Medications for Pain: Chapters 33-36
36 Questions
0 Views

Choose a study mode

Play Quiz
Study Flashcards
Spaced Repetition
Chat to lesson

Podcast

Play an AI-generated podcast conversation about this lesson

Questions and Answers

What is the primary mechanism of action for triptans like sumatriptan in the treatment of migraines?

  • They block pain signals at the spinal cord level.
  • They promote vasodilation of cranial blood vessels.
  • They inhibit the production of calcitonin gene-related peptide.
  • They activate specific serotonin receptors in the brain. (correct)

    • Why should patients wait 24 hours after taking triptans before using ergot alkaloids?

  • To avoid gastrointestinal side effects.
  • To prevent potential vasospastic reactions. (correct)
  • To ensure effective management of headache symptoms.
  • To allow adequate elimination of the triptan.

    • What adverse effect is commonly associated with beta blockers like propranolol in migraine prevention?

  • Tiredness. (correct)
  • Insomnia.
  • Increased heart rate.
  • Increased blood pressure.

    • Which neurochemical is believed to suppress migraines?

    <p>Serotonin.</p> Signup and view all the answers

    What is a common method of administration for ergotamine?

    <p>Oral, sublingual, rectal, or inhalation.</p> Signup and view all the answers

    Which preventative therapy for migraines may result in cognitive dysfunction as a side effect?

    <p>Topiramate.</p> Signup and view all the answers

    In patients with coronary artery disease risk factors, the use of triptans is contraindicated due to the risk of what?

    <p>Coronary vasospasm.</p> Signup and view all the answers

    What pharmacokinetic property describes the metabolism of sumatriptan?

    <p>Metabolized primarily in the liver with a half-life of 2.5 hours.</p> Signup and view all the answers

    Which of the following is true regarding the pharmacokinetics of ergotamine?

    <p>Metabolized by CYP3A4.</p> Signup and view all the answers

    What is the primary action of mu receptors when activated by opioids?

    <p>Analgesia and respiratory depression</p> Signup and view all the answers

    Which class of opioids functions as agonists for kappa receptors and antagonists for mu receptors?

    <p>Agonist-antagonists</p> Signup and view all the answers

    Which of the following opioids is metabolized by CYP3A4?

    <p>Fentanyl</p> Signup and view all the answers

    What is the most serious adverse effect associated with strong opioid agonists like morphine?

    <p>Respiratory depression</p> Signup and view all the answers

    How do agonist-antagonist opioids primarily differ from pure agonists?

    <p>They have less potential for abuse.</p> Signup and view all the answers

    Which of the following is a common adverse effect associated with the use of opioid medications?

    <p>Orthostatic hypotension</p> Signup and view all the answers

    What is a key nursing goal when administering opioids to minimize physical dependence?

    <p>Switch to nonopioid analgesics as soon as feasible</p> Signup and view all the answers

    Which opioid medication is known for having its analgesic effect through metabolism to morphine?

    <p>Codeine</p> Signup and view all the answers

    What effect does naloxone have when administered to a person who is physically dependent on opioids?

    <p>Severe withdrawal symptoms</p> Signup and view all the answers

    Which of the following best describes the pharmacokinetics of morphine?

    <p>Variable onset depending on route of administration</p> Signup and view all the answers

    What distinguishes moderate-strong opioid agonists from strong opioid agonists?

    <p>They have a lower potential for abuse.</p> Signup and view all the answers

    What is a primary use for opioid antagonists like naloxone?

    <p>Reverse opioid overdose effects</p> Signup and view all the answers

    What common risk is associated with opioid administration, particularly with long-term use?

    <p>Development of tolerance</p> Signup and view all the answers

    What is the specific role of COX-2 in the body?

    <p>Promotes inflammation and pain</p> Signup and view all the answers

    Which of the following is an advantage of using Celecoxib over first-generation NSAIDs?

    <p>Lower risk of gastrointestinal problems</p> Signup and view all the answers

    Which of the following is a common adverse effect associated with the use of non-aspirin NSAIDs?

    <p>Gastric distress and bleeding</p> Signup and view all the answers

    How does aspirin pharmacokinetics affect its therapeutic use?

    <p>Aspirin is quickly converted to salicylic acid, its active metabolite</p> Signup and view all the answers

    Which medication is contraindicated for individuals with a known hypersensitivity to NSAIDs?

    <p>Aspirin</p> Signup and view all the answers

    What primary effect differentiates acetaminophen from NSAIDs?

    <p>Acetaminophen can reduce fever without anti-inflammatory effects</p> Signup and view all the answers

    Which of the following interactions can increase the risk of adverse effects when using NSAIDs?

    <p>Co-administration with other anticoagulants</p> Signup and view all the answers

    What is one key characteristic of ibuprofen compared to aspirin?

    <p>It does not prevent myocardial infarctions</p> Signup and view all the answers

    What condition can result from acute acetaminophen poisoning?

    <p>Acute liver failure</p> Signup and view all the answers

    Which of the following is a significant adverse effect associated with high doses of aspirin?

    <p>Gastric bleeding</p> Signup and view all the answers

    What is the potential complication for a pregnant woman using NSAIDs?

    <p>Adverse effects on both mother and fetus</p> Signup and view all the answers

    What is a distinguishing factor of naproxen compared to other NSAIDs?

    <p>Has a longer half-life allowing less frequent dosing</p> Signup and view all the answers

    How does regular alcohol consumption affect the metabolism of acetaminophen?

    <p>It depletes glutathione, increasing toxicity risk.</p> Signup and view all the answers

    Which of the following is a common symptom of salicylism syndrome?

    <p>Tinnitus</p> Signup and view all the answers

    Study Notes

    Medications for Pain

    • Covers chapters 33, 34, and 36

    Non-Opioid Analgesics (Chapter 33)

    • Two types of non-steroidal anti-inflammatory drugs (NSAIDs)
      • First generation (Classical):
        • Non-selective COX inhibitors
        • Aspirin
        • Ibuprofen
        • Naproxen
        • Inhibit COX-1 & COX-2
        • Increase risk of peptic ulcers
        • Increase risk of bleeding
      • Second-generation (NEW):
        • Selective COX-2 Inhibitors
        • Celecoxib
        • Decrease risk of peptic ulcers
        • Increase risk of clotting

    What is COX?

    • Cyclooxygenase, an enzyme
    • COX 1 & COX 2
    • Found in all tissues
    • Regulates multiple processes using prostaglandins
      • Stomach COX-1 protects gastric mucosa
      • Platelets COX-1 stimulates aggregation
      • Uterus COX-1 causes contractions for delivery
      • Kidney COX-1 & 2 maintain renal blood flow
      • Tissue injury COX-2 promotes inflammation & pain
      • Vessels COX-2 causes vasodilation
      • Brain COX-2 mediates fever & perception of pain
      • Colon COX-2 promotes colorectal cancer

    COX Inhibitors

    • Uses:
      • Mild-moderate pain
      • Inflammation
      • Fever
      • Pre-menstrual symptoms
      • Protection against colon cancer
    • Two major categories:
      • Anti-inflammatories
        • NSAIDs - aspirin, ibuprofen, naproxen, celecoxib
      • Non anti-inflammatories
        • Acetaminophen

    First Gen NSAID - Prototype: Aspirin (ASA)

    • Uses: reduction of pain, fever, inflammation, MI prevention
    • MOA: irreversibly inhibits COX-1 and COX-2
    • Pharmacokinetics:
      • Absorption: PO: plain, buffered, enteric-coated
      • Metabolism: Short T1/2, is quickly converted to salicylic acid (SA), an active metabolite. SA's T1/2 is concentration-dependent.
      • Distribution: SA is highly bound to albumin, crosses all membranes easily
      • Excretion: SA by kidneys; dependent on pH
    • Adverse Effects:
      • GI - gastric distress, bleeding, ulcers
      • General excessive bleeding
      • Renal impairment
      • Salicylism Syndrome
      • Hypersensitivity (Do not give ASA to children or pregnant women. Contraindicated in patients with: peptic ulcer disease, bleeding disorders, ASA/NSAID hypersensitivity)
    • Interactions:
      • Other anticoagulants (warfarin, heparin)
      • Alcohol
      • Other NSAIDs (antiplatelet effect)
    • Toxicities
      • Salicylism Syndrome (develops slowly as ASA levels climb above the therapeutic range, s/sx: tinnitus, sweating, headache, dizziness; withhold aspirin until s/sx resolve, then at a reduced dose)
      • Acute Poisoning (s/sx: respiratory alkalosis, respiratory depression, acidosis, hyperthermia, sweating, dehydration, stupor, coma; an acute medical emergency; death related to respiratory failure; treatment is supportive)

    First Gen NSAID - Ibuprofen (Advil, Motrin)

    • Non-aspirin NSAID
    • MOA: Reversible inhibition of COX-1 and COX-2
    • Uses are the same as aspirin except: does not prevent MIs/CVAs; may increase CV risk.
    • Good choice for dysmenorrhea; is selective for COX in the uterine muscle
    • Less gastric bleeding than aspirin
    • Risk of renal impairment

    First Gen NSAID - Naproxen (Aleve, Anaprox)

    • Another non-aspirin NSAID
    • Fairly selective for COX-1, less incidence of GI problems and MI/CVA than other non-ASA NSAIDs
    • T1/2 of 12-17 hours, allows less frequent dosing
    • Otherwise, same as ibuprofen

    Second Gen NSAID - Celecoxib (Celebrex)

    • MOA: inhibits COX-2 only
    • Uses: arthritis, acute pain, dysmenorrhea
    • Less GI problems than 1st-generation NSAIDs
    • Increased risk of MIs and CVAs, can impair kidneys
    • Use lowest effective dose for shortest possible time
    • Not a good option for patients with heart disease

    Non-Anti-Inflammatory - Acetaminophen (Tylenol)

    • Uses:

      • Analgesia (pain reliever)
      • Antipyretic (fever reducer), preferred for children
      • No anti-inflammatory effects

    • MOA: COX inhibition, thought to be limited to the CNS

    • Pharmacokinetics:

      • Absorption: PO, PR, IV

    • Metabolism: In the liver by two pathways: major and minor;

      • Major pathway: Acetaminophen converted directly into nontoxic metabolites
      • Minor pathway: CYP450 converts acetaminophen to a toxic metabolite; Glutathione required to then convert toxic metabolite to nontoxic metabolite

    • 24-hour max for acetaminophen in adults: 4g

    • Watch for acetaminophen in combo medications; Regular alcohol consumption reduces the liver's ability to metabolize excessive doses of acetaminophen

    • Acetaminophen Toxicity:

      • Cause of 50% of acute liver failures
      • Manifestations of liver injury (hepatic necrosis) appear 48-72 hours after overdose
      • Early s/sx: N/V/D, sweating, abdominal pain/discomfort are initial signs
      • Late s/sx: Hepatic failure, coma, death
      • Antidote: acetylcysteine (Mucomyst) It substitutes for glutathione; 100% effective if given within 8-10 hours

    Drugs for Headaches (Chapter 36)

    • Headaches are a very common complaint. Mild, occasional headaches are often improved by over-the-counter (OTC) medications.
    • Types of headaches:
      • Tension-type
      • Cluster
      • Migraine

    Tension-type Headaches

    • Most common type
    • "headband", non-throbbing pain, tightness in head & neck
    • Abortive: Ibuprofen, naproxen, aspirin-butalbital, acetaminophen
    • Preventative: coping & relaxation skills, amitriptyline

    Cluster Headaches

    • Less common, mostly in males
    • Occur in a series of cluster attacks
    • Lasts 15 min – 2 hrs
    • Unilateral pain near eye, lacrimation, ptosis, nasal congestion, rhinorrhea
    • Abortive: Oxygen, sumatriptan
    • Preventative: betamethasone, verapamil, lithium

    Migraine Headaches

    • Throbbing, moderate-severe pain that may be unilateral or bilateral
    • May last for days
    • Associated with nausea/vomiting, photo/phonophobia
    • Aura vs. no aura
    • More common & more severe in females
    • Very debilitating
    • Migraine Patho:
      • Neurovascular problem
      • Vasodilation & inflammation of the cranial blood vessels
      • Many possible triggers
      • Two neurochemicals are involved:
        • Calcitonin gene-related peptide - CGRP (causes migraines?)
        • Serotonin/5-HT (suppresses migraines?)

    Abortive Therapy: Triptans (serotonin receptor agonists)

    • Prototype: Sumatriptan
    • Uses: Migraines & cluster headaches
    • MOA: bind to and activate specific subtypes of serotonin receptors in the brain, causing vasoconstriction
    • Pharmacokinetics:
      • Absorption: PO, SQ, inhalation
      • Metabolism: hepatic, T 1/2 = 2.5 hours
      • Follow maximum dosing instructions
    • Adverse Effects:
      • 50% experience chest "heaviness” – this is not angina pectoris!
      • Coronary vasospasm - this IS angina pectoris!
      • increased risk in patients with CAD risk factors
      • Teratogen
      • Interactions: Ergot Alkaloids cause vasospasm (wait 24 hrs), SSRI/SNRI may cause excessive serotonin syndrome

    Abortive Therapy: Ergot Alkaloids

    • Prototype: Ergotamine
    • Uses: Migraines & cluster headaches
    • MOA – several possibilities: activation of serotonin receptors, blockage of cranial inflammation, cranial vasoconstriction
    • Pharmacokinetics:
      • Absorption: PO, SL, PR, or inhalation
      • best absorption/distribution with PR and inhalation
      • Metabolism by CYP3A4, T 1/2 = 2 hours
    • Adverse Effects:
      • Rare at therapeutic doses
      • Possible nausea/vomiting
      • Risk of dependence
      • Triptans cause vasospastic reactions (wait 24 hrs)
      • CYP3A4 Inhibitors raise levels to dangerous levels to cause vasospasm

    Migraines: Preventative Therapy

    • In patients who have frequent or severe migraines, ongoing medicine to prevent them may be necessary. Daily dosing
    • Three common options:
      • Beta Blockers - propranolol (May cause tiredness, may exacerbate asthma)
      • Antiepileptics - topiramate (May cause fatigue and cognitive dysfunction)
      • Tricyclic Antidepressant - amitriptyline (May cause hypotension and anticholinergic effects)

    Opioid Medications (Chapter 34)

    • Opioid Analgesics
      • Endogenous opioid peptides: found in the central nervous system (CNS) and in peripheral tissues; serve as neurotransmitters, neurohormones, and neuromodulators
      • Opioids: drugs that have actions similar to endogenous opioid peptides, based on morphine

    Opioid Receptors

    • Mu - activation causes analgesia (pain relief), respiratory depression, euphoria, sedation, decreased GI motility, and eventual physical dependence
    • Kappa - activation causes analgesia, sedation, and decreased GI motility
    • Delta - no significant effects

    Classifications of Opioid Drugs

    • Pure Agonists: agonists for Mu and Kappa receptors (morphine, fentanyl, codeine, meperidine (Demerol), etc)
    • Agonist-Antagonists: antagonist for Mu, agonist for Kappa receptors (Pentazocine (Talwin), nalbuphine (Nubain))
    • Pure Antagonists: antagonists for Mu and Kappa (Naloxone (Narcan), naltrexone)

    Strong Opioid Agonists

    • Common drugs: morphine, hydromorphone, fentanyl, meperidine (Demerol), heroin, methadone
    • Morphine is the prototype
    • MOA: mimics endogenous opioids, activating mu and kappa receptors
    • Clinical uses: relief of moderate to severe pain (postoperative, cancer-related, labor/delivery, Mls)

    Strong Opioid Agonist: morphine

    • Pharmacokinetics/Distribution: can be given practically any route; onset and duration differ; small amount crosses BBB, best with scheduled administration depending on pain severity

    • Metabolism: affected by first-pass effect, liver inactivation

    • Adverse Effects:

      • Respiratory depression
      • Constipation (common)
      • Orthostatic hypotension
      • Urinary retention
      • Nausea/vomiting
      • Cough suppression
      • Toxicity: coma, respiratory depression, pinpoint

    • Drug Interactions

      • other CNS depressants
      • Anticholinergics
      • Antihypertensives
      • Agonist-antagonists
      • Antagonists

    • Physical Dependence

    • Intensity and duration of withdrawal syndrome depend on T 1/2 and degree of dependence on drug

    • Morphine short half-life means withdrawal is intense (7-10 days)

    • Initial reactions include yawning, rhinorrhea, sweating

    • Anorexia, irritability, tremor, gooseflesh, violent sneezing, N/V/D, abd cramping, bone & muscle pain, kicking movts

    Strong Opioid Agonist: fentanyl (Duragesic)

    • Strong opioid, about 100x more potent than morphine
    • Parenteral administration: for induction and maintenance of anesthesia
    • Transdermal administration: for persistent severe pain; usually reserved for patients tolerant
    • Metabolism: hepatic, by CYP3A4
    • Adverse effects same as morphine

    Moderate-Strong Opioid Agonists

    • Examples: codeine, oxycodone, hydrocodone
    • MOA is same as strong opioid agonists
    • Main difference: less analgesia and respiratory depression; less abuse potential than strong agonists
    • Many are co-formulated with APAP

    Moderate-Strong Agonist: Codeine

    • Uses: relief of mild to moderate pain, often co-formulated with acetaminophen; cough suppressant
    • Pharmacokinetics/Metabolism:
      • Absorption: PO most common method
      • Metabolism: liver metabolizes 10% of codeine to morphine
    • Adverse Effects: similar to morphine, increases with higher dosages, high dosages required for significant pain relief = dangerous side effects

    Agonist-Antagonist Opioids

    • Activate kappa receptors and block mu receptors
    • Provide analgesia without as many side effects as pure agonists
    • Less potential for abuse
    • If used to replace a long-term opioid agonist, could cause withdrawal symptoms

    Agonist-Antagonist: Pentazocine (Talwin)

    • MOA: Activates kappa receptors causing analgesia, sedation, and limited respiratory depression
    • Pharmacokinetics:
      • Absorption: PO administration
      • Metabolism: short T1/2; frequent dosing
    • Adverse Effects: many similar to morphine, but less respiratory depression; Increases cardiac workload; not a good choice for pain related to myocardial infarction
    • Physical dependence can develop but withdrawal is mild compared to pure opioid agonists

    Opioid Antagonists

    • MOA: block the opioid receptors
    • Uses: reversal of opioid overdose, relief of opioid-related constipation, and treatment of opioid addiction
    • No effect on their own; only used in combination with an opioid agonist

    Opioid Antagonist: Naloxone (Narcan)

    • Pharmacokinetics: 
      • Absorption highly affected by first-pass effect
    • given parenterally or intranasally
    • longer effects when given IM/SC
    • Metabolism: hepatic, T1/2 about hours
    • Adverse Effects: None on its own; if given to a person physically dependent on opioids, will cause immediate/severe withdrawal problems

    The Opioid Epidemic- Nursing Considerations

    • Nursing goals to minimize physical dependence and abuse of opioids
    • Assess pain and dosage sufficient to relieve pain
    • Administer lowest effective dose for shortest time needed
    • As pain diminishes, opioid dosages should be reduced
    • Switch patient to nonopioid analgesic as soon as possible

    Studying That Suits You

    Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

    Quiz Team

    Related Documents

    Medications for Pain, COX & Opioids, Headaches PDF

    Description

    This quiz covers key concepts from chapters 33, 34, and 36 regarding medications used for pain management. Focus is on non-opioid analgesics, including both first and second-generation NSAIDs and the role of cyclooxygenase enzymes. Test your knowledge on the benefits and risks associated with these medications.

    More Like This

    Use Quizgecko on...
    Browser
    Open
    Browser
    Browser