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Pharm Spring 2023 > Substance Use And Opioids > Flashcards

Substance Use And Opioids Flashcards

1
Q

What is the most clinically relevant opioid receptor

A

Mu
*mediates analgesia
*respiratory depression
*euphoria
*sedation
*miosis
*GI effects

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2
Q

What does the k (kappa) and delta opioid receptors mediate?

A

KOR
*mediates analgesia
*dysphoria
DOR
*mediates analgesia
*convulsions
*role in tolerance

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3
Q

When activating an opioid receptor what happens to the secondary signals?

A
  1. Reduce opening of voltage gates Ca2+ channels, thereby inhibiting calcium dependent neurotransmitter release
    *less excitation
  2. Stimulate K+ currents, bind open channels which will hyperpolarizes and inhibits postsynpatic neurons
    *not as many messages being sent
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4
Q

What are the components of the ascending pathway (pain transmission)

A
  1. Senses painful stimuli
  2. Transmits pain signal to cortex
  3. Opioids will decrease emotional signal to the brain AND
  4. Opioids will block sensory neuron signals (less pain sensations)
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5
Q

What happens to the potassium channels in the ascending pathway?

A
  1. Agonists open channels causing neuronal hyperpolarization
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6
Q

What are the components of the descending pathway (pain transmission)

A
  1. Modulates pain signal
    *opioids enchance inhibitory modulation (sensory)
    *less pain sensation
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7
Q

What happens to the calcium channels in the descending pathway?

A
  1. Agonists reduce channel opening, thereby inhibiting calcium dependent neurotransmitter release
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8
Q

How do the mechanisms of opioids work?

A
  1. Bind and stimulate open K+ channels causing hyperpolarization
    *less likely to fire
  2. Bind and reduce Ca2+ channel opening thereby blocking Ca- dependent neurotransmitter release
    *less excitatory signaling available
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9
Q

Opioids exert their analgesic effects in the human body by modulating the pain signal in both the ascending and descending pain pathways.

A

True

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10
Q

Definition of tolerance and dependency

A

Tolerance: higher opioid dose is needed to produce same level of analgesia
Dependency: chronic, relapsing brain disease characterized by compulsive drug seeking and use despite harmful consequences

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11
Q

Definition of addiction

A
  1. State where organism functions normally only in presence of substance
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12
Q

What effects will be shown with minimal/no tolerance, moderate tolerance, and rapid tolerance

A

Minimal
*pupillary miosis
Moderate tolerance
*constipation, emesis, analgesia, sedation
Rapid tolerance
*euphoria

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13
Q

What are the analgesic effects the opioids have?

A
  1. Continuous, dull pain better relived
  2. Opioids reduce sensory and emotional components of pain
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14
Q

What are the euphoric effects of opioids

A
  1. Pleasant feeling of well-being
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15
Q

What are the ‘respiratory depression’ effects of opioids?

A
  1. Primary consequence of opioid overdose
  2. Inhibition of respiratory controlling neurons in the brain stem
    *dose related
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16
Q

What are the hypotension effects of opioids

A
  1. Agonists stimulate histamine release thereby causing low BP
    *peripheral ad arterial vasodilation
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17
Q

What are the sedative opioid effects

A
  1. Drowsiness
  2. Mood alterations
  3. Mental clouding
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18
Q

What are other effects of opioids?

A
  1. Cough suppression (primary therapeutic effects)
  2. Miosis (pupil constriction)
  3. Emesis (N/V)
  4. Constipation
  5. Pruritis
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19
Q

Why does constipation happen while on an opioid?

A
  1. Opioid acts on nerves within the enteric nervous system to increase muscle tone and decrease peristaltic movement in small intestine and colon
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20
Q

What are the two predominate therapeutic uses of opioid medications?

  1. Analgesia
  2. Emesis
  3. Constipation
  4. Sedation
  5. Antitussive
A

*1 and 5

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21
Q

What is the “A” effects of opioids

A

Absorption
1. Modestly well GI absorption
2. Extensive first pass metabolism
3. Some are very lipohilic

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22
Q

What is the “D” effects of opioids

A

Distribution
1. 1/4 of morphine in plasma bound to proteins
2. Fails to redistribute into tissues very well

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23
Q

What is the “M” effect of opioids

A
  1. Morphine 6-glucuronide 2X potency as morphine
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24
Q

What is the “E” effects of opioids

A

Excretion
1. Glomerular filtration
2. Kidney ARDS in patient with significant renal hx

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25
Q

What are the neuropsychiatric opioid ARDS

A
  1. Sedation
  2. Clouded thoughts
  3. Euphoria
  4. Sleep-wake disturbances
  5. Mood changes
  6. Fatigue
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26
Q

What are the cardiopulmonary opioid ARDS

A
  1. Respiratory depression
  2. Dizziness
  3. Orthostatic hypotension
  4. Bronchoconstriction
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27
Q

What are the gastrointestinal opioid ADRs

A
  1. Nausea
  2. Vomiting
  3. Constipation
  4. Decreased GI motility
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28
Q

What are the ARDS of the urinary system and endocrine due to opioids

A

Urinary system
*urinary retention
Endocrine
*decreased testosterone levels
*reduced/absent menses
*hypogonadism
*infertility
*reduced libido

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29
Q

What are the allergic and immunologic ARDS

A
  1. Pruritus
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30
Q

What is the primary cause of morbidity to opioid therapy

A

Respiratory depression
*bc the duration of the opioid may be longer than analgesia

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31
Q

What type of patients should you monitor while on opioid therapy

A
  1. Asthma
  2. COPD
  3. Increased intracranial pressure
    *bc all the stages of breathing are being depressed
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32
Q

What are the risk factors of opioid induced respiratory depression?

A
  1. History of previous overdose
  2. Substance abuse
  3. Using large doses (>50 morphine milligram)
  4. Use with benzodiazepines (gabapentin, Pregabalin)
  5. Comorbid respiratory or psychiatric disease
33
Q

What SE do all opioids cause?

A
  1. Constipation
  2. Does not improve over time
    *anticipate and treat
    *no tolerance develops over time
    *if opioids are timed around the clock use prophylaxis
34
Q

What is the first line stool softener

A

Stimulant laxatives
1. Sienna
2. Bisacodyl

35
Q

What are the top 4 essential opioids ADE

A
  1. N/V
  2. Constipation
  3. Respiratory depression
  4. Sedation
36
Q

What drugs will cross react with on another

A

COD or MORPH in the name
*include heroin

37
Q

What is the onset of analgesia, duration of effect, and T 1/2 of morphine, Oxycodone, hydrocodone

A

Morphine
*onset = 20-40
*duration = 4 hours
*T 1/2 = 2
Oxy
*onset = 10-30
*duration = 3-6 hours
*T 1/2 = 3
Hydro
*onset = 10-20
*duration = 4-6 hours
*T 1/2 = 4 hours

38
Q

What is the onset of analgesia, duration of effect, and T 1/2 of oxymorphone, hydromorphone, methadone

A

Oxymorphone
*onset = 10-30
*duration = 4-6 hours
*T 1/2 = 9
Hydromorphone
*onset = 15-30
*duration = 4 hours
*T 1/2 = 2.5
Methadone
*onset = 10-15
*duration = 4-8 hours
*T 1/2 = 12-50 hours

39
Q

What is the onset of analgesia, duration of effect, and T 1/2 of Fentanyl transmucosal, IM, IV

A

Transmucosal
*onset = 5-10
*duration = 1-2 hours
*T 1/2 = 7
IM
*onset = 5-10
*duration = 1-2 hours
*T 1/2 = 4
IV
*onset = immediate
*duration = 30mins - 1 hour
*T 1/2 = 4 hours

40
Q

Which of the following are key side effects of oxycodone?

  1. Diarrhea
  2. Nausea
  3. Respiratory depression
  4. Excitation
  5. Sedation
A

*2, 3, 5

41
Q

What is tramadol (ultram) MOA

A
  1. Agonizes mu-opioid receptors to produce moderate analgesia
42
Q

What is the maximum dose of tramadol and the ADRs

A

Max = 300mg
ADRS
*constipation
*dizziness
*nausea
*somnolence

43
Q

What are the DDI of tramadol

A
  1. Caution with other drugs that can increase serotonin
    *SSRI, SNRI leads to serotonin syndrome
  2. Caution in patients with seizure disorder or taking anticonvulsants
44
Q

What are the components of methadone

A
  1. Long acting mu agonist
  2. Effective in severe chronic pain
  3. Very long half-life (50 hours)
    *sticks around after analgesia wears off
45
Q

What do equinanalgesic dose of methadone cause>

A
  1. It decreases progressively the higher of the previous opioid dose
46
Q

What opioid medication has a “quick on, quick off” pharmacokinetic profile?

A

Fentanyl

47
Q

How does age related to opioid therapy

A
  1. PD changes with aging
    *increase sensitivity to opioids
  2. Children <2 should not receive transdermal fentanyl
48
Q

How dos cognitive status relate to opioid therapy

A
  1. Ability to self-assess and report pain, take break-through analgesia
49
Q

How does pregnancy/breastfeeding relate to opioid therapy

A
  1. Opioids cross through the breast milk
  2. Developmental outcomes are unknown
50
Q

What genetic factors can effects opioid therapy

A
  1. CYP2D6
51
Q

What does dopamine mediate?

A
  1. Drug reinforcement by binding to D1 receptors in the NA (nucleus accumbens)
    *sensitizing dopaminergic neurons
    *all addictive substance increases dopamine in the NA
52
Q

What is the cycle of a SUD

A
  1. Drug use
    *dopamine surges
  2. Positive reinforcement
  3. Decrease use or wanting to stop
  4. Negative reinforcement
    *withdrawal symptoms
53
Q

What is the correct drug to use during intoxication / overdose phase

A

Naloxone
*will reserve the effect

54
Q

What are the correct drugs to use during the withdrawal phase?

A
  1. Methadone
  2. Buprenorphine
55
Q

What are the correct drugs to use during the maintenance phase

A
  1. Methadone
  2. Buprenorphine
  3. Naltrexone
    *keep system empty
56
Q

What is Naloxone (narcan)

A
  1. Opioid antagonist
    *used to treat overdose and prevent
  2. Injection (Naloxone)
  3. Nasal spray (narcan)
  4. Monthly IM (vivitrol) is naltrexone (maintenance)
57
Q

When to use then IV/IM/SubQ, or nasal spray

A

IV/IM/SubQ
*every 2-3 minutes (0.4 - 2mg)
Nasal spray
*every 2-3 minutes (4 to 8mg )

58
Q

Which of the following medications can be used for opioid withdrawal?
1. Methadone
2. Naloxone
3. Buprenorphine
4. Oxycodone
5. Clonidine

A

Methadone
Buprenorphine
Clonidine

59
Q

What is the MOA and SE of buprenorphine (belbuca)

A

MOA: partial mu opioid receptor agonist
SE
*sedation
*HTN
*N/V/D

60
Q

What are the warnings, and clinical pearls of buprenorphine (belbuca)

A

Warnings
*CNS depression
*hepatic events
*Qtc prolongation
Clinical pearls
*Subq requires 7 days of induction with PO
*must be in withdrawal
*oral cancer reported

61
Q

What are the contraindication of buprenorphine (belbuca)

A
  1. Respiratory depression
  2. GI obstruction
  3. Acute or severe asthma in unmonitored setting
62
Q

What are the clinical pearls and ADRs of methadone (dolophine, methadose)

A

Clinical pearls
*clinic records dont show in OARRS
ADRS
*QTc prolongation
*sedation
*respiratory depression

63
Q

What are the warnings of methadone (dolophine, methadose)

A
  1. Decompensated liver disease
  2. Concomitant substance use disorders
  3. Respiratory insufficiency
  4. Low levels of physical dependence to opioids
64
Q

What are the CI to methadone (dolophine, methadose)

A
  1. Respiratory depression
  2. Acute bronchial asthma or hypercapnia
  3. Known or suspected paralytic ileus
65
Q

What is the MOA and SE of naltrexone (ReVia PO, Vivitrol SR injection)

A

MOA = mu opioid receptor antagonist
SE
1. Nausea
2. Increased LFTs
3. Insomnia
4. Injection site reactions

66
Q

What are the warnings of naltrexone (ReVia PO, Vivitrol SR injection)

A
  1. Hepatotoxicity
  2. Suicidal thoughts ‘ depression
  3. Bleeding disorders (IM)
  4. Caution in renal impairment
67
Q

What are the clinical pearls of naltrexone (ReVia PO, Vivitrol SR injection)

A
  1. Can be used for both alcohol and opioid use disorders
  2. Not used for withdrawal, used to prevent euphoria in relapses
  3. Avoid with opioids or if in acute opioid withdrawal
68
Q

Which of the following medications should not be used in a patient with a prolonged QTc?
Buprenorphine
Naltrexone
Naloxone
Methadone

A

Buprenorphine
Methadone

69
Q

What is the treatment of alcohol intoxication mild-mod, severe

A

Mild/mod
1. Supportive care, symptom control, reassurance
Severe
1. Cardiac monitoring
2. Fluids
3. Respiratory support

70
Q

What should be used during severe alcohol intoxication

A
  1. Benzodiazepines (want to prevent seizures)
  2. Diazepam
  3. Lorazepam
  4. Midazolam
    *use thiamine before dextrose (or else there will be brain encephalopathy)
71
Q

What is wernicke-korsakoff syndrome

A

Caused from a thiamine deficiency, there will be
1. Mental confusion
2. Amnesia
3. Ataxia of gait
4. Nystagmus
5. Opthalmoparesis

72
Q

What can administration of glucose cause?

A
  1. Rapidly deplete existing thiamine stores
    *if pre-existing thiamine deficiency can precipitate wernicke disease
73
Q

How to treat wernicke-korsakoff syndrome

A
  1. Always give thiamine before dextrose-containing fluids
  2. Banana bag (thiamine + folate + multivitamin)
74
Q

What is the first line treatment of AUD

A
  1. Acamprosate
  2. Naltrexone
75
Q

What is the MOA and indication of use for acamprosate (Campari)

A

MOA = GABA agonist/glutamate antagonist
Indication
*moderate to severe AUD

76
Q

What is the dosage, SE, and CI of Acamprosate (Campari)

A

Dosage = 666TID
SE = anxiety/depression, diarrhea, insomnia, weakness, suicidal thoughts
CI = CrCl<30

77
Q

What is the MOA of disulfiram (Antabuse)

A

Aldehyde dehydrogenase inhibitor

78
Q

What are the clinical pearls of disulfiram (Antabuse)

A
  1. Need a BAC of zero

Pharm Spring 2023 (27 decks)

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