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NU 600

Exam 3 - Neuromuscular Transmission

What is the dose, onset, and duration of succinylcholine? Dose=1-1.5mg/kg up to 150mg; Onset=30-90sec; Duration=8-15min
Succinycholine is metabolized by what metabolic process? hydrolysis
Succinycholine increases pressures in what three areas of the body? cranial, ocular, abdominal
Succinylcholine attaches to ______ subunits. alpha
How much of a rise in potassium is seen with succinylcholine? +0.5meq/L
A depolarizing neuromuscular blockade is also referred to as a ___________. Phase I blockade
What is the manifestation of a Phase I Block? Fasciculations follows by flaccid paralysis
What medications potentiate and antagonize the action of succinylcholine? Potentiate=anticholinesterases; Antagonize=NDMR
What are the characteristics of a Phase I block seen on a PNS? a)decr. contraction in response to single twitch stim b)decr. amplitude but sustained response to cont. stim c)TOF ratio >0.7 d)absence of posttetanic facilitation e)augmentation of NMB with anticholinesterase
When will a Phase I block develop into a Phase II block? Repeat doses of sch (>2mg/kg) or w/sch infusion
Repeated doses of sch will lead to a Phase II block, describe this process. Postjxn membrane does not respond normally to ach even when postjxn membrane repolarizes
The duration of a Phase II block mimics the duration of action of a _______________. Nondepolarizing neuromuscular blocking drug
Alterations of what two electrolytes can augment the effects of NDNMBDs? High Mg, Low K
Administering an anticholinesterase drug in Phase I will ________ the blockade, while giving the same medication in Phase II will ________ the blockade. Enhance; antagonize
What anticholinesterase could be used to test the current level of blockade and what is the dose? Edrophonium; 0.1-0.2mg/kg
Define tachyphylaxis. Sudden and abrupt decreased response to a drug
Transition from a Phase I to Phase II block occurs at what dose of sch? 2-4mg/kg
vWhat type of drug can be used to antagonize a Phase II block? anticholinesterase
Where is plasma cholinesterase synthesized? liver
What are 3 causes of prolonged activity of sch? Decreased hepatic production of plasmacholinesterase, atypical plasmacholinesterase, severe and prolonged hepatic dz
Why does SCh have a brief duration of action? Rapid hydrolysis in plasma (before the NMJ)
Patients being treated with what 3 disease may be taking drugs that decrease plasma cholinesterase activity? Glaucoma (echothiophate), myasthenia gravis (neo-, pyrido- stigmine), cancer (nitrogen mustard, cyclophosphamide)
High levels of what hormone is associated with decreased plasmacholinesterase activity? What patient population is this effect seen in? estrogen; parturients at term
Give examples of two insecticides that decrease plasma cholinesterase activity? carbamate, organophosphates
How does Reglan influence plasma cholinesterase? Reduces its activity
What lab test can determine inherent activity of plasma cholinesterase? Dibucaine test
_____% inhibition of plasma cholinesterase activity after giving Dibucaine is considered a normal response. 80
What type of drug is Dibucaine? local anesthetic
What does the the Dibucaine test reflect and what is the normal value? The % of inhibited plasma cholinesterase; 80%
What is the Dibucaine %, incidence, and duration of action of NMB for the homozygous patient with decreased plasma cholinesterase activity? 20-40%; 1:3000; 4+ hours
What is the Dibucaine %, incidence, and duration of action of NMB for the heterozygous patient with decreased plasma cholinesterase activity? 60%; 1:500; up to 60min
What are the adverse effects of SCh? Dysrhythmias, hyperK, myalgia, myoglobinuria, incr. intragastric press., increased intraocular press., increased ICP, sustained skeletal muscle spasm
What are 3 cardiac dysrhythmias that could be seen with SCh? Bradycardia, junctional rhythm, sinus arrest
MH is an inherited disorder of what body system? skeletal muscleWhat
What is the trigger for MH? VAA and SCh
What role does calcium have in MH? Dysfunction in Ca reuptake mechanisms leads to 500 fold increase in intracellular calcium levels
What are the effects of intracellular flooding of calcium? sustained muscle contraction, severe hypoxia, lactic acidosis, membrane instability, rhabdomyolysis, ARF
The clinical features of MH are all features of a ____________ state. Hypermetabolic
What are the clinical features of MH? Masseter spasm, muscle rigidity, tachypnea, tachycardia, HTN, cardiac arrhythmias, myoglobinuria, increased creatinin phosphokinase
What are the steps to initiate in the treatment of MH? Administer Dantrolene, call for help, stop the VAA, 100% O2, manually hyperventilate, use a clean breathing system, abort surgery, cooling measures
What is the dose for dantrolene? 1mg/kg then 1-2.5mg/kg q10min until MH is controlled
What is the maximum dose for MH? 10mg/kg
What is dantrolene's method of action? Impairs calcium dependent muscle activity by decreasing intracellular calcium concentration
How is dantrolene prepared? 20mg dantrolene with 3gm mannitol mixed in 60ml water
Who first discovered the ACh neurotransmitter? Otto Loewi
What are the 2 different types of receptors that ACh acts upon? Nicotinic (ion-gated peptid) and muscarinic (G-protein coupled)
Which subunit of the nicotinic receptor does ACh bind? alpha subunit
Identify the different subunits on a nicotinic receptor? delta, beta, 2 alpha, gamma
What are two functions of G-protein coupled receptors? Help extracellular molecules travel to intracellular environment; signal transduction
What are the different subunits of G-protein coupled receptors? alpha, beta, gamma
Skeletal muscle is innervated by the ______. Motor neuron (motor nerve)
Where does the motor neuron arise from? ventral horn of spinal grey matter
What and from what is ACh manufactured? Manufactured in nerve terminal from acetate and choline
Where are acetate and choline derived from? acetate=acetyl-coA (mitochondria); choline=dietary intake and liver
What enzyme combines acetate and choline to form ACh? acetyl transferase
Where is ACh stored? Nerve terminal in quanta
Nicotinic cholinergic receptors are located on the __________ and contained within _________. Motor end plate; folds or gyri
What causes ACh release from the nerve terminal of the motor neuron? Influx of calcium into the nerve terminal, causing ACh vesicle to fuse with the nerve membrane and release ACh into the synaptic cleft
Each vesicle of ACh contains _________ molecules of ACh. 5,000-10,000
How many vesicles of ACh are released with each depolarization? 200-400
SCh is broken down by _________, ACh is broken down by __________. Plasma cholinesterase; acetylcholinesterase
What electrolyte is required for the release of ACh? Calcium
Created by: philip.truong
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