Pain Notes NSG 335
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This 5 page Class Notes was uploaded by Brieanna Phipps on Thursday January 28, 2016. The Class Notes belongs to NSG 335 at University of North Carolina - Wilmington taught by Dr. Sauer in Spring 2016. Since its upload, it has received 56 views. For similar materials see Pathology and Pharmacology in Nursing and Health Sciences at University of North Carolina - Wilmington.
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Date Created: 01/28/16
Four Phases of Pain 1. Transduction: starts when tissue is damaged or injured; nocioceptor fibers are activated 2. Transmission: the fibers are transmitted into the spinal cord and up to the brain 3. Perception: the actual awareness of the pain, which occurs in the cerebral cortex. Pain can be influenced by culture, sex, experience, and expectations. 4. Modulation: when substances are released that alter the pain experience, such as prostaglandins, bradykinin, histamine, and endorphins. -Prostaglandins increase pain. Some suppressants of prostaglandins are NSAIDS and Naproxen Neuromodulators -injury and inflammation will trigger these pain pathways -both excitatory and inhibitory -Excitatory: substance P, glutamate, somatostatin -Inhibitory: GABA, glycine, serotonin, norepinephrine, endorphins Clinical Descriptions of Pain -Pain threshold: point at which an individual starts to feel pain -Perceptual dominance: having pain at one part of the body may cause the threshold of pain to increase at another part of the body -Pain tolerance: amount of time or intensity that a person will go through before there is a start of pain responses Types of Pain -Acute: protective, lasts seconds to days -increased HR, BP, sweating, dilated pupils, increased BG, decreased gastric acid, slowed GI motility, decrease in blood flow -Somatic: skin, connective tissue and bone -Visceral: internal organs, abdomen, can be referred pain -Referred: felt somewhere other than point of origin -Chronic: lasts at least 3-6 months -persistent or intermittent -may occur suddenly or over a period of time -changes in behavior and psyche, not as much physiologic signs as you do with acute -Myofascial pain syndrome: injury to muscle causing spasms, tenderness and stiffness -Neuropathic Pain: occurs as an end result of trauma or injury to non- nociocpetor nerves; mostly chronic pain -Example of peripheral is diabetic neuropathy -Example of central is phantom limb Treatment of Pain -difference between anesthetics and analgesics are LOSS OF CONSCIOUSNESS Anesthetics -Lidocaine -Combined with epinephrine which prolongs effects -allergies are rare -accumulates in blood, can cause toxicity -metabolized through liver Analgesics -Opioid: drug with attributes like morphine -Opiate: has same substances that are found in morphine -Narcotic: illegal substance, CNS changes When one is injured, certain chemicals are released that provides a pain response, some drugs that inhibit these chemicals are: -Antihistamines -Prostaglandin inhibitors -Antidepressants -Substance P antagonists Opiate Agonists: Morphine, Codeine, Hydrocodone, Oxycodone, Methadone -ADRs: lightheadedness, sedation, confusion, hypotension, nausea, emesis, constipation -Serious ADRs: RESPIRATORY DEPRESSION; urinary retention, abuse, CNS depressant Opiate Partial Antagonists: Buprenorphine (Buprenex, Subutex), Butorphanol (Stadol), Nalbuphine (Nubain), Pentazocine (Talwin) -ADRs: clamminess, dizziness, sedation, diaphoresis, nausea, emesis, dry mouth, constipation -Serious ADRs: confusion, hallucinations, respiratory depression, abuse Pure Opioid Antagonists: Naloxone (Narcan) -reverses the effects of opioid overdose -lasts 20 minutes -Methylnaltrexone: used to relieve opioid constipation OPIOID AGONISTS: Morphine: derivative of the poppy seed -effects: pain relief, sedation, respiratory depression, cough reducers, slow GI, biliary colic, hypotension, miosis (pupillary constriction) -Not very lipid soluble -more effective for constant pain -NO loss of consciousness -Onset: IV-7 minutes IM-30 mins SQ: up to 90 mins Lasts for 4-5 hours -Can be more harmful to patients who have impaired lung function -Can make ICP rise. RR is low, so CO2 levels increase -Take SMALLER doses MORE often so sedation can be minimized -Hormone levels can change, as well as a decrease in immune function -Withdrawal is NOT lethal -Classic Triad of toxicity: coma, respiratory depression, and pinpoint pupils Fentanyl: 50-100X STRONGER THAN MORPHINE -same ADRs as morphine -“Azoles” INCREASE levels of fentanyl -patches can last up to 48-72 hours -peak effects is 24 HOURS -buccal tablets or lozenges are different in bioavailability -must be older than 18 years and opioid tolerant Meperidine (Demerol) -ACCUMULATION OF METABOLITE CAN PRODUCE TOXIC EFFECTS -lots of drug interactions -used to treat rigors and post-anesthesia shivering Methadone -used to treat opioid addiction -ELONGATES Q-T INTERVAL -DO NOT crush and snort or OD because it can cause respiratory depression and even death Hydromorphone -ADRs same as morphine WITH LESS N/V -make sure to distinguish IR from ER Codeine -combination with Tylenol or aspirin (Schedule III) -cough medicine (Schedule V) Oxycodone -with ASA: Percodan -with Tylenol: Percocet -Schedule II -metabolized in LIVER Hydrocodone -Schedule II -used as cough suppressant -can be combined with ASA, Tylenol, or Ibuprofen Pain Assessment: -anxiety, fear, depression, and anger can decrease pain tolerance NONOPIOID ANALGESICS Non-Opioid Centrally Acting Analgesics Tramadol (Ultram) -SUICIDE RISK Clonidine (Duraclon) Ziconotide (Prialt) Dexmedetomidine (Precedex) HEADACHES: can be brought on by fatigue, stress, sickness, tyramine sensitivity, alcohol, etc. -Ergotamine: treats vascular headaches with vasoconstriction -ADRS: dizziness, rhinitis, HTN, N/V, abdominal pain -caution w/ ‘-virs and ‘-azoles -Imitrex: treats migraines or cluster headaches -ADRs: dizziness, vertigo, warm tingling sensation, and injection site rxn -metabolized through LIVER -use caution with patients taking SSRIs or SSNRIs because of serotonin syndrome SEDATIVE-HYPNOTIC DRUGS -depresses CNS -used for anxiety and insomnia (INCREASES effects of opioids) -3 major groups 1. Barbituates (Secobarbital) 2. Benzodiazepines (Diazepam) 3. Benzo-like drugs (Zolpidem) Benzodiazepines -Diazempam (Valium) -Lorazepam (Ativan) -Alprazolam (Xanax) -LESS addictive than barbituates -lipid soluble-crosses the blood brain barrier easily -metabolized in LIVER -ADRs: hypotension, cardiac arrest, respiratory depression, daytime sleepiness, impaired memory after dose, -Schedule IV -ANTIDOTE: FLUMAZENIL (ROMAZICON)
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