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Pharm Block 2 > Pain Pharmacology (opioids) > Flashcards

Pain Pharmacology (opioids) Flashcards

1
Q

Define allodynia

A

Pain caused by a stimulus that does not normally provoke pain

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2
Q

Define analgesia

A

Absence of pain in response to stimulation which would normally be painful.

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3
Q

Define dysesthesia

A

Dysesthesia: An unpleasant abnormal sensation, whether spontaneous or evoked

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4
Q

Define Hyperalgesia

A

Hyperalgesia: Increased pain response to a stimulus that is normally painful

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5
Q

Define hyperesthesia

A

Hyperesthesia:Increased sensitivity to stimulation, excluding the special senses.

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6
Q

Define hyperpathia

A

Hyperpathia: Increased pain reaction to any stimulus, with increased threshold

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7
Q

Define paresthesia

A

Paresthesia: An abnormal sensation, whether spontaneous or evoked

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8
Q

Define hypesthesia

A

Hypesthesia: Decreased sensitivity to stimulation, excluding the special senses.

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9
Q

What is first pain and how is it transmitted?

A

First pain is carried by well myelinated peripheral nerve fibers that enter the dorsal horn of the spinal cord

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10
Q

Where are endorphins found?

A

From frontal/insular cortex & limbic system

- Role in descending modulation

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11
Q

Where is NE found?

A

From locus coeruleus (pons)

- Role in descending modulation

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12
Q

What are the main side effects of NSAIDS?

A

Tinnitis, renal, inhibits platelet function

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13
Q

What is the mechanism of action of NSAIDS?

A

Inhibition of prostaglandin production (anti-inflammatory) from arachadonic acid
- Reversible or irreversible acetylation of cyclooxgenase (COX- especially COX 2)

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14
Q

What is the mechanism of action of peripheral prostaglandins?

A

Contribute to hyperalgesia:

  • Sensitization of nerve endings to:
    • Mediators (histamine, bradykinin)
    • Non-nociceptive stimuli (touch)
  • Induce COX-2
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15
Q

What is the mechanisms of action of central prostaglandins?

A

Direct action at spinal cord

- Enhanced nociception at terminal sensory neurons of dorsal horn

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16
Q

What are the different classifications of NSAIDS?

A
  • Carboxylic acids
  • Enolic Acids
  • Cox-2 inhibitors
  • Analine Derivatives (ie tylenol/aceteminophen)
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17
Q

What are the various types of carboxylic acids?

A

Salicylic Acids & Esters
Acetic Acids
Propionic Acids
Antrancillic Acids

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18
Q

What type of NSAID is aspirin?

A

Aspirin is a salicylic acid. It irreversibly inactivates COX via acetylation

  • Platelets cannot synthesize new COX (no nucleus) unlike other cells
  • Effect lasts life of platelet = 10-14 days
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19
Q

Name 3 acetic acid derivatives.

A
  • Indomethacin
  • Diclofenac
  • Ketorolac (Toradol)
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20
Q

What is the primary use of indomethacin?

A

Primarily used for: acute gout & osteoarthritis

  • IV formulation FDA approved for closure of persistent patent ductus arterioles
  • Concentration in synovial fluid is equal to plasma (within 5 hours)
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21
Q

What are the main side effects of indomethacin?

A

High incidence of side effects, requiring short term dosing

Gastritis, renal dysfunction

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22
Q

What is the mechanism of action of indomethacin?

A

More potent inhibitor of COX than aspirin

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23
Q

What is the mechanism of action of diclofenac?

A

COX-2 selectivity (similar to Celebrex)

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24
Q

What should be monitored in patients in diclofenac?

A

Hepatotoxicity should be monitored

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25
Q

What is the primary use of diclofenac?

A

Significant post-operative pain relief

- Accumulates in synovial fluid (effect is considerably longer than half life of 1-2 hrs)

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26
Q

What is the mechanism of action of ketorolac?

A

Mechanism of Action: Non-selective COX inhibitor

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27
Q

What is the clinical use of ketoralac?

A

Short-term management of pain, can be administered IV, very strong analgesic, post-surgical pain

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28
Q

What are the adverse drug reactions of ketoralac?

A
  • Use must be limited to less than 5 days
  • Increased risk of allergic reactions in persons with asthma
  • Can precipitate/exacerbate renal failure
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29
Q

What important interactions should be considered in patients on ketoralac?

A

Adverse GI effects increased by other NSAIDs, use with acetaminophen increases liver toxicity

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30
Q

Name 3 proprionic acids.

A

1) Naproxen (ie midol, aleve)
2) Ibuprofen (Advil, Motrin)
3) Oxaprozin (daypro)

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31
Q

What are the primary benefits of naproxen?

A
  • Less GI irritation compared to aspirin

- Possibly less CV risk compared to other NSAIDs

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32
Q

What is Ibuprofen (Advil, Motrin) proven effective in?

A

-Headache and migraine, menstrual pain, and acute postoperative pain

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33
Q

What are the main side effects of ibuprofen?

A

GI side effects (nausea/dyspesia) at higher doses

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34
Q

What are the mechanisms of action of oxaprozin?

A
  • In addition to good nonselective COX-1&2 activity, additional mechanisms identified:
    • NF-ᴋB & metalloproteinase inhibition
    • Endogenous cannabinoid modulation
  • Long acting medication – once daily dosing
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35
Q

What is Oxaprozin used for?

A

Superior analgesia & QOL with refractory shoulder pain compared to diclofenac in one study
- uses readily into inflamed synovial tissues

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36
Q

Name an enolic acid.

A

Meloxicam (Mobic)

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37
Q

What is the mechanism of action of meloxicam?

A

COX-2 preferential, especially at low doses

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38
Q

What are the benefits of meloxicam?

A
  • As effective as piroxicam (Feldene), diclofenac, & naproxen, but with fewer GI symptoms
  • Lower perforations, obstructions, bleeds
  • Not altered by renal or hepatic insufficiency
  • Dose adjustment not needed in elderly
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39
Q

Name a coxib.

A

Celecoxib (Celebrex)

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40
Q

What is the mechanism of action of celecoxib?

A

Selective COX-2 inhibitor and synthesis of PGs causing pain, fever and inflammation

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41
Q

What is the clinical use of celecoxib?

A

Mild to moderate pain

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42
Q

What are the adverse drug reactions of celecoxib?

A

GI bleeding but may be less than nonselective COX inhibitors.

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43
Q

What interactions should be noted in patients on celecoxib?

A
  • Levels increased by drugs that inhibit cytochrome P450 2C9
  • Decreases effects of angiotensin-converting enzyme inhibitors and diuretics
  • Increases lithium levels.
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44
Q

What are the benefits of celecoxib?

A

Does not interfere with platelet aggregation

  • Perioperative administration possible without increased bleeding
  • Less GI & CV complications
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45
Q

What is the main contraindication of celecoxib?

A

Contraindicated w/ sulfa allergy

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46
Q

Name an analine derivative.

A

Acetaminophen (Tylenol)

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47
Q

What is the mechanism of action of acetaminophen?

A
  • Not entirely clear; may act centrally to inhibit cyclooxygenases
  • Lacks antiplatelet activity
  • Inhibits central prostaglandin synthesis with minimal effect peripherally (weak anti-inflammatory effect)
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48
Q

What is the clinical use of acetaminophen?

A

Mild to moderate pain, fever

- Safest and most cost-effective nonopioid analgesic

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49
Q

What are the adverse drug reactions of acetaminophen?

A

None usually, overdose can cause fatal hepatic failure especially in combination with alcohol

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50
Q

What interactions should be noted in patients on acetaminophen?

A

Additive liver toxicity with NSAIDs.

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51
Q

Describe the pharmacokinetics of acetaminophen.

A
  • Peak serum concentrations 0.5-3 hrs (orally)
  • Only 10%–50% is protein bound and has an estimated
  • Half-life = 2-3 hrs, duration of action 4-6 hrs
  • Metabolized in the liver
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52
Q

What is the major concern of all NSAIDS?

A 
All NSAIDs (including Aspirin) may induce hypersensitivity reactions
   - Related to the inhibition of PG synthesis
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53
Q

What are the two types of NSAID induced hypersensitivity reactions?

A

1) Syndrome of asthmatic attacks
- Patients with vasomotor rhinitis, nasal polyposis, and bronchial asthma
2) Syndrome of urticaria and angioedema
- Prostaglandin E2 is a bronchodilator
- Stabilizes histamine stores in mastocytes, inhibiting inflammatory response

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54
Q

What are the major GI effects of NSAIDS?

A
  • Gastric distress
  • Superficial mucosal lesion
  • Serious Ulceration
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55
Q

What increases the risk of GI effects related to NSAIDS?

A

SSRIs increase risk 12-15 fold

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56
Q

What are the renal effects of NSAIDS?

A
  • Renal impairment

- Acute renal failure

57
Q

What are the risk factors for renal effects related to NSAID use?

A
  • Chronic NSAID use
  • High-dose/multiple NSAIDs
  • Volume depletion
  • CHF, vascular disease
  • Hyperreninemia
  • Shock
  • Sepsis
  • SLE
  • Hepatic disease
  • Sodium depletion
  • Nephrotic syndrome
  • Diuresis
  • Concomitant drug therapy (diuretics, ACE inhibitors, beta blockers, potassium supplements)
  • Advanced age
58
Q

What is the proposed mechanism of renal impairment with NSAID use?

A

Decrease in prostaglandin production–> reduced renal blood flow –> medullary ischemia

59
Q

What causes the hepatic effects of NSAIDS?

A
  • Rare complication of most NSAIDs

- Dose-related toxicity - aspirin & acetaminophen

60
Q

What is the mechanism of action of the hepatic effects of NSAIDS?

A
  • Almost entirely metabolized in the liver
  • Depletion of hepatocyte glutathione –> accumulation of the toxic metabolite NAPQI –> mitochondrial dysfunction, and alteration of innate immunity
61
Q

What are the risk factors for hepatic side effects due to NSAIDS?

A

Concomitant depression, chronic pain, alcohol or narcotic use, and/or using several preparations simultaneously

62
Q

What are the cardiac effects of NSAIDS?

A
  • 10 fold increase in heart failure exacerbation
    • induce systemic vasoconstriction: increase after load and decrease cardiac contractility and decrease cardiac output
  • Hypertension
  • MI
63
Q

What are the other side effects of NSAIDS?

A
  • Impaired fracture healing
  • Interference with Aspirin
    • Competition for COX-1 binding of platelets
    • Administered NSAIDs 2 hours after aspirin
    • No interference with COX-2 inhibitors
64
Q

Why should NSAIDS be avoided in the 3rd trimester?

A

Avoid NSAIDs in 3rd trimester

=> in utero constriction of the fetal ductus arteriosus

65
Q

What are the effects of NSAIDS at term?

A
  • May delay labor onset 3-10 days
  • May cause serious pulmonary vascular disease
  • Increased bruising of newborn
66
Q

Which NSAIDS are approved for children?

A

naproxen, ibuprofen, aspirin

67
Q

Why should NSAIDS be avoided in pediatric viral cases?

A

Avoid w/ viral illness –>Reyes Syndrome (especially Aspirin)

68
Q

What risks of NSAIDS are pertinent in the elderly population?

A
  • Hypoalbuminemia –> toxicity
  • Longer half-lives of some NSAIDs
  • Higher risk for drug interaction
69
Q

How do NSAIDS interact with lithium and warfarin?

A
  • Lithium: may increase lithium plasma levels and decrease its renal clearance
  • Warfarin: may increase the risk for bleeding
70
Q

What is the class and mechanism of action of Gabapentin/pregablin?

A

Class: Anticonvulsants

Mechanism of Action: preventing Ca++ influx in dorsal horn

71
Q

What are the clinical uses of gabapentin?

A

Neuropathic pain.

- Can be used prn

72
Q

What are the adverse drug reactions of gabapentin?

A

Dizziness, fatigue, weight gain, drowsiness, and peripheral edema
* BUT NO INTERACTIONS

73
Q

What is the mechanism of action of tricyclic antidepressants (TCA)?

A

Mechanism of Action: Norepinephrine and serotonin reuptake inhibitors

74
Q

What is the clinical use of TCAs?

A

Neuropathic pain, appetite stimulant, sleep aide

75
Q

What are the adverse drug reactions of TCAs?

A

Innumerable- sedation, increased appetite, dry mouth, sexual dysfunction, orthostatic hypotension

76
Q

What are the major interactions of TCAs?

A
  • Use with caution in elderly.
  • Chronic pain patients do not want to gain weight.
  • Use with caution with other serotonin reuptake inhibitors
77
Q

What SNRIs are used in pain management?

A

Venlafexine, duloxetine, milnaciprin

78
Q

What is the mechanism of action of SNRIs?

A

Norepinephrine and serotonin reuptake inhibitors

79
Q

What are the clinical uses of SNRIs?

A

Neuropathic pain, appetite stimulant, sleep aide, depression, anxiety

80
Q

What is the major side effect of SNRIs?

A

Many- appetite stimulation

81
Q

What are the primary interactions of SNRIs?

A
  • Chronic pain patients do not want to gain weight.

- Use with caution with other serotonin reuptake inhibitors

82
Q

Name 2 natural forms of opium.

A

1) Codeine

2) Morphine

83
Q

Name 5 types of semisynthetic opioids.

A

1) Hydrocodone
2) Oxycodone
3) Hydromorphone
4) Oxymorphone
5) Buprenorphine

84
Q

Name 5 types of synthetic opioids.

A

1) Meperidine
2) Fentanyl
3) Sufentanil
4) Methadone
5) Propoxyphene

85
Q

What is the mechanism of action of morphine?

A

Prototypic mu opioid receptor agonist

86
Q

What are the adverse side effects of morphine?

A

Sedation, confusion, constipation, respiratory depression, sexual dysfunction, fracture, physical dependence (withdrawal syndrome), abuse, misuse, addiction, infection, tumors

87
Q

What are the major interactions for patients on morphine?

A
  • Additive effects with CNS depressants
  • MAO inhibitors can cause severe or fatal reactions
  • Can be used in patients with hepatic failure
88
Q

What is the mechanism of action of meperidine?

A

mu opioid receptor agonist => same as morphine

89
Q

What is the clinic use of meperidine?

A

Clinical Use: Severe pain. Not recommended for routine use!

90
Q

What are the adverse drug reactions of meperidine?

A

ADRs: Same as morphine plus increased heart rate

91
Q

What are the major interactions for patients on meperidine?

A

MAO inhibitors can cause severe or fatal reactions

92
Q

What is a distinguishing factor of meperidine that is different from other opioids?

A

Causes mydriasis while all other opioids cause meiosis.

93
Q

What is oxycodone?

A

Strong Opioid analgesic

94
Q

What are the major adverse drug reactions of oxycodone?

A

Sedation, confusion, constipation, respiratory depression, sexual dysfunction, fracture, physical dependence (withdrawal syndrome), abuse, misuse, addiction, infection, tumors

95
Q

What are the interactions of oxycodone?

A

Interactions: Additive effects with CNS depressants

96
Q

How is oxycodone metabolized?

A
  • Metabolized to oxymorphone by CYP2D6 and noroxycodone by CYP3A4
  • Oxycodone and noroxycodone are excreted in urine unchanged and oxymorphone is conjugated and excreted
  • Concentrated in breast milk
    • Breastfed infants may receive 10% of therapeutic infant dose
97
Q

What is the half life of oxycodone?

A

T ½ 2-3 hours

  • longer half life in hepatic disease
  • safer for patients with renal disease
98
Q

What is the mechanism of action of oxymorphone?

A
  • Oxymorphone is a strong Opioid analgesic used for severe pain and with the same ADRs as morphine
  • Mechanism of Action: Works in modulation phase of nociception.
99
Q

What are the interactions associated with oxymorphone?

A

Interactions: Additive effects with CNS depressants

100
Q

How does oxymorphone compare to morphine and oxycodone?

A
  • Metabolic end product of oxycodone.

- High abuse potential. Twice as strong as morphine

101
Q

What is the mechanism of action of Methadone?

A
  • Methadone is a strong opioid analgesic.
  • Mechanism of Action: Works in modulation phase of nociception. Has NMDA receptor antagonist properties. Can inhibit the reuptake of serotonin. Long elimination half life.
102
Q

What are the adverse drug reactions of methadone?

A

Same as morphine plus => Can prolong QTc and cause arrhythmia (get EKG before use)

103
Q

What are the interactions of methadone?

A

Additive effects with CNS depressants. Beware using with other serotonin reuptake inhibitors

104
Q

What is methadone used for?

A
  • severe pain

- used to treat addiction

105
Q

In what population should we use methadone cautiously?

A

Exercise tremendous caution in using in elderly

106
Q

Describe the major pharmacokinetic concern with methadone.

A

Pharmacokinetics indicate dose should not be increased more frequently than every 14 days

107
Q

What is the importance of the two enantiomers of Methadone?

A

Two enantiomers- Levo mu agonist and dextro blocks NMDA receptor

108
Q

Describe the pharmacokinetics/dynamics of methadone.

A
  • Bioavailability range broad and variable 40-90% due to variable expression of CYP3A4 and CYP3A5
  • T ½ beta 8.5-47 hours
  • Variable potency dependant on dosage
109
Q

What is the mechanism of action of fentanyl?

A
  • Strong Opioid analgesic
  • Mechanism of Action: Works in modulation phase of nociception.
    • 80 times stronger than morphine
110
Q

What is the clinical use of fentanyl?

A

severe pain

111
Q

What are the adverse drug reactions of fentanyl?

A

Same as morphine

112
Q

What are the major interactions of fentanyl?

A

Additive effects with CNS depressants

113
Q

What is the major hepatic effect of fentanyl?

A

Hepatic failure alters skin permeability and regional blood flow to skin so can alter absorption of patches

114
Q

What is the mechanism of action of hydrocodone?

A
  • Not as potent analgesic as others

- Mechanism of Action: Works in modulation phase of nociception.

115
Q

What is the clinical use of hydrocodone?

A

severe pain

116
Q

What are the ADR of hydrocodone?

A

same as morphine

117
Q

What interactions should be considered for hydrocodone?

A

Additive effects with CNS depressants

118
Q

What is the most abused prescription drug in the U.S.?

A

Hydrocodone

119
Q

What is the mechanism of action of hydromorphone?

A

Mechanism of Action: Works in modulation phase of nociception to treat severe pain but 7.5 times more potent than morphine

120
Q

What is the clinical use of hydromorphone?

A

severe pain with similar ADR as morphine

121
Q

What are the major drug interactions of hydromorphone?

A

Additive effects with CNS depressants

122
Q

In what patient group is hydromorphone effective in?

A

Useful in renal failure patients

123
Q

How does hydromorphone act in hepatic disease?

A
  • Reduced first pass clearance because of shunting and increased bioavailability
  • Avoid sustained release versions
124
Q

What is the mechanism of action of tapentadol?

A
  • Strong Opioid analgesic

- Mechanism of Action: Works in modulation phase of nociception.

125
Q

What is the clinical use of tapentadol?

A

Clinical Use: Severe pain. May be more useful to treat neuropathic pain

126
Q

What are the adverse drug effects of taptentadol?

A

Same as morphine plus inhibits reuptake of norepinephrine and to a much lesser degree serotonin
- Additive effects with CNS depressants

127
Q

What is the mechanism of action of tramadol?

A
  • Not as potent analgesic as others and used in MODERATE pain
  • Mechanism of Action: Works in modulation phase of nociception and inhibits reuptake of norepinephrine and serotonin.
128
Q

What adverse drug reactions are associated with tramadol?

A

Beware combing with methadone or antidepressants that inhibit the reuptake of serotonin
- Interactions: Additive effects with CNS depressants

129
Q

What is the mechanism of action of naloxone?

A

Mechanism of Action: Competitively blocks mu, kappa and delta opioid receptors; rapidly reverses effects of opioid agonists.

130
Q

What is the clinical use of naloxone?

A

Clinical Use: Opioid overdose, opioid dependence.

- Can precipitate withdrawal in opioid-dependent persons

131
Q

What are the major interactions of naloxone?

A

Interactions: Large, repeated doses are needed to antagonize mixed agonist-antagonist opioids, Naltrexone has a longer half-life.

132
Q

What is Buprenorphine used for?

A

Used to treat opioid addiction/ moderate to severe pain.

- 30 times as potent as morphine (24 mg of buprenorphine is equivalent to 720 mg of morphine)

133
Q

What is the safest drug to use in the hepatorenal system?

A

Buprenorphine

134
Q

What is the mechanism of action of buprenorphine?

A

Buprenorphine is a mixed agonist/antagonist blocks the activity of other opiates and induces withdrawal in opiate dependent individuals who are currently physically dependent on another opiate.

135
Q

What may be safer in elderly than NSAIDS?

A

Opioids
- Begin opioids cautiously, titrate carefully, monitor frequently because elderly are more susceptible to side effects

136
Q

What methods are most commonly used to test for drugs?

A

Initial (immunoassay-screening) and confirmatory (gas chromatography-mass spectrometry

137
Q

What food product contains trace amounts of codeine and morphine?

A
  • Poppy seeds contain trace amounts of morphine and codeine
  • It is possible to obtain levels high enough to result in positive GC/MS for morphine and codeine
    • Morphine levels greater than 1000 ng/ml and no codeine detected (not just below cut-off levels) are not compatible with poppy ingestion.
138
Q

How do we differentiate morphine use from poppy seed consumption?

A

Morphine is not metabolized into codeine

Pharm Block 2 (15 decks)

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