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Pharmacology > Lecture 8 - Opioids > Flashcards

Lecture 8 - Opioids Flashcards

1
Q

Describe the analgesic pain ladder:

Step 1 - Mild

A

non-narcotics
1st choice = ASA
Alternatives = acetaminophen or NSAID

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2
Q

Describe the analgesic pain ladder:

Step 2 - Mild to Moderate

A

non-narcotics + weak narcotics
1st choice = ASA + codeien
Alternatives = codeine or Acetaminophen + codeine

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3
Q

Describe the analgesic pain ladder:

Step 3 - Moderate to Severe

A

moderate strength narcotics
1st choice = codeine or morphine
Alternatives = oxycodone, levorphanol, anileridine, oxymorphone

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4
Q

Describe the analgesic pain ladder:

Step 4 - Severe

A

strong narcotics
1st choice = morphine
Alternatives = methadone, hydromorphone

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5
Q

List 3 endogenous opioids

A
  • endorphines
  • enkaphalins
  • dynorphins
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6
Q

Describe endorphins

A
  • from pituitary and hypothalamus
  • polypeptides
  • from poropiomelanocortin and prodynorphin
  • potent analgesics
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7
Q

Describe enkephalins

A
  • from proenkephalin and prodynorphin
  • pentapeptide ligands
  • involved in modulated pain response
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8
Q

Describe dynorphins

A
  • from proenkephalin B
  • polypeptides
  • physiological role not yet understood
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9
Q

Are opioids direct neurotransmitters?

A

No - they just make the neuron more likely to fire - but are not directly neurotransmitters

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10
Q

Describe the 3 Mechanisms of action?

A

1 - hyper polarization of nerves by opening K+/Ca2+ channels in 1st (receptor to medulla) and 2nd order neurons (medulla to thalamus)

2 - inhibition of ascending pathways in the CNS

3 - excitation of descending adrenergic and seratonergic pathways

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11
Q

What can opioids be used for?

A
  • pain control
  • sedation and anxiolysis
  • can be used before anesthesia
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12
Q

What is the #1 cause of opioid death?

A

depression of respiration

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13
Q

List the 7 pharmacological effects of opioids

A

1 - inhibition of pain and pain perception
2 - sedation and anxiolysis
-drowsiness and lethargy
-cognitive impairment
-relaxation inhibition of pain
3 - depression of respiration (main cause of death from opioid overdose)
4 - cough suppression (opioids suppress the cough centre in the brain)
5 - reduction of intestinal motility (codeine used to treat diarrhea)
6 - pupillary constriction (KEY SYMPTOM OF OVERDOSE)
7 - nausea and vomiting (first stimulated, then inhibited)

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14
Q

_____ are used for pain, diarrhea, coughing, panic breathing (COPD)

A

opioids

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15
Q

What 3 things do we dose opioids by ?

A

by the mouth
by the clock
by the ladder

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16
Q

Briefly explain the WHO pain ladder (slide 8)

A

0-3: mild pain

  • acetaminophen
  • NSAIDs
  • maybe caffeine

4-6: moderate pain
-codeine (mild opioid)

7-10: severe pain
-morphine (strong opioid)

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17
Q

If you are increasing to a stronger or different pain med, do you discontinue the original medication?

A

no
never
not in a million years

  • *never stop the lower pain control!
  • pain meds work by different mechanisms so you always want to keep the pain controlled and don’t want to take away any form of pain management
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18
Q

By the mouth:

-Oral dosing is ___ effective than IV

A

less

*because of first pass metabolism

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19
Q

Describe 3 points of by the mouth

A

1 - oral dosing has longer term effect requiring less frequent doses
2 - oral dosing avoids the highs and thus is less addictive
3 - oral dosing is safer in terms of overdose

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20
Q

Describe 3 points of by the clock

A

1 - uses less drug. It takes more drug to bring pain down than it does to maintain a person pain-free (maintain dosing)
2 - avoids the euphoria associated with release of pain, so less addictive potential
3 - avoids the development of chronic pain syndrome (from pain pathway rewirling)

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21
Q

What is the #1 problem with dosing by the clock?

A

Pt does not want to comply because they do not feel pain and do not want to become addicted

*have to explain to pt that by dosing by the clock, you are actually reducing risk of addiction

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22
Q

Describe points of by the ladder

A

1 - it assures that the safest and least potent drug required for any specific case is used
2 - avoids addictive potential because opioids (and strong opioids) are not used until required

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23
Q

_____ - weakest commonly used opioid and has the least addiction risk

A

codeine

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24
Q

codeine has ___% of potency of morphine

A

10

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25
Q

Potency of codeine is so ___, it is has it’s own special step on the pain ladder (possibly now shared with tramadol)

A

low

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26
Q

What is codeine used for?

A

pain
diarrhea
coughing
inhibit breathing

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27
Q

_____ = unique weak opioid agonist

A

tramadol

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28
Q

What is the main downside to tramadol?

A

expensive

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29
Q

Unlike other opioids, tramadol has two complementary mechanisms: describe them

A

1 - like other opioids, activates the micro-opioid receptor

2 - weak inhibitor of norepinephrine and serotonin reuptake

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30
Q

Tramadol has ____ potential for addiction and shows greater pain control

A

less

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31
Q

Oral dose of morphine has relatively ___ availability

A

poor (approx 20-30%)

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32
Q

onset of oral morphine?

A

15-60 mins

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33
Q

duration of action of oral morphine?

A

3-6 hours

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34
Q

IV morphine is ____ as potent as oral morphine

A

twice

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35
Q

duration of action for IV morphine?

A

almost immediate to 2 hours (high population variability)

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36
Q

Is oxycodone more potent than morphine?

A

yes up to 2X more potent

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37
Q

Oral bioavailability of oxycodone?

A

80% (remember that morphine has 20-30% oral bioavailability)

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38
Q

Oxycodone has a slightly ____ half-life than morphine

A

greater

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39
Q

You give oxycodone at ___ the dose of morphine for the equivalent effect

A

half

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40
Q

slow release form of oxycodone = ?

A

OxyContin

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41
Q

Oxycodone + tylenol = ?

A

Percocet

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42
Q

Oral hydromorphone onset = ?

A

15-30 mins

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43
Q

IV hydromorphone duration of action ?

A

3-4 hours

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44
Q

Peak effect of hydromorphone = ?

A

30-60 mins

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45
Q

Is hydromorphone stronger than morphine = ?

A

yes - 5X as potent

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46
Q

Where is hydromorphone used?

A

surgical settings for moderate to severe pain (cancer, bone trauma, burns, etc.)

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47
Q

Fentanyl is highly ______

A

lipophilic

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48
Q

Fentanyl is very _____

A

potent

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49
Q

Fentanyl comes as what dosage forms?

A

transdermal (patch)
sublingual
intravenous (rarely)

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50
Q

Fentanyl has ___ times the analgesic potency of morphine

A

80

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51
Q

Fentanyl has ___ times the analgesic potency of hydromorphone

A

10

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52
Q

latency of sublingual fentanyl?

A

7-12 mins

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53
Q

duration of sublingual fentanyl?

A

1-2 hours

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54
Q

What is sublingual fentanyl used for?

A

acute but temporary pain (fast onset, short duration) such as debriding wounds and breakthrough pain in palliative care

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55
Q

latency of transdermal fentanyl ?

A

12-17 hours

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56
Q

duration of transdermal fentanyl ?

A

72-96 hours

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57
Q

What is transdermal pain used for?

A

used in more severe pain (cancer, palliative care)

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58
Q

Sufentanyl is __x more potent than fentanyl

A

10

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59
Q

Naltrexone is an oral opioid ____

A

INHIBITOR

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60
Q

Naltrexone is a ??

A

reverse agonist (kind of considered an antagonist)

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61
Q

latency of naltrexone ?

A

15-30 mins

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62
Q

duration of naltrexone ?

A

24-72 hours

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63
Q

peak of naltrexone ?

A

6-12 hours

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64
Q

How does naltrexone work?

A

reverses the psychotomimetic effects of opiate agonists, reverses hypotension and cardiovascular instability

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65
Q

naltrexone is not highly effective in treating ??

A

opioid addiction

mainly due to compliance

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66
Q

naltrexone is effective to some extent in treating ??

A

alcohol addiction

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67
Q

Naloxone (Narcan) is a ?

A

potent opioid antagonist

68
Q

Naloxone (Narcan) has a strucure almost identical to ?

A

oxymorphone

69
Q

Naloxone (Narcan) very quickly blocks ?

A

opioid binding

70
Q

When is Naloxone (Narcan) used?

A

in emergency situations such as respiratory depression in clinical situations or heroin overdose

71
Q

Naloxone (Narcan) has a ____ half life

72
Q

Naloxone (Narcan) blocks all major effects of _____

A

opioids (including pain control)

73
Q

Describe methadone’s half life

A

very long but variable

  • up to 5 days
  • but effective for only 6-12 hours
74
Q

Is methadone more potent than morphine?

A

yes - at least 10X more potent

75
Q

Although methadone is less addictive, it is a greater risk for ?

A

accidental overdose

76
Q

Can any pharmacist dispense methadone?

A

not everyone - it requires special training and licensure

77
Q

What is methadone primarily used for?

A

narcotic maintenance

-so like weening addicts off of narcotics/opioids

78
Q

Dosing schedule is based on ??

A

time, not pain!

by the clock!

79
Q

What is the rule for switching opioids?

A

30% rule

if you switch to a new opioid - you calculate the dose that would be equivalent and then use 30% less

80
Q

Why do you use the 30% rule?

A

because for some unknown reason when you start a new drug, it can be more effective than when you have continued use of a drug

*this is done to prevent overdose

81
Q

Why would you ever rotate opioids?

A

to improve analgesia

82
Q

When would you discontinue therapy?

A
  • when there is intolerable or unacceptable side-effects (myoclonus-neurotoxic effect, respiratory depression, level of conscience) with little or no evidence of analgesia
  • high doses of opioids without analgesia
  • there is evidence of addiction
  • there is no evidence of any effort to increase function in the face of reasonable analgesia
83
Q

Define tolerance

A

reduced potency of analgesic effects of opioids following repeated administration

84
Q

What is the negative consequence with tolerance?

A

increased doses are necessary to produce pain relief - this increases risk of dependence and addiction

85
Q

Define physical dependence

A

normal response to chronic opioid administration

86
Q

List signs of dependence that would be evident with opioid withdrawl

A 
yawning
sweating
tremor
fever
increased HR
insomnia
muscle/abdominal cramps
dilated pupils
87
Q

How do you avoid dependence?

A

decrease dose by 20-30% per day

88
Q

_____ = psychological dependece

89
Q

Define addiction

A

a pattern of drug use characterized by a … craving for opioids … manifest .. [by] compulsive drug-seeking behaviour leading to .. overwhelming involvement in use and procurement of the drugs

90
Q

List 3 ways to deal with tolerance

A
  • prevent dose escalation
  • use a medication holiday following slow withdrawal
  • plan for this at the beginning of treatment
91
Q

List some other effects of opioids on the body

A
  • causes vomiting by stimulating the chemoreceptor trigger zone in the brainstem - then depresses vomiting
  • pinpoint pupils - no tolerance
  • vasodilation - flushing of skin and decrease in blood pressure
  • methadone causes sweating
  • constipation
  • decreases sex hormones in males and females - decreases libido and fertility
92
Q

Pain works by 3 different pathways: describe them

A

1 - descending inhibitory pathways (NE, seretonin, enkephalins)

  • TCAs
  • SSRIs
  • SNRIs
  • alpha adrenergic agents
  • opioids
  • tramadol

2 - peripheral sensitization (Na+)

3 - central sensitization
(Ca2+, NMDA)

93
Q

What works on pain in the descending inhibitory pathways?

A

NE and S are pain mediators - inhibit pain signals from reaching the higher levels of brain

-part of the modulatory system in the spinal cord and brain

94
Q

Drug classes that work on the descending inhibitory pathways for pain?

A

1 - antidepressants

  • TCAs
  • SSRIs
  • SNRIs

2 - alpha 2 adrenergic agonists

3-opioids (esp tramadol)

95
Q

How do TCAs work on descending inhibitory pathways?

A
  • increases serotonin and/or NE in the synapse by inhibiting reuptake
  • takes 1-3 weeks for pain control so used for chronic pain
  • may have anticholinergic effects (dry mouth, dry eyes, etc.)
  • more effective for conditions like diabetic neuropathy than other anti-depressants
96
Q

Examples of TCAs

A

nortriptyline

amitryptyline

97
Q

What is the 1st line treatment for neuropathic pain?

A

nortriptyline

98
Q

How do SSRIs work on descending inhibitory pathways?

A

-specific inhibitor of Serotonin reuptake

99
Q

Side effects of SSRIs

A
  • suicide
  • impaired platelet aggregation
  • CNS depression
  • QT prolongation
  • serotonin syndrome
  • SIADH/hyponatremia
  • sexual dysfunction
100
Q

examples of SSRIs

A

paroxetine (paxil)
fluoxetine (prozac)
sertraline (zoloft)

101
Q

How do SNRIs work on descending inhibitory pathways?

A
  • serotonin and norepinephrine reuptake inhibitors

- also weakly inhibits dopamine reuptake

102
Q

side effects of SNRIs??

A
  • suicide
  • impaired platelet aggregation
  • CNS depression
  • hypercholesterolemia
  • hypertension
  • serotonin syndrome
  • sexual dysfunction
  • SIADH/ hyponatremia
  • QT prolongation
103
Q

example of SNRI

A

venlafaxine

104
Q

What is venlafaxine used for?

A

neuropathic pain

DM neuropathy

105
Q

onset of venlafaxine ?

A

1-2 weeks

max 6

106
Q

common adverse effects of venlafaxine?

A

nausea
dizziness
drowsiness

107
Q

How do alpha 2 adrenergic agonists work on descending inhibitory pathways?

A
  • stimulate alpha-adrenoreceptors in brainstem - activating inhibitory neuron thus reducing sympathetic outflow of CNS
  • prevents pain signal transmission
108
Q

examples of alpha adrenergic agonists?

A
  • clonidine (Catapres)

- tizanidine (Zanaflex)

109
Q

What is clonidine used for?

A

neuropathic pain that is not responding to other treatment

110
Q

Unlabeled uses of clonidine?

A
  • heroin or nicotine withdrawal
  • dysmenorrhea
  • menopausal vasomotor symptoms
  • migraine prophylaxis
111
Q

routes available for clonidine?

A

epidural infusion
oral
transdermal

112
Q

side effects of clonidine

A

bradycardia

CNS and respiratory depression

hypotension

113
Q

Tizanidine is used to treat?

A
  • tension type headache
  • back pain
  • neuropathic pain
  • myosfascial pains
114
Q

Is tizaidine better than clonidine?

A

Yes

  • less side effects
  • less likely to cause hypotension
  • better tolerated than clonidine
115
Q

Peripheral sensitization - caused by?

A

sodium channels on nerves

-neuropathic pain triggered by spontaneous peripheral nerve activity mediated by sodium channels

116
Q

Causes of pain through peripheral sensitization ?

A

-local tissue injury
-ischemia
etc

releasing inflammatory factors thereby increasing Na channels leading to excitability of the nerve

117
Q

Medication classes which dampen the peripheral sensitization include?

A
  • carbamazepine
  • TCAs
  • Topiramate
  • Lidocaine
118
Q

How does carbamazepine (Tegretol) work on peripheral sensitization?

A
  • anticonvulsant
  • limits influx of Na+ ions across the cell membrane
  • trigeminal or glossopharyngeal neuralgia and neuropathic pain
119
Q

How does Topiramate (Topamax) work on peripheral sensitization?

A
  • anticonvulsant

- limits influx of sodium ions across the cell membrane, antagonizes glutamate receptors

120
Q

Adverse effects of Topiramate?

A
  • dizziness
  • ataxia
  • somnolence (strong desire for sleep)
  • psychomotor slowing
  • parasthesia
  • weight loss
121
Q

What do you need to monitor for topiramate?

A

electrolytes

kidney function

122
Q

How does lidocaine work on peripheral sensitization?

A

-topical application reduces discharge of small afferent nerve fibres by blocking voltage gated Na channels (decreases membrane permeability)

123
Q

Lidocaine comes as?

A

gel

transdermal patch

124
Q

What is lidocaine used for?

A

post-herpetic neuralgia or

peripheral neuropathic or other aetiologies

125
Q

Side effects of lidocaine?

A

arrythmias
seizures
coma
respiratory depression or death

with patch:

  • application site erythema
  • swelling
  • burning
  • discomfort
126
Q

Describe central sensitization-1?

A

calcium channels

  • occurs in the dorsal horn of the spinal cord
  • release of excitatory neurotransmitters (incl. glutamate and substance P)
  • increased calcium transport causes spontaneous impulses (APs) - pain message sent to brain
127
Q

What types of medication decrease Ca channel activity?

A

GBP - gabapentin

PreGab - pregabalin

128
Q

Describe central sensitization-2?

A

NMDA receptor

  • occurs in the dorsal horn of the spinal cord
  • release of excitatory neurotransmitters (including glutamate and substance P)
129
Q

What medications work on central sensitization 2 ?

A

medications that are NMDA antagonists (decrease nerve impulse)

  • ketamine
  • dextromethorphan
  • methadone
130
Q

How does Ketamine (Kelatar) work on central sensitization?

A

NMDA receptor antagonist

  • decreases central sensitization and modulation by lowering the threshold for nerve transduction and reduces the effects of substance P
  • also targets the opioid receptor, Na and K channels to reduce pain (dissociative agent)
131
Q

common adverse rxn of ketamine ?

A

local skin rxns

132
Q

Describe how dextromethorphan (Robitussin) works on central sensitization ?

A

low affinity uncompetitive NMDA antagonist - high doses needed (45-400 mg/day)

  • also binds opioid receptors
  • short half life (2-4 hours)
133
Q

side effects of dextromethorphan (Robitussin)

A

serotonin syndrome (if in combination with other antidepressants)

  • rash
  • nausea/vomiting
  • drowsiness/sedation
  • constipation/diarrhea
  • confusion
  • nervousness
  • closed eye hallucinations
134
Q

Describe how methadone works on central sensitization

A
  • mu and delta opioid agonist
  • also blocks NMDA receptor
  • inhibits reuptake of NE
  • crossing BBB rapidly
  • lipophilic so distributes in muscle and fat
  • high bioavailability
135
Q

side effects of methadone?

A
  • CNS & respiratory depression
  • QT prolongation
  • constipation
  • nausea and vomiting
  • dizziness and disorientation
136
Q

What is gout?

A

caused by accumulation of uric acid crystals in joints

137
Q

What is gout associated with?

A

ingesting red meat, cheese, wine (large intakes of purines)

138
Q

gout a.k.a. ?

A

rich man’s disease

139
Q

Uric acid production pathway

A

purine nucleotides (dietary and cellular)

inosinic acid

hypoxanthine
(xanthine oxidase)
xanthine
(xanthine oxidase)
uric acid
140
Q

Drug therapy of gout?

A
  • cholchicine
  • allopurinol
  • probenecid
  • NSAIDs (indomethacin)
141
Q

Describe colchicine

A
  • weak anti-inflammatory agent
  • not analgesic or antipyretic
  • impairs PMN motility and chemotaxis and thus inflammatory response to urate crystals
  • dose to toxicity - nausea, vomiting, diarrhea, abdominal cramping, may cause death
  • no effect on plasma or urinary uric acid
  • may be considered for low dose continuous prophylactic therapy
  • decreases motility of immune cells
  • doesn’t affect underlying disease
  • just reduces inflammation
142
Q

Describe allopurinol

A
  • xanthine oxidase inhibitor
  • reduces urate formation
  • active metabolite (oxypurinol/alloxanthine)
  • risk of hypoxanthine stones
143
Q

What is allopurinol used for?

A

-for prophylaxis when acute gouty attacks happen frequently

144
Q

Caution with alloupurinol?

A

fluid intake

acute attack of gout

145
Q

adverse events with allopurinol

A 
allergic rxns
bone marrow
suppression
liver toxicity
renal toxicity
146
Q

Describe NSAIDs (indomethacin)

A
  • most common type of drug given for all kinds of arthritis
  • drug of choice for gouty arthritis
  • less toxic than colchicine with short term use
  • not uricosuric
  • affords symptomatic relief
  • GI side effects with indomethacin
147
Q

How do NSAIDs (indomethacin) work?

A

decreases inflammation

helps with uric acid formation a little bit

148
Q

How does Probenecid work?

A
  • uricosuric: inhibits reabsorption of uric acid (decreases amount of uric acid in the blood)
  • half-life dose dependent
  • highly protein bound
  • inhibits excretion of other acidic drugs
  • caution: renal urate stones (fluid intake)
149
Q

Define: local anesthetic

A
  • an agent that interrupts pain impulses in a specific region of the body without a loss of patient consciousness
  • normally, the process is completely reversible - the agent doe snot produce any residual effect on the nerve fibre
150
Q

end in “caine” = ?

A

sodium channel blocker

  • decrease nerve sensitization
  • decrease pain
151
Q

Where are local anesthetics used?

A

to render a specific portion of the body insensitive to pain

152
Q

How do local anesthetics work?

A

interfere with nerve impulse transmission to specific areas of the body

153
Q

Do you lose consciousness with local anesthetics?

154
Q

Describe topical anesthetics

A
  • applied directly to skin or mucous membranes

- creams, solutions, ointments, gels, ophthalmic drops, lozenges, suppositories

155
Q

Describe parenteral anesthetics

A

injected into the CNS by various spinal injection techniques

156
Q

Describe surface anesthesia

A
  • this type of anesthesia is accomplished by the application of a local anesthetic to skin or mucous membranes
  • surface anesthesia is used to relieve itching, burning, and surface pain (ex minor sunburns)
157
Q

Describe nerve block anesthesia

A
  • local anesthetic is injected around a nerve that leads to the operative site
  • usually more concentrated forms of local anesthetic solutions are used for this type of anesthesia
158
Q

Describe peridural anesthesia

A

this type of anesthesia is accomplished by injecting a local anesthetic into the peridural space (one of the coverings of the spinal cord)

159
Q

Describe spinal anesthesia

A

the local anesthetic is injected into the subarachnoid space of the spinal cord

160
Q

List the 5 types of local anesthesia

A
  • epidural
  • infiltration
  • nerve block
  • spinal
  • topical
161
Q

Describe the drug effects of local anesthesia

A
  • first, autonomic activity is lost
  • then pain and other sensory functions are lost
  • motor activity is the last to be lost
  • as local agents wear off, they do so in reverse order (motor, sensory, then autonomic activity are restored)
162
Q

Indications of local anesthetics ?

A
  • surfical, dental, and diagnostic procedures
  • treatment of certain types of pain:
  • infiltration anesthesia
  • nerve bock anesthesia
163
Q

Indication for infiltration anesthesia

A
  • minor surgical and dental procedures
    • injection of the anesthetic solution intradermally, subcutaneously, or submucosally across the path of nerves supplying the target area
    • may be given in a circular pattern around the operative area
164
Q

Indication for nerve block anesthesia

A
  • surgical, dental and diagnostic procedures
    • also used for therapeutic management of pain
    • the anesthetic agent is injected directly into or around the nerve trunks or nerve ganglia that supply the area to be numbed
165
Q

adverse side effects of local anesthetics ?

A

-usually limited

adverse effects result if:

  • inadvertent intravascular injection occurs
  • excessive dose or rate of injection is given
  • slow metabolic breakdown
  • injection into a highly vascular tissue

Pharmacology (21 decks)

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