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104 Cards in this Set
- Front
- Back
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Acute Pain
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Associated with trauma or surgery
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Chronic Benign Pain (time frame)
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Greater than 3 months
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Chronic Benign Pain
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Depression, sense of helplessness, and hopelessness
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Somatic Pain characteristics
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throbbing, stabbing, localized
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Somatic Pain Rx
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Narcotics, NSAIDS, nerve blockers
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Visceral Pain Origin
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Kidneys, Intestines, Liver (thoracic and abdominal structures)
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Visceral Pain Characteristics
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Aching, throbbin, sharp, gnawing,crampy
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Visceral Pain Treatment
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narcotics, NSAIDS, nerve blockers, antiemetics
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Neuropathic Pain characteristics
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burning, aching, numbing, tingling, constant
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Neuropathic Pain treatment
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antidepressants (LYRICA, CYMBALTA), anticonvulsants (GABAPENTIN)
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Sympathetic System Pain characteristics
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occuring when no pain should be felt
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Sympathetic system pain treatment
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nerve blockers
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Narcotics
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Pain modulating chemicals that cause insensibility or stupor
Main effects of CNS and GI tract (lesser=peripheral tissue) |
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Natural Opiod Peptides
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endorphins, enkaphalins, dynorphins
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Natural Opiod Receptors
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Mu (morphine and strong opiod agonists) ,
Kappa (mixed opiod agonsists/antagonists), Delta (No drugs currently work on delta) |
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Anecdote to Opiod Overdose
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Opioid antagonists : block the effects of opioid
agonists and are used to reverse adverse drug reactions, such as respiratory and CNS depression, produced by those drugs. Unfortunately, by reversing the analgesic effect, they also cause the patient’s pain to recur. |
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Effects of Narcotics
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Analgesia, Sedation, Euphoria, Dysphoria, potential for DEPENDENCE AND TOLERANCE
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Mu receptors
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analgesia, sedation, euphoria, respiratory depression, physical dependence, constipation
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Kappa receptors
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analgesia, respiratory depression, anxiety, strange thoughts, nightmares, hallucinations
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Delta receptors
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analgesia without many adverse effects
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Opiod agonist MOA
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Mimics the action of endogenous opiod peptides that bind at opiod receptors in the antinociceptive pathway
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Opiod agonist metabolism site
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Liver
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Gold standard opiod agonist
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Morphine
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Schedule 3 Opiod agonists
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Codeine, Hydrocodone, Propoxyphene, Sufentanil
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Schedule 2 Opiod agonists
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Morphine sulfate, methadone, fantanyl, oxycodone, meperidine, hyromorphone
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Opiod effects on CVS
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Decreased myocardial O2 demands; vasodilation and hypotension (MONA AND LONA)
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Opiod preferred for hepatic and renal impairment (ex. cirrhosis, liver damage, cancer)
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Fentanyl - PATCH; doesn't need cytochrome p450 to break down); patch changed every 2-3 days
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Mild to moderate Opiod
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C3
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Strong Opiod agonsts (severe pain)
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C2
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Therapeutic uses of Opiods
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analgesics, MI, antitussives, pulmonary edema, antidiarrheal, adjunct to anesthesia
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Relative Contraindications & Precautions to with Opiod Use
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1. Avoid mixed agonist/antagonist in pts on full agonists-precipitate withdrawal
2. Do not use in patients with head injuries-depression 3. Chronic use during pregnancy may result in a dependent offspring 4. In pts with underlying respiratory dysfunction, respiratory failure can occur 5. Half-lives increased in patients with hepatic or renal dysfunction |
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Adverse effects of Opiod agonists
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constipation, Respiratory and CNS depression, flushing, orthostatic hypotension, pupil constriction, seizures, tachycardia, delirium, Nausea and vomiting
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Treatment of constipation due to opiod agonist
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Can give dulcolax (stool softener)or high fiber and laxatives to reduce effect
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Treatment of N/V due to opiod agonist
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Can use metoclopramide, prochlorperazine or trimethobenzamide short term.
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Treatment of respiratory depression due to opiod agonist
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Naloxone (opiod antagonist)
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Opiod dependency
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Physican dependence begins after a few weeks with withdrawal symptoms if the drug is abruptly discontinued; MORPHINE AND HYDROMORPHINE HIGH DEPENDENCY; Can do opiod rotation to prevent dependency
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Drug alternative for Heroin
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Methodone (PO, INJ)
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Meperidine (Demerol)
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Use caution with CNS AND RENAL DYSFUNCTION; Can accumulate over time
meperidine is metabolized to normeperidine, a toxic metabolite with a longer half -life than meperidine. This metabolite accumulates in patients with renal failure and may lead to CNS excitation and seizures. Administration of meperidine for more than 48 hours increases the risk of neurotoxicity and seizures from buildup of normeperidine. Use within 14 days of MAOI can cause life-threatening drug interaction |
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Mixed Agonist- Antagonist MOA
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mixed opioid agonist-antagonists, have agonist and
antagonist properties. The agonist component relieves pain, while the antagonist component decreases the risk of toxicity and drug dependence. These mixed opioid agonist -antagonists reduce the risk of respiratory depression and drug abuse. |
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Opiod agonist Antitussive
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Low dose codeine (Promethazine+codeine good for persistent cough)
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Opiod agonist ADRs
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The use of opioid agonists with other drugs that also decrease respirations, such as
alcohol, sedatives, hypnotics, and anesthetics, increases the patient’s risk of severe respiratory depression. Taking tricyclic antidepressants, phenothiazines, or anticholinergics with opioid agonists may cause severe constipation and urine retention. Drugs that may affect opioid analgesic activity include amitriptyline, diazepam, phenytoin, protease inhibitors, and rifampin. Drugs that may be affected by opioid analgesics include carbamazepine, warfarin, beta-adrenergic blockers, and calcium channel blockers. |
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Mixed opiod agonist-antagonist MOA
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Binds as a weak agonist to the kappa receptor and weak antagonist to the Mu receptor
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Buprenorphine
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Mixed opiod agonist-antagonist
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Butorphanol
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Mixed opiod agonist-antagonist
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Nalbuphine
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Mixed opiod agonist-antagonist
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Pentazocine hydrochloride
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Mixed opiod agonist-antagonist
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Benefits of Mixed opiod agonist-antagonists
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Produces pain relief without as severe of side effects (LESS CNS DISTURBANCES); decreased dependency and abuse factor
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Mixed opiod agonist-antagonist adverse reactions
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Nausea, vomiting, light-headedness, sedation, and euphoria
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Childbirth analgesia
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Mixed opiod agonist-antagonist
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Opiod abuse and the use of Mixed opiod agonist-antagonist
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Patients who abuse opioids shouldn’t receive mixed opioid agonist -antagonists because
these drugs can cause symptoms of withdrawal. |
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Heroin addiction rx
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Buprenorphine + Naltrexone reduces heroin addiction
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Naloxone
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Opiod Antagonist
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Naltrexone
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Opiod Antagonist
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Opiod Antagonist MOA
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Act by occupying opiod receptors, displacing opiods attached to opiate receptors and preventing opiods from binding to these sites (STRONGER AFFINITY TO OPIATE RECEPTOR SITES)
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DOC for opiod overdose
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Naloxone
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Side effects Naloxine
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N/V, HTN, tachycardia
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Rx+ psychotherapy to treat drug abuse (ex. alcohol dependence)
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Naltrexone
Managing naltrexone therapy for drug addiction To prevent acute withdrawal during treatment for opioid addiction, plan to use naltrexone as part of a comprehensive rehabilitation program. Keep in mind the following guidelines: Don’t give naltrexone until a negative naloxone challenge test is obtained. Don’t give naltrexone to a patient who’s receiving an opioid agonist, addicted to an opioid agonist, or in the acute phase of opioid withdrawal because acute withdrawal symptoms may occur or worsen. For a patient who’s addicted to a short -acting opioid, such as heroin or meperidine, wait at least 7 days after the last opioid dose before starting naltrexone. For a patient who’s addicted to a longer -acting opioid, such as methadone, wait at least 10 days after the last opioid dose before starting naltrexone. During naltrexone therapy, be alert for signs of opioid withdrawal, such as drug craving, confusion, drowsiness, visual hallucinations, abdominal pain, vomiting, diarrhea, fever, chills, tachypnea, diaphoresis, salivation, lacrimation, runny nose, and mydriasis. |
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Naltrexone Side effects
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edema, hypertension, palpitations, SOB, anxiety, depression, disorientation, HA, N/V, constipation
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Preoccupation with drugs
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Sign of narcotic addiction
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Refusal of medication tapers
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Sign of narcotic addiction
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Strong preference for a specific opiod
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Sign of narcotic addiction
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Medication often not taken as prescribed
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Sign of narcotic addiction
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Decrease in ability to function
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Sign of narcotic addiction
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Tendency to rely on multiple prescribers and pharmacies to conceal behavior
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Sign of narcotic addiction
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3Before administering buprenorphine, the nurse asks the patient if he has used opiates.
That’s because administering a mixed opioid agonist -antagonist to a patient dependent on opioid agonists may cause which reaction ? A. Hypersensitivity reaction B. Withdrawal symptoms C. Urinary incontinence D. Respiratory depression |
b. withdrawal symptoms
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What is somatic pain?
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Somatic pain is the aching, throbbing pain of skeletal muscles, fascia, ligaments, vessels, and joints.
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What is visceral pain?
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Visceral pain is dull and aching pain resulting from stimulation of nerve endings in smooth muscle or
sympathetically innervated organs. Visceral pain is difficult locate. |
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Name an advantage of a nonnarcotic analgesic
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Non addictive
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Classic migraine components
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Prodrome, aura, headache, headache relief, postdrome
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Symptom indicating onset
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Prodrome
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Subjective sensation or motor phenomenon that precedes onset of migraine
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Aura (examples: flashing lights, shimmering heat waves, bright lights, dark holes in visual fields, blurred vision)
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Cause of Migraine HA
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Decreased levels of serotonin causes excessive vasodilation in cranial arteries
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Abortive therapy
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therapy for migraine HA; taken after migraine occurs, taken at first sign such as aura or HA
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anticonvulsants
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Prophylactic Migraine therapy
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Beta blockers
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Prophylactic Migraine therapy
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Calcium channel blockers = (Nifedipine)
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Prophylactic Migraine therapy
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estrogen
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Prophylactic Migraine therapy
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feverfew
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Prophylactic Migraine therapy
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NSAIDS (tylenol, ibuprofen, aleve, aspirin)
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Prophylactic Migraine therapy
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SSRIs
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Prophylactic Migraine therapy
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Tricyclic Antidepressants (amitriptyline)
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Prophylactic Migraine therapy
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Beta Blockers (propranolol, timolol)
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Prophylactic Migraine therapy
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Anticonvulsants (Divalpurex Sodium, Topiramate)
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Prophylactic Migraine therapy
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Ergot MOA
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Promotes constriction and reduces the amplitude of pulsations; affects blood flow by depressing the vasomotor center
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Ergot Side effects
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NV, weakness of legs, tachycardia, peripheral vasoconstriction angina like pain
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First line therapy migraine
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triptans
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Triptan MOA
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Activates serotonin 1b and 1d causing vasoconstriction; NO EFFECT ON OTHER RECEPTORS
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Triptan contraindications
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Coronary Artery Disease (vasoconstrictor!!!)
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Triptan Side effects
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vasoconstriction, tingling and paresthesias, warmth in the head, chest and limbs, fatigue, vertigo
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butalbital-acetaminophen-caffeine
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Fioricet
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butalbital-aspirin-caffeine
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fiorinal
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Isometheptene-dichloralphenazone-acetaminophen
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midrin; analgesic, sedative, vasoconstrictor; MILD TO MODERATE HAs
Take 2 capsules at onset; 1 ever 1-2 hrs until pain stops; up to 5 capsules in 12 hours |
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chlorpromazine
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antiemetic
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metoclopramide (REGLAN)
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antiemetic
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prochlorperazine
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antiemetic
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Tramadol
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Given for PAIN or MIGRAINE; high success when given with NSAIDS;
Slow onset of action, potential for addiction CONTRAINDICATED IN SEIZURES |
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Contraindications triptans
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cerebrovascular disease, CAD, ischemic heart disease
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Dextroamphetamine
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CNS stimulant (ADHD, ADD); Narcolepsy
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Lisdexamfetamine
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CNS stimulant (ADHD, ADD)
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Methylphenidate
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CNS stimulant (ADHD, ADD); narcolepsy
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Mixed amphetamine salts
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CNS stimulant (ADD); not given to ADHD
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Atomoxetine
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CNS stimulant (ADHD, ADD); NOT A CONTROLLED SUBSTANCE
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Modafenil
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CNS stimulant (ADHD, ADD); not a controlled substance
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CNS stimulants MOA
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Increase levels of dopamine and NE by:
blocking the reuptake of Da and NE Enhancing the presynaptic release Inhibiting MAO |
