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Autonomics-1.8
Pharmocology-Autonomics1.8/NMB's(Nm)
| Question | Answer |
|---|---|
| NMB structure/chemistry? | quaternary ammonium groups, bind to alpha subunit of cholinergic receptors at NMJ. Poor oral absorption and aviods CNS penetration |
| Succinylcholine structure? | 2 Ach molecules, flexible structure |
| Benzylisoquinoline derivatives structure? | bulky, rigid (Tubocurarine, mivacurarium) |
| Aminosteroidal compounds structure? | bulky, rigid structure (pancuronium, vacuronium) |
| two types of MOA for NMB? | depolarizing noncompetative, non-depolarizing competative |
| D/NC NMB prototype? | succinylcholine |
| succinylcholine? | binds Ach receptor cause persistant depolarization of NM endplate. Hydrolysis is slower by pseudocholinesterase so longer depolarization and breif excitation may elicit fasciculations |
| 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 |
| ND/C NMB prototypes? | tubocurarine, pancuronium (also metocurine, vecuromium, Atracurium) |
| tubocurarine, pancuronium? | bind postsynaptic receptor and compete with Ach to prevent binding resulting in block. They can be reversed with a AchE inhibitor (neostigmine) |
| what is a AchE inhibitor? | neostigmine |
| NMB effects on autonomic ganglia? | in ganglia and adrenal medulla, partial block may lead to hypotension and/or tachycardia |
| NMB effects on Muscarinic receptors? | vagolytic action: tachycardia. |
| succinylcholine may have what effect on muscarinic receptors? | vagal stimulation producing bradycardia or sympathetic ganglia stimulation causing hypertension and tachycardia |
| atracurium and cisatracurium elimination? | hoffmann elmination; spontaneous degredation in the plasma |
| mivacurium duration of action? | short due to plasma cholinesterases |
| ND/C pharmacodynamics? | rapid onset of blockade; flacid paralysis, first affected small rapid moving muscles (head/neck) ultimately respiratory |
| 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 |
| Excretion of NMB? | metabolized by plasma cholinesterases are short acting. Other routes are longer acting. |
| Patient Factors? | doses for obese patients based on lean body mass. Neonates require more NMB due to receptor immaturity. Elderly require less. |
| pharmocodynamics of ND NMB? | motor weakness then flacid paralysis of the small rapidly moving muscles (eye) followed by limbs, neck and trunk |
| 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. |
| CV effects of NMB? | vagolytic, ganglionic blockade. Hypotension due to peripherial dilation from histamine release and sympathetic ganglionic block. |
| NMB on CNS? | no signifigant effect, can increase IC pressure for unknown reason (assoc with succ) |
| effects of tubocurarine in CV? | hypotension secondary to histamine release and block ganglia |
| effects of pancuronium in CV? | cause dose dependent tachycardia and HTN from vagolytic effects and block reuptake of NE. |
| effects of succinylcholine in CV? | brady or tachydysrythmias. Similar to Ach and induced catacholamine release. (succinylcholine is agonist/antagonist) |
| when succinylcholine is contraindicated? | nodal or ventricular cardiac arrythmias |
| muscle faciculation in NMB? | can prevent with ND NMB |
| hyperkalemia in NMB? | succinylcholine can cause efflux and transient elevation in serum K. |
| succinylcholine with hyperkalemia contraindicated in NMB? | burn pts, acute neurologic, severe intraabdominal infections, cardiac arrythmia, skeletal muscle atrophy |
| 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) |
| 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. |
| what drugs antagonize NMB? | Ca with a AchE inhibitor antagonizes aminoglycoside antibiotics, AchE inhibitors alone, Ca salts to antagonize Ca chanel blockers. |
| 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. |
| AchE inhibitors? | neostigmine and pyridostigmine, but too much will lead to excessive Ach release and prolonged depolarization |
| 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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lmh9p4
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