on κ receptors and is a weak
antagonist at μ and δ receptors

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74
Q

Pentazocine (Talwin) Indications

A

Pentazocine promotes analgesia by activating
receptors in the spinal cord, and it is used to relieve
Moderate pain

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75
Q

Pentazocine (Talwin) Dosage

A

25-50mg every 3-4h

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76
Q

Pentazocine (Talwin)

A

Weak opioid only available in combination with a
nonopioid analgesic (acetaminophen) or an opioid
anatagonist (naloxone)

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77
Q

Suboxone (Buprenorphine/naloxone) MOA

A

.

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78
Q

Suboxone (Buprenorphine/naloxone) Indications

A

Used to maintain addicts, requires special license

Good option for addicts with true pain

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79
Q

Suboxone (Buprenorphine/naloxone) Side Effects

A

GI absorption of naloxone is negligible

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80
Q

Suboxone (Buprenorphine/naloxone) characteristics

A

Can’t be abused due to naloxone administration if taken

parenterally

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81
Q

Naloxone (Narcan) Antagonist

A

Antagonist
Competitive antagonist at μ, κ, and δ, receptors,
with a tenfold higher affinity for μ than for κ
receptors

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82
Q

Naloxone (Narcan) Indications

A

Used to reverse the coma and respiratory depression of
opioid overdose. It rapidly displaces all receptor-bound
opioid molecules and, therefore, is able to reverse
the effect of a morphine overdose

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83
Q

Naloxone (Narcan) Half life

A

Half-life of 30 to 81 minutes

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84
Q

Tramadol (Ultram) Schedule

A

Schedule II controlled

substance

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85
Q

Tramadol (Ultram) MOA

A

Acts through monoceminergic (like TCA) and
opioid (central) mechanism to block pain
perception
Weak mu opioid receptor agonist and SSNRI
Weak inhibitor of norepinephrine and serotonin
reuptake
A centrally acting analgesic that binds to the μ- opioid receptor. The drug undergoes extensive
metabolism via CYP450 2D6, leading to an active
metabolite that has a much higher affinity for the
μ receptor than the parent compound.
In addition, it weakly inhibits reuptake of
norepinephrine and serotonin. Major mechanism,
which is thought to account for

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86
Q

Tramadol (Ultram) Indications

A

Used to manage moderate to moderately severe pain
Neuropathic pain
Fibromyalgia
Immediate release: relief of moderate to moderately
severe pain
Extended release: relief of moderate to moderately severe
chronic pain in patients requiring continuous around the
clock analgesia

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87
Q

Tramadol (Ultram) Side Effects

A

Nausea, Sedation, Constipation,
Seizures, Headache, Tremor, Dry
mouth Urinary retention, increase risk suicide
Fewer side effects than morphine. The risk of respiratory depression is lower at equianalgesic doses; the risk of fatal respiratory depression is minimal at appropriate
oral dosing, and limited essentially to patients
with severe renal failure.
Tramadol has a low abuse potential,however,
Nausea and vomiting occur at the same rate as with other opioids
Tramadol should also be avoided in patients taking
MAOIs.
Serotonin syndrome (caution with MAOI’s, TCA’s and
SSRI’s

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88
Q

Tramadol (Ultram) Dosage

A

50-100mg 4x daily
25mg/d initially, titrated to 25mg 4x daily over 3d, then to 50-100mg every 4-6h; maximum dose of 400mg/d
Extended release tablets can be started at dose of 100mg/d and slowly titrated to a maximum of
300mg/d

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89
Q

Tramadol (Ultram) Metabolism and Excretion

A

Metabolized with one pharmacologically active metabolite, M1
Reduce dose in pts with hepatic dysfunction and in older
patients
Adjust dose for hepatic, renal disease and elderly

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90
Q

Tapentadol MOA

A

a centrally acting analgesic that binds the μ- opioid receptor and is also a norepinephrine
reuptake inhibitor that is believed to create an
additive effect to the opioid actions

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91
Q

Tapentadol Indications

A

Used to manage moderate to severe pain, both chronic

and acute.

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92
Q

Tapentadol Avoided in what patients

A

Tapentadol should be avoided in patients currently taking MAOIs and those who have taken MAOIs within the last 14 days

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93
Q

Tricyclic Antidepressants (TCA) MOA

A

Theorized that the analgesic properties are
associated with their action as SNRI
TCAs with the greatest effect upon serotonin
seem to have the greatest analgesic effect.
Inhibit NE and 5-HT reuptake leading to increased
descending inhibition of pain pathways
Also block sodium channels, alpha-adrenergic,
muscarinic (cholinergic), and histaminergic
pathways

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94
Q

Tricyclic Antidepressants compared to SSRI

Onset

A

Analgesic effect (superior to SSRIs)
- Independent of their effect on clinical depression
- Onset of analgesia with TCA ranges from 3-7 days
- Analgesia tends to occur at lower doses and plasma
levels than that needed for antidepressant effects

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95
Q

TCA Side Effects

A

Sedation (1-3hrs after ingestion)
Contraindicated in patients with severe cardiac disease, particularly conduction disturbances, obtain a
pretreatment ECG
Avoid in pts w/ GI dysfunction
Orthostatic hypotension, anticholinergic effects, weight gain, sexual dysfunction, restlessness

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96
Q

Signs of TCA Toxicity

A

Hyperthermia, Tachycardia, Seizures

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97
Q

TCA Metabolism and Excretion

A

Metabolized via CYP2D6 isoenzyme

Excreted in urine

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98
Q

Tricyclic side effects

A

.

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99
Q

Tricyclic Guidelines

A

.

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100
Q

Amitriptyline (Elavil)

A

Tertiary amine

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101
Q

Amitriptyline (Elavil) Side Effect

A

Has the most Anticholinergic side effects (dry mouth, orthostatic hypotension, constipation, urinary retention, Insomnia, restlessness)

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102
Q

Amitriptyline (Elavil) Dosage

A

100-150mg/day (25-150mg/day)
Neuropathic pain: initial dose of 10- 25mg at bedtime titrated by 10-25mg per week until response or a
maximum of 150mg/day
Anticholinergic SE reduce by starting low doses qhs and slowly titrated to higher dose or using
secondary amine

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103
Q

Tertiary amine TCA

A

Imipramine , Tripramine, Clomipramine, Doxepin, Amitriptyline

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104
Q

Secondary amine TCA

A

Desipramine, Nortriptyline, Protriptyline, Amoxapine

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105
Q

Desipramine Side Effect

A

Fewer anticholinergic side effects Lower sedating effect

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106
Q

Desipramine Dosage

A

200-250mg/day (10-150mg/day) Neuropathic pain: initial dose of 10- 25mg at bedtime titrated by 10-25
mg per week until response or a
maximum of 150mg/day
Time to Effect: 6 week
Safe in older pts but starting dose reduced by ½

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107
Q

Nortriptyline Side Effect

A

Fewer side effects

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108
Q

Nortriptyline Dosage

A

100-150mg/day (30-150mg/day) Neuropathic pain: initial dose of 10-25mg at bedtime titrated by 10-25
mg per week until response or a
maximum of 150mg/day
Time to Effect: 6 week
Fewer anticholinergic side effects
Safe in older pts but starting dose reduced by ½

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109
Q

Trazadone MOA

A

Inhibits serotonin uptake and blocks serotonin

5HT2 receptors, Alpha-1-receptor antagonist

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110
Q

Trazadone Indications

A

At low dose, it is used as an

adjunct for insomnia

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111
Q

Trazadone Side Effect

A

Sedation

Orthostatic Hypotension

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112
Q

Duloxetine (Cymbalta) MOA

A

NE and 5-HT reuptake inhibitor

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113
Q

Duloxetine (Cymbalta) Indications

A 
Chronic Musculoskeletal Pain
(Discomfort from Chronic Low Back Pain and Osteoarthritis)
Diabetic Peripheral Neuropathy
Fibromyalgia
DM and depression
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114
Q

Duloxetine (Cymbalta) Side Effects

A

Nausea, Dry mouth, Insomia, Drowsiness, Constipation, Fatigue, Dizziness
SIADH(rare)
Sucide
Hepatoxicity
SEs are reduced by administering 30mg daily for one week before increasing to 60mg daily
duloxetine does not cause QTc interval prolongation,

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115
Q

Duloxetine (Cymbalta) Dose

A

20 to 60 mg daily or bid
60-120mg/day (Reduce dose if CrCl< 30 ml/min)
Chronic Musculoskeletal Pain: 30mg/day for 1 week to target of 60mg/day

Diabetic Peripheral Neuropathy: the initial and target dose is 60mg/day

Fibromyalgia: 30mg/day for 1 week to a target dose of 60mg/day
Time to Effect: 4 week

116
Q

Duloxetine (Cymbalta) Metabolism and Excretion

A

Liver metabolism and excreted in urine/feces (70/30)
Associated with transaminase elevation
Avoid in: MAOI’s or phenothiazine use, narrow-angle glaucoma, alcohol use
Avoided in patients with hepatic or severe renal insufficiency

117
Q

Milnacipran (Savella) MOA

A

,

118
Q

Milnacipran (Savella) Indication

A

Fibromyalgia

119
Q

Milnacipran (Savella) Dose

A 
Fibromyalgia: dose titrated as follow 
Day 1: 12.5 mg
Day 2 -3: 12.5mg twice daily
Day 4-7: 25mg twice daily
Target dose is 50mg twice daily
120
Q

Venlafaxine (Effexor) MOA

A

NE and 5-HT reuptake inhibitor

121
Q

Venlafaxine (Effexor) Indication

A

Painful Diabetic Peripheral Neuropathy

Painful polyneuropathies of different origin but NOT Post Herpetic Neuralgia

122
Q

Venlafaxine (Effexor) Side Effect

A

Prescribe with caution in patients with cardiac disease
Nausea, headache, somnolence, insomnia
Suicidality, seizures, SIADH, HTN, mania, arrhythmia, serotonin syndrome, blood dyscrasia’s
Monitor EKG though less concerning than TCA
Avoid with MAOI’s

123
Q

Venlafaxine (Effexor) Dose

A

150-225mg/day (37.5- 225 mg/day)
25mg daily and titrate

Neuropathic Pain: initial doses of 37.5mg once or twice daily titrated by 75mg weekly to response or a maximum dose of 225mg/day
Time to Effect: 4-6 week

124
Q

Venlafaxine (Effexor) Metabolism and Excretion

A

Liver metabolism, urine excretion

Reduce the dose by 25-50% in patients with mild to moderate renal impairment and 50% in hepatic impairment

125
Q

Fluoxetine (Prozac) MOA

A

Serotonin Reuptake Inhibitor

126
Q

Fluoxetine (Prozac) Indications

A

Fibromyalgia
Peripheral Neuropathy
Not preferred for neuropathic pain

127
Q

Fluoxetine (Prozac) Side Effect

A

,

128
Q

Fluoxetine (Prozac) Dose

A

Fibromyalgia: usual dose is 20-80mg/day

Peripheral Neuropathy: usual dose is 20-40 mg/day

129
Q

Paroxetine (Paxil)

A

.

130
Q

Paroxetine (Paxil)

A

.

131
Q

Paroxetine (Paxil)

A

.

132
Q

Paroxetine (Paxil)

A

.

133
Q

Paroxetine (Paxil)

A

.

134
Q

Carbamazepine (Carbatrol, Tegretol) MOA

A

Blocking sodium channels

135
Q

Carbamazepine (Carbatrol, Tegretol) Indications

A

Trigeminal neuralgia and bipolar disorder.

136
Q

Carbamazepine (Carbatrol, Tegretol) Side Effects

A

Hyponatremia, drowsiness, fatigue, dizziness, and blurred vision. Drug use has also been associated with Stevens-Johnson syndrome. Blood dyscrasias: neutropenia,
leukopenia, thrombocytopenia, pancytopenia, and anemias
Cause bone marrow suppression or hepatotoxicity. A CBC and LFT should be obtained at baseline
Use with caution in patients with hepatic impairment

137
Q

Carbamazepine (Carbatrol, Tegretol) Dose

A

200mg tid
Neuropathic pain: 100mg 2x daily titrated slowly to response or a maximum of 1200mg/day
Time to Effect: 4 week

138
Q

Carbamazepine (Carbatrol, Tegretol) Excretion and Metabolism

A

CYP3A4 system, urine/feces (70/30)

139
Q

Carbamazepine (Carbatrol, Tegretol) effects on drugs

A

Induces metabolism of many drugs (warfarin, CCB’s, OCP’s, HIV, azoles, other AEDs, etc)
Mycins, cimetidine, and propoxyphene increase CBZ levels

140
Q

Carbamazepine (Carbatrol, Tegretol) and Bicuculline

A

Bicuculline antagonizes its antinociceptive effect

141
Q

Oxcarbazepine (Trileptal) MOA

A

Blocks Na+ channels

an analogue of carbamazepine

142
Q

Oxcarbazepine (Trileptal) Indications

A

.

143
Q

Oxcarbazepine (Trileptal) Side Effect

A

Nausea, rash, hyponatremia, headache, sedation, dizziness, vertigo, ataxia, and
Diplopia, weight gain and edema, GI symptoms, fatigue, allergic rxn

May cause hyponatremia; monitoring of serum sodium levels may be necessary

144
Q

Oxcarbazepine (Trileptal) Doses

A

Diabetic Neuropathy: 150-300 mg/day titrated to response or a maximum dose of 1800mg/day; the usual effective dose is 900-1200mg/day. Start 75-150mg BID and titrate weekly as tolerated to effect, max 1200 BID

Neuralgia: 300mg 2or 3 times daily titrated to response or a maximum of 2000mg/day

145
Q

Oxcarbazepine (Trileptal) Metabolism and Excretion

A

Dose adjusted in patients with renal impairment

146
Q

Gabapentin (Neurontin) MOA

A

Unknown MAO
Thought to inhibit voltage dependent calcium channels at the alpha 2- delta subunit and inhibit neurotransmitter release
An analog of GABA. However, it does not act at GABA receptors, and it neither enhances GABA actions nor is converted to GABA.

147
Q

Gabapentin (Neurontin) Indications

A

Neuropathic pain conditions

Postherpetic Neuralgia
Diabetic Neuropathy

First-line drug for treatment of PHN and PDN

148
Q

Gabapentin (Neurontin) Side Effects

A

Mild drowsiness, dizziness, ataxia, weight gain, and diarrhea. Few drug interactions.

149
Q

Gabapentin (Neurontin) Dose

A

2400-3600mg/day (dose 3 or 4 times daily)
Reduce dose if CrCl < 60ml/min

Neuropathic Pain: 100-300mg at bedtime titrated weekly in increments of 300mg/day to response or a maximum dose of 3600mg/day divided 3 times daily

Fibromylagia: 300mg at bedtime titrated slowly to 1200mg/day

Time to Effect: 4 week

150
Q

Gabapentin (Neurontin)

A

Dose must be adjusted in patients with renal impairment
Excreted in urine unchanged
Lower dose in renal insufficiency

151
Q

Lamotrigine (Lamictal) MOA

A

Blocks sodium channels as well as high voltage–dependent calcium channels

152
Q

Lamotrigine (Lamictal) Indications

A

Reduce the symptoms of complex regional pain syndrome (type 1), with the sudomotor changes seen in this condition being alleviated along with pain and allodynia.

153
Q

Lamotrigine (Lamictal) Side Effects

A

Nausea, drowsiness, dizziness, headache, and diplopia. Rash (Stevens-Johnson syndrome—potentially life-threatening). Broad spectrum of antiseizure activity.
Lamotrigine is associated with rare but serious skin reactions
Rapid titration to high serum concentrations of lamotrigine have been reported to cause a rash, which in some patients may progress to a serious, life-threatening reaction
Caution with OCP’s

154
Q

Lamotrigine (Lamictal) Dosage

A

100-200 mg bid
(Use reduce dose in significant renal impairment)

Neuropathic pain: 50mg/day for 2 weeks followed by 50 mg twice daily for 2 weeks then titrate by 100mg/day every week to response or a maximum dose of 600mg/day (the immediate release formulation is administered in 2 divided doses)
Time to Effect: 6-8 week

155
Q

Lamotrigine (Lamictal) Metabolism and Excretion

A

Dose should be reduced and titrated carefully in patients with impaired hepatic or renal function

156
Q

Pregabalin (Lyrica) Schedule

A

Schedule V

157
Q

Pregabalin (Lyrica) MOA

A

Binds to the α2 -δ site, an auxiliary subunit of voltage-gated calcium channels in the CNS, inhibiting excitatory neurotransmitter release.

A lipophilic GABA analog to facilitate diffusion across the blood brain barrier

158
Q

Pregabalin (Lyrica) Indications

A

Diabetic peripheral neuropathy,

Postherpetic Neuralgia, Fibromyalgia.

159
Q

Pregabalin (Lyrica) Side Effect

A

Common: Constipation, Dizziness, Blurred vision, Dry mouth, Sedation
Weight gain, somnolence, , headache, weight gain, diplopia, and ataxia.
One hundred percent renal elimination.
rhabdomyolysis (rarely)

160
Q

Pregabalin (Lyrica) Dosage

A

300-600 mg/day (dose 2 or 3 x daily)
Reduced dose if CrCl < 60ml/min
Fibromyalgia: initial dose of 150mg/day divided twice daily may be increased to 300mg/day within 1 week and titrated to a maximum dose of 450mg/day
Diabetic Peripheral Neuropathy: initial dose of 150mg/day divided 3 times daily may be increased to a maximum dose of 300mg/day within 1 week. Maximum dose of 600mg/day
Time to Effect: 4-6 week
Postherpetic Neuralgia: initial dose of 150mg/day divided 2-3x daily may be increased to 300mg/day within 1 week and titrated to a maximum dose of 600mg/day

161
Q

Pregabalin (Lyrica) Dosage Metabolism and Excretion

A

Reduce doe in patients with renal dysfunction

Renal excretion, no liver metabolism

162
Q

Topiramate MOA

A

Blocks voltage-dependent sodium channels, and it has been shown to
increase the frequency of chloride channel opening by binding to the
GABA-A receptor agonist. High-voltage calcium currents (L type) are reduced by topiramate . It is a carbonic anhydrase inhibitor and may act at glutamate (NMDA) sites

163
Q

Topiramate Indications

A

Migraine.

164
Q

Topiramate Side Effects

A

Paresthesia, weight loss, nervousness, depression, anorexia, anxiety, tremor,
cognitive complaints, headache, and oligohidrosis. Few drug interactions.
Broad spectrum of antiseizure activity.

Interacts with OCP’s, DM meds, AED’s

165
Q

Topiramate Dosage

A

150-200mg bid
Reduced dose if CrCl < 70ml/min

25mg daily, titrate weekly to max 200mg/d
Time to Effect: 12 week

166
Q

Topiramate Metabolism and Excretion

A

Minimal liver metabolism, urine excretion

167
Q

Valproate (Depakote) MOA

A

sodium channel blockade, blockade of GABA transaminase, and action at the T-type calcium channels.

168
Q

Valproate (Depakote) Indications

A

Anti-epileptic

169
Q

Valproate (Depakote) Side Effects

A

Weight gain, easy bruising, nausea, tremor, hair loss, weight gain, GI upset, liver damage, alopecia, and sedation. Hepatic failure, pancreatitis, and teratogenic effects have been observed. Broad spectrum of antiseizure activity.

170
Q

Valproate (Depakote) Dosage

A

1000- 1200 mg/day (dose 2 or 3 x daily)
125mg QD-TID, max 500 TID

Reduce starting dose; max dose= 60 mg/kg/day
Diabetic Neuropathy: usual dose of 500mg to 1200mg/day
Time to Effect: 4 week

171
Q

Valproate (Depakote) Metabolism and Excretion

A

Use with caution in patients with hepatic impairment
CYP2C9 inhibitor, urine excretion mostly
Interacts with other meds via CYP450 system and protein binding (aspirin/warfarin)

172
Q

Clonazepam (Klonopin) MOA

A

Benzodiazepine—which

binds to the GABAB receptor

173
Q

Clonazepam (Klonopin) Indication

A

Utilized to treat various neuropathic pain syndrome and lower extremity muscle conditions. Useful effect in treatment of the shooting pain associated with phantom limb pain
Useful in pts w/ anxiolysis
It belongs to the benzodiazepine group of drugs,
anxiolysis and muscle relaxation may also be
produced by its use

174
Q

Clonazepam (Klonopin) Side Effect

A

Somnolence is a predominant side effect, and with this drug’s long half-life, daytime sedation may complicate use.

175
Q

Clonazepam (Klonopin) Dosage

A

,

176
Q

Clonazepam (Klonopin) Metabolism and Excretion

A

.

177
Q

Muscle Relaxants –> Sedatives

A 
	Carisoprodol (Soma)
	Methacarbamol (Robaxin)
	Orphenadrine (Norflex)
	Metaxalone (Skelaxin)
	Cyclobenzaprine (Flexeril)
178
Q

Muscle Relaxants actually relaxes muscles

A 
	Baclofen
	Benzodiazepines
	Tizanidine
	Dantrolene
	Botox
179
Q

Baclofen MOA

A

a muscle relaxant that is believed to affect GABA receptors at the level of the spinal cord.
the ρ-chlorophenyl derivative of
GABA. Baclofen is a GABAB agonist

180
Q

Baclofen Indications

A

used for muscle spasms and spasticity, neuropathic pain

181
Q

Baclofen Side Effects

A

Sedation, weakness, and confusion.

Abrupt cessation may cause a withdrawal syndrome, such as hallucinations, anxiety, tachycardia,or seizures

182
Q

Baclofen Dosage

A

Spasticity/ Pain: Initial dose of 5mg 3x daily increased in 5mg dose increments every 3 days to response or a maximum dose of 80mg/day
used intra-thecally

183
Q

Baclofen Metabolism and Excretion

A

Use with caution in patient with renal dysfunction; dosage reduction may be necessary

184
Q

Baclofen Contraindicated in patients

A

with history of seizures

185
Q

Cyclobenzaprine (Flexeril) MOA

A

structurally similar to
TCAs and, as such, demonstrates significant
anticholinergic side effects

Centrally acting

186
Q

Cyclobenzaprine (Flexeril) Indications

A

Nocturnal Muscle spasm

187
Q

Cyclobenzaprine (Flexeril) Side Effects

A

anticholinergic side effects, including
lethargy and agitation, although it usually
does not appear to produce significant dysrhythmias beyond sinus tachycardia. Elderly patients seem to tolerate cyclobenzaprine less well and may develop hallucinations as well as significant anticholinergic side effects, such as sedation.

Side effects: Drowsiness	, Cardiac dysrhythmias	
–	Anticholinergic
»	Dry mouth
»	 Blurred vision
»	Urine retention
»	Constipation
»	Increased intraocular pressure
188
Q

Cyclobenzaprine (Flexeril) Dosage

A

Spasm: Initial dose of 5mg 3x daily increased to 7.5- 10mg 3x/day; the
Extended release capsule should be initiated at 15mg/day and may be increased to 30mg/day

Fibromyalgia: 10-30 mg at bedtime

189
Q

Cyclobenzaprine (Flexeril) Metabolism and Excretion

A

Use with caution in patients with hepatic impairment; do not use the extended release capsule formulation in theses patients

190
Q

Carisoprodol (Soma) MOA

A

Act as indirect agonists at the GABAA receptor, yielding CNS chloride ion channel conduction effects similar to benzodiazepines. Therefore, flumazenil may be a potentially useful antidote to carisoprodol toxicity.

Precursor of meprobamate – an anxiolytic
Centrally active

191
Q

Carisoprodol (Soma) Indications

A

Useful for the short-term treatment of acute musculoskeletal disorders,
especially in combination with acetaminophen, aspirin, or NSAIDs.

192
Q

Carisoprodol (Soma) Side Effects

A

Poor metabolizers of mephenytoin have a diminished ability to metabolize carisoprodol
and therefore may be at increased risk of
developing concentration-dependent side effects (eg, drowsiness, hypotension, CNS depression) at “usual” adult doses.

 Side effects:
– Sedation, drowsiness, dependence
– Withdrawal like any other CNS depressant w/d
 Addictive, please avoid. Junkies love to combine with hydrocodone

193
Q

Carisoprodol (Soma) Dosage

A

350mg three times daily

194
Q

Carisoprodol (Soma) Metabolism and Excretion

A

Carisoprodol is primarily metabolized in the liver to several metabolites, including meprobamate by N-dealkylation via CYP2C19.

195
Q

Methocarbamol (Robaxin) MOA

A

Centrally active general CNS depressant

196
Q

Methocarbamol (Robaxin) Indications

A

MS
Clinical effects:
Reduction of muscle spasms

197
Q

Methocarbamol (Robaxin) Side Effects

A

drowsiness

198
Q

Methocarbamol (Robaxin) Dosage

A

1000- 1500mg four times daily

199
Q

Metaxalone (Skelaxin) MOA

A

.

200
Q

Metaxalone (Skelaxin) Indications

A

Reduction in muscle spasm through CNS depression

201
Q

Metaxalone (Skelaxin) Side Effects

A

Nausea
Drowsiness
Dizziness

202
Q

Metaxalone (Skelaxin) Dosage

A

Daily dosage: 400-800 mg tid

203
Q

Orphenadrine (Norflex) MOA

A

Analog of diphenhydramine

Thought to work through central atropine like effects

204
Q

Orphenadrine (Norflex) Indications

A

Given IV for antispasticity trials

205
Q

Orphenadrine (Norflex) Side Effects

A

Anticholinergic

Rare aplastic anemia

206
Q

Orphenadrine (Norflex) Dosage

A

Daily dosage: 100 mg bid

207
Q

Dantrolene MOA

A

Suppresses excitation contraction coupling by binding the ryanodine receptor and decreases intracellular calcium

208
Q

Dantrolene Indications

A

treatment for NMS, MH, SS

209
Q

Dantrolene Side Effects

A

sedation, hypersensitivity, pleural effusion and pericarditis, liver toxicity, seizures

210
Q

Dantrolene Dosage

A

Start 25mg daily and titrate to effect as tolerated in 7 day intervals

211
Q

Clonidine MOA

A

Reduces neurotransmitter release and sympathetic tone, decreases BP

212
Q

Clonidine Indications

A

Best indication in sympathetically mediated pain

Complex regional pain syndrome, cancer pain, headaches, postherpetic neuralgia, peripheral neuropathy

213
Q

Clonidine Side Effects

A

.

214
Q

Clonidine Dosage

A

Available in oral, transdermal, and epidural or intrathecal use form.

For pain, start 0.05mg daily to BID and titrate as tolerated

215
Q

Tizanidine (Zanaflex) MOA

A

Agonist at the α2- adrenoreceptor.

imidazoline derivative that is structurally related to clonidine

216
Q

Tizanidine (Zanaflex) Indications

A

Useful for painful consitions involving Muscle Spasticity

neuropathic pain

217
Q

Tizanidine (Zanaflex) Side Effects

A

Somnolence, dry mouth, dizziness, asthenia

Hepatotoxicity, hypotension, hallucinations

218
Q

Tizanidine (Zanaflex) Dosage

A

Spasticity: Initial dose of 4mg/day increased in 2-4 mg dose increments
over 2-4 weeks; the usual dose is 8 mg every 6-8 hours with a maximum dose of 36mg/day

219
Q

Tizanidine (Zanaflex) Metabolism and Excretion

A

Metabolism of tizanidine occurs primarily in the liver through oxidative processes, and
metabolites of the parent compound have no activity. Excretion of tizanidine and its metabolites occurs primarily
via the kidneys (53%-66%).
Reduced dose in patients with renal dysfunction
Use with caution in patients with hepatic impairment
Caution with SSRI’s (inhibit metabolism), especially fluvoxamine (Luvox), and ciprofloxacin
Metabolized by the liver, excretion in urine and feces

220
Q

 Glutamate is the major excitatory neurotransmitter and works via several receptors

A

– NMDA
– AMPA/kainate
– Metabotropic receptors (G protein and kinase cascade)

221
Q

 NMDA felt to be involved in neuroplastic changes

A

of developing chronic pain states

222
Q

NMDA antagonists

A

– Dextromethorphan
– Memantine and Amantadine
– Methadone and Propoxyphene
– Ketamine

223
Q

Dextromethorphan

A

A synthetic cough depressant that has relatively
no analgesic action and a relatively low potential for
abuse in usual antitussive doses

224
Q

Capsacin MOA

A

Alkaloid Active components of chili peppers.
A member of the vanilloid family that binds to the
TRPV1 receptor
Depletes presynaptic substance P

225
Q

Capsacin Indications

A 
Chronic musculoskeletal or 
neuropathic pain 
Postherpetic Neuralgia 
HIV neuropathy 
Diabetic neuropathy
226
Q

Capsacin Side Effects

A

Burning
Stinging
Erythema

227
Q

Capsacin Dosage

A 
Commercially available in 0.025% 
and 0.075% concentration. Higher 
concentration patch (8%) 
Patch administered as a single 60 
mins application 
Cream must be applied 3-4x per 
day over the entire painful area for 
up to 6-8 wks before optimal pain 
relief can be achieved
228
Q

Capsacin Applications

A

Apply to painful area with gloves and avoid application to
anywhere else especially the eyes and mucous
membranes
May be useful in combination with local anesthetics by
increasing intra-neuronal access for the LA

229
Q

Lidocaine Patch (5%) Indications

A

Postherpetic Neuralgia
Allodynia
Peripheral Neuropathic pain

230
Q

Lidocaine Patch (5%) MOA

A

.

231
Q

Lidocaine Patch (5%) Side Effect

A

Edema, erythema, abnormal

sensation, exfoliation

232
Q

Lidocaine Patch (5%) Dosage

A

Its used 12 hours ON and 12 hours OFF.

233
Q

Botulinum Toxin

A

Botulinum Toxin Type A

Potent neutotoxin

234
Q

Botulinum Toxin

A

Postherpetic Neuralgia

235
Q

NSAIDS MOA

A

NSAIDs are weak organic acids, consisting in one or two aromatic rings connected to an acidic functional group.
Inhibits the prostaglandin G/H synthase enzymes (COX), therefore inhibiting the synthesis of prostaglandin E, prostacyclin, and thromboxane.
Inhibit COX-1 inhibit the synthesis of TXA2
inhibit platelets  prolonged bleeding time mild
below the upper limits of normal.
Inhibit COX-1 NSAIDs act mainly in the periphery, but they may have a central effect.
COX-2 induction within the spinal cord may play an important role in central sensitization.

The acute antihyperalgesic action of NSAIDs has been show to be mediated by the inhibition of constitutive spinal COX-2, which has been found to be upregulated
in response to inflammation

Act as antipyretic, analgesic, and anti inflammatory

236
Q

NSAIDS Indications

A 
Nociceptive Pain 
Indicated for mild to 
moderate pain, particularly of 
somatic origin. 
Used for soft tissue injury, 
strains, sprains, headaches, 
and arthritis
237
Q

NSAIDS Side Effects

A

Main SEs: Inhibition of platelets, GI insult (dyspepsia and gastric ulceration, food helps), renal insult, and CV effects. In the kidney, prostaglandins help to maintain GFR and blood flow. They also contribute to the
modulation of renin release, excretion of water, and tubular ion transport. NSAIDs may
decrease rapidly the GFR, release of renin, which can progress to renal failure. Sodium, water retention, hyperkalemia, hypertension, acute papillary necrosis, chronic interstitial nephritis, and nephrotic syndrome can also occur. Nephrotoxcity includes reversible renal insufficiency due to renal vasoconstriction, acute interstitial nephritis , ATN in pt with low renal perfusion
NSAIDs rarely cause potentially fatal hepatic necrosis and notable
increases (ALT) or (AST) 3x. Rare cases of severe hepatic reactions, including jaundice and fatal fulminant hepatitis, liver necrosis, and hepatic failure (some with fatal outcome

238
Q

NSAIDS

A

.

239
Q

NSAIDS

A

.

240
Q

NSAIDS

A

.

241
Q

COX-2 inhibitors (Coxibs).

A

.

242
Q

COX-2 inhibitors (Coxibs) Indications

A

A good choice if there is any history of GI symptoms.
Coxibs are associated with less GI toxicity than standard
NSAIDs, since they do not inhibit the constitutive
COX-1 and therefore the production of the
cytoprotective PGI2 in the stomach mucosa.

243
Q

COX-2 inhibitors (Coxibs) Side Effects

A

There is a possible increased risk of MI and thrombotic stroke events associated with the continuosly long-term use of coxibs. (rofecoxib and valdecoxib being withdrawn from the market). Coxibs (COX-2 inhibitors) have similar renal effects to NSAIDs. Increase serum warfarin levels
Associated with less GI toxicity than standard NSAIDs but they are more expensive
COX-2 is not present in platetelets, and coxibs are not associated with platelet dysfunction.
Celecoxib and valdecoxib are contraindicated in patients allergic to sulfonamides

244
Q

COX-2 inhibitors (Coxibs) Dosage

A

Unlike ibuprofen, naproxen, and ketorolac, celecoxib does not interfere with the inhibition of platelet COX-1
activity and function by aspirin. Doses above 200mg per day have been associated with increase cardiovascular risk. high doses of celecoxib (400mg/day or more) should be avoided.

245
Q

COX-2 inhibitors (Coxibs)

A

.

246
Q

Ketorolac (Tordadol) Indications

A

Has been used as a short term alternative (less than 5 days) to opioids, for moderate to severe pain.

247
Q

Ketorolac (Tordadol) MOA

A

potent analgesic, poor anti-inflammatory

248
Q

Non-acetylated salicylates (Salsalate and Choline

magnesium trisalicylate) MOA

A

Nonacidic prodrug metabolized to a structural analogue of naproxen

249
Q

Non-acetylated salicylates (Salsalate and Choline

magnesium trisalicylate) Side Effects

A

Minimally toxic to the GI tract, and it is the choice when GI side effects are a special concern

250
Q

Acetaminophen MOA

A

An aniline derivative Induced analgesia is centrally mediated but has peripheral mechanism of action NOT anti-inflammatory

251
Q

Acetaminophen Indications

A

Drug of choice for relieving mild to moderate

musculoskeletal pain. Hip or knee osteoarthritis

252
Q

Acetaminophen Side Effects

A

The liver receives the major insult from acetaminophen toxicity, with the predominant lesion being acute centrilobular hepatic necrosis. Relative contraindications: liver disease or heavy alcohol use. Max dose in these patients is 2g per day

253
Q

Acetaminophen Dosage

A

OTC FDA lists the maximum daily dose
to be 4g per day but manufactures uses maximum daily dose to 3 to 3.25g per day Caution with narcotic combos
Acetaminophen overdose can lead to severe
hepatotoxicity

254
Q

Acetaminophen Metabolism and Excretion

A

It is suggested the use of the glutathione precursor of N-acetylcysteine for the treatment of acetaminophen intoxication in efforts to maintain hepatic reduced
glutathione concentrations and adrenergic agonists may lower hepatic glutathione
significantly

255
Q

Aspirin MOA

A

Covalently acetylates COX-1 and COX-2,
irreversibly inhibiting COX activity
Irreversibly inhibit platelet aggregation for lifetime of the platelet (4-7 days) Inhibition of platelet COX-1 (COX-2 is expressed only in
megakaryocytes) last for the lifetime of the
platelet, 8 to 12 days (10 days average) after
therapy has been stopped.

256
Q

Aspirin Indications

A

.

257
Q

Aspirin Side Effects

A

ASA and other salicylates are contraindicated in children and young adults (younger than 20 years) with fever associated with viral illness, owing to the association with Reye syndrome. Sensitivity of platelets to inhibition by low doses of aspirin, as low as 30 mg/d is related to their presystemic inhibition in the portal circulation before aspirin is deacetylated to salicylate on first pass through the liver. Patient allergic to ASA may also be allergic to other NSAIDs

258
Q

Aspirin Dosage

A

Aspirin because of its irreversible antiplatelet effect should be stopped 10 days before elective surgery.

259
Q

Diflunisal MOA

A

a difluorophenyl derivative of salicylic acid, more potent than aspirin

260
Q

Diflunisal Indications

A

Used primarily as analgesic in osteoarthritis and musculoskeletal sprains, where is 3 to 4 times more potent than ASA

261
Q

Diflunisal Side Effects

A

It also produces fewer and less intense GI and antiplatelet effects than ASA.

262
Q

Indomethacin Indications

A

Reserve for challenging patients or those with known disease, ie gout, RA, etc

263
Q

Indomethacin Side Effects

A

Intolerance limits its dosing to short-term. It also may have a direct, COX-independent vasoconstrictor effect. increased risk of MI and stroke, Very potent and worse side effect profile

264
Q

Indomethacin Dosage

A

10 to 40 times more

potent inhibitor of COX than ASA

265
Q

Diclofenac Side Effects

A

Diclofenac is available in combination with
misoprostol, retaining the efficacy of diclofenac while reducing the frequency of GI toxicity; higher incidence of hepatotoxicity

266
Q

Diclofenac Dosage

A 
Topical gel (voltaren 1%) and patch  (flector) 
more potent than ASA; its  potency against COX-2 is substantially greater  than that of indomethacin, naproxen, or several  other NSAIDs.
267
Q

Calcitonin Indications

A

Used as an adjuvant drugs for Phantom limb pain, Sympathetically maintained pain, Cancer bone pain, Osteoporosis pain

268
Q

Ziconotide MOA

A

non-opioid and non-NSAID analgesic
A synthetic drug with an amino acid sequence
derived from marine sea snail venom (a conopeptide), binds to a neutral N-type Ca channels

269
Q

Ziconotide Indications

A

Intrathecal analgesic therapy reserved for intractable severe pain

270
Q

Ziconotide Side Effects

A

Black Box warning of neurologic impairment and psychiatric symptoms

271
Q

Ziconotide Dosage

A

Effective when given IV or orally

272
Q

Botulinum MOA

A

two clinically available botulinum toxins in the United States are botulinum toxin type A and botulinum toxin type B.
Most evident mechanism of botulinum toxin-induced analgesia is via reduction of muscle spasm by cholinergic chemodenervation
at motor end plates and by inhibition of gamma motor endings in muscle spindles

273
Q

Botulinum Indications

A

Diminished pain in patients with painful muscle spasms or cervical dystonia by
diminishing muscle tone, it is also felt that botulinum toxin may itself possess analgesic
properties

274
Q

Botulinum

A

.

275
Q

Corticosteroids (glucocorticoids) MOA

A

.

276
Q

Corticosteroids (glucocorticoids) Indications

A

Most effective in nociceptive syndromes

277
Q

Corticosteroids (glucocorticoids) Side Effects

A 
Corticosteroids increase the risk of  glaucoma by raising the intraocular  pressure (IOP) when administered  exogenously. ESIs were noted to cause a significant increase in the blood 
glucose levels in diabetics,  Mania/anxiety, Adrenal suppression, Exacerbation of 
myasthenia gravis, Glaucoma
Side Effects 
 Kaposi’s sarcoma 
 Myopathy 
 Psychiatric disturbances 
 Adrenal suppression 
 Bronchospasm 
 Delayed wound healing 
 Immunosuppression 
 Osteoporosis 
 AVN 
 Fluid retention 
 Hypertension 
 Hyperglycemia 
 GI ulceration 
 exacerbation of MG 
 Increased IOP 
 Cushings 
 Tissue atrophy 
 Anaphylaxis
278
Q

Corticosteroids (glucocorticoids) Dosage

A

For epidural injection, a crystalline depot for is used to allow for prolonged release of the
medication over time. These particles can occlude blood vessels and lead to cord infarction and stroke, especially with cervical
transforaminals . Also can cause arachnoiditis

279
Q

Calcitonin/bisphosphonates indications

A

helpful in reducing pain due to bony metastases helpful in chronic neuropathic
pain states – CRPS, phantom pain

280
Q

Pharmacological Treatment of Fibromyalgia

A 
Gabapentin 
Duloxetine- less effective 
Amitriptyline- less effective
Pregabalin- CCB
Cyclobenzaprine
Tizanidine 
TPI - less effective
281
Q

Treatment of CRPS

A

Amitriptyline 10–75 mg/day Once a day (at night) Sedation, anticholinergic effects

Nortriptyline 10–75 mg Once a day (at night) Sedation, anticholinergic effects

Desipramine 10–75 mg/day Once a day (at night) Least sedative/anticholinergic effects

Venlafaxine 37.5–340 mg/day BID–TID

282
Q

Anticholinergic Effects Mnemonic

A

Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter.

Hot as a hare: increased body temperature
Blind as a bat: mydriasis (dilated pupils)
Dry as a bone: dry mouth, dry eyes, decreased sweat
Red as a beet: flushed face
Mad as a hatter: delirium

283
Q

Diabetic Neuropathy Treatment

A

Duloxetine
Gabapentin and pregabalin effective in diabetic neuropathy and postherpetic
neuralgia (PHN)

284
Q

Anticonvulsants for CRPS

A

Gabapentin 900–3600 mg/day TID Somnolence, memory impairment,
tremors

Pregabalin 150–600 mg/day BID–TID Dizziness, somnolence, peripheral
edema

Carbamazepine 100–1000 mg/day BID–QID Ataxia, sedation, nausea, liver
damage, skin rash, bone marrow

285
Q

Opioid for CRPS

A

Morphine (extended release) 15–60 mg BID–TID Nausea, vomiting, constipation,
sedation, pruritus

Oxycodone (extended release) 10–60 mg BID–TID Nausea, vomiting, constipation,
sedation, pruritus

Methadone 5–20 mg BID–TID Nausea, vomiting, constipation, sedation, pruritus

Pharmacology of Chronic Pain Management (2 decks)

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