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Adv Pharm I > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

Types of pain

A

Nociceptive

Neuropathic/functional

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2
Q

Nociceptive pain

A

Caused by damage to body tissue, secondary to noxious stimuli

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3
Q

Neuropathic/functional pain

A

Disengaged from noxious stimuli or healing; Described in terms of chronic pain, result of nerve damage or abnormal operation of nervous system

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4
Q

Postherpetic neuralgia - pain type?

A

Neuropathic/functional pain

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5
Q

Diabetic neuropathy - type of pain?

A

Neuropathic/functional

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6
Q

Neuropathic pain

A

Result of nerve damage

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7
Q

Pain regulated by -

A

Excitatory & inhibitory neurotransmitters in response to stimuli

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8
Q

Perception of pain - 3 systems?

A
  1. Afferent pathways
  2. CNS
  3. Efferent pathways
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9
Q

Afferent pathway

A

send signals to spinal cord

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10
Q

CNS system involvement in pain pathway

A

discriminate & localize pain, arouse & alert (fight/flight), motivational factors

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11
Q

Efferent pathway

A

Modulate pain sensation

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12
Q

Pathophysiology - 4 stages of pain

A
  1. Stimulation
  2. Transmission
  3. Perception
  4. Modulation
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13
Q

Pain - Stimulation pathophysiology

A

Involves stimulation of free nerve endings - nociceptors

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14
Q

Pain - Transmission pathophysiology

A

Afferent fibers synapse into various layers of the spinal cords dorsal horn - pain impulses transmitted to brain stem — thalamus via ascending pathways — then finally to CNS

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15
Q

Ascending transmission pathway

A

Peripheral pain receptors to spinal cord to medulla to brain stem to midbrain to cortex

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16
Q

Pain - perception pathophysiology

A

The point at which pain becomes a conscious experience

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17
Q

Pain - modulation

A

Initiation of the anti-nociceptive system

Endogenous opiate system in CNS releases “endorphins”

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18
Q

Location of pain modulation

A

Descending system - inhibits pain transmission at dorsal horn

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19
Q

Neuropathic pain

A

Rewiring of pain circuits - anatomically and biochemically

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20
Q

The goal of managing pain

A

Reduce peripheral sensation (the cause) and decrease central stimulation

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21
Q

Pain severity vs. therapy measurement

A

Numerical assessment unless cognitive deficit or children - use face scale

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22
Q

Mild pain scale

A

1-3

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23
Q

Mild pain treatment

A

APAP, aspirin, NSAID, COX-2 inhibitors

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24
Q

Moderate pain scale

A

4-7

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25
Q

Moderate pain treatment

A

NSAID, opioid + APAP, tramadol

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26
Q

Severe pain scale

A

8-10

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27
Q

Severe pain treatment

A

Opioids

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28
Q

Reason for combination therapy (opioid + another Rx)

A
  1. Take advantage of the synergistic effect on pain

2. To limit the dose

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29
Q

Benefits of non-opioids

A

Availability, additive therapy when combined with opioids, inexpensive, low abuse

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30
Q

Only true “pain killers”

A

NSAIDs - decreasing inflammation (large cause of pain)

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31
Q

Disadvantages of non-opioids

A

Effects are “capped”, not effective at a certain pain level, side effects - can be toxic, limited parenteral availability

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32
Q

APAP

A

Tylenol

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33
Q

Tylenol - MOA

A

Believed to inhibit synthesis of prostaglandins in CNS; work peripherally to block pain impulse generation

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34
Q

Tylenol Dose

A

325-650 mg Q4H or 1000 mg q6h

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35
Q

Maximum dose of Tylenol/day

A

4 grams/day

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36
Q

Maximum Tylenol dose for liver impairment/alcoholism

A

2grams/day

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37
Q

Dosage forms of Tylenol

A

PO, PR, IV ($$$)

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38
Q

Tylenol black box warning

A

Hepatotoxicity and failure with excessive doses (>4g/day)

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39
Q

COX

A

Enzyme - cycle-oxygenase

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40
Q

COX binds to

A

Arachidonic acid

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41
Q

Arachidonic acid

A

Inflammatory mediator released in setting of tissue injury

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42
Q

COX-1 and COX-2

A

Isoenzymes

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43
Q

COX-1 pathway

A

Generates cytoprotective prostaglandins and thromboxane

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44
Q

COX-1 pathway location

A

GI, kidney, lung

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45
Q

COX-1 pathway effects

A

Platelet aggregation, vasoconstriction

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46
Q

COX-2 pathway

A

Inflammatory prostaglandins and prostacyclin

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47
Q

COX-2 effects

A

Inflammation, pain, antiplatelet, vasodilation

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48
Q

What pathway is blocked from NSAIDs?

A

COX-1 and COX-2

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49
Q

Salicylates

A

Aspirin

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50
Q

Aspirin MOA

A

Irreversibly binds to COX-1 and COX-2 enzymes

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51
Q

Aspirin properties

A

Analgesia, anti-inflammatory, antipyretic, antiplatelet

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52
Q

Aspirin - harmful

A

Antiplatelet - irreversible. Prevents synthesis of thromboxane A

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53
Q

Thromboxane A

A

Vasoconstrictor & inducer of platelet aggregation

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54
Q

Aspirin onset

A

15-20 min

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55
Q

Aspirin peak

A

1-3 hours

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56
Q

Aspirin duration

A

3-6 hours

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57
Q

Aspirin half life

A

3 hours

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58
Q

Aspirin elimination

A

Urine and liver

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59
Q

Aspirin adverse events

A

GI irritation and bleeding (ulcers), dizziness, deafness, tinnitus (salicylism) with high doses, Reye’s syndrome

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60
Q

Reye’s syndrome

A

Liver disorder and encephalopathy - occurs in children with viral infections

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61
Q

Aspirin - unique adverse effect

A

Asthamtics - increase risk of bronchospasm, urticaria, angioedema

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62
Q

Aspirin contraindication

A

Active peptic ulcer, history of GI bleed, hypersensitivity to aspirin or NSAID

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63
Q

Aspirin safety

A

Avoid use with recent surgery

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64
Q

NSAIDs general properties

A

Same as aspirin: analgesic, anti-inflammatory, antipyretic, antiplatelet (reversible)

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65
Q

Different property in general NSAID vs. aspirin

A

General NSAID: antiplatelet (reversible)

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66
Q

Ibuprofen maximum dosage/day

A

2400 mg

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67
Q

Indomethacin max dose/day

A

200 mg

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68
Q

Ketorolac max dose/day

A

120 mg

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69
Q

Naproxen max dose/day

A

600 mg

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70
Q

Common NSAIDs

A

Ibuprofen, indomethacin, ketorolac, naproxen

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71
Q

NSAID adverse effects - cardio

A

Fluid retention, hypertension, edema

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72
Q

NSAID - adverse effects - GI

A

Irritation, ulcers, bleeding, perforation

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73
Q

NSAIDs adverse effects - respiratory

A

Bronchospasm

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74
Q

NSAIDs adverse effects - skin

A

Rash

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75
Q

NSAIDs adverse effects - renal

A

Insufficiency or failure

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76
Q

NSAIDs - avoid with?

A

Other nephrotoxic drugs

77
Q

Nephrotoxic drugs

A

Diuretics - furosemide, hydrochlorothiazide; Ace inhibitors

78
Q

Black box warnings - NSAIDs

A

Potential adverse CV thrombotic events (MI and stroke), GI ulceration/bleeding/perforation, Tx of periop pain in setting of CABG

79
Q

Toradol

A

Ketorolac

80
Q

Ketorolac indication

A

Short-term management of moderate to severe pain

81
Q

Routes - ketorolac

A

Parenteral (IV/IM) or PO

82
Q

Ketorolac adverse events

A

Severe bleeding post-op, renal failure

83
Q

Maximum length of therapy for toradol

A

5 days

84
Q

COX-2 Inhibitor

A

Celecoxib

85
Q

Celebrex

A

Celecoxib

86
Q

Advantage of Celebrex

A

Minimal GI side effects, no effect on platelet aggregation

87
Q

Disadvantages of Celebrex

A

Renal dysfunction, avoid with “sulfa-allergy”, CARDIOVASCULAR EVENTS

88
Q

NSAID selectivity, most to least

A

Celecoxib, meloxicam/diclofenac, ibuprofen/naproxen, aspirin

89
Q

All NSAIDs increase the risk of

A

Major Adverse Cardiac Events

90
Q

Dose dependent

A

Dose-effect of NSAIDs…try to take as little as possible to minimize cardiac adverse effects

91
Q

Phenanthrenes

A

Morphine, hydromorphone, levorphenol, oxymorphone, codeine, hydrocodone, oxycodone

92
Q

Phenylpiperidines

A

Meperidine, fentanyl, sufentanil, alfentanyl, remifentanyl

93
Q

Phenylheptanes

A

Methadone

94
Q

Morphine is eliminated how?

A

Renal —— KNOW THIS

95
Q

Morphine routes of administration

A

PO, PR, IV, IM, SubQ, epidural, intro the cal

96
Q

Morphine PO Dosing

A

15-30 q4h PRN

97
Q

Morphine dosing IV

A

2-4 mg q4h PRN

98
Q

Active metabolites of Morphine

A
  1. 6-glucuronide: active analgesia

2. 3-glucuronide: myoclonus, confusion, hallucinations

99
Q

Histamine release

A

Hypotension, Pruritis

100
Q

Unique morphine related effect

A

Histamine release

101
Q

Histamine Release

A

Hypotension, Pruritis

102
Q

Hydromorphone formulations

A

PO, PR, IV, IM, SubQ, epidural

103
Q

Hydromorphone formulations

A

PO, PR, IV, IM, SubQ, epidural

104
Q

Hydromorphone half life

A

2-3 hours

105
Q

Hydromorphone metabolism

A

Primarily non-renal, no active metabolites

106
Q

Alternative agent for morphine in patient with advanced CKD, concerned of accumulation of morphine in the setting of lack of renal elimination

A

Hydromorphone

107
Q

Hydromorphone dosing PO

A

2-4 mg q4-q6 PRN

108
Q

Hydromorphone dosing IV

A

0.2-1 mg q2-3h PRN

109
Q

Methadone - used for?

A

Chronic Pain

110
Q

Reason Methadone is used for withdrawal

A

Long analgesic half life, even longer occupation of opiate receptor/preventing cravings

111
Q

Methadone Route of administration

A

PO, IV, IM, SubQ

112
Q

Methadone Dosing PO

A

2.5 mg q8-12h

113
Q

Methadone Dosing IV

A

2.5-10 mg q8-12h

114
Q

Methadone metabolism

A

Renally cleared

115
Q

Unique feature of Methadone

A

Prolong QTc - hold or reduce dose if QTc greater than or equal to 500

116
Q

When should caution be used when prescribing methadone?

A

In combination with other medications that could cause prolongation of QTc interval

117
Q

Methadone Cautions

A

Lowers threshold of seizures - use caution in patients with history; serotoninergic effects

118
Q

Methadone Metabolism

A

Biphasic elimination - analgesic half life: 8-12h; terminal half-life: 24-36h

119
Q

Meperidine routes of administration

A

PO, IV, IM, SubQ

120
Q

Meperidine Dose

A

IV: 50-150 mg q4-q6h

121
Q

Meperidine Metabolism

A

Renal

122
Q

Meperidine Metabolite

A

Active metabolite: normeperidine

123
Q

Side effect of normeperidine

A

Anxiety, seizures, tremors

124
Q

Increased risk of active metabolite when?

A

Renal dysfunction, preexisting CNS dysfunction, prolonged use > 48h, high cumulative doses

125
Q

Meperidine alternative uses

A

Post-op shivering

126
Q

Side effects of meperidine

A

Serotoninergic effects

127
Q

Codeine route of administration

A

PO

128
Q

Codeine dosage

A

15-60 mg q4h PRN

129
Q

Codeine metabolism

A

Converted to morphine (active metabolite)

130
Q

Codeine Metabolism Route

A

Major CYP 2D6 substrate (metabolizer variants)

131
Q

Codeine side effects

A

Antitussive

132
Q

Codeine tolerance

A

Weak agonist - low risk for abuse

133
Q

Hydrocodone route of administration

A

PO

134
Q

Hydrocodone dosage

A

5-10 mg q4-q6h PRN

135
Q

Hydrocodone metabolism

A

Metabolized to hydromorphine

136
Q

Hydrocodone metabolized via which route

A

CYP2D6

137
Q

Hydrocodone is used when?

A

Acute moderate to severe pain in patients with limited opioid use

138
Q

Hydrocodone is available as?

A

Immediate release combination product with APAP (Vicodin), ibuprofen (vicoprofen), OR extended release (Zohydro ER, Hysingla ER)

139
Q

Fentanyl route of administration

A

Transdermal, IV, lozenge, buccal, intranasal, sublingual, epidural

140
Q

Fentanyl dosage IV

A

25-50 mcg q2-3h

141
Q

Fentanyl Metabolism

A

Via CYP3A4

142
Q

Preferred agent for pain in liver failure

A

Fentanyl

143
Q

Why does fentanyl have a rapid onset?

A

High potency, lipid solubility

144
Q

Adverse effects of fentanyl

A

Bradycardia, chest wall rigidity

145
Q

Antagonists

A

Naloxone, naltrexone, methylnaltrexone

146
Q

Naloxone is used to?

A

Reverse toxic effects of agonists and agonists-antagonists

147
Q

Naloxone dosage

A

Repeated dosing maybe necessary based upon half-life of agonist

148
Q

Naloxone metabolism

A

Poor systemic bioavailability d/t extensive first pass

149
Q

Oral Naloxone

A

May be used to prevent opioid induced constipation

150
Q

Naltrexone uses

A

Not for acute reversal of toxic effects

151
Q

Naltrexone routes of administration

A

IM depot and PO (opioid dependence)

152
Q

Naltrexone brand name

A

Vivitrol

153
Q

Naltrexone side effects

A

Hepatotoxic

154
Q

Methylnaltrexone Brand Name

A

Relistor

155
Q

Methylnaltrexone route of administration

A

SubQ

156
Q

Methylnaltrexone is not used for?

A

Acute reversal of toxic effects

157
Q

Methylnaltrexone is used for?

A

To treat opioid induced constipation with chronic opioid use

158
Q

Methylnaltrexone metabolism

A

Renally eliminated

159
Q

Methylnaltrexone risk of?

A

GI perforation

160
Q

Methylnaltrexone acts on?

A

Peripheral mu receptors - GI tract; does NOT cross BBB

161
Q

Opioid conversion - Morphine 10 IV

A

30 PO

162
Q

Opioid conversion - Hydromorphone 1.5 IV

A

7.5 PO

163
Q

Tramadol MOA

A

Weak opiate mu receptor binding, inhibition of norepinephrine and serotonin reuptake

164
Q

Tramadol route of administration

A

PO

165
Q

Tramadol dosage

A

25-100 mg q4-q6h PRN

166
Q

Tramadol Metabolism Route

A

CYP 2D6

167
Q

Tramadol is cleared by?

A

Renal and hepatic

168
Q

Advantages of tramadol

A

Less respiratory depression, GI dysmotility

169
Q

Tramadol adverse effects

A

Decreases seizure threshold, drug intxn (CYP, serotonin)

170
Q

Opioid Adverse Effects

A

Respiratory Depression, sedation, constipation

171
Q

Less serious adverse effects of opioids

A

Itching

172
Q

Which adverse effect of opioids is persistent?

A

Constipation

173
Q

Because of respiratory depression from opioids, what is an increased risk?

A

Cardiac insult

174
Q

Tolerance of opioids

A

Dose increase required to maintain similar analgesia

175
Q

Tolerance Development

A

High/Moderate/None

176
Q

Chronic pain regimen

A

Long acting opioid with a short acting opioid for breakthrough pain

177
Q

Short acting opioid for breakthrough pain (chronic pain regimen) - calculated how?

A

10-15% of total daily dose of regularly scheduled opioid & offer immediate release formulation q2-4h PRN

178
Q

When would you increase the long-acting dose opioid for someone on a chronic pain regimen?

A

If patient uses greater than or equal to 3 doses of break thru Rx per day

179
Q

Which drug would you avoid in the elderly?

A

Morphine

180
Q

A patient with liver disease will react how to Codeine?

A

Activity of codeine may be decreased due to decreased conversion

181
Q

What is the preferred medication for pain in liver disease patients?

A

Fentanyl

182
Q

Which drug would you avoid in patients with kidney disease?

A

Morphine and codeine

183
Q

Treatment strategy for neuropathic pain?

A

SSNRI, tricyclics antidepressants, calcium channel a2 “something” ligand

184
Q

SSNRI

A

duloxetine, venlafaxine

185
Q

Tricyclic antidepressants

A

Nortriptyline, despiramine

186
Q

Calcium channel a2 Ligands

A

Gabapentin, pregabalin

187
Q

How do you start therapy for patients beginning gapabentin or pregabalin?

A

Start slow and titrate to effect

188
Q

Adverse effects of gabapentin or pregabalin?

A

CNS depression, dizziness, somnolence, abnormal gait

189
Q

Who should you be wary of while taking gabapentin or pregabalin?

A

Accumulation in renally impaired patients

Adv Pharm I (8 decks)

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