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Med Surg 1

Chapter 12 - Pain Management

Addiction Chronic neurologic and biologic disease defined by pain specialists and characterized by behaviors that include: impaired control over drug use, compulsive use, continued use despite harm, and craving to use the opioid for effects other than pain relief.
Adjuvant Analgesic Agent Drug that has a primary indication other than pain but is an analgesic agent for some painful conditions.
Agonist-Antagonist Type of opioid that binds to the kappa opioid receptor side acting as an agonist and simultaneously to the mu opioid receptor site acting as an antagonist.
Allodynia Pain due to a stimulus that does not normally provoke pain, such as touch; typically experienced in the skin around areas affected by nerve injury and commonly seen with many neuropathic pain syndromes.
Breakthrough Pain Transitory increase in pain that occurs on a background of otherwise controlled persistent pain.
Ceiling Effect Analgesic doe above which further dose increment produce no change in effect.
Central Sensitization Key central mechanism of neuropathic pain. Abnormal hyprexcitability of central neurons in spinal cord, which results from complex changes induced by incoming afferent barrages of nociceptors.
Comfort-Function Goal Pain rating identified by the individual patient above which the patient experiences interference with function and quality of life.
Efficacy Extent to which a drug or another treatment "works" and can produce the effect in question.
Half-Life Time it takes for the plasma concentration to be reduced by 50%.
Hydrophilic Readily absorbed in aqueous solution.
Intraspinal "Within the Spine". Refers to spaces or potential spaces surrounding the spinal cord into which medications can be administered.
Lipophilic Readily absorbed in fatty tissues.
Metabolite Product of biochemical reactions during drug metabolism.
Mu Agonist Any opioid that binds to the mu opioid receptor subtype and produces analgesic effects.
Neuropathic Pain Pain sustained by injury or dysfunction of the peripheral or central nervous systems and distinctly different from nociceptive pain. Pathophysiologic Pain.
Neuroplasticity Ability of peripheral and central nervous systems to change both structure and function as a result of noxious stimuli.
Nociceptive Pain Pain that is sustained by ongoing activation of the sensory system that conducts the perception of noxious stimuli. Implies existence of damage to somatic or visceral tissues sufficient to activate nociceptive system. Physiologic Pain.
Nociceptor Type of primary afferent neuron that has the ability to respond to a noxious stimulus or to a stimulus that would be noxious if prolonged.
Harmful Endocrine Effects of Unrelieved Pain Increased glucagon Decreased insulin
Harmful Cardiovascular Effects of Unrelieved Pain Increased heart rate, cardiac workload, peripheral vascular resistance, systemic vascular resistance, coronary vascular resistance, & myocardial oxygen consumption. Hypertension. Hypercoagulation. Deep vein thrombosis.
Harmful Respiratory Effects of Unrelieved Pain Decreased flows & volumes, & cough. Atelectasis. Shunting. Hypoxemia. Sputum Retention. Infection.
Harmful Genitourinary Effects of Unrelieved Pain Decreased urinary output. Urinary retention. Fluid overload. Hypokalemia.
Transduction Processes by which noxious stimuli activate primary afferent neurons.
Prostaglandins Lipid compounds that initiate inflammatory responses that increase tissue swelling & pain at site of injury.
Cyclo-oxygenase Acts on arachidonic acid to produce prostaglandins. COX
Types of NSAIDs Ibuprofen Naproxen Diclofenac Ketorolac Celecoxib
Types of NSAIDs that Block Cox-1 & Cox-2 Ibuprofen Naproxen Diclofenac Ketorolac
Cox-2 Selective NSAID Celecoxib
A-delta fibers Lightly myelinated & faster conducting. Endings detect thermal & mechanical injury. Allow relatively quick localization of pain. Responsible for rapid reflex withdrawal from painful stimulus.
C Fibers Unmyelinated fibers that are slow impulse conductors & respond to chemical, thermal, & mechanical stimuli. Produce poorly localized & often aching or burning pain.
A-beta Fibers Largest of fibers & respond to touch, movement, & vibration but do not normally transmit pain.
Transmission Second process involved in nociception.
Ketamine NMDA receptor antagonist. Produces analgesia by preventing glutamate from binding to NMDA receptor sites.
Glutamate Key transmitter because it binds to the N-methyl-D-aspartate (NMDA) receptor & promotes pain transmission.
Methadone Binds to opioid receptor sites & has NMDA antagonist properties.
Perception Third process involved in nociception. Result of neural activity associated with transmission of noxiuos stimuli. Requires activation of higher brain structures for the occurrence of awareness, emotions, & drives associated with pain.
Serotonin & Norepinephrine Inhibitory neurotransmitters that are released in the spinal cord & brain stem in descending fibers.
Patient-Controlled Analgesia Interactive method of pain management that allows patients to treat their pain by self-administering doses of analgesic agents.
Recommended Dose of Acetaminophen 1000mg every 6 hours for a maximum of 4000mg in patients weighing more than 50kg.
30-60 Minutes Onset of PO Morphine
5-10 Minutes Onset of IV Morphine.
60-90 Minutes Peak of PO Morphine.
15-30 Minutes Peak of IV Morphine.
3-6 Hours Duration of PO Morphine.
3-4 Hours Duration of IV Morphine.
5 Minutes Onset of OT Fentanyl.
3-5 Minutes Onset of IV Fentanyl.
15 Minutes Peak of OT Fentanyl.
15-30 Minutes Peak of IV Fentanyl.
2-5 Hours Duration of OT Fentanyl.
2 Hours Duration of IV Fentanyl.
15-30 Minutes Onset of PO Hydromorphone.
5 Minutes Onset of IV Hydromorphone.
30-90 Minutes Peak of PO Hydromorphone.
10-20 Minutes Peak of IV Hydromorphone.
3-4 Hours Duration of PO Hydromorphone.
3-4 Hours Duration of IV Hydromorphone.
Tolerance Process characterized by decreasing effects of a drug at its previous dose, or the need for a higher dose of drug to maintain an effect.
Titration Upward or downward adjustment of the amount of an analgesic agent.
Self-Report Ability of an individual to give report.
Refractory Nonresponsive or resistant to therapeutic interventions such as analgesic agents.
Preemptive Analgesic Agents Pre-Injury pain treatments to prevent the establishment of peripheral and central sensitization of pain.
Placebo Any medication or procedure that produces effect in patient because of its implicit or explicit intent & not because of its specific physical or chemical properties.
Physical Dependence Body's normal response to administration of opioid for 2 or more weeks. Withdrawal symptoms may occur if abruptly stopped or antagonist is administered.
Peripheral Sensitization Key peripheral mechanism of neuropathic pain occurs when changes in the number & location of ion channels.
Opioid Tolerance Denotes person who has taken opioids long enough at doses high enough to develop tolerance to many of opioids effects.
Opioid Naive Denotes person who has not recently taken enough opioid on a regular enough basis to become tolerant to opioids effects.
Opioid-Induced Hyperanalgesia Phenomenon in which exposure to an opioid induces increased sensitivity, or a lowered threshold, to the neural activity conducting pain perception.
Opioid Dose-Sparing Effect Occurs when a nonopioid or adjuvant is added to an opioid, allowing the opioid dose to be lowered without diminishing analgesic effects.
Opioid Refers to codeine, morphine, and other natural, semisynthetic, and synthetic drugs that relieve pain by binding to multiple types of opioid receptors.
NSAID Acronym for nonsteroidal anti-inflammatory drug.
Nonopioid Refers to analgesic agents that include acetaminophen and nonsteroidal anti-inflammatory drugs.
Created by: danatmock
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