Pharmocology-Autonomics1.8/NMB's(Nm)
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| NMB structure/chemistry? | quaternary ammonium groups, bind to alpha subunit of cholinergic receptors at NMJ. Poor oral absorption and aviods CNS penetration
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| Succinylcholine structure? | 2 Ach molecules, flexible structure
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| Benzylisoquinoline derivatives structure? | bulky, rigid (Tubocurarine, mivacurarium)
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| Aminosteroidal compounds structure? | bulky, rigid structure (pancuronium, vacuronium)
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| two types of MOA for NMB? | depolarizing noncompetative, non-depolarizing competative
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| D/NC NMB prototype? | succinylcholine
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| succinylcholine? | binds Ach receptor cause persistant depolarization of NM endplate. Hydrolysis is slower by pseudocholinesterase so longer depolarization and breif excitation may elicit fasciculations
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| D/NC phase I block, phase II block and dual block? | I: initial phase followed my block of transmission and flacid paralysis, II: D to Nondepolarizing, secondary to desensitization and return potential to nml. duel: simultaneous phaseI and phaseII block during use of succinylcholine
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| ND/C NMB prototypes? | tubocurarine, pancuronium (also metocurine, vecuromium, Atracurium)
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| tubocurarine, pancuronium? | bind postsynaptic receptor and compete with Ach to prevent binding resulting in block. They can be reversed with a AchE inhibitor (neostigmine)
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| what is a AchE inhibitor? | neostigmine
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| NMB effects on autonomic ganglia? | in ganglia and adrenal medulla, partial block may lead to hypotension and/or tachycardia
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| NMB effects on Muscarinic receptors? | vagolytic action: tachycardia.
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| succinylcholine may have what effect on muscarinic receptors? | vagal stimulation producing bradycardia or sympathetic ganglia stimulation causing hypertension and tachycardia
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| atracurium and cisatracurium elimination? | hoffmann elmination; spontaneous degredation in the plasma
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| mivacurium duration of action? | short due to plasma cholinesterases
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| ND/C pharmacodynamics? | rapid onset of blockade; flacid paralysis, first affected small rapid moving muscles (head/neck) ultimately respiratory
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| distribution of NMB? | approximate ECF, breif duration of paralysis is due to initial dose and when doses repeated, tissues become saturated and metabolism and excretion influence duration of action
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| Excretion of NMB? | metabolized by plasma cholinesterases are short acting. Other routes are longer acting.
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| Patient Factors? | doses for obese patients based on lean body mass. Neonates require more NMB due to receptor immaturity. Elderly require less.
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| pharmocodynamics of ND NMB? | motor weakness then flacid paralysis of the small rapidly moving muscles (eye) followed by limbs, neck and trunk
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| pharmocodynamics of D NMBs? | succinlylcholine evokes transient fasciculations over the chest and abdomen, then will affect the neck, arms, and leg muscles. Slight facial involvment.
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| CV effects of NMB? | vagolytic, ganglionic blockade. Hypotension due to peripherial dilation from histamine release and sympathetic ganglionic block.
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| NMB on CNS? | no signifigant effect, can increase IC pressure for unknown reason (assoc with succ)
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| effects of tubocurarine in CV? | hypotension secondary to histamine release and block ganglia
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| effects of pancuronium in CV? | cause dose dependent tachycardia and HTN from vagolytic effects and block reuptake of NE.
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| effects of succinylcholine in CV? | brady or tachydysrythmias. Similar to Ach and induced catacholamine release. (succinylcholine is agonist/antagonist)
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| when succinylcholine is contraindicated? | nodal or ventricular cardiac arrythmias
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| muscle faciculation in NMB? | can prevent with ND NMB
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| hyperkalemia in NMB? | succinylcholine can cause efflux and transient elevation in serum K.
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| succinylcholine with hyperkalemia contraindicated in NMB? | burn pts, acute neurologic, severe intraabdominal infections, cardiac arrythmia, skeletal muscle atrophy
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| what other effects can NMB have? | hyperkalemia, muscle faciculations, masseter muscle ridigity, inc IOC pressure (aviod in open eye injury and some glaucoma), inc IC pressure, malignant hyperthermia, profound long-lasting muscle atropy (assoc with large dose chronic use)
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| drugs that enhance NMB? | anesthetics act synergistically with ND NMB. Aminoglycoside antibiotics inhibit Ach release to produce NMB. Ca channel blocker enhance D and ND NMB.
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| what drugs antagonize NMB? | Ca with a AchE inhibitor antagonizes aminoglycoside antibiotics, AchE inhibitors alone, Ca salts to antagonize Ca chanel blockers.
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| Reversal of NMB? | AchE inhibitors, also cause excessive salivation, inc GI motility, bradycardia. Should be given with atropine or glycopyrrolate to antagonize Ach muscarinic effects.
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| AchE inhibitors? | neostigmine and pyridostigmine, but too much will lead to excessive Ach release and prolonged depolarization
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| therapudic use of NMB? | adjuvent to general or local anesthesia for skeletal muscle relaxation, facilitate tracheal muscle intubation, long term mechanical ventilation, rapid control of epilepticus
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