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.
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.
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.
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
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.
Components of nonverbal inidactor of pain
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
Why pain should be the fifth vital sign?
To raise awareness of pain and emphasize pain relief.
(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.
Patient Controlled Analgesia - pump are effective and safe way to deliver opiods by IV. epudural or subcutaneous routes.
Morphine usualy used
used for mild pain or in conjuction with opioids. Reduces amount of opioi he patient requieres.
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...
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)
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.
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
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.
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
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.
Appropriate routes of administration of morphine
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.
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
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
Adverse reactions of opioid with other classes of drugs
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.
These agents (eg, antihistamines, tricyclic antidepressants, atropine-like drugs) can exacerbate morphine-induced constipation and urinary retention.
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
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.
Clinical manifestations and reatment of opioid tocisity
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 consists primarily of ventilatory support and giving an opioid antagonist. Traditionally, naloxone [Narcan] has been the antagonist of choice
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.
Strong opioid agonists
Fentanyl: parenteral, transdermal, transmucosla,
Alfentanil and Sufentanil
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.
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.
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.
Clinical use of opioids
Avoiding withdrawal reaction
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
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.
Use and actions of opioid antagonists
pg. 278-279 in Pharmocology.
Component of a thorogh pain assessment.
COMPRIHENSIVE INITIAL 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?
PHISICAL AND NEUROLOGC EXAMINATIONS
palpation, nonverbla cues, reffered pain should be assest. neurologic complications.
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