Module 8/N110

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Module 8/N110
2011-10-23 01:51:35
30 Wilk 28 29 Lehne

Pain management, Opioid analgesics
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  1. CLassification of Pain?
    • Origin of pain
    • Cause
    • Duration
    • Quality of pain
  2. Origin of pain
    • refers to the site where paoin is felt, and not necessarily the source of pain.
    • Superficial pain (cutaneous): damage to sup. tissue. Injuri is super. it can cause significant short-term pain.
    • Visceral pain: stimulation of deep internal receptors. In abdominal cavity, cranium or thorax. Can be local, achy discomfort to more wide spread, intermittent(vremennaya, nepostoyanaya), and crampy pain. Ex. menses cramps, labor pain, gastric infec, bowel disordes, organ cancers
    • Deep Somatic pain: originates in the ligaments, tendons, nerves, blood vessels, and bones. More diffuse and lasts longer. ex. fracture, sprain, arthritis, bone cancer.
    • Radiating pain: starts at the origin but extends to other locations.
    • Referred: occurs in an area that is distant from the original site. ex. during heart attack the pain felt in the arm, jaw.
    • Phantom: pain percieved to originate from an area thathas been surgically removed.
    • Psychogenic: pain that is believed to arise from the mind. Can be as sever as from a phisical cause.
  3. Cause of pain
    • 2 types of cause of phisical pain that differ in the way they affect the patient and how they are treated.
    • Nociceptive pain: most common type. Nociceptors(pain receptors) respond to stimuli that arepotentially damaging ex. result of noxious thermal, chemical or mechanical types of injury, in trauma, surgery, or inflmation. 2 types: visceral and somatic.
    • Neuropathic pain: Complex and often chronic. Pain results from when injury to one or more nerves results in repeated transmission of pain signals even in the absence of painful stimuli. ex. diabees, stroke, tumor, viral infection. Prescribed neuropathic pain meds. Described as burning, numbness, itching, "pins and needles" prichkling pain.
  4. Duration of Pain
    • Acute pain: Lasts up to 6 months
    • releved when its cause is identified and treated
    • Mild to severe
    • Fight or flights raction
    • Behaviors - restless, anxious, crying, rubbing/holding area
    • Client verbalizes pain
    • Chronic pain: lasts more than 6 months -pain continues beyond normal healing and ore exists without pathylogy to explain it
    • Can be progressive
    • Mild to severe
    • Vital signs normal
    • Onset can be gradual
    • May not report pain
    • Maybe difficult to describe
    • Behavior may not show pain
    • Intractable pain: is chronic and highly resistant to relief.
  5. Qulity of pain
    sharp, dull, aching, throbbing, stabbing, burnin, ripping, searing or tingling, cramping. Episodic, intermittent, constant. Intensity - mild, distracting, moderate, sever intolerable.
  6. Physiology of Pain
    • Transduction: activation of nocicepors by stimuli to mechanical, thermal and chemical potential damaging. Mechanical - phisical damage, frictions, surgical insicions, pressure. Thermal stimuli - from esposure to estreme heat or cold. Chemical - internal or external. ex. external - lemon juice on an open area on a skin. Internal - a chemical changes that happen in the body for ex. during myocardial infarction.
    • Transmission: pain massages are conducted to the spinal cord along iether of two types of fibers:
    • A-delta: fast pain impulses from mechanical and thermal stimuli.Pleasurable stimuli to skin recepors, such as from massage, also stimulate A-delta fiber.
    • C fibers: unmyulinate fibers trasmit slow pain impulses , dull, diffuse pain impulses from mechanical, thermal and chemical stimuli. Lingering(prodolzhitel'naya) pain from pumped knee
  7. What is perception and misperceptions of the clients' pain experience?
    • Perception: involves the recognition and definition of paoin in the forntal cortex.
    • Pain threshold: it is the point at which the brain recognizes and defines a stimulus as pain. The lowest intensity at which a person can percieve Repeated experience wih pain can reduce a patient's threshold.
    • Pain tolerance: is the duration or intesity of pain that a person is willing to endure(terpet'). Extreme sensitivity to pain - hyperalgesia
    • Modulation process: changes the perception of pain by either facilitating or inhibiting pain signals. 2 Mechanisms:
    • Endogenous alnalgesia system: when a pain is recived in the brain, than brain sends back impulses that trigger the relseas of endogenous opiods which are blocking the continuing pain impulses and provide pain relief. Endogenous opiods are naturally occuring analgesic neutroasmitters tha inhibit the transmission of pain impulses. They are enkephalisn, dynorphins, beta endorpihns. These opiods bind to opiate receptor sites in the central and peripheral nervous sytem at receptor sites, sedignated as mu and kappa. These sites are also invloved in reception when patients take pain medicines.
    • Gate control theory: Two impulses cannot occupy the same nurve. pain that travels along slow fibers C fibers go through open gates to rich the brain, when the source of pain is stimulated by touch the gate to pain closes and opens to sensation of touch.
  8. Components of nonverbal inidactor of pain
    • Faciale expressions
    • Vocalizations - nosy braething, profanity(rugatel'stvo) verbaly abusive language
    • Change in physical activity - disruptive behavior
    • CHnages in routines
    • Mental status changes
    • Physiological cues include elevated blood pressure, respiraiton, and pulse
    • Absence of cues dose not mean that pain is absent
    • Use direct question - close-ended
  9. Why pain should be the fifth vital sign?
    To raise awareness of pain and emphasize pain relief.
  10. Principles of effective pain management
    • Believe the subjective reportof pain
    • Obtaning apain hisotry: Onset, location, aggravating/alleviating factors.
    • Identify any knowledge deficits: fear of addciton, any other fears and beliefs that can interfear with affective pain management
    • Focused assessment
    • Actively listen to the patient's report of pain
    • Support the patient in maintaning an active role in treatment by including her as paor ot the pain management team
    • Provide prescribed analgesics promptly
    • Assess for response to analgesics and nonpharmocological measure, including level of sedation.
    • Alter the treatment if pain is not adequatly relieved.
    • Reduce anxiety and fear by offering explanations about care and medications.
    • Assess nonverbal signs of pain
    • Use pain scales
  11. Non-pharmocological intervention for pain (pg.736 in Wilk 1)
    • Cutaneous Stimulation: works best on pain that is localized and not diffuse
    • Prescribe cutaneous stimulations: TENS - transcutaneous nerve stimulator. Acupancture - stimulates endogenouse alagesia system. Chiropractic
    • Others: massage, heat/cold, change positions
    • Cognitive-Behavioral Interventions: attempts to alter patterns of negative thoughts and to encourage more adaptive thoughts, emotions, and actions. Used to dicrease depression and anxiety
    • Distructions
    • Relaxation
    • Guided Imagery
    • Deep breathing
    • Pacing
  12. Pharmocological intervension of pain
    • (1) Non-narcotic analgesics (aspirin, Tylenol, NSAIDS-nonsteroidla anti-inflammatory drugs ex. asprin and ibeprofen)
    • (a) Used for mild to moderate pain and for acute or chronic pain.
    • (b) Works best on muscle and joint pain.
    • (c) Produces analgesia at the peripheral nervous system.
    • (d) Major Side-effects - Nausea, vomiting, increased bleeding tendencies.
    • (2) Narcotic analgesic (morphine, codiene, demerol)
    • (a) Used for severe pain.
    • (b) In sufficient dose, considered capable of relieving pain, in most cases
    • (c) Analgesia produced at the entral nervous system
    • (d) Major side-effect - nausea, vomitting, constipation, drawsiness.Large doses - resp. depression and hypotension.
    • (3) Other medications (antidepressants, anticonvulsants)
    • (a) Used usually in combination with opioids especially when there is a neurologic component as one of the causes of the pain.
    • (b) Mechanism of action not clearly understood, may block pain transmission or may suppress abnormal nerve endings from injury to nerve tissue (anticonvulsant).
    • natural and synthetic compounds that relieve pain.Find pain receptor sites to bind with and block the pain impulse.- mimics actions of endogenous opiods in body.
    • Mu agonists stimulate mu receptors and are used for acute, chronic, and cancer pain. Codeine, mophine, delaudid, fentanyl, methadone oxycodone. No maximum daily dose limit. Rapid onset and short duration.
    • Agonist-antagonists: stimulate some opioid receptors but block others. Mixed. For moderate to sever acute pain. Should not be in combo with mu agonists
    • Opioids are most effective for visceral pain and not for neurological.
  14. PCA
    • Patient Controlled Analgesia - pump are effective and safe way to deliver opiods by IV. epudural or subcutaneous routes.
    • Morphine usualy used
  15. Adjuvant Analgesics
    • used for mild pain or in conjuction with opioids. Reduces amount of opioi he patient requieres.
    • Drugs are: anticonvulsants, antidepressants, local anesthetics, topical agents, psychostimulants, muscle relaxants, neuroleptics, corticosteroids.
    • Used to manage neuropathic pain.
  16. Differentiate between opioids and narcotics
    • Opioid: is a general term defined as any drug, naturalor syntehtic, that has actions similar to those of mophine. Mimics actions of endogenoous opioids of our body
    • Narcotic: has been used to mean an analgesic, a CNS depresant, any drug capable of causing physical dependence. Alos referd as a drug such as cocaine, marijuana...
  17. Classes of opioid reseptor sites
    • Opioidanalgesics act primarily by activating mu receptors, although they also produce wake acivation of kappa receptors. Opioid analgesics do not interact with delta receptors.
    • Mu: most important. response to activation of mu receptors include analgesia, respiratory deression, euphoria, sedation. Also, phisical dependence
    • Kappa: can produce analgesia and sedation. may underlie psychotomimetic effects (psychotic alterlation of behavior or personality)
    • Delta
  18. Classification of drugs that act at opioid receptor sites.
    • Drugs that act at opioid receptors are classified on the basis of how they affect receptor function.
    • At each type of receptor, a drug can act in one of threeways - as agonist, partaial agonist, or antagonist (partial agonist is a drug that produces low to moderate receptor activation when administered alone, but will block the actions of a full agonist if the two are given together)
    • Opioid Agonists: activate mu and kappa receptors. Produce analgesia, euphoria, sedation, respiratory depression, physical dependence, constipation. Can be strong - morhpine or moderate - strong - chodeine
    • Agonist-Antagonist Opioids: 4 available - pentazocine, nalbuphine, butorphanol, and buprenorphine. When administred along, the agonist-antagonist will produce analgesia. If given with opioid agonist, the drug can antagonize(block mu) analgesia caused by the pure agonist. Blocking mu, activating kappa.
    • Opioid Antagonists: blocks mu and kappa receptors. do not produce analgesia or any of the other effects caused by opioid agonists. Their principal use is reversal of respiratory and CNS depression caused by overdose with opioid agonists. Ex. methylnatrexone - treated opioid induced constipation. Nolaxon.
  19. Discuss the therapeutic use of morphine
    • Strong opioid analgesics - releaves moderate to stong pain. more effective to constant and dull pain.
    • Effect of analgesia, sedation, euphoria, respiratory depression, cough suppression, and suppression of bowel motility
    • . In addition to relieving pain, the drug causes drowsiness, mental clouding, anxiety reduction, and a sense of well-being. Through actions in the CNS and periphery, morphine can cause respiratory depression, constipation, urinary retention, orthostatic hypotension, emesis, miosis, cough suppression, and biliary colic. With prolonged use, the drug produces tolerance and physical dependence.
    • The ability of morphine to cause mental clouding, sedation, euphoria, and anxiety reduction can contribute to relief of pain
  20. Mechanism of analgesic action
    • Mimic the actions of endogenous opiois.primarily at mu receptors
    • Both: produce analgesia, share structural similarites, bind to the same receptors in th CNS, both bind to receptors located in brian and spainal cord associated with perception of pain, can be blocked by the same antagonist: naloxone.
  21. Adverse effects of opioid analgesia
    • Respiratory depression: the most serios, in overdose death is due to respiratory arrest. Prolonged use - tolorance developes. Assess resp rate before admin, if less than 12 withhold the opioid. Other drugs and alochol can increase resp depression.
    • Constipation: supress intestinal contractions, inhibits the secretion of fluids ino the intestinal lumen, incrase the tone of an anal sphinceter. To help with constipation can increase phisical exersie, fiber intak, fluids, laxatives, and drug that helps by blocking opioid receptors in he intestine which cannot cross the blood-brain barriers.
    • Orthostatic Hypotension: lowers blood pressure by dilating peripheral veins and arterioles. Dropes significantly when pateint standup
    • Urinary Retention: suppressing awareness of bladder stimuli. Could be catheterized. Decreases urine production by decreasing renal blood flow and promoting release of antidiuretic hormone.
    • Cough supression: suppresssion of sponteneous cough may leand to accumulation of secretions in the airway. patients should be instructed to cough at regular intervals
    • Biliary Colic - spasm of bile duct
    • Emesis - nosia vomiting
    • Elevation of intracnaila pressue: due to low resp
    • Euporia/Dysphoria: Euphoria- exaggereated sense of well being. Dysphoria - sence of anxiety and unease in patients who doesn't have pain
    • Sedataion
    • Miosis: pupilary constriciton. impair vision
    • Neurotoxicity: cause delirium,agitation, ...main risk factors renal impairment, cognitive impariemnt,
    • Adverse effect from Prolonged use: hormonal changes and alterationof immune function.
  22. Appropriate routes of administration of morphine
    • Oral
    • IM
    • IV
    • subQ
    • Epidural
    • Intrathecal
  23. Difirenciate between drug tolerance and physical dependence.
    • Tolerance: state in which a larger dose ir requied to produce the same response that could formerly be elicited by a smaller dose. Tolerance to resp. depression. but constipation and miosis remain a problem
    • Cross-tolerance: if you tolerant to one opioid you will develope tolerance to other opioid agonists.
    • Phisical dependence: abstinence syndrome if drug use is abruptly stopped. Not seen in treating acuetly.
  24. Define abuse liability and the controlled substance act
    • subjected to abused largely becuase of theri ability to cuase plseasurable experiences. Phisical dependence contirbutes to abuse.
    • The abuse liability of the opioids is reflected in their classification under the Controlled Substances Act
  25. Populations that required special precautions with the use of opioids
    • Decreased Respiratory Reserve: in patients with asthma, emphysema, kyphoscoliosis, chronic cor pulmonale, and extreme obesity
    • Pregnancy: fetal dependance
    • Labor and Delivery: can supress uterine contractions and cause resp. depression in neonate reversed by naloxone
    • Head Injury: Head injury can cause respiratory depression accompanied by elevation of ICP. Morphine can exacerbate these symptoms. In addition, since miosis, mental clouding, and vomiting can be valuable diagnostic signs following head injury, and since morphine can cause these same effects, use of opioids can confound(sputivat') diagnosis.
    • Other preacations: pg. 266
  26. Adverse reactions of opioid with other classes of drugs
    • CNS Depressants.
    • All drugs with CNS-depressant actions (eg, barbiturates, benzodiazepines, alcohol) can intensify sedation and respiratory depression caused by morphine and other opioids. Outpatients should be warned against use of alcohol and all other CNS depressants.
    • Anticholinergic Drugs.
    • These agents (eg, antihistamines, tricyclic antidepressants, atropine-like drugs) can exacerbate morphine-induced constipation and urinary retention.
    • Hypotensive Drugs.
    • Antihypertensive drugs and other drugs that lower blood pressure can exacerbate morphineinduced hypotension.
    • Monoamine Oxidase Inhibitors.
    • The combination of meperidine (a morphine-like drug) with a monoamine oxidase (MAO) inhibitor has produced a syndrome characterized by excitation, delirium, hyperpyrexia, convulsions, and severe respiratory depression. Deaths have occurred
    • Agonist-angagonist: These drugs (eg, pentazocine, buprenorphine) can precipitate a withdrawal syndrome if given to an individual physically dependent on a pure opioid agonist
  27. Beneficial interaction of opioids with other classes of drugs
    Opioid antagonists (eg, naloxone) can counteract most actions of morphine and other pure opioid agonists. Opioid antagonists are employed primarily to treat opioid overdose. The actions and uses of the opioid antagonists are discussed in detail later in the chapter.

    Other Interactions.Antiemetics of the phenothiazine type (eg, promethazine [Phenergan]) may be combined with opioids to reduce nausea and vomiting. Amphetamines, clonidine, and dextromethorphan can enhance opioid-induced analgesia. Amphetamines can also offset sedation.
  28. Clinical manifestations and reatment of opioid tocisity
    • Clinical Manifestations.
    • Opioid overdose produces a classic triad of signs: coma, respiratory depression, and pinpoint pupils. Coma is profound, and the patient cannot be aroused. Respiratory rate may be as low as 2 to 4 breaths per minute. Although the pupils are constricted initially, they may dilate as hypoxia sets in (secondary to respiratory depression). Hypoxia may cause blood pressure to fall. Prolonged hypoxia may result in shock. When death occurs, respiratory arrest is almost always the immediate cause.
    • Treatment.
    • Treatment consists primarily of ventilatory support and giving an opioid antagonist. Traditionally, naloxone [Narcan] has been the antagonist of choice
  29. Guidelines of dosage and administration
    • High doses are required for patients with a low tolerance to pain or with extremely painful disorders. Patients with sharp, stabbing pain need higher doses than patients with dull pain. Elderly adults generally require lower doses than younger adults. Neonates require relatively low doses because their blood-brain barrier is not fully developed. For all patients, dosage should be reduced as pain subsides. Outpatients should be warned not to increase dosage without consulting the physician.
    • Before an opioid is administered, respiratory rate, blood pressure, and pulse rate should be determined. The drug should be withheld and the prescriber notified if respiratory rate is at or below 12 breaths per minute, if blood pressure is significantly below the pretreatment value, or if pulse rate is significantly above or below the pretreatment value.
    • As a rule, opioids should be administered on a fixed schedule
    • Oral: for patients with chronic, sever pain. Usualy higher(pass through the liver) Should not drink alchohol - can accelerate release of phorphine from this formulation.
    • Intramuscular and SubQ - not recomended. painful and unreliable.
    • Intravenous: inject slowely. Rapid injeciton can cause cardian and resp arrest.
    • Epidural and intrethecal: onset is rapid and lasts up to 24 hours.
  30. Strong opioid agonists
    • Fentanyl: parenteral, transdermal, transmucosla,
    • Alfentanil and Sufentanil
    • Remifentanil
    • Meperidine: as morhpine. short half life
    • Methadone: long action
    • Heroin: Not legal in the US. more lipid soluble. Converted to morphine in the brain.
    • Hydrophone, oxymorphone and Lavorphanol: like morphine, moderate to sever pain. Schedule II agents.
  31. Moderate to strong Opioids agonists
    • produce less analgesia and respiratory depression than morphine and have a somewhat lower potential for abuse.
    • Codein:by mouth, limited side effects, 10% in the liver converted to morhpine. made with non opioid analgesics
    • Oxycodone: actions equl to codein.
    • Hydrocodone: most widely prescribed in the US. as a cholesterol-lowering drug and as an antibiotic. ony available in combinations with other drugs. Vicodine, Vicorofin, Lortab.
    • Propoxyphene: analgesic effect equal to aspirin. toxic psychosis. fatal.
  32. Agonist-antagonist opioids
    • 4 available, have low potential for abuse, less resp depression, less analgesic effects.
    • Pentazocine: for mild to moderate pain. less effectivce than morphine. acts as an agonist at kappa receptors and as an antagonist at mu receptors. By activation kappa receptors the drug produces analgesia, sedation, resp depression - limited. Little to no euphoria. anxiety, strange thoughts, nightmares, hallucinations from activation of kappa receptors. Increase cardiac work.
    • Nalbuphine: aganist at kappa receptors and antagonist at mu. Similar to pantazocine. low abuse potential and is no under controlled substance ACT.
    • Butorphanol: similar to pentazocine.
    • Buprenorphine: differs significantly from other opiod agonist-antagonists. partial agonist at mu receptors and an antagonist at kappa receptors. similar to morphine effect but significant toleranc has not been observed. sever resp deprs has not been absorved. can cause liver damage. Schedule III. Used to treat opioid addiction. The only opioid that can not be treated with naloxone to treat toxicity.
  33. Clinical use of opioids
    • Pain assessment
    • Dosage Determination
    • Dosing schedule
    • Avoiding withdrawal reaction
  34. Physical dependance, abuse, and addiction
    • physical dependence is a state in which an abstinence syndrome will occur if the dependence-producing drug is abruptly withdrawn. Physical dependence should NOT be equated with addiction
    • Abuse: Abuse can be broadly defined as drug use that is inconsistent with medical or social norms. By this definition, abuse is determined primarily by the reason for drug use and by the setting in which that use occurs—and not by the pharmacologic properties of the drug itself
    • Addiction: can be defined as a behavior pattern characterized by continued use of a psychoactive substance despite physical, psychologic, or social harm. Note that nowhere in this definition is addiction equated with physical dependence. In fact, physical dependence is not even part of the definition
  35. Patient-controlled analgesia
    Patient-controlled analgesia (PCA) is a method of drug delivery that permits the patient to self-administer parenteral (transdermal, IV, subQ, epidural) opioids on an “as-needed” basis. PCA has been employed primarily for relief of pain in postoperative patients. Other candidates include patients experiencing pain caused by cancer, trauma, myocardial infarction, vaso-occlusive sickle cell crisis, and labor. As discussed below, PCA offers several advantages over opioids administered by the nurse.
  36. Use and actions of opioid antagonists
    pg. 278-279 in Pharmocology.
  37. Component of a thorogh pain assessment.
    • Onset and temporal pattern—When did your pain begin? How often does it occur? Has the intensity increased, decreased, or remained constant? Does the intensity vary throughout the day
    • Location—Where is your pain? Do you feel pain in more than one place? Ask patients to point to the exact location of the pain, either on themselves, on you, or on a full-body drawing.
    • Quality—What does your pain feel like? Is it sharp or dull? Does it ache? Is it shooting or stabbing? Burning or tingling? These questions can help distinguish neuropathic pain from nociceptive pain.
    • Intensity—On a scale of 0 to 10, with 0 being no pain and 10 the most intense pain you can imagine, how would you rank your pain now? How would you rank your pain at its worst? And at its best? A pain intensity scale (see below) can be very helpful for this assessment.
    • Modulating factors—What makes your pain worse? What makes it better?
    • Previous treatment—What treatments have you tried to relieve your pain (eg, analgesics, acupuncture, relaxation techniques)? Are they effective now? If not, were they ever effective in the past?
    • Impact—How does the pain affect your ability to function, both physically and socially? For example, does the pain interfere with your general mobility, work, eating, sleeping, socializing, or sex life?
    • palpation, nonverbla cues, reffered pain should be assest. neurologic complications.
    • imaging studies
    • of patient and family's
    • The impact of significant pain on the patient in the past
    • The patient's usual coping responses to pain and stress
    • The patient's preferences regarding pain management methods
    • The patient's concerns about using opioids and other controlled substances (anxiolytics, stimulants)
    • Changes in the patient's mood (anxiety, depression) brought on by cancer and pain
    • The impact of cancer and its treatment on the family
    • The level of care the family can provide and the potential need for outside help (eg, hospice)
  38. Barriers to effecive pain mnagement
    • more pain than they have or report less
    • some are unable to report at all
    • Cultural and language diferences
    • fear addiction to opioids
    • tough it out
    • fear pain signifies diseas progression
    • fear they may be denied sufficient pain medication and to ensure adequate dosing, report mor pain than they actually have.
    • behavior and facial espression may be poort indicator of paoin status.
    • nonverbal patietns.
    • Table 29-1 on page 286 in Lehne