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NEUROMUSCULAR BLOCKING DRUGS
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ARE NEUROMUSCULAR BLOCKERS ANESTHETICS?
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Barry NMB Slides
Barry NMB slides
| Question | Answer |
|---|---|
| NEUROMUSCULAR BLOCKING DRUGS | AKA: Muscle relaxants or paralytics.Interfere with transmission of nerve impulses at the NMJ.Help facilitate intubation.Provide optimal surgical conditions and patient safety (primary reason for use) |
| ARE NEUROMUSCULAR BLOCKERS ANESTHETICS? | NO NO NO!!!NEVER use in a under anesthetized patient! |
| ARE NEUROMUSCULAR BLOCKERS ALWAYS PART OF THE ANESTHETIC PLAN? | NO: Can often achieve relaxation with regional or deep inhalation anesthetics, or a mixed anesthetic technique.In fact, some surgeries necessitate NOT using them (thyroid, breast, facial) |
| NEUROMUSCULAR TRANSMISSION | Consists of: A prejunctional motor nerve ending, A synapse, and a highly folded post junctional membrane. |
| ACTION POTENTIAL | Moves along nerve terminal.CA++ influx into nerve cytoplasm.Vesicles release ACH.ACH diffuses across synaptic cleft to bind with NICOTINIC CHOLINERGIC RECEPTORS. |
| WHAT ARE THE 5 NICOTINIC CHOLINERGIC RECEPTOR SUBUNITS? | 2 Alpha (primary) Only subunit capable of binding ACH.1 Beta1 Gamma1 Delta |
| WHAT HAPPENS WHEN ACH OCCUPIES BOTH OF THE ALPHA SUBUNITS ON A NICOTINIC CHOLINGERGIC RECEPTOR? | A conformational change occurs.This allows NA+ (and CA++) to flow in and K+ to flow out (on the post-junctional side)Muscle contracts.ACH is metabolized off of the receptor.Ion channels close.End plate repolarizes. |
| HOW IS ACH METABOLIZED? | Ach is hydrolyzed by the enzyme acetylcholinesterase (aka: true cholinesterase) |
| WHERE IS ACETYLCHOLINESTERASE FOUND? | In the folds of the endplates of the neuromuscular junction. |
| WHAT IS ACETYLCHOLINESTERASE HYDROLYZED INTO? | Acetic Acid and Choline (reuptake results in the synthesis of more ACH)(Danelle said that this is a board question) |
| WHAT ARE THE TWO CLASSESS OF NMB'S? | Depolarizing and Non-Depoalrizing |
| WHICH NMB IS A DEPOLARIZER? | Succinylcholine |
| Depolarizer MOA | Mimic ACH: Binds to ACH receptor to generate an action potential and muscle contraction.ACH receptor agonist.Not metabolized by acetylcholinesterase = high conc at the synapse for a long period of time.Prolonged depolarization=fasiculations. |
| SUCCINYLCHOLINE | The only depolarizing NMB.Rapid onset: 30-60sec.Short duration: 3-10 min.Dose: 1-1.5 mg/kg IV and 4-5mg/kg in children.20mg IV to tx laryngospam. |
| WHY DOES SUCCINYLCHOLINE HAVE A SHORT DURATION OF ACTION? | Upon entering the circulation, Succinylcholine is metabolized by pseudocholinesterase into succinylmonocholine. Only a fraction of it makes it to the receptor. |
| WHAT DOES SUCCINYLCHOLINE DO ONCE IT GETS TO ITS RECEPTOR? | It binds to 2-alpha subunits and causes depolarization. It is sustained b/c metabolism is slower than ACH.Blockade occurs b/c membrane can not repolarize.This is a Phase 1 block. Will see fasiculations. |
| WHAT IS A PHASE 2 BLOCK? | Can occur with a single dose of Succinylcholine.Usually due to repeated doses or infusion of >3-5mg/kg IV.Resembles a nondepolarizing block b/c ionic and conformational changes create a prolonged membrane depolarizaiton. |
| WHAT HAPPENS WITH A DECREASED AMOUNT OF PLASMA CHOLINESTERASE? | These patients can not efficiently metabolize Succinylcholine. They are unable to hyrolyze the ester bonds.Can cause severe liver disease.Unable to metabolize anticholinesterase in insecticides, drugs for myasthenia gravis and some chemo drugs. |
| WHAT IS ATYPICAL PLASMA CHOLINESTERASE? |
Created by:
Christine.scott1
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