pathophysiologic issues with depolarizing and non depolarizing NMB agents
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| What are the 5 drugs associated with resistance to non depolarizing NMB agents | Phenytoin (Dilantin), Corticosteroids, Aminophylline, Theophylline, Fursosemide (1 - 4 mg/kg dosages)
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| Why does Phenytoin (Dilantin) cause shorter duration of non depolarizing NMB agents? | increased metabolism due to induction of cytochrome P-450 or decreased activity of acetylcholinesterase
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| How long is the duration of Rocuronium (Zemuron) in patients taking Phenytoin (Dilantin)? | 4 - 7 minutes (20% of normal duration)
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| How long is the duration of Vecuronium (Norcuron) in patients taking Phenytoin (Dilantin)? | 16 - 22 minutes (37% of normal duration)
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| How long is the duration of Pancuronium (Pavulon) in patients taking Phenytoin (Dilantin)? | 24 - 36 minutes (40% of normal duration)
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| Chronic use of Corticosteroids has been reported to cause resistance to the ___________ class of non depolarizing NMBs. | steroidal
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| Why are Aminophylline and Theophylline associated with resistance to non depolarizing NMB? | they inhibit phosphodiesterase, increasing the cAMP needed to make and release ACh. more ACh = greater dose of NMB needed to compete
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| Why do large doses (1 - 4 mg/kg) of Furosemide (Lasix) cause resistance to non depolarizing NMB? | inhibits phosphodiesterase and increases cAMP needed to make and release ACh, so more ACh = greater dose of NMB needed to compete
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| Why are burn patients resistant to non depolarizing NMB? | caused by decreased sensitivity (affinity) of post junctional receptors to either ACh or non depolarizing NMB
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| When does the resistance to non depolarizing NMB in burn patients begin and how long does it last? | begins 10 days after injury, peaks at 40 days and declines after 60 days; requires > 30% or more BSA burned
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| How does hyperkalemia affect non depolarizing and depolarizing NMB agents? | non depolarizing = resistance;
depolarizing = sensitivity
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| How does hypokalemia affect non depolarizing and depolarizing NMB agents? | non depolarizing = sensitivity;
depolarizing = resistance
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| How does hypermagnesemia affect blockade by non depolarizing NMB agents? | decreases release of ACh from pre junctional receptors causing an enhanced block
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| How does hypernatremia affect blockade by NMB agents? | dehydration causes decreased volume of distribution, so prolonged blockade r/t more drug reaching receptors
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| How does significant hypothermia affect blockade by NMB agents? | prolongs duration by slowing metabolism via kidneys, liver, and Hofmann elimination and plasma esterases
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| How do volatile anesthetics enhance the effect of non depolarizing NMBs? | volatiles decrease skeletal muscle tone, so requires less dose of NMB to produce same effect; weaker twitches and stronger blockade; can be used to our advantage.
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| How do local anesthetics enhance the effect of non depolarizing NMBs? | they interfere with release of ACh from pre junctional receptors, block ion channels and directly suppress skeletal muscle tone
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| How do certain antibiotics enhance the effect of non depolarizing NMBs? | magnesium type effect (anti calcium = decreased release of ACh)
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| What antibiotics increase sensitivity to non depolarizing NMBs? | aminoglycosides: genatmycin, neomycin, streptomycin, kanamycin, amikacin, tobramycin, and vancomycin too
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| What antibiotics have no effect on blockade by NMBs? | penicillins and cephalosporins
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| Why does lidocaine enhance the effect of non depolarizing NMBs? | blocks pre junctional release of ACh
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| True or False: Quinidine (an anti arrhythmic drug) prolongs blockade by both non depolarizing and depolarizing NMBs. | true
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| Although Lithium has a variable effect on blockade by non depolarizing NMB, why does it cause a prolonged onset and duration of depolarizing NMB? | acts similarly to sodium ion. influx hypopolarizes membrane and potentiates depolarizing NMBs (SCh)
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| Why does Lasix (in doses < 1 mg/kg) enhance blockade by non depolarizing NMBs? | decreased cAMP production, so less ACh released
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| Does cyclosporine (anti rejection drug) cause sensitivity or resistance to non depolarizing NMBs? | sensitivity (prolonged blockade)
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| How does the administration of SCh affect the blockade by a non depolarizing NMB? | it enhances the block (deepens it) but does not prolong it. so it reduces the dose of the non depolarizing NMB needed.
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| What must you always check for after administration of Succinylcholine but before administration of any non depolarizing NMB? | return of twitches
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| Combination of non depolarizing NMB causes a __________ effect, allowing for a smaller doses of each. | synergistic
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| Do Verapamil and other calcium channel blocking drugs cause sensitivity or resistance to non depolarizing NMBs? | sensitivity
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| Doe acute administration of Hydrocortisone potentiate or lessen a blockade by a non depolarizing NMB? | potentiate
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| The antihypertensive drugs Trimethaphan and Hexamethonium cause prolongation of blockade by depolarizing and non depolarizing NMB agents, Why? | inhibit plasma cholinesterase activity and cause relaxation on their own
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| What groups of patients will typically receive aminoglycoside antibiotics during anesthetic? | GU cases = gentamycin
suspected endocarditis = clindamycin
allergic to PCNs or cephalosporins = vancomycin
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| Succinylcholine administration for intubation ________ dose required of non depolarizing NMB | reduces
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| Untreated myasthenia gravis patients are ________ to non depolarizing NMBs because they have _______ receptors for which to compete | sensitive
decreased
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| Treated myasthenia gravis patients are ________ to non depolarizing NMBs | resistant
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| Treated myasthenia gravis patients are sensitive to Succinylcholine. Why? | because part of treatment is anticholinesterase drugs which inhibit plasma cholinesterase needed to metabolize SCh
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| Myasthenic Syndrome or Eaton Lambert is seen in what kind of cancer? | oat cell carcinoma of the lungs
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| What is an autoimmune disease where presynaptic calcium channels are destroyed by antibodies | Myasthenic syndrome (Eaton Lambert)
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| Why are anticholinesterase drugs ineffective in Myasthenic Syndrome (Eaton Lambert) patients? | because there is no ACh released into the NMJ
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| Myasthenic Syndrome (Eaton Lambert) patients are _____ sensitive to NMB agents (both SCh and non depolarizers) than myasthenia gravis patients. | more
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| What would be the goal when giving non depolarizing NMB agent to myotonia dystrophica patient? | dose them in order to avoid giving reversal. reversal drug = increase of ACh = possible prolonged contraction in these patients
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| Succinylcholine causes prolonged muscle contraction in patients with _______ ________ | myotonia dystrophica
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| Why is pediatric dosing for non depolarizing NMB essentially unchanged from adult dosing despite increased sensitivity in pediatric patients? | pediatric patients have a larger volume of distribution
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| With regard to non depolarizing NMB, elderly patients typically have _______ duration and ________ onset time. | prolonged duration
prolonged onset time
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| Obese patients typically have _______ blockade with non depolarizing NMBs | prolonged (especially with Vecuronium)
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| Rocuronium (Zemuron) dose is based on ______ body weight | ideal
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| Succinylcholine dose is based on _______ body weight | total
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Created by:
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