Chapter 26 Opioid agonist, opiod antagonist, and antimigraine agents Flashcards
Opioid agonists MEDS
Morphine, Codeine, Fentanyl, Hydrocodone, Hydromorphone, Meperidine, Methadone, Oxycodone, Oxymorphone, Tapentadol ,Tramadol
MOA opioid agonist
Opioid agonists stimulate opioid receptors in the CNS, specifically mu and kappa receptors.
Mu-receptor effects:
Analgesia, euphoria, respiratory depression, pupil constriction, and physical dependence.
Kappa-receptor effects:
Analgesia, sedation, and dysphoria.
Opioids alter pain perception by modulating pain signal transmission in the brain and spinal cord.
Indications for opioid agonists
Relief of moderate to severe acute or chronic pain.
Preoperative medication to reduce anxiety and pain.
Adjunct to anesthesia
for additional sedation and pain control.
Management of severe pain conditions, including cancer pain and post-surgical pain
Pharmacokinetics opioid agonists
Absorption: Well absorbed through oral, IM, IV, subcutaneous, transdermal, and intrathecal routes.
Metabolism: Mostly in the liver.
Excretion: Primarily through urine and bile.
Half-life of Morphine: 1.5 to 2 hours.
CI opioid agonist
Allergy to opioids.
Severe respiratory disorders (e.g., COPD, asthma, emphysema) due to respiratory depression risk.
Acute or severe GI conditions (e.g., paralytic ileus, biliary tract disease) as opioids slow motility.
Head injuries, cerebral vascular disease, alcohol use disorder, or delirium tremens (opioids may exacerbate CNS depression).
Preg and lactation: Use with caution due to risk of neonatal opioid withdrawal syndrome
AE opioid agonists
CNS Effects: Light-headedness, dizziness, sedation, confusion, psychoses, anxiety, hallucinations.
Respiratory Depression: Apnea, circulatory depression, respiratory arrest, shock.
Cardiovascular (CV) Effects:
Orthostatic hypotension, tachycardia, cardiac arrest.
Gastrointestinal (GI) Effects:
Nausea, vomiting, constipation, biliary spasm.
Genitourinary (GU) Effects:
Urinary retention, ureteral spasms, loss of libido.
Pupil Constriction: Causes miosis.
Physical Dependence: Long-term use can lead to opioid addiction and withdrawal syndrome.
DDI opioid agonists
CNS Depressants (barbiturates, benzodiazepines, alcohol, phenothiazines, MAOIs): Increased risk of respiratory depression, sedation, and coma.
Tapentadol + SSRIs, MAOIs, TCAs, St.
John’s Wort: Risk of serotonin syndrome, a potentially fatal condition.
Anticholinergic Agents: May exacerbate constipation and urinary retention.
Antihypertensive Drugs: Increased risk of hypotension and orthostatic hypotension.
Nursing interventions for opioid agonists
Assessment:
- Assess for contraindications, including respiratory
dysfunction, liver or kidney disease, head trauma, and
pregnancy.
- Monitor CNS effects, such as sedation, confusion,
dizziness, and hallucinations.
- Check vital signs (respiratory rate, blood pressure, heart
rate) to detect respiratory depression or hypotension.
- Evaluate bowel function to monitor for constipation.
- Assess urinary output to detect urinary retention.
Interventions:
- Administer IV opioids slowly to reduce risk of
hypotension and respiratory depression.
- Monitor respiratory rate (hold if < 12 breaths/min).
- Encourage fiber intake and hydration to prevent
constipation.
- Ensure patient safety (fall precautions due to sedation
and dizziness).
- Educate patients on opioid dependence risks and the
importance of gradual tapering.
Patient Teaching:
- Take opioids exactly as prescribed to avoid addiction and overdose.
- Do not mix opioids with alcohol or other CNS depressants.
- Report signs of respiratory distress, confusion, or extreme drowsiness.
- Increase fiber and fluids to prevent constipation.
- Avoid operating heavy machinery due to drowsiness and
dizziness risks.
Opioid Agonist- Antagonists MEDS
Buprenorphine(Buprenex)
Butorphanol (generic)
Nalbuphine (generic)
Pentazocine (available only in combination with naloxone)
MOA opioid agonist-antagonist
These drugs act as partial agonists at mu-opioid receptors and antagonists at kappa-opioid receptors.
They produce analgesia, sedation, and euphoria but can also cause hallucinations and impaired mental function.
Their antagonistic properties may induce withdrawal in opioid- dependent patients.
Indications Opioid Agonist- Antagonists
Moderate to severe pain requiring opioid therapy.
Treatment of opioid use disorder (buprenorphine).
Pain relief during labor and delivery (nalbuphine).
Pharmacokinetics Opioid AA
Buprenorphine: Available in IM, IV, oral, transdermal, and transmucosal forms.
Butorphanol: Available IM, IV, and as a nasal spray.
Nalbuphine: Administered parenterally (subcutaneous, IM, IV).
Pentazocine: Only available in oral combination form with naloxone.
Metabolized in the liver, excreted in urine or feces.
Crosses the placenta and enters breast milk.
CI to Opioid AA
Allergy to opioid agonist-antagonists.
Sulfite allergy (for nalbuphine).
Physical dependence on opioids (can trigger withdrawal syndrome).
Use with caution in:
- Respiratory disorders (COPD,
asthma, sleep apnea) due to risk
of respiratory depression.
- Cardiac conditions (MI, CAD,
hypertension) due to stimulatory
effects.
- Renal or hepatic dysfunction
(may affect drug metabolism and
clearance).
- Pregnancy and lactation (risk of
neonatal opioid withdrawal syndrome).
AE opioid AA
Central Nervous System (CNS):
Light-headedness, dizziness, sedation, hallucinations, psychoses, anxiety, fear.
Respiratory Effects: Respiratory depression, apnea, suppression of cough reflex.
Gastrointestinal (GI): Nausea, vomiting, constipation, biliary spasms.
Genitourinary (GU): Urinary retention, ureteral spasms, loss of libido.
Physical and psychological dependence are possible, but less likely than with full opioid agonists.
DDI Opioid AA
CNS depressants (barbiturates, alcohol, benzodiazepines): Increased risk of respiratory depression, sedation, and coma.
Use in opioid-dependent patients: May precipitate withdrawal symptoms, including hypertension, vomiting, anxiety, and fever.
Patients switching from opioid agonists to opioid agonist-antagonists require careful monitoring.
Nursing interventions Opioid AA
Assessment:
- Assess for contraindications, including opioid dependence, respiratory disorders, cardiovascular conditions, and hepatic/renal dysfunction.
- Monitor CNS effects, including hallucinations, sedation, and dizziness.
- Check respiratory rate and oxygen saturation (hold if respiratory rate < 12 breaths/min).
- Assess bowel function (constipation risk) and urinary output (urinary retention risk).
Interventions:
- Monitor for withdrawal symptoms in opioid-dependent patients.
- Educate on avoiding alcohol and CNS depressants.
- Ensure fall precautions due to dizziness and sedation.
- Titrate doses carefully to prevent severe sedation or
withdrawal reactions.
- Monitor pain relief effectiveness and adjust treatment if
necessary.
Patient Teaching:
- Take the medication exactly as prescribed.
- Avoid alcohol and sedatives to prevent excessive CNS
depression.
- Report any signs of withdrawal, hallucinations, or
difficulty breathing.
- Use caution when driving or operating heavy
machinery.
- Maintain hydration and fiber intake to prevent
constipation.
Opioid Antagonists MEDS
Naloxone (generic)
Naltrexone (Vivitrol)
Methylnaltrexone and other opioid antagonists for opioid- induced constipation
MOA opioid antagonist
Block opioid receptors to reverse opioid effects such as respiratory depression, sedation, and hypotension.
Do not produce analgesic effects but can induce withdrawal symptoms in opioid-dependent individuals.
Indication opioid antagonist
Reversal of opioid- induced respiratory depression and sedation.
Treatment of opioid overdose.
Management of opioid dependence (naltrexone).
Pharmacokinetics opioid antagonist
Naloxone: Administered parenterally (IM, IV, or subcutaneous); not absorbed orally.
Naltrexone: Well absorbed orally.
Metabolism: Hepatic metabolism.
Excretion: Primarily in the urine.
Half-Life: Shorter than most opioids, so repeat dosing may be required.
CI opioid antagonist
Known hypersensitivity to opioid antagonists.
Use with caution in pregnancy and lactation, as it may cause withdrawal symptoms in the fetus or newborn.
Use with caution in patients with a history of opioid dependence, as it can precipitate acute withdrawal.
AE opioid antagonist
Opioid Withdrawal Symptoms (Opioid Abstinence Syndrome): Nausea, vomiting, sweating, tachycardia, hypertension, tremors, and anxiety.
CNS Effects: Agitation, restlessness, nervousness.
Cardiovascular (CV) Effects: Tachycardia, dysrhythmias, blood pressure fluctuations, pulmonary edema.
DDI opioid antagonist
Higher doses of opioid antagonists may be required to reverse the effects of:
- Buprenorphine
- Butorphanol
- Nalbuphine
- Pentazocine (opioid
agonist-antagonists).
Nursing interventions opioid antagonist
Assessment:
- Assess for opioid overdose signs (respiratory depression, pinpoint pupils, unresponsiveness).
- Monitor respiratory status and oxygen levels closely.
- Evaluate cardiovascular status, including heart rate and
blood pressure.
- Check for opioid dependence history, as administration
may trigger withdrawal.
Interventions:
- Ensure airway patency and provide artificial ventilation if necessary.
- Monitor continuously for opioid withdrawal symptoms.
- Be prepared for repeated dosing, as opioid antagonists
have shorter half-lives than most opioids.
- Provide comfort and support to help patients cope with
withdrawal symptoms.
Patient Teaching:
- Inform patients and families about opioid reversal effects.
- Warn about potential withdrawal symptoms in opioid- dependent individuals.
- Educate caregivers on how to use naloxone auto- injectors in emergency settings.
- Ensure opioid-dependent patients are aware that opioid antagonists block opioid effects and may reduce pain relief from prescribed opioids.
Ergot derivatives MEDs
Dihydroergotamine
(Migranal, D.H.E. 45)
Ergotamine (Ergomar)
MOA ergot
Block alpha-adrenergic and serotonin receptor sites in the brain
Cause vasoconstriction of cranial blood vessels, reducing blood flow and hyperperfusion.
Reduce cranial artery pulsation, which helps alleviate migraine symptoms.
Indication of ergot
Prevention or treatment of migraine and vascular headaches.
Dihydroergotamine (parenteral form) is also approved for cluster headaches.
Pharmacokinetics ergot
Rapidly absorbed from multiple routes, with an onset of 15 to 30 minutes.
Metabolized in the liver and excreted primarily in bile.
Administration Routes:
- Dihydroergota
mine: Nasal
spray, IM, IV.
- Ergotamine:
Sublingual (for rapid absorption).
- Cafergot: Oral form that
combines ergotamine with caffeine to enhance GI absorption.
CI ergot
Allergy to ergot preparations (to prevent hypersensitivity reactions).
Coronary artery disease (CAD), hypertension, or peripheral vascular disease, as these conditions could be worsened by vasoconstriction.
Liver impairment, which may affect drug metabolism.
Pregnancy and lactation, as ergot derivatives may cause fetal harm or neonatal complications.
Ergotism (toxic effects in infants) has been reported, causing vomiting, diarrhea, and seizures.
Use with caution in:
- Pruritus, as vasoconstriction may worsen symptoms.
- Malnutrition, as these drugs stimulate the chemoreceptor trigger zone (CTZ), potentially causing severe GI reactions that exacerbate malnutrition.
AE ergots
CNS Effects: Numbness, tingling in extremities, muscle pain.
Cardiovascular (CV) Effects: Pulselessness, weakness, chest pain, arrhythmias, localized edema, MI.
Gastrointestinal (GI) Effects: Nausea, vomiting, diarrhea (due to CTZ stimulation).
Ergotism Syndrome: Nausea, vomiting, severe thirst, hypoperfusion, chest pain, blood pressure changes, confusion, drug dependency, and withdrawal syndrome.
DDI ergot
Ergot Derivatives + Beta- Blockers: Increased risk of peripheral ischemia and gangrene.
Ergot Derivatives + Triptans:
- Risk of severe
vasospasm, which can worsen cardiovascular complications.
- These drugs should not be taken together.
Nursing interventions Ergot
Assessment:
- Assess for contraindications, including CAD, hypertension, liver dysfunction, and pregnancy
- Monitor for complaints of extremity numbness and tingling, which may indicate vasoconstriction effects.
- Check cardiovascular status, including pulse, blood pressure, and ECG.
- Inspect for localized edema, itching, or skin breakdown, as vasoconstriction may impair circulation.
Interventions:
- Administer at the first sign of a migraine for best results.
- Monitor blood pressure closely in patients with a history
of cardiovascular disease.
- Avoid beta-blockers or triptans to prevent severe
vasospasm or ischemia.
- Educate patients on signs of ergotism (nausea, thirst,
confusion, chest pain) and when to seek medical attention.
- Ensure proper hydration and monitor for GI effects, as
nausea and vomiting may be severe.
Patient Teaching:
- Take medication at the onset of migraine symptoms to maximize effectiveness.
- Avoid taking ergot derivatives with beta-blockers or triptans due to the risk of severe vasoconstriction and ischemic complications.
- Report any numbness, tingling, or signs of cardiovascular distress (chest pain, weakness, severe headache) immediately.
- Do not use during pregnancy—discuss contraception options with healthcare providers.
- Monitor for signs of ergotism (nausea, vomiting, muscle pain, confusion).
Triptans MEDS
Almotriptan (generic)
Eletriptan (Relpax)
Frovatriptan (Frova)
Naratriptan (Amerge)
Rizatriptan (Maxalt, Maxalt-MLT) Sumatriptan (Imitrex)
Zolmitriptan (Zomig, Zomig-ZMT).
MOA triptans
Bind to selective serotonin receptor sites in cranial blood vessels, causing vasoconstriction.
Reduce neurogenic inflammation, which is involved in migraine pathology.
Do not have the extensive vascular and gastrointestinal effects of ergot derivatives.
Indications triptans
Acute migraine treatment (not for prevention).
Sumatriptan is also indicated for cluster headaches (subcutaneous route).
Naratriptan, rizatriptan, zolmitriptan, and eletriptan are for oral use in acute migraine relief.
Rizatriptan and zolmitriptan are available as fast- dissolving tablets.
Pharmacokinetics triptans
Rapidly absorbed from various administration routes.
Metabolized in the liver (sumatriptan by monoamine oxidase).
Excreted in the urine.
Cross the placenta and enter breast milk.
Half-life of Sumatriptan: 115 minutes.
CI to triptans
Allergy to triptans (to avoid hypersensitivity reactions).
Pregnancy, as triptans can cause vasoconstriction that may harm the fetus.
Active coronary artery disease (CAD) or angina, which may be worsened by the vasoconstrictive effects of triptans.
Use with caution in:
- Older adults (due to underlying vascular disease risks).
- Patients with risk factors for CAD.
- Patients with renal or hepatic dysfunction, as metabolism and excretion may be affected.
AE triptans
Central Nervous System (CNS): Numbness, tingling, dizziness, weakness, myalgia, vertigo.
Cardiovascular (CV): Blood pressure alterations, chest tightness or pressure.
Gastrointestinal (GI): Dysphagia, abdominal discomfort.
Injection site reactions (for sumatriptan subcutaneous administration).
DDI triptans
Triptans + Ergot Derivatives: Increased risk of prolonged vasoconstrictive reactions.
Triptans + Monoamine Oxidase Inhibitors (MAOIs): Risk of severe adverse effects—triptans should not be taken within 2 weeks of MAOI discontinuation.
Triptans + Selective Serotonin Reuptake Inhibitors (SSRIs) or Serotonergic Medications: Risk of serotonin syndrome, a potentially fatal condition.
Nursing interventions triptans
Assessment:
- Evaluate for CAD risk factors, hypertension, or prior cardiovascular disease before prescribing triptans.
- Monitor for numbness, tingling, dizziness, and signs of serotonin syndrome (agitation, hallucinations, tachycardia, hyperreflexia).
- Check renal and hepatic function before prescribing triptans.
Interventions:
- Administer at the onset of a migraine (not for prophylaxis).
- Avoid giving with ergot derivatives or MAOIs due to drug interactions.
- Monitor blood pressure closely, especially in patients with CAD risk.
- Provide environmental modifications (reduce noise, dim lights) to enhance drug effectiveness.
Patient Teaching:
- Take triptans at the first sign of a migraine.
- Fast-dissolving tablets should be placed on the tongue
and allowed to dissolve before swallowing.
- Do not take more than two doses in 24 hours.
- Avoid triptans if pregnant or planning pregnancy.
- Report chest pain, severe dizziness, or signs of serotonin
syndrome immediately.
Calcitonin Gene- Related Peptide (CGRP) Inhibitors and Serotonin Agonists - >MEDS
CGRP inhibitors:
Rimegepant (Nurtec ODT)
Ubrogepant (Ubrelvy)
(Monoclonal Antibodies): Eptinezumab-jjmr (Vyepti) Erenumab-aooe (Aimovig) Fremanezumab-vfrm (Ajovy) Galcanezumab-gnlm (Emgality)
Serotonin Agonist:
Lasmiditan (Reyvow).
MOA CGRP
CGRP Inhibitors:
CGRP is a potent vasodilator released during migraine attacks.
There are two types of CGRP inhibitors: - Gepants block CGRP receptors, treating acute migraines.
- Monoclonal antibodies target either the receptor or the CGRP peptide, used for migraine prevention.
Serotonin Agonist:
A highly selective serotonin receptor agonist for acute migraine treatment.
Less vasoconstriction compared to triptans, making it safer for patients with cardiovascular risks.
Indications CGRP
Gepants: Acute migraine treatment.
Monoclonal Antibodies:
Migraine prevention; galcanezumab also treats cluster headaches.
Serotonin Agonist:
Acute migraine treatment, with or without aura.
Pharmacokinetics CGRP
Gepants:
Oral/Sublingual administration, absorbed in 1.5 hours.
Metabolized partially in the liver, mostly excreted in bile and feces.
Monoclonal Antibodies: Injected subcutaneously or intravenously.
Long half-life (27– 31 days), allowing for less frequent dosing.
Serotonin Agonist:
Oral administration, absorbed in ~2 hours.
Metabolized inside and outside the liver, eliminated renally.
Half-life: ~6 hours.
CI to CGRP
Known allergy to CGRP inhibitors or serotonin agonists (risk of hypersensitivity).
Pregnancy: Lasmiditan and gepants may cause fetal harm (animal studies).
Monoclonal antibodies have not shown fetal harm but lack human data.
Use with caution in:
- Renal/hepatic dysfunction, which may affect drug metabolism.
- CNS disorders (lasmiditan
causes sedation).
AE CGRP
Gepants: Nausea, hypersensitivity reactions.
Monoclonal Antibodies: Injection site reactions, hypersensitivity reactions.
Serotonin Agonist: Dizziness, fatigue, paresthesia, sedation (Schedule V controlled substance).
DDI CGRP
Gepants:
- May inhibit Pgp or BCRP transporters avoid other drugs metabolized this way.
- CYP3A4 inducers/inhibitors affect metabolism, requiring dose adjustments.
Serotonin Agonist:
Avoid CNS depressants, heart rate-lowering medications, and serotonergic drugs (risk of increased adverse effects).
Nursing interventions CGRP
Assessment:
- Screen for allergies to prevent hypersensitivity reactions.
- Monitor CNS effects (dizziness, sedation) with
lasmiditan.
- Assess liver and kidney function, especially for gepants.
- Check for pregnancy status due to fetal risk with
lasmiditan and gepants.
Interventions:
- Ensure proper administration (oral/sublingual for gepants, injection for monoclonal antibodies).
- Monitor for injection site reactions with monoclonal antibodies.
- Avoid CNS depressants with lasmiditan to prevent excessive sedation.
- Educate about delayed onset of monoclonal antibody CGRP inhibitors, as they take time to work.
Patient Teaching:
- Take CGRP inhibitors as directed (daily for prevention, as needed for acute relief).
- Lasmiditan causes sedation—avoid driving for at least 8 hours after taking it.
- Report severe hypersensitivity reactions (rash, difficulty breathing, swelling).
- Do not use CGRP inhibitors or lasmiditan during pregnancy unless absolutely necessary.
