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283 Cards in this Set
- Front
- Back
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What is the trade name for remifentanil?
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ultiva
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What are the 3 narcotic antagonists?
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naloxone (narcan)
naltrexone (trexane) nalmafene (revex) |
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The body has endogenous chemicals that relieve pain, called ______.
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enkephalins
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Why do we have pain?
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warning sign of tissue damage in the body
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These chemicals stimulate pain producing neurons:
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substance P, bradykinin, ACh
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nociception
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perception of pain
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The pain impulse goes up the spinal cord in the ______ tract to the thalamus. The thalamus acts as a _____ system, causing awareness in the brain, producing a response. The descending tract tells the body to _______ from the painful stimuli.
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spinothalamic, relay, withdraw
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Along every pain pathway, there is an ability to
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suppress it!
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The term "pro" means
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precursor
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The predominant effects of narcotics are seen in these 2 body systems: ______.
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CNS and GI
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Since there are more opiate receptors in the gut than the CNS, there is this side effect
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constipation
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These 4 groups of chemicals in the body that relieve pain in the CNS and GI tract
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enkephalins, endorphins, dynorphins, endomorphins
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Enkephalins are classified according to their _____ amino acid.
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terminal
(Ex: leu enkephalin and met enkephalin) |
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The precursor to enkephalins is
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proenkephalin A
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These are the anatomic locations of what opioid group?
amygdala, hypothalamus, pituitary gland, periaqueductal gray matter, rostroventral medulla, rexed's laminae I, II, V, X; GI tract, SNS, adrenal medulla |
enkephalin locations
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What is the beta endorphin precursor?
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pro-opiomelanocortin
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What are the anatomic locations of beta endorphins?
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arcuate nucleus of basal hypothalamus, pituitary gland, nucleus of solitary tract, periaqueductal gray matter, locus ceruleus
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What are the 2 types of dynorphins
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dynorphin and alpha neoendorphin
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What is the dynorphin precursor?
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prodynorphin
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Endomorphin 1 and 2 have an _____ precursor and both dynorphins and endomorphins have similar distribution to _____.
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unknown, enkephalins
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What is the ending amino acid sequence for endomorphin 1
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trp-phe-NH2
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What is the ending amino acid sequence for endomorphin 2
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phe-phe-NH2
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Opioid peptide precursors are ______ or ____ into active endogenous chemicals when the body ____.
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cleaved or catalyzed, needs it
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The current literature suggests ____pain relief as most effective mgmt.
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multimodal therapy
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Why is multimodal therapy so lovely?
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aims to decrease the dose of any single agent, thus improving antinociception and reducing side effects
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What are some of your choices for multimodal pain therapy cocktail?
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cox-2 inhibitors, local anesthetics, opioids, NSAIDs, alpha 2 agonists
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_______ sparing is a key goal of multimodal therapy. This will reduce the associated complications of:
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opioid,
incr morbidity and length of stay |
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Multimodal analgesia aims to avoid _____(several)______ from excessive narcotic dosing.
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sedation, resp depression, constipation, pruritis, PONV, dependence, tolerance
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By using multimodal therapy, you _____ the pain transmission pathway at numerous points, in both ___ and ____ nervous systems.
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interrupt, peripheral, central
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Which drugs interrupt pain pathway at brain level?
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opioids, alpha agonists, centrally acting analgesics, cox and nsaid anti-inflammatory agents
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Which drugs interrupt pain pathway at spinal cord level?
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local anesthetics, opioids, alpha 2 agonists, anti-inflam nsaids and cox 2 inhib.
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Which drugs interrupt pain pathway at PNS level
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local anesthetics
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Which drugs interrupt pain pathway at tissue level?
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local anesthetics, opioids, anti-inflam. cox2 inhib. and nsaids
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What is the mechanism of action for opiates?
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agonist at opiate receptors which produces a decr pain transmitter release, resulting in analgesia
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NSAIDs inhibit ______ mediator release. (BK, 5HT, PGs)
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inflammatory mediator
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Opiates inhibit ________ of transmission neuron and ____ release, relieving pain.
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excitation, neuropeptide (SP, CGRP)
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5HT, BK, CGRP, NA, NGF, NO, NSAID, PG, and SP are all modulatory mechanisms/neurotransmitters in the ______ pathway.
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nociceptive
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The mu opioid receptor prefers what endogenous ligands?
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Beta endorphin, met and leu enkephalin
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The delta opiate receptor prefers what endogenous ligands?
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met and leu enkephalin
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The kappa opiate receptor prefers what endogenous ligand?
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dynorphin
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The ORL1/non-opioid like receptor prefers what endogenous ligand?
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nociceptin
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______ travels across the synapse between neurons to transmit a pain signal. _____ that travel down the neuron must signal for its release.
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Substance P, electrical impulses
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When the ____ receptors on the pre-synaptic neuron are activated, a comformational change prevents release of ______.
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opiate, substance P
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The brain signals for the release of _____ during unusually traumatic events.
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endorphins
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What are the 3 subtypes of opiate receptors?
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mu, kappa and delta
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The amount of pain relief is ALWAYS proportional to the amount of _____ that accompanies it.
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respiratory depression
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When people receive opiates that aren't in pain, interestingly it can cause _____.
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dysphoria
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Narcotics (do/don't) produce anesthesia (LOC).
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don't
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Under narcotics, the patient needs a higher ____ to drive the same respiratory rate.
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CO2 level
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_____ is seen w repeated narcotic administration, and it can be seen in as little as ____ hours.
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physical dependence/addiction, 24-48
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These 2 side effects are not lessened with repeated admin of narcotics:
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constipation and miosis -- you will always get them
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Once you develop opiate tolerance, you also develop
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a cross-tolerance against all opiate drugs.
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The endogenous ligands endomorphin 1 and 2, met enkephalin, and dynorphin A and B both act on this receptor:
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mu (OP3)
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Mu receptors are seen at these sites:
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peripheral inflammation, pre and post synaptic neurons in spinal cord, periaqueduct grey matter, limbic system, caudate putamen, thalamus, cerebral cortex
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The endogenous ligands dynorphin A and B and beta endorphins both act on this receptor
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kappa (OP1)
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Kappa receptors are seen at these sites:
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nucleus raphe magnus (midbrain), hypothalamus, spinal cord
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Leu and met enkephalins, and beta endorphins are the endogenous ligands for this receptor:
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delta (OP2)
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These are the sites where delta receptors are found:
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olfactory centers, cerebral cortex, nucleus accumbens, caudate putamen, spinal cord
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Orphanin FQ (nociceptin) is the endogenous ligand for what receptor?
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orphan/nonopiate/ORL-1
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What are the sites of non opiate receptors?
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nucleus raphe magnus, spinal cord, and afferent neurons
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Drugs cannot differentiate between ____ and ____ opioid receptors, and affect both equally, causing both pain relief and resp depression
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mu 1 and mu 2
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These 3 drugs are antagonists to all opioid receptors
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naloxone, naltrexone, and nalmafene
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List the effects (Both desirable and undesirable) of mu 1 and mu 2
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analgesia (supraspinal and spinal), euphoria, low abuse potential - mu1, physical dependence mu 2, miosis, bradycardia, hypothermia, urine retention, pruritis, skeletal muscle rigidity, biliary spasm, depr ventillation, mucho constipation
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What are the 3 main agonists of mu 1 and 2 receptors?
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endorphins, morphine, synthetic opioids
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List the effects of kappa receptors
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analgesia (spinal and supraspinal), dysphoria, sedation, low abuse potential, miosis, mediate anti shivering effects w demerol
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____ is the kappa receptor agonist.
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dynorphins
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What are the effects of delta receptors?
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analgesia (supraspinal and spinal), depressed ventillation, physical dependence and constipation, urine retention
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_____ is the delta receptor agonist.
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enkephalin
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______ provokes maximal biological response, ____ provokes submaximal response even at high doses w limited efficacy, and _____ reverses biological response to opioids.
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full agonist, partial agonist, antagonist
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Along w the amount of analgesia and respiratory depression you produce w a given amt of narcotic, you also develop the same proportionate ____.
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addiction liability.
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Phenanthrene alkaloids have the potential to release ______ or provoke an _____ reaction.
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histamine, allergic
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The 2 types of phenanthrene alkaloids are
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naturally occuring (morphine, codiene, thebaine) and semi synthetic (heroin, vicodan, dilaudid, oxycontin, oxymorphone)
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4 types of synthetic opioids:
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1. morphinan derivatives (levorphanol, butorphanol, nalbuphine)
2. piperidine derivatives (anilinopeperidines, phenylpiperidines) 3. methadone derivatives 4. benzmorphans (pentazocine) |
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examples of anilinopiperidines
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meperidine and loperamide
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examples of phenylpiperidines
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fentanyl, sufentanil, alfentanil, remifentanil
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This type of narcotic does not release histamines, so it is better for asthmatics
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phenylpiperidines
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Patients are likely to have cross-allergies _____, but not likely to also be allergic to ____.
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within a class, a different class
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These are normal effects of narcotics, not to be confused w allergies...
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n/v, itching, rash (neck, chest, BUE), euphoria
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Potency ratios are estimates relative to ____ as one and are purely guidelines.
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morphine sulfate
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Dosages are variable, depending upon...
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the patient's condition, other drugs administered and pain levels
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High dose opioids do not provide all of the requirements of _______. Supplemental drugs may be needed to guarantee ______, relaxation and sympathetic control.
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general anesthesia, amnesia/unconsciousness
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______ is subjective.
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potency
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____ is the most potent opiate and ____ is the least potent opiate.
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sufentanil, codeine
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Phenanthrene derivatives are all metabolized in the _____ by _____. Metabolism is subject to influence by enzyme ___ and ____.
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liver, CYP450, inhibitors and inducers
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This is the only opioid w a toxic metabolite, which causes seizures.
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meperidine --> normeperidine metabolite causes seizures
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____ is metabolized in the plasma by RBC esterase, making it VERY short acting!
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remifentanil
ester group makes it susceptible to hydrolysis in plasma -- easily metabolized |
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Toxicity from normeperidine metabolite is most often seen when
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prolonged administration
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Narcotics are _____ drugs with a relatively _____ half life.
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basic, short
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Because remifentanil has such a short half life (5-10 min), it is fast acting and fast clearing, intended for this type of administration
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continuous infusion
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The volume of distribution is used to determine ____ and ____. It is very low for alfentanil and remifentanil because they don't distribute as widely in the body as the others.
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half life and dosing intervals
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Lipid solubility ____ the volume of distribution.
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increases!
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The ______ is constricted by narcotics, causing inability to drain bile and increased biliary pressure, leading to biliary colic.
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sphincter of Odi
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Per the dose response curve, the greatest concentration of anesthesia is required during this activity:
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intubation -- greater than skin incision or closure!!
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Narcotics are better for ______ pain than managing ____ pain.
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acute rather than chronic/neuropathic
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Since narcotics do not produce anesthesia/LOC, provider must also give..
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anesthetic
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Analgesia works in the brain and spinal cord to inhibit _______.
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release of pain chemicals -- opioid agonists inhibit pain pathways
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The vasodilation side effect of opioids is most common in _____ that release ____.
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phenanthrenes, histamine
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miosis
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pinpoint pupils
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Narcotics produce a smooth muscle spasm, especially in the _____ and ____ of GI tract. Slowed GI and biliary function results in ____ and ____.
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sphincters and smooth muscles,
biliary colic and constipation |
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Urinary retention w opioids occurs due to influence of this nerve, tightening urinary sphincters.
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vagal
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You can always count on these 3 effects of long term opioid use
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tolerance, physical dependence, constipation
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CV effects of narcotics are minimal, but do produce ______ due to the vagotonic effect on the heart, as well as _____.
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bradycardia, postural hypotension
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What is the #1 cause of PONV??
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opiates!
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Opiates have a ____ Effect with nusea and vomiting...some parts of the brain stimulate it and others suppress it.
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dual effect
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This chemoreceptor senses O2, CO2, and pH to influence respiration. There is no blood-brain barrier, so it can react w a quick response and cause nausea and vomiting.
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CTZ- chemotactic trigger zone
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If you stimulate the CTZ there is a _____ nausea and vomiting reaction.
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fast!
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For more chronic/long term nausea and vomiting, like in pregnancy, the _____ in the back of the brain is stimulated.
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vomiting center
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Opiates stimulate the _____ and suppress the _____.
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CTZ, vomiting center
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During which dose are pts more likely to experience nausea and vomiting?
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first dose -- decreases w repeated administration
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Which pt population has the most common nausea and vomiting after receiving opiates?
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ambulatory (Compared to supine)
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Which neurotransmitters inhibit the CTZ?
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dopamine agonists (droperidol, most potent), serotonin agonists (zofran), histamine agonists, ACh muscarinic antagonists, benzos and propofol
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The CTZ stimulates the
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vomiting center
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What stimulates the CTZ?
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opiates and vestibular portion of CN8
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What stimulates the vomiting center?
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GI distension, pharynx, higher centers, mediastinum
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The CTZ is located in the ____. The vomiting center receives input from the CTZ as well as peripheral sites via the ____.
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postrema of the brain stem, vagus nerve
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What steroid serves as a good antiemetic?
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decadron 4 mg
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What are the anesthetic risk factors for PONV
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volatile agents, N20, opioids, high doses of neostigmine
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What are the patient risk factors for PONV?
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female, history of PONV and motion sickness, pain, high anxiety level
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What are surgical risk factors of PONV?
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long OR procedures, certain types of surgery (intra-abdominal, major gynecologic- fertility, laparoscopic, breast, ENT, strabismus eye sx)
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Droperidol should be used for PONV when
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other first line drugs fail
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Can anesthesia/OR doses of dexmethasone cause avascular necrosis of the femoral head?
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no bad side effects when given in one PONV prophylaxis dose -- problems result from chronic use
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What is the best pharmacological approach to PONV?
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since etiology is mutifactorial, combo drug therapy is more effective
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3 strategies to minimize PONV
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1. identify high risk pts
2. avoid emetogenic stimuli (etomidate, n20, IAs, opioids -- try using NSAIDs and local) 3. multimodal therapy (antiemetics, TIVA w propofol, adequate hydration, effective analgesia, anxiolytics/benzos, nonpharm techniques - acupuncture) |
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Nausea is more prevalent w which hydration status?
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hypovolemia
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If a pt has > 4 PONV risk factors, it is recommended to ...
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use antiemetics and TIVA w propofol, dexaOpmethasone
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How does smoking affect PONV?
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nonsmokers more prone to PONV
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Opiates shift the CO2 reponse curve to the ____. Pt is also less sensitive to O2, but moreso with CO2.
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right
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Opiates decrease resp center sensitivity to changes in _____, the resp center doesn't respond and there is resulting _____.
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CO2, resp depression
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Opioid (fentanyl, dilaudid, vicodan, methadone, codiene, morphine) antitussive effects help with...
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ventilator tolerance
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During opioid administration, it takes a much greater _____ to increase alveolar ventilation. This is most detrimental at what part of the OR case?
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Pa CO2, at the end of the case when you're trying to extubate!
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When moving toward extubation, the provider should allow the patient to _____ CO2, open the ______, and let the patient try to stimulate spontaneous breathing response. This helps to determine ____.
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build up, APL, depth of anesthesia
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Pt respiration may become depressed again after extubation when
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they are not being stimulated post-operatively
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What is the muscular side effect of high dose narcotic admin such as intraoperatively?
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muscle rigidity - chest wall tightness
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Risk factors for chest muscle rigidity
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high dose narcotic, speedy admin, N20 co-admin, elderly, absence of muscle relaxants
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Opiates most likely to cause muscle rigidity
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alfentanil and remifentanil
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Problems with muscle rigidity after opiate admin
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impairs spontaneous and controlled ventilation, glottic closure, may occur long after last administration, decr lung compliance and FRC, incr ICP and PA pressure and CVP and PVR
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How do I treat muscle rigidity assoc w opioids?
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muscle relaxants! succinylcholine, narcan, thiopental, benzos, alpha 2 agonists
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When does opioid induced rigidity most often occur?
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right after LOC
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If you try to mask ventilate a pt experienced significant narcotic induced muscle rigidity before giving muscle relaxants, you will..
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insufflate the stomach by accident, inadequate oxygenation and ventillation
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Miosis (pinpoint pupils) occur because of _____ stimulation of the parasympathetic oculomotor nerve.
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ciliary ganglia
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Opioids abolish cortical inhibition of the _____, causing papillary constriction.
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edinger-westphal nucleus
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How does use of fentanyl, alfentanil, sufentanil, during induction affect the eyes?
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prevents incr IOP
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Opioids ______ thermoregulatory thresholds.
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reduce
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____ is a unique opioid that can effectively terminate shivering.
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meperidine
also precedex! |
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Meperidine reduces shiver threshold at the ____ Receptor.
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kappa
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Morphine induced itching is mediated by the ____ Receptor. It can be treated w administration of _____, suggesting a ____-mediated central mechanism for pruritis.
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mu, narcan, receptor
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By giving a _____ opioid w low to medium efficacy at both mu and kappa receptors (nalbuphine and butorphanol) help to maintain kappa analgesia and antagonize mu itching.
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mixed
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Pruritis secondary to cholestasis is ameliorated by
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opioid antagonists
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The opiate that most increases biliary pressure is
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fentanyl
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What is the treatment for biliary colic induced by opioids?
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atropine or glyopyrolate (anti-cholinergic/anti-vagal)
nitroglycerine (smooth muscle relaxant) glucagon (dilates sphincters, relaxes smooth muscles) narcan (reverses narcotic -- no analgesia now!) |
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This is the most potent opioid, should be given after obtaining an airway first, and is reserved for big extensive ORs
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sufentanil
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This opioid has a shorter half life and lower volume of distribution than fentanyl, making it more ideal in outpatient settings.
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alfentanil
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This opioid should be given by continuous infusion, wears off quickly w the shortest half life and duration of action, and is metabolized by nonesterase dependent hydrolysis in the plasma.
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remifentanil
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In obese patients, opioid dose should be based on
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ideal body weight or lean body mass, rather than total body weight
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Tolerance of an IV infusion opioid can develop in as little as 2 hrs, requiring
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increase in dose/gtt rate
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It is (Safe/unsafe) to give narcan to a pt without narcotic onboard, causing this side effect:
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safe, appetite suppression
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Naltrexone is abused as
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a diet pill
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If narc antagonist doesn't last as long as the narcotic..
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the pt becomes renarcotized and requires additional dose
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Naltrexone is given for _____ programs to deter further abuse, and pts receiving it require _____.
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etoh and opiate withdrawal programs, more narcotic acutely
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Possible complications of narcan
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HTN, CVA, pulm edema, cardiac arrest, death, vtach, vfib
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Methods of administration of fentanyl
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transdermal
oral mucosal (pill or lolly) intranasal transpulmonary |
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Opioid induced bowel dysfunction includes...
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1. decr GI motility and emptying
2. decr pyloric tone 3. decr enzymatic secretion 4. inhibition of small and large bowel propulsion 5. incr fluid and electrolyte absorption 6. incr nonpropulsive segmental contractions 7. incr anal sphincter tone |
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Clinical GI effects of opioids
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decr appetite, incr gerd, NV, delayed digestion, constipation, delayed absorption of meds, straining, incomplete evacuation, bloating, abd distension, spasm/abd cramps/pain
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What action do alvimopan and methylnaltrexone have?
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opioid antagonists that only act peripherally, so they decr GI side effects of narcotics but maintain pain control in brain and avoid withdrawal
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Giving highest opioid dose in the beginning of the case when pt has most pain is called
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front loading
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This is any natural or synthetic compound that has effects similar to hose of morphine or acts as agonist at same receptors to which morphine binds
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opioid
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Local anesthetics act by
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interrupting transmission of all nerve impulses, including pain
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NSAIDs and asa act by
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decreasing pathological processes leading to pain
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Opioid analgesics act primarily to alter the ____ of pain as a ____ entity.
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perception, noxious
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The classical pharmacological effects of morphine, like analgesia and resp depr, are mediated by ___ receptors.
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mu
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___ receptors shrae a number of effects w mu receptors and also prevent shivering.
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kappa
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____ Receptors are responsible for mediating analgesic effects of endogenous opioid peptides, esp in spinal cord.
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delta
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Doses of opioids that are sufficient to produce apnea and profound analgesia do not necessarily produce ____ in healthy individuals.
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sleep
must also give anesthetic! |
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_____ can be produced due to merperidine metabolite normeperidine. This is most likely after ____ dose or if pt is in ____ Failure and retains metabolite.
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seizures - potent convulsant,
large, renal |
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Opioids produce a dose-related depr of ventilatory response to CO2 by direct effect on ventilatory centers in the _____.
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medulla
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Pts drive to breathe may be abnormal despite an apparently normal ____ and state of _____.
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RR and consciousness
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_____ further depresses the response to CO2 and potentiates opioid resp depr.
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Sleep
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Equianalgesic doses of all opioids produce equivalent amts of
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ventilatory depression -- none are more or less dangerous than morphine in this regard
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Tolerant individuals are unlikely to become
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apneic
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It is dificult to reverse resp depression without also reversing
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analgesia
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Opioids suppress cough by depressing cough centers in the
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medulla
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____ is a pathognomonic sign of opioid OD
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pinpoint pupils (miosis)
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Opioids cause direct stim of the CTZ, located in the _____.
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postrema on the floor of the fourth ventricle
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The most common drugs to cause lead pipe muscle rigidity are -------. may also cause constriction of laryngeal and pharyngeal muscles
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fentanyl, alfentanil, sufentanil, remifentanil
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Opioid anesthesia in critically ill pts w cardiac ischemia or failure is beneficial because
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minimal myocardial effects, bradycardia and peripheral vasodilation
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Not in potent opioids, but in morphine, there may be a noimmunological release of ______, from tissue mast cells, leading to local itching, redness and hives, flushing.
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histamine
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Opioids decrease the passage of liquids and solids at every level of the ____, termed opioid ____ dysfunction
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GI tract, bowel
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|
Urinary effects of opioids
|
incr contractions of ureter,
relieve pain from ureteral stones, decr detrusor contraction in response to bladder distension, incr tone of urinary sphincter |
|
|
Even though opioids have no specific teratogenic effects...
|
chronic maternal opioid use leads to fetal physical dependence -- neonatal withdrawal (Can be fatal)
|
|
|
Meperidine is (more/less) lipid soluble than morphine, making it (faster/slower) than morphine, with a (longer/shorter) duration.
|
more, faster, shorter
|
|
|
Patients receiving MAOIs and meperidine may suffer __________ (clonus, agitation, hyperreflexia, hyperthermia)
|
serotoninergic crisis
|
|
|
Dilaudid is (water/lipid) soluble, making it ideal for chonic users w high tolerance or pain pumps, as well as selective spinal analgesia.
|
water
|
|
|
Methadone is a synthetic mu opioid with ____ bioavailability. After repeated oral doses, pt may be subject to ______.
|
very high oral bioavailability,
accumulation |
|
|
Methadone is great in the community setting/ post op pain mgmt because
|
less euphoria and interruption of ADLs
|
|
|
Fentanyl is ____ soluble, giving it rapid onset and short duration. In low doses, the drug is quickly ______, and in high doses the drug is _____.
|
lipid,
redistributed, long-acting |
|
|
Sufentanil is (more/less) potent and lipid soluble than fentanyl, intended for ____ OR cases.
|
more,
long! |
|
|
Methadone is a synthetic mu opioid with ____ bioavailability. After repeated oral doses, pt may be subject to ______.
|
very high oral bioavailability,
accumulation |
|
|
Methadone is a synthetic mu opioid with ____ bioavailability. After repeated oral doses, pt may be subject to ______.
|
very high oral bioavailability,
accumulation |
|
|
Remifentanil is metabolized in the plasma and has a very short half life, leading to _____ accumulation.
|
essentially none
|
|
|
Drawback of remifentanils short duration
|
pts expected to have post op pain must receive longer acting opioid prior to d/c remi gtt
|
|
|
Co-admin of opioids potentiates the sedative/hypnotic effects of ______. This way, opioids can aid in _____ emergence -- lower doses of volatile agents needed.
|
barbs, benzos and propofol,
more rapid |
|
|
_____ is usually a reliable sign of increasing opioid effect if the case permits spontaneous ventilation. _____ is also a useful cardiac sign.
|
decreasing RR or depth,
incr BP |
|
|
Naloxone works as a competitive antagonist at all opioid receptors, but the most at ____ receptors. Since the block is reversible and competitive, it may be overcome by ____.
|
mu, adding more agonist
|
|
|
Opioid antagonist onset and duration is ___ and ____. This is shorter than all opioids durations except ____.
|
rapid and brief,
remifentanil |
|
|
Dose of narcan
|
0.4 mg IV
|
|
|
_____ are always in the body (Constitutive) and ____ are released when tissue is damaged (inductive/reactionary enzyme).
|
COX 1,
COX 2 |
|
|
____ acts on platelets (TXA2) and the stomach (PGE2).
|
COX1
|
|
|
____ acts on blood vessels and kidneys.
|
COX 2
|
|
|
Types of non-narcotic analgesics
|
asa
acetaminophen (tylenol, paracetamol) ibuprofen (advil, dolgesic, motrin, saleto, caldolor IV) naproxen (naprosyn) indomethacin (indocin) ketorolac (toradol) celecoxib (celebrex - only cox 2 inhibitor) |
|
|
Since celecoxib is a cox 2 inhibitor, it is able to protect the _____ but increases ____ side effects.
|
stomach, cardiovasc (MI)
|
|
|
All non narcotic analgesics are _____ and ____. However, all but acetaminophen are ____.
|
antipyretic and analgesic,
anti-inflammatory |
|
|
Primary mechanism by which NSAIDs exert analgesia is through inhibition of ____ and synthesis of ____, which are important mediators of peripheral sensitization and hyperalgesia.
|
COX, prostaglandins
|
|
|
Cox 1 is ____ and Cox 2 is ____.
|
constitutive, inducible
|
|
|
Cox 1 participates in
|
platelet aggregation, hemostasis, gastric mucosal protection
|
|
|
Cox 2 participates in
|
pain, inflammation, fever
|
|
|
Asa is a noncompetitive inhibitor of ______, which is irreversible. It takes 6-8 days to make replacements. Pts should stop taking asa 1 wk before surgery unless ____.
|
platelets, at high risk for MI
|
|
|
NSAIDs serve as an effective adjunct for ____, and can be given through these routes.
|
opioids,
PO, IV |
|
|
NSAIDs (not acetaminophen) reduce opioid related side effects of ____.
|
nausea, vomiting and sedation
|
|
|
Due to inhibition of cox and prostaglandins, some perioperative side effects of nsaids include
|
decr hemostasis,
renal dysfunction, GI hemorrhage, deleterious effects on bone healing and osteogenesis |
|
|
Perioperative NSAIDs are most likely to affect renal function in patients with these high risks
|
hypovolemia, abnormal renal fxn, abnormal serum electrolytes
|
|
|
NSAID induced renal dysfunction occurs due to _____ dilating the renal vascular beds and mediating diuretic and natriuretic renal effects.
|
prostaglandins
|
|
|
In patients w asa-induced asthma, they should not be given
|
asa, NSAID, or tylenol
|
|
|
Types of non-narcotic analgesics
|
asa
acetaminophen (tylenol, paracetamol) ibuprofen (advil, dolgesic, motrin, saleto, caldolor IV) naproxen (naprosyn) indomethacin (indocin) ketorolac (toradol) celecoxib (celebrex - only cox 2 inhibitor) |
|
|
How do cox 2 inhibitors affect bone and wound healing?
|
interfere w fracture healing -- incomplete unions and nonunions
|
|
|
Since celecoxib is a cox 2 inhibitor, it is able to protect the _____ but increases ____ side effects.
|
stomach, cardiovasc (MI)
|
|
|
All non narcotic analgesics are _____ and ____. However, all but acetaminophen are ____.
|
antipyretic and analgesic,
anti-inflammatory |
|
|
Primary mechanism by which NSAIDs exert analgesia is through inhibition of ____ and synthesis of ____, which are important mediators of peripheral sensitization and hyperalgesia.
|
COX, prostaglandins
|
|
|
Cox 1 is ____ and Cox 2 is ____.
|
constitutive, inducible
|
|
|
Pts w sulfonamide allergy should not receive
|
celecoxib
|
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol is contraindicated in patients with serum ____ concentrations indicating advanced ____ impairment.
|
creatinine, renal
|
|
|
Toradol can be given via these routes
|
IM, IV, spinal block
|
|
|
Toradol is contraindicated in patients with serum ____ concentrations indicating advanced ____ impairment.
|
creatinine, renal
|
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
Toradol can be given via these routes
|
IM, IV, spinal block
|
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
cox-2 inhibitors (celecoxib or valdecoxib) are contraindicated in patients with
|
hypersensitivity to the med,
asthma, urticaria, or allergic type reactions (Asa triad) after taking asa or nsaids |
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol is contraindicated in patients with serum ____ concentrations indicating advanced ____ impairment.
|
creatinine, renal
|
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol can be given via these routes
|
IM, IV, spinal block
|
|
|
Toradol is contraindicated in patients with serum ____ concentrations indicating advanced ____ impairment.
|
creatinine, renal
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol should be used w caution in patients w ____ because it is a potent inhibitor of prostaglandin synthesis.
|
impaired renal fxn or history of kidney dz.
|
|
|
Toradol can be given via these routes
|
IM, IV, spinal block
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol is contraindicated in patients with serum ____ concentrations indicating advanced ____ impairment.
|
creatinine, renal
|
|
|
Toradol is contraindicated in patients with serum ____ concentrations indicating advanced ____ impairment.
|
creatinine, renal
|
|
|
Toradol and its metabolites are eliminated primarily via the ____.
|
kidneys
|
|
|
Toradol is contraindicated in patients with serum ____ concentrations indicating advanced ____ impairment.
|
creatinine, renal
|
|
|
The IV form of tylenol is called _____, and is approved for use as _____.
|
ofirmev (cadence),
pain mgmt and fever reduction |
|
|
_____ Was the first nsaid to become available IV, and is marketed for short term use <5days. In the elderly pop especially, there is risk of GI bleeding, ulceration or perforation.
|
toradol
|
|
|
IV ibuprofen is called _____, is good for treating mild to moderate pain, and may cause ____ and ____ toxicity.
|
caldolor,
renal, GI |
|
|
Overdose of tylenol causes serious or fatal ____ injury, especially in fasting patients.
|
liver
|
|
|
Tylenol overdose is treated with
|
n-acetylcysteine
|
|
|
Tylenol can increase the anticoagulant effects in a drug interaction with
|
coumadin
|
|
|
IV tylenol has been shown to have ___ sparing effect.
|
opioid
|
|
|
Why do they mix oral morphine w naltrexone?
|
so that it cannot be crushed for recreational abuse -- only works in pill form!
|
|
|
The most potent opioid outside the OR is
|
dilaudid
|
|
|
In patients taking an MAOI, meperidine can cause severe ___ and ___.
|
encephalopathy, death
|
