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107 Cards in this Set
- Front
- Back
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How does morphine depress respiration?
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reduces the sensitivity of the brainstem to CO2
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Why does the respiratory depression associated with morphine have a slower onset and a longer duration than fentanyl?
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fentanyl is more lipid soluble it gets into the CNS more quickly and gets out more quickly
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What lasts longer the respiratory depression associated with narcotics or the analgesia?
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respiratory depression
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How is morphine metabolized?
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metabolized into glucuronic acid in hepatic and extra hepatic sites
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What are side effects of morphine?
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reduces sympathetic tone with resultant orthostatic hypotension and syncope, causes histamine release, ventilatory depression
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How does respiratory depression with morphine differ when morphine is given epidurally?
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biphasic, initial depression due to systemic absorption at about 1 hr and then a later depression due to cerebral migration which occurs at about six to eight hours
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How can you treat right upper quadrant abdominal pain due to narcotics?
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narcan
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How potent is meperidine compared to morphine?
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1/10th
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What is different about the absorption of meperidine compared to morphine?
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meperidine is well absorbed from the GI tract
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How should you adjust meperidine doses in liver failure and why?
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give decreased dose because it is highly metabolized on first pass through the liver
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Why do elderly patients have increased sensitivity to meperidine?
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less protein binding and therefore greater bioavailability
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What are problems with meperidine?
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negative inotropic effects, orthostatic hypotension, tachycardia
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How potent is fentanyl compared to morphine?
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100 times more potent than morphine
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Why does fentanyl have a rapid onset and short duration?
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due to its lipid solubility
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How is fentanyl metabolized and eliminated?
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hepatic metabolism and renal excretion
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What is the cause of alfentanil's rapid onset and short duration?
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rapid onset is due to low pKa and short duration is due to low volume of distribution(low lipid solubility and greater protein binding) and extensive hepatic metabolism
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What is the dose of alfentanil?
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10-50 ug/kg
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What is the onset of action of alfentail, fentanyl?
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alfentanil: 1-2 minutes, fentanyl: 5-6 minutes
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Why should you be cautious about using alfentanil in patients with liver failure?
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elimination half life is markedly increased
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How does the potency of remi compare to fentanyl?
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similar
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What is the time to peak effect of remifentanil?
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1-2 min
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What is the typical infusion dose of remifentanil?
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0.1 mcg/kg/min-0.5 mcg/kg/min
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What is the typical infusion dose of sufentanil?
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bolus 1mcg/kg, infusion of 0.5 mcg/kg/hr
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What is the typical infusion dose of fentanyl?
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bolus 10 mcg/kg and infusion of 1-2 mcg/kg/hr
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What is the typical infusion dose of alfentanil?
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bolus 10-50 mcg/kg and infusion of 0.5-1.5 mcg/kg/min
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How is atracurium metabolized?
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hoffman elimination and nonspecific ester hydrolysis
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How does the potency of cisatracurium compare to atracurium?
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3 times more potent than atracurium
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What is the clinical duration of cisatracurium?
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1 hour
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What is the dose of cisatracurium?
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0.2 mg/kg
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How is pancuronium eliminated?
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80% eliminated unchanged in the urine(also undergoes significant hepatic metabolism)
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What is the lipid solubility of pancuronium?
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highly ionized and has limited lipid solubility
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How long after administering rocuronium does maximal neuromuscular blockade occur?
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60-90s
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What is the duration of action of rocuronium?
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30min
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How is rocuronium eliminated?
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biliary excretion
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How is doxacurium and pipecuronium eliminated?
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renal clearance
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What type of neuromuscular blockers are doxacurium and pipercuronium?
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both are long acting, doxacurium is a bisquaternary ammonium compound; pipercuronium is a steroidal
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How is the dosing of pipercuronium different in infants versus children and adults?
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potency is increased and duration of action is shortened
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How is vecuronium metabolized and excreted?
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hepatic metabolism and biliary excretion
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How is vecuronium affected in liver failure?
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elimination half life is increased at 0.2 mg/kg but not at 0.1 mg/kg
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How does magnesium affect neuromuscular block?
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decreases the release of acetylcholine from the nerve terminal and it decreases the sensitivity of the end-plate to the effects of ACh
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Name some drugs and electrolytes that prolong neuromuscular block?
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Li, Na, Mag, antibiotics, botulinum, procaine, decreased Ca and decreased K
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What is the connection of prostaglandings, arachidonic acid, COX, lipooxygenase, and phospholipase enzyme?
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prostaglandins are derived from arachidonic acid by COX or lipooxygenase, arachidonic acid release from cell membranes is stimulated by phospholipase enzyme
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What reaction is catalyzed by COX?
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arachidonic acid to endoperoxides
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What is the function of thromboxane synthetase?
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endoperoxides are converted to either thromboxane or prostacyclin by enzymes thromboxane synthetase
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what is the function of thromboxane?
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stimulates platelet aggregation by inhibiting adenylate cyclase and decreasing c-AMP
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What is the function of prostacyclin?
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stimulates production of cAMP and decreases platelet adhesiveness and aggregation
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What does lipoxygenase facilitate?
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conversion of arachidonic acid to the eventual production of leukotrienes
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How does aspirin impair platelet aggregation?
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inhibits cyclooxygenase and prevents the formation of thromboxane, a potent platelet aggregator
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What are the benefits of celocoxib over other NSAIDs?
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low risk of stomach ulceration, no effect on platelets and bleeding time
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What dose of morphine and demerol is comparable to 50mg toradol?
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50mg meperidine, 6mg morphine
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What is the half-life of ketorolac?
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6 hours
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What are contraindications of ketorolac?
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bronchospasm, angioedema, nasal polyps, concurrent use of other NSAIDs, know allergy to aspirin, history of GI bleeding
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What are the effects of echinacea?
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immunostimulation properties, hepatotoxicity
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What are the dangers of using garlic?
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decreased platelet aggregation, may augment the effects of warfarin, heparin, NSAIDs, asa
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What are the effects of ginger?
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prolongs bleeding time secondary to inhibition of thromboxane synthetase (has been used for nausea, vomiting, motion sickness, and vertigo, hyperemesis gravidarum)
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What is garlic used for?
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vasodilation and hypocholesterolemic activity(studies on both are lacking)
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What is ginko used for?
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intermittent claudication, tinnitus, memory loss, and impotence
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What are the risks of ginkgo?
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bleeding, should also be avoided with the concomitant use of anticonvulsants and TCAs as it decreases the effectiveness of these agents
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What are risks of ginseng?
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hypertension, bleeding, hypoglycemic effect and should be avoided in patients on insulin or oral hypoglycemics, should not be used with MAOIs as manic episodes have resulted from this combination
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What is St. John's Wort used for and what are the side effects?
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uses: anxiety, depression, and sleep disorders; side effect: photosensitivity
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What are the uses and side effects of kava kava?
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uses: anxiety; side effects: hepatotoxicity, depression, suicide
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What are the effects of Ma Huang(ephedra)?
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positive inotropic and chronotropic effects, bronchodilator,
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What are the side effects of Ma Huang(ephedra)?
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HTN, tachycardia, dysrhythmias, MI and CVA, periop hyper and hypotension
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What are causes of parkinsonism?
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drugs, viral encephalitis, and atherosclerosis
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What drugs inhibit or prevent the action of dopamine in the basal ganglion leading to a parkinson like effects?
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phenothiazine, reglan, butyrophenones(droperidol)
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What are treatments of parkinsonism?
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L-dopa, anticholinergics(benztropine, procyclidine, biperiden), bromocriptine
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Is ondansetron safe to use in patients with parkinsonism?
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yes it has no effect on dopamine receptors
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What are the doses of phenytoin?
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100-500mg or 10-15mg/kg
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How do benzos, barbs, theophylline and antacids affect phenytoin?
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benzos cause increased sensitivity to phenytoin; barbs, theophylline, and antacids cause decreased sensitivity to phenytoin
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What drugs have decreased effectiveness when used with phenytoin?
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nondepolarizing muscle relaxants, steroids, lasix, dopamine
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What are risks of using phenytoin by rapid IV bolus?
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bradycardia, hypotension, cardiac arrest
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What is the use of phenytoin?
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anticonvulsant, refractory Vtach or digoxin induced arrhythmias
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What are side effects of droperidol?
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state of cataleptic immobility, hallucinations, loss of body image, hypotension(secondary to alpha adrenergic blockade), QT prolongation, torsades, and EPS
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What is the dose of droperidol used for nausea?
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0.6-1.2mg
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What is the dose of versed for premedication?
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0.05-0.1mg/kg
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What are side effects of etomidate?
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pain on injection, myoclonic activity, postoperative N/V and adrenal suppression
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What is the dose and side effects of methohexital?
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1-2mg/kg; pain on injection and hiccoughing
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What is the induction dose of midazolam?
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0.2-0.3 mg/kg
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What happens to heart rate with rapid IV administration of thiopental?
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tachycardia
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How is propofol available commercially?
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1% solution in aqueous solution of 10% soybean oil, 2.25% glycerol, and 1.2% purified egg phosphatide
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How does propofol affect neuromonitoring?
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decrease in frequency with an increase in beta activity on EEG, induction doses can produce epileptiform activity, increases the latency and decreases the amplitude of somatosensory evoked potentials
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What are induction doses of thiopental?
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3-6mg/kg
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How is the dose of thiopental changed in the elderly?
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slow passage of thiopental from central to peripheral compartments which result in higher plasma concentrations of thiopental for brain distribution, creating greater anesthetic effects in elderly
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What are contraindications for flumazenil?
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patients on benzos to control life threatening increased ICP or status and patients withdrawing from cyclic antidepressants
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When is alprostadil beneficial?
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infants with congenital cardiac defects who have restricted pulmonary or systemic blood flow and who depend on a PDA for adequate oxygenation and lower body perfusion(pulmonary atresia, pulmonary stenosis, tetrology of fallot, coarctation of the aorta, transposition of the great vessels)
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What infants that require a patent ductus arteriosus respond best to prostaglandins?
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low initial PO2 and are 4 days old or less
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Why is PGE1 given by continuous IV infusion?
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due to it's rapid metabolism
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What are the most serious adverse effects of alprostadil?
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apnea, bradycardia, hypotension, fever
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What are the effects of alprostadil?
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vasodilation, inhibition of platelet aggregation, stimulation of intestinal and uterine smooth muscle
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What is the role of alprostadil in the setting of liver transplantation?
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fulminant hepatic and primary non-function postop may be effective by increasing liver blood flow and making liver cells more resistant to ischemic injury, also beneficial in hepatic failure due to tylenol, hep B
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What drugs should be avoided for 4 weeks after administering echothiophate?
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SCh, procaine, chloroprocaine, cocaine, tetracaine
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In what conditions is pseudocholinesterase increased?
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obesity and goiter
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In what conditions is pseudocholinesterase decreased?
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burns, liver disease, organophosphates, echothiophate, malnutrition, pregnancy
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What drugs inhibit pseudocholinesterase?
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anticholinesterases, echothiophate, pancuronium
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Why is SCh contraindicated in skeletal muscle myopathies?
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patients can experience rhabdomyolysis, hyperkalemia, and cardiac arrest
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What are complications of TPN?
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hypo and hyperglycemia, hypercarbia, hypophosphatemia, fatty acid deficiency, metabolic acidosis, sepsis
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What are effects of hypophosphatemia?
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left sift of the oxy-hemoglobin dissociation curve, respiratory failure, postop muscle weakness
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What should you do in a patient on TPN with failure to wean and concern for carbon dioxide retention?
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may be related to glucose load which results in excessive CO2 production, in this circumstance patient may benefit from greater proportion of calories coming from intralipid rather than glucose
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What should you start prior to discontinuing TPN?
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glucose containing solution
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What patients are at greatest risk of cyanide toxicity from SNP?
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nutritionally deficient in cobalamines(vit B12)
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What is the treatment of cyanide toxicity?
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sodium nitrite or thiosulfate, hyroxycobalamine in the setting of abnormal renal function
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How can you decrease the risk of cyanide toxicity when giving SNP?
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propranolol, captopril
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What are adverse effect of SNP?
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CN- and thiocyanate toxicity, rebound htn, intracranial htn, blood coagulation abnormalities, increased pulmonary shunting, hypothyroidism
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What is the mechanism of fenoldapam?
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dopamine receptor agonist with vasodilating properties in coronary, renal, mesenteric, and peripheral arteries
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What are the benefits of fenoldapam over SNP?
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not light sensitive, does not result in toxic metabolites, increases renal blood flow, glomerular filtration, promotes natriuresis and free water elimination
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How does fenoldapam affect MAP, SVR, PCWP, CI, HR?
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decreases MAP, SVR, PCWR while increasing CI without changing HR
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What is the elimination half-life of fenoldapam and where is it eliminated?
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90% of the drug is eliminated in the urine with a half-life of 5-10min
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