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Unit III: The Nervous System

Review: Drug-Receptor Interactions. What is a receptor?Drugs bind to receptor and cause specific activity of cell to be either enhances or inhibited.What is:An AgonistA Partial AgonistAn Antagonist. Pain Management. What is essential to successfully manage pain?What does pain management therapy depend upon? Describe a comprehensive pain assessment.How is pain classified?.

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Unit III: The Nervous System

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    1. Unit III: The Nervous System Chapter 18 Drugs for Control of Pain

    2. Review: Drug-Receptor Interactions What is a receptor? Drugs bind to receptor and cause specific activity of cell to be either enhances or inhibited. What is: An Agonist A Partial Agonist An Antagonist Receptor: “cellular macromolecule to which a medication binds to initiate its effect” ; most are proteins; drugs attach in a specific manner (lock and key) Bound drugs can either directly enhance or inhibit a cell or may initiate a second messenger event which will start a biochemical cascade which will initiate the drug action by stimulating or inhibiting normal cell activity. Agonist: same response as endogenous substance; stimulates a particular receptor Partial agonist: produces weaker, or less efficacious response that an agonist Antagonist: prevents endogenous chemical from acting; blocks receptorsReceptor: “cellular macromolecule to which a medication binds to initiate its effect” ; most are proteins; drugs attach in a specific manner (lock and key) Bound drugs can either directly enhance or inhibit a cell or may initiate a second messenger event which will start a biochemical cascade which will initiate the drug action by stimulating or inhibiting normal cell activity. Agonist: same response as endogenous substance; stimulates a particular receptor Partial agonist: produces weaker, or less efficacious response that an agonist Antagonist: prevents endogenous chemical from acting; blocks receptors

    3. Pain Management What is essential to successfully manage pain? What does pain management therapy depend upon? Describe a comprehensive pain assessment. How is pain classified? To successfully manage pain Must accurately assess the degree of pain experienced and the potential underlying disorders that may be causing pain Therapy is dependent upon: nature and character of pain Comprehensive pain assessment includes: Onset and duration Location Intensity Quality Relief measures (facilitating factors) Contributing symptoms (precipitating factors) Effects of pain on client Client expectations Classifications: Acute vs. Chronic Nociceptor vs. neuropathic Other sources include cancer pain or idiopathic pain To successfully manage pain Must accurately assess the degree of pain experienced and the potential underlying disorders that may be causing pain Therapy is dependent upon: nature and character of pain Comprehensive pain assessment includes: Onset and duration Location Intensity Quality Relief measures (facilitating factors) Contributing symptoms (precipitating factors) Effects of pain on client Client expectations Classifications: Acute vs. Chronic Nociceptor vs. neuropathic Other sources include cancer pain or idiopathic pain

    4. Compare and Contrast Nociceptor Pain and Neuropathic Pain Nociceptor Injury to tissues Somatic: sharp, localized sensations Visceral : generalized, dull, throbbing or aching Responds well to conventional pain relief medications Neuropathic Injury to nerves Burning, shooting or numb Less therapeutic response to conventional pain relief medications

    5. Nonpharmacologic Techniques May replace or be an adjunct to pharmacotherapy How does the concurrent use of nonpharmacologic therapies impact pharmacotherapy? Impact– may allow for lower medication doses and possibly fewer side effects Impact– may allow for lower medication doses and possibly fewer side effects

    6. Neural Mechanism of Pain Pain receptor (nociceptor) is stimulated Nerve impulse signaling pain is sent to spinal cord along Ad (myelinated, signal sharp, well-defined pain) and C (unmyelinated, conduct dull, poorly localized pain) fibers Neurotransmitters pass message along to next neuron Opioids (enkephalins, dynorphins, endorphins) Serotonic Norepinephrine Descending neurotransmitters have an inhibitory effect and modify sensory information at level of spinal cord This process of the pain signal beginning at nociceptors within the peripheral tissues and proceeding to the CNS allows several opportunities (targets) for pharmacologic intervention Pain receptor (nociceptor) is stimulated Nerve impulse signaling pain is sent to spinal cord along Ad (myelinated, signal sharp, well-defined pain) and C (unmyelinated, conduct dull, poorly localized pain) fibers Neurotransmitters pass message along to next neuron Opioids (enkephalins, dynorphins, endorphins) Serotonic Norepinephrine Descending neurotransmitters have an inhibitory effect and modify sensory information at level of spinal cord This process of the pain signal beginning at nociceptors within the peripheral tissues and proceeding to the CNS allows several opportunities (targets) for pharmacologic intervention

    7. Analgesics Classes of Pain Medications NSAIDs Opioids Action results from interaction with receptors Mu-1 and Mu-2 Kappa Sigma Delta Epsilon Non-steroidal anti-inflammatory drugs: Aspirin and Ibuprophen Opioids- natural (opiates) or synthetic morphine-like substances; aka: narcotics The mu and kappa receptors are most important to pain management Non-steroidal anti-inflammatory drugs: Aspirin and Ibuprophen Opioids- natural (opiates) or synthetic morphine-like substances; aka: narcotics The mu and kappa receptors are most important to pain management

    8. Compare and Contrast Responses Mu Analgesia Decreased GI motility Euphoria Physical dependence Respiratory depression Sedation Kappa Analgesia Decreased GI motility Miosis Sedation Miosis: constriction of the pupil secondary to contraction of the iris What is similar? Both cause analgesia, decreased gi motility, and sedation What is different? Kappa causes miosis and doesn’t cause euphoria, physical dependence, or respiratory depression Mu does not cause miosisMiosis: constriction of the pupil secondary to contraction of the iris What is similar? Both cause analgesia, decreased gi motility, and sedation What is different? Kappa causes miosis and doesn’t cause euphoria, physical dependence, or respiratory depression Mu does not cause miosis

    9. Prototype Opioid: Morphine See box on page 228 Produces analgesia, cough suppression and decreased GI motility CNS depressant Adverse effects Respiratory depression Sedation Nausea and vomiting CNS effect: Sedation Euphoria Intense relaxation Euphoria and relaxation are key reasons the drug is abusedCNS effect: Sedation Euphoria Intense relaxation Euphoria and relaxation are key reasons the drug is abused

    10. Risk of Dependence All narcotic (opioid) analgesics have the potential to cause physical and psychological dependence. What factors increase the likelihood of developing dependence Factors Larger doses over extended period of timeFactors Larger doses over extended period of time

    11. Case Study Mr. J, a 56-year-old, had an inguinal hernia repair through ambulatory surgery. His discharge medications included Vicodin (hydrocodone 5 mg and acetaminophen 500 mg) one or two tablets every 4 hours prn. What is the drug classification for this medication? Analgesic: opioid and non-opioidAnalgesic: opioid and non-opioid

    12. Combination Drugs Opioid + non-opioid (non-narcotic) analgesics What is the reason to combine these medications? What are the benefits of combined analgesics? Reasons: Together they have a synergistic effect (one substance augments or adds to the activity of the other) Benefits: Can use a lower dose of the narcotic and avoid dependence and avoid or decrease opioid related side effects Reasons: Together they have a synergistic effect (one substance augments or adds to the activity of the other) Benefits: Can use a lower dose of the narcotic and avoid dependence and avoid or decrease opioid related side effects

    13. Nursing Considerations: Opioids Carefully monitor client’s condition Provide education as it relates to the prescribed drug treatment Assess current and past history Diagnostics Baseline and continuing VS Comprehensive pain assessment before administration Assess for presence or history of: Severe respiratory disorders Increased ICP Seizures Liver or renal disease Allergies Current meds (especially alcohol and CNS depressants) Diagnostics: CBC LFT– ALT, AST, Amylase, bilirubin RFT VS: monitoring for respiratory depression cause by mu receptor activation; monitor for decreased LOC Assess for presence or history of: Severe respiratory disorders Increased ICP Seizures Liver or renal disease Allergies Current meds (especially alcohol and CNS depressants) Diagnostics: CBC LFT– ALT, AST, Amylase, bilirubin RFT VS: monitoring for respiratory depression cause by mu receptor activation; monitor for decreased LOC

    14. Nursing Considerations: Opioids Have narcotic antagonist and resuscitative equipment available Ensure safety Monitor for urinary retention Can cause constipation and Nausea/Vomiting Do not administer in infectious diarrheal illnesses Narcotic antagonist: naloxone hydrochloride (Narcan) Safety: bed in low position, side rails up Closely monitor I&O and check for bladder distention Will need to institute measures to prevent or treat constipation Antiemetics can be used to treat n/v GI pathogens produce toxins which are shed in the stool, constipation or decreased gi motility would cause the toxins to build up Narcotic antagonist: naloxone hydrochloride (Narcan) Safety: bed in low position, side rails up Closely monitor I&O and check for bladder distention Will need to institute measures to prevent or treat constipation Antiemetics can be used to treat n/v GI pathogens produce toxins which are shed in the stool, constipation or decreased gi motility would cause the toxins to build up

    15. Contraindications: Opioids Hypersensitivity Do not administer if: Acute asthma or upper respiratory obstruction Respiratory rate < 12

    16. Case Study Miss N, 86-years-old, weighs 96 lbs. They physician has ordered 10 mg of morphine sulfate IM for acute abdominal pain. Your are familiar with the drug and know that the ED50 is 10 mg. Miss N’s VS are: 98.6°- 80 – 22, 120/80. Thirty minutes after administering the medication you return to evaluate its effectiveness. You note that Miss N had a decrease in LOC and VS are 98.6° - 68 – 8, 112/60.

    17. Case Study Questions What will you do first? What other things must be done? Was a medication error made? What factors may have contributed to Miss N’s response? First: Stimulate breathing Prepare to administer naloxone (Narcan)– opioid antagonist to block opioid activity and reverse symptoms of opioid toxicity or overdose Other things: Closely monitor respiratory status Be prepared to initiate resuscitation Error? The order was for 10 mg which is the standard dose Contributing factors: Age and weight of the patient Renal and hepatic function may have been impaired She was outside the 50% who respond to the standard (ED50) dose First: Stimulate breathing Prepare to administer naloxone (Narcan)– opioid antagonist to block opioid activity and reverse symptoms of opioid toxicity or overdose Other things: Closely monitor respiratory status Be prepared to initiate resuscitation Error? The order was for 10 mg which is the standard dose Contributing factors: Age and weight of the patient Renal and hepatic function may have been impaired She was outside the 50% who respond to the standard (ED50) dose

    18. Nursing Role: Opioid Antagonist Therapy Carefully monitor patient condition Provide education as it relates to prescribed drug treatment Administer if RR < 10 Have resuscitative equipment immediately accessible Gather good medical history Underlying cardiovascular disease

    19. Nursing Role: Opioid Antagonist Therapy Use cautiously in patients physically dependent upon opioids Comprehensive pain assessment before administration and during treatment VS every 3-5 minutes ABGs, ECG Monitor for drowsiness, tremors, hyperventilation, VT and loss of analgesia Opioid dependent patients will experience more severe opioid withdrawal symptoms after receiving an opioid antagonist Monitor for s/s of opioid withdrawal: cramping, vomiting, HTN, anxietyOpioid dependent patients will experience more severe opioid withdrawal symptoms after receiving an opioid antagonist Monitor for s/s of opioid withdrawal: cramping, vomiting, HTN, anxiety

    20. Opioid Antagonist Drugs Prototype: naloxone hydrochloride (Narcan) See box p. 231 Naltrexone Used for treatment of addiction Monitor for side effects during RX VS q 3 – 5 min Continuous assessment of respiratory and cardiac function Side effects: (opioid withdrawal s/s)- increased thirst, chills, fever, joint/muscle pain, CNS stimulation, drowsiness, dizziness, confusion, seizures, headache, n/v, diarrrhea, rash, tachycardia, tachypnea, pulmonary edema, wheezing)Side effects: (opioid withdrawal s/s)- increased thirst, chills, fever, joint/muscle pain, CNS stimulation, drowsiness, dizziness, confusion, seizures, headache, n/v, diarrrhea, rash, tachycardia, tachypnea, pulmonary edema, wheezing)

    21. Compare and Contrast Opioid Tolerance and Opioid Dependence How is opioid dependence treated? Tolerance: biologic condition; body adapts to substance after repeated administration Over time higher doses are required to produce the same initial effect Common for substances that affect the CNS Natural consequence, not evidence of addiction Dependence: When a person has an overwhelming desire to take a drug and cannot stop Higher and more frequent doses quickly cause physical dependence As an individual develops tolerance, dosages will be increased in amount and frequency and physical dependence is more likely Treatment: Methadone (Dolophine) maintenance Does not cure dependence Must continue drug to avoid withdrawal symptoms Allows individual to return to productive work and social relationships Tolerance: biologic condition; body adapts to substance after repeated administration Over time higher doses are required to produce the same initial effect Common for substances that affect the CNS Natural consequence, not evidence of addiction Dependence: When a person has an overwhelming desire to take a drug and cannot stop Higher and more frequent doses quickly cause physical dependence As an individual develops tolerance, dosages will be increased in amount and frequency and physical dependence is more likely Treatment: Methadone (Dolophine) maintenance Does not cure dependence Must continue drug to avoid withdrawal symptoms Allows individual to return to productive work and social relationships

    22. Non-opioid Analgesics Acetaminophen NSAIDs Ibuprofen and ibuprofen type Salicylates: ASA Centrally acting agents Clonidine (Catapres) Tramadol (Ultram) Acetaminophen– analgesic and anti-pyretic, not an anti-inflammatory; Prototype- see box p 479 Ibuprofen Analgesic, anti-inflammatory, and anti-pyretic activity Inhibit cyclooxygenase (enzyme responsible for formation of prostaglandins) Less effect on COX-1 so produces less gastric bleeding Drug of choice for mild to moderate pain (esp. pain associated with inflammation) Inhibit pain mediators at nociceptor level (peripheral)– figure 18.3. p. 234 Long term use can reduce renal function (damages nephrons) Tissue damage occurs Chemical mediators are released (histamine, potassium ions, hydrogen ions, bradykinin, and prostaglandins) Bradykinins are associated with sensory impulse of pain and prostaglandins induce pain through formation of free radicals Salicylates ASA is prototype, see box p. 235 Inhibits both COX-1 and COX-2– so is more likely to cause peptic ulcer and GI bleeding and Acute renal failureAcetaminophen– analgesic and anti-pyretic, not an anti-inflammatory; Prototype- see box p 479 Ibuprofen Analgesic, anti-inflammatory, and anti-pyretic activity Inhibit cyclooxygenase (enzyme responsible for formation of prostaglandins) Less effect on COX-1 so produces less gastric bleeding Drug of choice for mild to moderate pain (esp. pain associated with inflammation) Inhibit pain mediators at nociceptor level (peripheral)– figure 18.3. p. 234 Long term use can reduce renal function (damages nephrons) Tissue damage occurs Chemical mediators are released (histamine, potassium ions, hydrogen ions, bradykinin, and prostaglandins) Bradykinins are associated with sensory impulse of pain and prostaglandins induce pain through formation of free radicals Salicylates ASA is prototype, see box p. 235 Inhibits both COX-1 and COX-2– so is more likely to cause peptic ulcer and GI bleeding and Acute renal failure

    23. Nursing Role: Non-opioid Analgesics Thorough assessment Monitoring Diagnostics Baseline and continuing comprehensive pain assessment Give with food and plenty of fluids Do not crush enteric coated tablets Use extreme caution with ASA in children and teenagers Assess for presence or history of: Hypersensitivity Bleeding disorders Peptic ulcer disease Severe renal/hepatic disease Pregnancy Monitor for: Nephrotoxicity Blood dyscrasias Hepatitis Allergic response n/v; anorexia; dizziness; drowsiness Diagnostics: (assess before and during pharmacotherapy) RFTs- BUN, creatinine LFTs- AST, ALT Hemoglobin ASA: Implicated in development of Reye’s syndrome Toxicity can develop rapidly in febrile and dehydrated children Assess for presence or history of: Hypersensitivity Bleeding disorders Peptic ulcer disease Severe renal/hepatic disease Pregnancy Monitor for: Nephrotoxicity Blood dyscrasias Hepatitis Allergic response n/v; anorexia; dizziness; drowsiness Diagnostics: (assess before and during pharmacotherapy) RFTs- BUN, creatinine LFTs- AST, ALT Hemoglobin ASA: Implicated in development of Reye’s syndrome Toxicity can develop rapidly in febrile and dehydrated children

    24. Headaches Two major types: Tension Migraine Migraine treatment goals: Stop migraine in progress Prevent migraine from occuring Tension: Self-limiting Treated with OTC analgesics Migraine: Painful headache caused by dilation of intracranial vessels Accompanied by n/v Sometimes preceded by aura Often associated with triggers Tension: Self-limiting Treated with OTC analgesics Migraine: Painful headache caused by dilation of intracranial vessels Accompanied by n/v Sometimes preceded by aura Often associated with triggers

    25. Migraine Treatment Triptans Ergot alkaloids Ergot alkaloids are a Category X drug. What does that mean? Triptans and ergot alkaloids are serotonin agonists To terminate migraine: Start with OTC acetaminophen or NSAIDs If unable to abort– triptans (sumatriptan {Imitrex}) If unresponsive to triptans– ergot alkaloids Category X: Teratogenic; harmful to fetus, do not use in pregnancy Triptans and ergot alkaloids are serotonin agonists To terminate migraine: Start with OTC acetaminophen or NSAIDs If unable to abort– triptans (sumatriptan {Imitrex}) If unresponsive to triptans– ergot alkaloids Category X: Teratogenic; harmful to fetus, do not use in pregnancy

    26. Migraine Prophylaxis Will be used if person has high incidence of migraines and is unresponsive to drugs to abort migraine. Beta blocker Propranolol (Inderal) Tricyclic antidepressant Amitriptyline hydrochloride (Elavil) Amitriptyline is drug of choice if accompanying mood disorder and insomnia Table 18.4, p. 238 May also prescribe calcium channel blocker, or depakote (antiseizure medication)Amitriptyline is drug of choice if accompanying mood disorder and insomnia Table 18.4, p. 238 May also prescribe calcium channel blocker, or depakote (antiseizure medication)

    27. Role of Nurse: Migraine Pharmacotherapy Carefully monitor client’s condition Provide education as it related to prescribed drug treatment Gather data Assess Alter environment Monitor for possible side effects Gather data: Frequency and intensity Presence or history of: MI, angina, HTN, renal or liver disease, diabetes, pregnancy Assess: Apical pulse, RR, BP Stress level and coping Hypersensitivity Use of MAOIs, SSRIs (can increase effect of triptans) Neuro status (LOC, blurred vision, n/v, tingling in extremities Provide: Quiet, calm environment with decreased noise and subdued lighting Limit disruptions Decrease neural stimulation Cold packs Side effects: Dizziness, drowsiness, vasoconstriction, warming sensation, tingling, light headedness, weakness, neck stiffness Gather data: Frequency and intensity Presence or history of: MI, angina, HTN, renal or liver disease, diabetes, pregnancy Assess: Apical pulse, RR, BP Stress level and coping Hypersensitivity Use of MAOIs, SSRIs (can increase effect of triptans) Neuro status (LOC, blurred vision, n/v, tingling in extremities Provide: Quiet, calm environment with decreased noise and subdued lighting Limit disruptions Decrease neural stimulation Cold packs Side effects: Dizziness, drowsiness, vasoconstriction, warming sensation, tingling, light headedness, weakness, neck stiffness

    28. Contraindications to Anti-migraine Therapy Hypertension Myocardial ischemia Coronary artery disease History of MI Dysrhythmias or heart failure High-risk CAD profile Diabetes Ergot alkaloids Promote vasoconstriction Side effects include: n/v, weakness in legs, myalgia, numbness and tingling in fingers and toes, angina-like pain, tachycardia Toxicity is evidenced by peripheral artery constriction (cold, pale and numb extremity with muscle pain) Long term use can cause physical dependenceErgot alkaloids Promote vasoconstriction Side effects include: n/v, weakness in legs, myalgia, numbness and tingling in fingers and toes, angina-like pain, tachycardia Toxicity is evidenced by peripheral artery constriction (cold, pale and numb extremity with muscle pain) Long term use can cause physical dependence

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