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Pharmacology for APRN > Pain Management and OUD > Flashcards

Pain Management and OUD Flashcards

1
Q

What area of the brain do opioids effect?

A

They produce feelings of pleasure by activating the ventral tegmental area and releasing dopamine from the nucleus accumbens

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2
Q

What is a PDMP?

A

Prescription Drug Monitoring Program is an electronic database that relays information on filled prescriptions for controlled substances and can assist in identifying opioid misuse in an individual patient.

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3
Q

Buprenorphine MOA

A

Partial agonist of the mu receptor.
Weak kappa receptor antagonist.
Delta receptor agonist.
Potent analgesic acting on the CNS producing a ceiling effect on respiratory depression.

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4
Q

Buprenorphine Pharmacokinetics

A

Bioavailability: PO = high first-pass effect, SL bypasses the first-pass effect.
Absorption: Peak effect 3-4 hours
Distribution: highly lipophilic, crosses blood-brain barrier
Metabolism: metabolism by cytochrome CYP3A4 enzymes after it enters the body and forms an active metabolite, norbuprenorphine, with weak intrinsic activity.
Half-Life: 38 hours
Excretion: fecal excretion
Urine: high levels of norbuprenorphine metabolite.

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5
Q

Buprenorphine Dosing

A

SL: 2-4mg and titrate up to 8mg-24mg
IM: 300mg extended release monthly
Induction: when patients experience mild to moderate withdrawal symptoms

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6
Q

Buprenorphine Special Considerations

A

Renal: no contraindication
Liver: reduced dose to prevent toxicity

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7
Q

Buprenorphine Adverse Effects

A

Anticholinergic: CNS depression, QT prolongation, HypoTN, lowered Sz threshold.
N/V, Drowsy, Dizzy, HA, memory loss, diaphoresis, dry mouth, myosis, sexual adverse effects, urinary retention.

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8
Q

CYP3A4 Agonists = metabolize Buprenorphine Faster

A

Carbamazapine
Phenytoin
Rifampin

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9
Q

CYP3A4 Antagonists = metabolize Buprenorphine Slowly

A

fluvoxamine
ketoconazole
indinavir
erythromycin
saquinavir

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10
Q

Buprenorphine vs Methadone

A

The drug is safer even at high doses.
Optional therapeutic doses can be achieved relatively quickly.
There is a lower risk of substance misuse and diversion.
The drug is associated with less stigma than methadone.
Patients can obtain the medication from any healthcare provider, eliminating the need for specialized methadone clinics.
Due to its partial opioid receptor agonist activity, buprenorphine is less likely to cause euphoria compared to full agonists such as methadone or morphine, reducing the likelihood of misuse or diversion.
Buprenorphine treatment typically lasts 3 to 6 months or even 1 to 2 years, whereas methadone treatment is often lifelong.

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11
Q

Buprenorphine/Naloxone MOA

A

Buprenorphine is a long-acting opioid that binds with high affinity at the mu receptor.
Naloxone is a pure opioid receptor antagonist combined with buprenorphine to reduce abuse potential.[3] Naloxone competes and displaces other opioids from the mu, kappa, and delta receptors, diminishing their effects.

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12
Q

Buprenorphine/Naloxone Pharmacokinetics

A

Absorption: Bioavailability is higher for SL for buprenorphine and lower for Naloxone.
Distribution: Buprenorphine high plasma binding, Naloxone weak plasma binding
Metabolism: metabolism by cytochrome CYP3A4 enzymes after it enters the body and forms an active metabolite, norbuprenorphine, with weak intrinsic activity.
Half-Life: 38 hours
Excretion: fecal excretion
Urine: high levels of norbuprenorphine metabolite.

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13
Q

Anticholinergics to avoid while on Buprenorphine/Naloxone

A

Benztropine, oxybutynin, diphenhydramine, scopolamine, antipsychotics, and tricyclic antidepressants as they can increase the risk of urinary retention and constipation

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14
Q

MOA’s to avoid while on buprenorphine/naloxone

A

Phenelzine, tranylcypromine, and linezolid with opioids, including buprenorphine, may result in serotonin syndrome.

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15
Q

Methadone MOA

A

Binds to opiate receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression. Methadone has also been shown to have N-methyl-D-aspartate (NMDA) receptor antagonism.

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16
Q

Methadone Pharmacokinetics

A

Onset of action: Oral: Analgesic: 0.5 to 1 hour; Parenteral: 10 to 20 minutes.
Peak effect: Parenteral: 1 to 2 hours; Oral: Continuous dosing: 3 to 5 days.
Distribution: Lipophilic, highly protein bound.
Metabolism: Hepatic; N-demethylation primarily via CYP3A4, CYP2B6, CYP2C19, CYP2C9, and CYP2D6 to inactive metabolites.
Excretion: Urine

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17
Q

Methadone Adverse Effects

A

Anticholinergic: CNS depression, QT prolongation, HypoTN, lowered Sz threshold.
N/V, Drowsy, Dizzy, HA, memory loss, diaphoresis, dry mouth, myosis, sexual adverse effects, urinary retention.

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18
Q

Methadone Dosing Precautions

A

Dose cautiously if renal or liver impairment is present

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19
Q

Why is Methadone effective in treating OUD?

A

It reduces cravings. Methadone is effective in treating OUD due to its very long half-life, which reduces cravings and dulls the euphoric effects of other opioid agonists. Because of its full mu opioid agonist properties, methadone is also efficacious in pain control and is thought to be less likely to produce tolerance due to its antagonistic effects at the N-methyl-d-aspartate (NMDA) receptor.

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20
Q

Which medication is not routinely used in the management of chronic pain?

A

Naltrexone: Medications used in OUD include buprenorphine, methadone, and naltrexone. Naltrexone, an opioid antagonist, is not routinely used in the management of chronic pain.

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21
Q

Patient Education on OUD treatment

A

Proper administration.
Discuss common side effects.
Drug take-back programs

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22
Q

Pain Definition

A

“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

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23
Q

Nociceptive Pain

A

Occurs as a result of nerve receptor stimulation following a mechanical, thermal, or chemical insult.
Includes: Somatic, visceral, and central pain.

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24
Q

Somatic Pain

A

Nociceptive pain associated with muscle, skin, or bone injury.

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25
Q

Visceral Pain

A

Nociceptive pain associated with the visceral organs.

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26
Q

Central Pain

A

Nociceptive pain that is from MS, SCI’s, Migraine, and Post-stroke syndrome

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27
Q

Neuropathic Pain

A

Caused by abnormal signal processes in the CNS.

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28
Q

Peripheral Pain

A

Neuropathic pain that is from DM and postherpetic neuralgia.

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29
Q

Inflammatory Pain

A

A subtype of nociceptive pain that results from the release of proinflammatory cytokines at the site of tissue injury.
Present in acute pain and chronic pain.

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30
Q

A patient complains of pain from a migraine. How would the practitioner classify this type of pain?

A

Central Neuropathic Pain: Examples of central neuropathic pain syndromes include pain from multiple sclerosis, spinal cord injuries, migraine, and poststroke syndrome. Peripheral neuropathies include pain from diabetes and postherpetic neuralgia. Inflammatory pain may be present in acute pain from bruises or infection and chronically in pain from rheumatoid arthritis or osteoarthritis. Somatic pain is associated with muscle, skin, or bone injury and is often well localized.

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31
Q

Acute Pain Classification

A

Sudden onset, usually subsides quickly. Characterized by sharply localized sensations with an identifiable cause.

32
Q

Chronic pain classification

A

Pain persisting beyond the normal time and despite efforts to diagnose and treat original condition/injury.
Peripheral and central sensitization of pathways occurs.

33
Q

Cancer-Related Pain Classification

A

Pain associated with a malignancy that can result from the disease itself or damage to secondary tissue.
Pain secondary to direct tumor involvement of bone, nerves, viscera, or soft tissue.

34
Q

Chronic Non-Cancer Pain Classification

A

Persistent pain in patients not affected by cancer
Ex: Osteoarthritis, fibromyalgia

35
Q

Breakthrough Pain Classification

A

A transitory pain seen in conjunction with chronic pain, where moderate-to-severe pain occurs in patients with otherwise well-controlled pain.
Brief, lasting minutes to hours and interfering with functioning and quality of life.

36
Q

Transduction phase of Nociception

A

Nociceptor activation due to mechanical, thermal, or chemical injury; nerve endings are activated through the release of various excitatory chemical neurotransmitters.

37
Q

Transmission stage of Nociception

A

An action potential transmitted via the myelinated A-delta and unmyelinated C fibers, by way of the dorsal root ganglia, synapsing in the dorsal horn of the spinal cord.

38
Q

Perception stage of Nociception

A

Nociceptive information travels through different areas of the CNS to the brain where the pain is perceived; perception is the end result of the pain transmission to the brain.

39
Q

Modulation stage of Nociception

A

Involves serotonin and norepinephrine. Pain modulation occurs at various levels of the CNS; endogenous opioids work through binding of opioid receptors in the periphery and the CNS.

40
Q

What stage of nociception is occurring when neurotransmitters in the dorsal horn directly or indirectly depolarize the second-order neurons?

A

Transmission: During transmission, neurotransmitters in the dorsal horn directly or indirectly depolarize the second-order neurons, facilitating transmission of information to the brain and leading to the perception of pain. During transduction, nerve endings are activated through the release of various excitatory chemical neurotransmitters. Perception is the end result of the pain transmission to the brain. Pain modulation occurs at various levels of the CNS, where endogenous opioids bind opioid receptors in both the periphery and CNS.

41
Q

Peripheral Sensitization

A

When pain receptors in the periphery are continually stimulated, the threshold for stimulation becomes lowered and increased nerve firing occurs.

42
Q

Central Sensitization

A

Defined as “an amplification of neural signaling within the CNS that elicits pain hypersensitivity”

43
Q

Chemical pain Mediators: Identify

A

Neurotransmitters, norepinephrine, serotonin, histamine, and polypeptides such as bradykinin, prostaglandins, and substance P.

44
Q

Chemical pain Mediators: Role

A

Activating and sensitizing nociceptors and increasing neuronal excitability.
Exitatory amino acids, glutamate, and aspartate, along with substance P facilitate activation of second-order neurons in the dorsal horn primarily through activation of the N-methyl-d-aspartate (NMDA) receptors.

45
Q

A practitioner conducting a pain assessment asks the patient “is the pain consistent or intermittent?” What character of pain is the practitioner assessing?

A

Temporal Pattern: The temporal pattern describes whether the pain is constant or intermittent and if it is associated with movement. Quality describes what the pain feels like (sharp, stabbing, burning). Region refers to the location of the pain. Severity is derived from the pain assessment and reflects the intensity of the pain.

46
Q

SE’s common to opioids

A

Sedation, confusion, respiratory depression, itching, N/V, constipation.

47
Q

Common Co-analgesics

A

Antidepressants, Anticonvulsants, Sodium-Channel Blockers, NMDA-receptor antagonists, Skeletal muscle relaxants, antispastic agents.

48
Q

What type of pain are cannabinoids safe to use with minimal side effects?

A

Chronic Pain. Cannabinoids have been studied in the treatment of chronic pain in patients with neuropathic pain, fibromyalgia, rheumatoid arthritis, and mixed chronic pain. Current evidence suggests that cannabinoids are safe with minimal side effects and are effective in reducing neuropathic pain specifically in fibromyalgia and rheumatoid arthritis.

49
Q

Endocannabinoid System work on what Pain receptors?

A

CB1 and CB2

50
Q

Dronabinol (Marinol) Indications

A

Indicated for the treatment of anorexia associated with weight loss in acquired immunodeficiency syndrome (AIDS) patients and for the treatment of chemotherapy-induced nausea and vomiting.

51
Q

Dronabinol (Marinol) Adverse Events

A

Most common adverse reactions (≥3%) are abdominal pain, dizziness, euphoria, nausea, paranoid reaction, somnolence, thinking abnormal, and vomiting.

52
Q

Nabilone (Cesamet) Indications

A

Treatment of nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments.
Similar to dronabinol, nabilone also has psychotomimetic reactions, which are not normally observed with other antiemetic agents.

53
Q

Nabilone (Cesamet) Adverse Events

A

Early in treatment, euphoria and hypotension may occur, as well as impaired cognition. Delayed adverse reactions include depression, ataxia, and orthostatic hypotension. Less severe adverse reactions include drowsiness, headache, vertigo/dizziness, insomnia and/or fatigue, asthenia, and dry mouth.

54
Q

Cannabidiol (CBD, Epidiolex) Indications

A

98% pure plant-derived oral CBD solution with a Food and Drug Administration (FDA)–approved indication for the treatment of seizures associated with Lennox-Gastaut Syndrome (LGS) or Dravet Syndrome (DS) in pediatric patients 2 years of age and older.
It is the first plant-derived cannabis product approved by the FDA and is considered a nonpsychoactive cannabinoid.

55
Q

Which medication has been approved by the FDA for the treatment of seizures associated with LGS in pediatric patients 2 years of age or older?

A

CBD. CBD solution with an FDA-approved indication for the treatment of seizures associated with LGS. Dronabinol (Marinol; Syndros) is a synthetic tetrahydrocannabinol (THC) product which is indicated for the treatment of anorexia associated with weight loss in AIDS patients and for the treatment of chemotherapy-induced nausea and vomiting. Nabilone (Cesamet) is a synthetic derivative of THC, approved by the FDA for the treatment of nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments. Sativex is indicated for the “symptom improvement in adult patients with moderate-to-severe spasticity due to multiple sclerosis (MS) who have not responded adequately to other anti-spasticity medication” (Sativex Prescribing Info).

56
Q

THC/CBD (Sativex, Nabiximols) Indications

A

Sativex is indicated for the “symptom improvement in adult patients with moderate-to-severe spasticity due to multiple sclerosis (MS) who have not responded adequately to other anti-spasticity medication”

57
Q

Allodynia Definition

A

Pain caused from sensory stimuli that is not normally painful.
Caused by nerve or CNS injury
Ex: Diabetic neuropathy

58
Q

Hyperalgesia Definition

A

Heightened response to pain, extreme sensitivity, extreme response to pain caused when there is damage to the nerves or chemical changes to the nerve pathway.
Central Sensitization is the end result.
Ex: Fibromyalgia, complex regional pain syndrome

59
Q

WHO Pain Ladder for Mild Pain

A

Nonopioid plus adjuvant therapy

60
Q

WHO Pain Ladder for Mild to Moderate Pain

A

“Weak” opioid or multimodal opioid plus/minus Non-opioid plus/minus adjuvant therapy

61
Q

WHO Pain Ladder for Moderate to Severe Pain

A

“Strong” Opioid plus/minus non-opioid plus/minus adjuvant therapy

62
Q

WHO Pain Ladder for Severe to Very Severe breakthrough pain

A

Interventional treatments plus/minus non-opioid plus/minus adjuvant therapy

63
Q

X-Waiver Details for Buprenorphine Prescriptions - New Legal Development Details

A

Congress passed the Omnibus Bill, which included the removal of the federal requirement for clinicians to submit a Notice of Intent (AKA a waiver) to prescribe buprenorphine for the treatment of opioid use disorder as part of theMainstreaming Addiction Treatment Act.
Clinicians who have a current DEA registration with Schedule III authority may now prescribe buprenorphine if permitted by state law.

64
Q

Buprenorphine for Chronic Pain Considerations

A

Patients who have previously been prescribed opioids and those who are opioid naive.

65
Q

Central Sensitization to Pain: Definition

A

A process that occurs in chronic pain states.
Results from CNS changes.
May lead to allodynia, hyperalgesia, persistant pain, referred pain.
PREVENTION: adequate treatment of acute pain

66
Q

Xylazine (Tranq) MOA

A

Alpha-2 adrenergic agonist found as an adulterant of fentanyl
Does not respond to naloxone!

67
Q

Xylazine (Tranq) withdrawal treatment

A

Benzodiazepines for resultant anxiety issues.
Antipsychotics
Wound management (wounds at site of injections)

68
Q

Enzyme Definition

A

Proteins that act as a biologic catalyst helping chemical reactions speed along and then biotransform

69
Q

Substrate Definition

A

The reactants that engage with enzymes. This causes the enzyme to change shape allowing the substrate to separate and release as it changes into products, which are then also released.

70
Q

Sensitive Substrates that fall into CYP1A2

A

Caffeine, Melatonin, Duloxetine, Clozapine, Theophylline, Ramelteon, Tizanidine

71
Q

CYP1A2 Inhibitors - Increase the AUC (area under the curve) of sensitive substrates of a given metabolic pathway

A

Ciprofloxacin, Fluvoxamine, Cimetidine, OCP’s, Allopurinol, Acyclovir

72
Q

CYP1A2 Inducers - Decrease the AUC (area under the curve) of sensitive substrates of a given metabolic pathway

A

Phenytoin, Smoking, Cruciferous vegetables: Broccoli, Brussel Sprouts, Char-grilled meat, tobacco

73
Q

The role of P-glycoprotein (P-gp) in drug transportation

A

Functions as a transmembrane efflux pump - pumps substrates from inside to the outside of the cell.
Impacts plasma and tissue concentrations.
Determines the uptake and efflux of drugs.

74
Q

Drugs that are substrates of P-gp

A

Apixaban, Dabigatran, Edoxaban, Rivaroxaban, Colchicine, Digoxin, Tacrolimus

75
Q

Drugs that are Inhibitors of the P-gp Drug efflux pump

A

Increase serum concentrations of the drugs that are substrates for P-gp
Amiodarone, all macrolides, ketoconazole, carvedilol, tamoxifen, verapamil, CBD

76
Q

Drugs that are Inducers of the P-gp Drug efflux pump

A

Decrease serum concentrations of substrates of P-gp
Carbamazepine, Green Tea, St. John’s Wort, Phenytoin, Rifampin

Pharmacology for APRN (11 decks)

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