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Anes. Pharm I Test 1

pathophysiologic issues with depolarizing and non depolarizing NMB agents

QuestionAnswer
What are the 5 drugs associated with resistance to non depolarizing NMB agents Phenytoin (Dilantin), Corticosteroids, Aminophylline, Theophylline, Fursosemide (1 - 4 mg/kg dosages)
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
How long is the duration of Rocuronium (Zemuron) in patients taking Phenytoin (Dilantin)? 4 - 7 minutes (20% of normal duration)
How long is the duration of Vecuronium (Norcuron) in patients taking Phenytoin (Dilantin)? 16 - 22 minutes (37% of normal duration)
How long is the duration of Pancuronium (Pavulon) in patients taking Phenytoin (Dilantin)? 24 - 36 minutes (40% of normal duration)
Chronic use of Corticosteroids has been reported to cause resistance to the ___________ class of non depolarizing NMBs. steroidal
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
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
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
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
How does hyperkalemia affect non depolarizing and depolarizing NMB agents? non depolarizing = resistance; depolarizing = sensitivity
How does hypokalemia affect non depolarizing and depolarizing NMB agents? non depolarizing = sensitivity; depolarizing = resistance
How does hypermagnesemia affect blockade by non depolarizing NMB agents? decreases release of ACh from pre junctional receptors causing an enhanced block
How does hypernatremia affect blockade by NMB agents? dehydration causes decreased volume of distribution, so prolonged blockade r/t more drug reaching receptors
How does significant hypothermia affect blockade by NMB agents? prolongs duration by slowing metabolism via kidneys, liver, and Hofmann elimination and plasma esterases
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.
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
How do certain antibiotics enhance the effect of non depolarizing NMBs? magnesium type effect (anti calcium = decreased release of ACh)
What antibiotics increase sensitivity to non depolarizing NMBs? aminoglycosides: genatmycin, neomycin, streptomycin, kanamycin, amikacin, tobramycin, and vancomycin too
What antibiotics have no effect on blockade by NMBs? penicillins and cephalosporins
Why does lidocaine enhance the effect of non depolarizing NMBs? blocks pre junctional release of ACh
True or False: Quinidine (an anti arrhythmic drug) prolongs blockade by both non depolarizing and depolarizing NMBs. true
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)
Why does Lasix (in doses < 1 mg/kg) enhance blockade by non depolarizing NMBs? decreased cAMP production, so less ACh released
Does cyclosporine (anti rejection drug) cause sensitivity or resistance to non depolarizing NMBs? sensitivity (prolonged blockade)
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.
What must you always check for after administration of Succinylcholine but before administration of any non depolarizing NMB? return of twitches
Combination of non depolarizing NMB causes a __________ effect, allowing for a smaller doses of each. synergistic
Do Verapamil and other calcium channel blocking drugs cause sensitivity or resistance to non depolarizing NMBs? sensitivity
Doe acute administration of Hydrocortisone potentiate or lessen a blockade by a non depolarizing NMB? potentiate
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
What groups of patients will typically receive aminoglycoside antibiotics during anesthetic? GU cases = gentamycin suspected endocarditis = clindamycin allergic to PCNs or cephalosporins = vancomycin
Succinylcholine administration for intubation ________ dose required of non depolarizing NMB reduces
Untreated myasthenia gravis patients are ________ to non depolarizing NMBs because they have _______ receptors for which to compete sensitive decreased
Treated myasthenia gravis patients are ________ to non depolarizing NMBs resistant
Treated myasthenia gravis patients are sensitive to Succinylcholine. Why? because part of treatment is anticholinesterase drugs which inhibit plasma cholinesterase needed to metabolize SCh
Myasthenic Syndrome or Eaton Lambert is seen in what kind of cancer? oat cell carcinoma of the lungs
What is an autoimmune disease where presynaptic calcium channels are destroyed by antibodies Myasthenic syndrome (Eaton Lambert)
Why are anticholinesterase drugs ineffective in Myasthenic Syndrome (Eaton Lambert) patients? because there is no ACh released into the NMJ
Myasthenic Syndrome (Eaton Lambert) patients are _____ sensitive to NMB agents (both SCh and non depolarizers) than myasthenia gravis patients. more
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
Succinylcholine causes prolonged muscle contraction in patients with _______ ________ myotonia dystrophica
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
With regard to non depolarizing NMB, elderly patients typically have _______ duration and ________ onset time. prolonged duration prolonged onset time
Obese patients typically have _______ blockade with non depolarizing NMBs prolonged (especially with Vecuronium)
Rocuronium (Zemuron) dose is based on ______ body weight ideal
Succinylcholine dose is based on _______ body weight total
Created by: Mary Beth