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NU 600
Exam 4 - Opioids and Induction Agents
| Question | Answer |
|---|---|
| T/F: Pain is thought to be always unpleasant. | True |
| Objective signs of pain are based on _______, while subjective signs of pain are based on ________. | Vital signs; experiences |
| What does tissue injury activate and what does this result in? | Activates inflammatory mediators and results in increased sensitivity of nociceptors |
| Where do peripheral nociceptors carry pain signals to? | Dorsal horn of the spinal cord |
| Output neurons from the dorsal horn ascend the spinal cord after crossing into what feature? | Anterior lateral quadrant |
| Pain impulses ascend via what two fibers and in what tract? | Alpha and Delta fibers in the spinothalamic tract |
| Prior to terminating in the somatosensory cortex, what structure do Alpha and Delta fibers enter? | Thalamus |
| Where do somatosensory fibers terminate? | Primary somatosensory cortex |
| What is the general method of action of opioids? | Block transmission of pain by decreasing action potentials of sensory neurons |
| What channels do opioids affect? | Sodium, potassium, calcium |
| How does pain affect the SNS? | Increases SNS tone |
| How does pain affect global O2 demand? | Increases |
| In what 3 ways does pain affect breathing? | Hypoventilation, atalectasis, decreased cough |
| What two hormones do opioids reduce? | Adrenocorticotropic, cortisol |
| How do opioids contribute to dynamic fluid stability? | Decrease stress response |
| True/False: Opioids have negative cardiac effects and should be used sparingly. | False = cardiac friendly and can be used in large doses |
| Which enzyme is inhibited by opioid binding? | Adenylate cyclase |
| The neuron is (hyper/hypo)-polarized as a result of opioid binding. | Hyper-polarized |
| The presynaptic effects of opioids blocks the release of what 3 neurotransmitters? | Dopamine, norepinephrine, substance P |
| Mu I receptors are located (above/below) the spinal cord. | Above |
| (Mu I/Mu II) receptors provide supraspinal analgesia. | Mu I |
| What are the side effects of Mu I receptor stimulation? | Euphoria, miosis, pruritis, urinary retention, N/V |
| What are the negative side effects of Mu II receptors? (4) | Sedation, bradycardia, respiratory depression, ileus |
| Apnea and hypoventilation are caused by stimulation of (Mu I/Mu II receptors). | Mu II |
| (Mu I/Mu II) receptors are associated with more side effects. | Mu II |
| Delta, Kappa, and Sigma are types of _______ receptors. | opiate |
| Mu activity and dependence are related to stimulation of (Delta/Kappa/Sigma). | Delta |
| What are the responses of kappa receptor stimulation? | Spinal analgesia; sedation; myosis |
| What are the responses of sigma receptor stimulation? | Dysphria, hypertonia |
| How much more potent is fentanyl over morphine? | 100x |
| Fentanyl has a/an (stable/unstable) cardiac profile. | Stable |
| Fentanyl ideal as a (primary/adjunct) analgesic. | Adjunct |
| Fentanyl is associated with more (Mu I/Mu II) symptoms. | Mu II |
| Which medication is associated with chest wall rigidity? | Fentanyl |
| All opioids have the capability of causing _______. | Nausea |
| What is the Vd for fentanyl? | 4L/kg |
| What is the onset and duration of effect fentanyl? | Onset=immediate; Duration=30min to 1hr |
| The ½ life of fentanyl is _____ minutes. | 219 |
| Fentanyl undergoes 1st pass effect in the ______. | Lungs |
| How much of the initial dose of fentanyl is metabolized in the lungs? | 75% |
| Fentanyl metabolites are (active/inactive). | Inactive |
| How much fentanyl is cleared in the urine? How much is excreted unchanged in urine? | 75%; 10% |
| 1st pass metabolism of fentanyl occurs in the ________. | Liver |
| Describe the mechanism by which fentanyl’s effects may be prolonged. | Continuous infusion or boluses lead to saturation of inactive tissues |
| What should be given in the event of chest wall rigidity with fentanyl? | NMB |
| What are the low, moderate, and large doses for fentanyl? | 1-3mcg/kg; 3-10mcg/kg; 50-150mcg/kg |
| Name the scenarios in which low, moderate, and large doses of fentanyl would be used. | L=minor procedures; M=DL or w/surgical stimulation; L=cardiac anesthesia |
| Moderate dosing of fentanyl blunts the ______ pathway. | Nociceptive |
| What dose of fentanyl is required to blunt the response to directly laryngoscopy? | 3-10mcg/kg |
| Fentanyl is associated with the release of what 2 hormones? | Prolactin, HGH |
| What are the non-analgesic effects of fentanyl? | Respiratory depression, bradycardia, euphoria, sedation, dysmotility, prolactin and growth hormone release |
| Where are Mu receptors located in the body? | Cerebral cortex, thalamus, hypothalamus, midbrain and medulla, dorsal horn, gut, peripheral tissues |
| What neurological effect are Kappa receptors associated with? | Dysphoria |
| Kappa receptors have (weaker/stronger) analgesic and respiratory effects than Delta and Mu receptors. | Weaker |
| Pain is generally (under/over) reported in the elderly. | Under |
| What are three systems breakdowns that affect the dosing of analgesics for the elderly? | GI malabsorption, decreased hepatic fxn, decreased CYP enzymes |
| What is the effect of the GG variant of the A118A polymorphism in men? | Lower pain threshold |
| Men have lower pain threshold d/t what genetic variant? | GG variant of Au8A |
| Chronic ETOH use leads to enzyme (induction/inhibtion). | Induction |
| Give an example of cross tolerance. | Chronic ETOH leads to enzyme induction, requiring higher doses of pain medication for effect |
| Which opiate analgesic is least affected by genetic variability of the CYP system? | Fentanyl |
| What are the 5 methods of administration for fentanyl? | PO, IV, intrathecal, epidural, transdermal |
| What does preemptive analgesia decrease? | Sensitization of the CNS to pain impulses |
| When should pre-emptive analgesia be given? | Almost any time: upfront prior to painful stimuli, intra-operatively, after discharge home |
| What are the benefits of multimodal analgesia vs. opiate analgesia? | Improved pain relief, reduced SE, opiate sparing |
| What are three types of medications used with multimodal therapy? | NSAIDS, COX2 inhibitors, APAP |
| What does the Equianalgesic Theory state? | Doses of different opioids can provide equivalent pain relief |
| 10mg IV morphine = _____ mg IV dilaudid = _____ mcg IV fentanyl. | 1.5; 100 |
| Which medication serves as the “Gold Standard” for opioids? | Morphine |
| What type of metabolism does morphine undergo? | Phase II glucuronidation |
| Name the 2 metabolites of morphine and describe the differences. | Morphine-6-glucuronide=active=1/4 potency of morphine; morphine-3-glucuronide=inactive |
| Which pain receptors exhibit characteristics for physical dependence/abuse potential, and which do not? | High abuse potential=MuII/Delta; Low abuse potential=MuI, Kappa |
| Inhibition of peristalsis, nausea, and vomiting are associated with which pain receptor? | MuII |
| Which pain receptor exhibits diuretic symptoms when stimulated? | Kappa |
| Which pain receptor inhibits the release of vasopressin? | Kappa |
| Which pain receptor is associated with psychomimetic (i.e. hallucinations, delirium) reactions? | Kappa |
| Individuals with (renal/liver) failure are at risk for increased levels of active morpine metabolites. | Renal |
| What is the ½ life for morphine and its active metabolite? | Morphine=114min, M6G=173min |
| Sufentanil is a _______ derivative. | Phenylpiperidine |
| Sufentanil is _______ times more effective than fentanyl. | 10 |
| In what surgical scenarios is sufentanil used? | High dose cardiac and spinal procedures |
| Which opioid is ideal for continuous infusions? | Sufentanil |
| How are fentanyl and sufentanil dosed? | mcg/kg/hr |
| Which opiate has the highest lipophilic profile? Sufentanil | sufentanil |
| The bolus dose of sufentanil is _________ mcg. | 10-25 |
| In spinal cases, when should sufentanil be stopped? | 40min before expected wake-up |
| After sufentanil is stopped, _______ should continue running at _____________ to GA. | Propofol; 150mcg,kg,min |
| Post-op pain control is better obtained with periop use of (sufentanil/remifentanil). | Sufentanil |
| Which opioid does not undergo organ-dependent elimination? | Remifentanil |
| True/False: Remifentanil is effective as a bolus because of its rapid onset. | False = infusion only d/t profound apnea |
| How is remifentanil metabolized? | Ester hydrolysis by tissue and blood esterases |
| Remifentanil (does/does not) depend on plasma cholinesterase for metabolism. | Does not |
| What is the onset, duration of effect and ½ life of remifentanil? | Immediate; 5-10min; 10-20min |
| Renal and hepatic issues (do/do not) affect metabolism of remifentanil. | Do not |
| What classification of opioid is dilaudid and when is it used? | Intermediate acting semisynthetic used for moderate to severe pain |
| The onset of dilaudid is ______ min with a duration of ______ hrs. | 5; 4-5 |
| What are two significant benefits of dilaudid? | No active metabolites and diminished SE profile |
| Demerol is a member of the _______ group. | Phenylpiperidine |
| Demerol forms (active/inactive) metabolites. | Active |
| What is the active metabolite of demerol and what can it cause? | Normeperidine; seizures |
| Which opioid has pro-epileptic qualities? | Meperidine |
| In what patients is demerol not recommended for use? | Sickle cell, CNS d/o, renal failure, children |
| What is the post-op dose of meperidine used for rigors? | 6.25mg -> 12.5mg -> 25mg |
| Meperidine is potentially lethal when combined with what other class of medications? | MAOIs |
| What two physiological symptoms may result from the use of meperidine with MAOIs? | Hypotension, respiratory depression |
| Besides Mu receptors, receptors in what other areas may contribute to respiratory depression? | Cortical and brainstem |
| What is the potential problem with narcotic use in cholangiograms? | Biliary spasms |
| Which is the better indicator for patient satisfaction: PONV or post-op pain? | PONV |
| Nausea is triggered by stimulation of what three receptors? Dopamine, serotonin, histamine | Dopamine, serotonin, histamine |
| (Men/Women) are more prone to PONV. | Women |
| What is the classification of nalbuphine? | Synthetic opioid agonist-antagonist |
| Nalbuphine is a _____ receptor agonist, and a _______ receptor antagonist. | Kappa, Mu |
| What are the possible benefits of nalbuphine if used during a cholangiogram? | Reverses respiratory depression and sphincter of Oddi spasm |
| Nalbuphine is equipotent to which opiate? | Morphine |
| Buprenorphine is a/an (agonist/partial-agonist) of the ______ receptor. | Partial-agonist; Mu |
| The effects of buprenorphine can last up to _______ hrs. | 8 |
| What are two characteristics of the relationship between buprenorphine and naloxone? | Buprenorphine not readily reversed by naloxone; used together in drug rehab |
| Which medication is often paired with naloxone in its use for drug rehabiliation? | Buprenorphine |
| Buprenorphine can cause withdrawal symptoms in what types of patients? | Patients who have been receiving Mu opioid agonists |
| What type of receptor does Narcan primarily influence? | Mu |
| Besides Mu receptors, what other receptors are affected by Narcan? | Kappa and Delta |
| What is the serum ½ life of Narcan? | 64 minutes |
| Narcan blocks both ______ and ______ opioids. | Endogenous; exogenous |
| _______ administration can precipitate flash pulmonary edema. | Narcan |
| True/False: The effects of Narcan last as long as opioids. | False – does not last as long |
| What is the drawback to rapid administration of Narcan? | Acute w/d manifested as sz, dysrhythmias, intense pain |
| How is Narcan prepared for administration? | 1amp (0.4mg/ml) is diluted in a syringe of 10cc NS to yield 40mcg/ml |
| After dilution in a 10cc syringe, how much and how often is Narcan administered? | 0.5-1.0ml q5min until desired effect is achieved |
| What is the benefit of the anesthesia method of naloxone administration? | Antagonizes only the MuII receptor (sedation, respiratory depression) while analgesia is maintained |
| What does the anesthesia method of Narcan administration reduce? | The dramatic effect of Mu agonism reversal |
| What are the physiologic effects of rapid Mu agonism reversal? | Acute narcotic w/d, seizures, flash pulmonary edema |
| What is the classification of Precedex? | Highly selective and potent alpha-2 adrenergic agonist |
| Precedex is ______ times more selective for alpha-2 receptors than clonidine. | 10 |
| What is Precedex an isomer of? | It is a dextro isomer of medetomidine |
| What are the 3 sites of action of dexmedetomidine? | Brain, spinal cord, autonomic nerves |
| What are the CNS effects of dexmedetomidine? | Sedation/hypnosis, anxiolysis, analgesia |
| What are the autonomic effects of dexmedetomidine? | Decreased sympathetic activity (i.e. decreased BP and HR) |
| Post-op controlled ventilation may be achieved with an infusion of _________. | Dexmedetomidine |
| What is the reversal medication for dexmedetomidine? | Atipamezole |
| What are the benefits of dexmedetomidine for children in anesthesia? | Effective for emergence agitation/delirium |
| Name 2 different alpha-2 agonist medications. | Dexmedetomidine & clonidine |
| What does dexmedetomidine inhibit that gives it vasodilating properties? | Catecholamines and renin |
| Induction agents (can/cannot) be utilized for TIVA. | Induction agents (can/cannot) be utilized for TIVA. can |
| What types of surgical cases benefit from TIVA? | Cases involving neuro-monitoring |
| What is the keystone of barbiturate induction agents? | Sodium thiopental |
| What is STP derived from? | Barbituric acid |
| Barbituric acid (does/does not) have CNS activity. | does not |
| What provides barbituric acid with its sedative hypnotic effects? | Changes at the 2 and 5 carbon positions |
| How are pro-epileptic effects of barbiturates obtained? | Methyl radical substitution on the #5 carbon |
| How are anti-convulsive effects achieved with phenobarbital? | Phenol group addition at #5 carbon |
| True/False: Barbituratic inductiona agents do not burn on injection. | False |
| What is the trade name for methohexital? | Brevital |
| What does addition of a phenol group to the #5 carbon of phenobarbital produce? | Enhanced anti-convulsive properties |
| Where is the sulfur placed that produces sodium thiopental? | #2 carbon |
| What does the sulfur addition in STP produce? | Increased hypnotic potency, fast onset, shortened duration |
| What is the trade name for sodium pentothal? | Thiopental |
| What medication has been used for physician assisted suicide? | Pentobarbital |
| What is the trade name for pentobarbital? | Nembutal |
| Which channels does the barbiturate-GABA relationship influence and how does it affect these channels? | Influences duration of chloride channel opening (hyperpolarization) |
| What creates the hangover effect from barbiturate administration? | High fat affinity (reservoirs) |
| What is the primary determinant of barbiturate distribution? What other factors play a role in distribution? | Lipid solubility; cardiac output, blood volume, protein binding ionization |
| What is the cause of cessation of effects with barbiturates? | Redistribution away from CNS |
| What should be used to calculate barbiturate dosing. | Lean body mass (not actual body weight) |
| Barbiturates (do/do not) provide analgesia. | Do not |
| Barbiturates (do/do not) obtund airway reflexes. | Do not |
| What is the difference between transient and global ischemia in terms of barbiturates? | Barbiturates may offer protection w/focal, little benefit w/global |
| True/False: Methohexital is effective for muscle relaxation on induction. | False = induces involuntary muscle contractions |
| Which patient population are barbiturates contraindicated in? | Patients with inducible porphyria’s (Vampire’s Dz) |
| What reaction can thiobarbiturates cause? | Mast cell histamine release |
| True/False: Oxybarbiturates are implicated in mast cell mediated histamine release. | False |
| What is the treatment for extravasation d/t barbiturate administration? | 1% procaine and local application of heat for pain |
| What are the building blocks for heme and what body systems do they affect? | Porphyrins; skin and nervous |
| What steps are taken in the event that a barbiturate is injected into an artery? | Sympathetic block to affected area; heparinization; alpha-adrenergic antagonist for vasopasms |
| What is the classification of etomidate? | Carboxylated imidazole |
| What induction agent is water soluble in storage, then molecularly changes to become lipid soluble after injection? | Etomidate |
| What is similar about etomidate and barbiturates in regards to adverse drug reactions? | Can cause inducible porphyrias |
| What three types of medications can be given to blunt hyperdynamic responses? | BZD, sevoflurane, beta-blocker |
| What is a drawback and benefit of ketamine in relation to dysrhythmias? | May reverse digitalis induced dysrhythmias; may predispose myocardium to dysrhythmias when local anesthetics w/epinephrine are used |
| What should be given simultaneously with ketamine to reduce its adverse effects? | Antisialogogue b/c ketamine increases oral/bronchial secretions |
| What induction medication leaves upper airway reflexes intact? | Ketamine |
| What must simultaneously be given with ketamine and why? | Antisialogogue d/t increased oral and bronchial secretions |
| What are two pulmonary benefits of ketamine? | Leaves upper airway reflexes intact; potent bronchodilator |
| What are the effects of ketamine on pulmonary vasculature? | Increases pulmonary vascular resistance, leading to increased RV workload |
| What induction agent has been effective as treatment for status asthmaticus? | ketamine |
| What is the classification of propofol? | Non-barbiturate sedative hypnotic |
| Where does propofol primarily exert its influence? | GABA receptors |
| What does the 1st pass pulmonary effect of propofol yield? | 2,6 – diisopropoyl – 1,4 |
| SSEPs (are/are not) significantly altered by propofol. | are not |
| Unused portions of a propofol should be discarded within _______ hours of opening. | 6 |
Created by:
philip.truong
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