Neuromuscular Physiology and Pharmacology (Valley)
Terms in this set (44)
Motor nerves/efferents exit the ____ cord and and sensory nerves/afferents enter the ________ cord
Motor/efferent nerves exit the vential cord and Sensory/afferent nerves enter the dorsal cord
What is the name of the molecule that metabolized acetylcholine
Acetylcholinesterase, it breaks Ach down into choline and acetate by hydrolysis
Side note: give the dermatomes for nipples, xiphoid, and belly button
Xiphoid = T7
Belly Button = T10
What is the purpose of presynaptic nicotinic receptors.
They response to acetylcholine by increasing teh sunthesis of Ach and mobilization of Ach containing vesicles. A positive feedback mechanism (prevents Ach depletion and accounts for fade)
do both alpha subunits of the nicotinic Ach receptor need to be occupied by Ach to open the ion channel (nicotinic receptor has 5 subunits)
Yes, both alpha subunits must be occupied by Ach, sodium and calcium influx and potassium effluxes
After Ach is metabolized the ______ is transported back into the nerve terminal where it is used to resynthesize Ach
the choline is transported back into the nerve terminal to make more Ach
__________ comes in, neurotransmitters go out
Calcium comes in, neurotransmitters go out
Hypocalcemia is associated with a decreased release of ________
a decreased release of neurotransmitters (hypercalcemia = increased release)
_________ magnesemia is associated with an increase in the amount of neurotransmitter relased
Hypomagnesemia = increased neurotransmitter release (the opposite of calcium)
Calcium and magnesium are _______ at presynaptic nerve terminals
They are antagonistic
In addition to Ach, acetylcholinesterase also degrades what other substances
ester local anesthetics, neostigmine, edrophonium, remifentanil, and esmolol
Is succinylcholine metabolized by acetylcholinesterase
No, this is why it can provide a depolarizing block as it keeps the cells in an absolute refractory period until plasma cholinesterases metabolize it
Notes on nondepolarizing / phase 2 block
M.O.A. = competitive inhibition,
fade follows high frequency stimulation,
post tetanic facilitation,
antagonized by anticholinesterases,
Succinylycholine is two Ach molecules put together, Notes on depolarizing / phase 1 block
decreased single twitch height,
response to high frequency stimulation is maintained,
antagonized by nondepolarizers,
potentiated by anticholinesterase,
muscle fasciculations precede block
Does the presynaptic action of succs enhance or reduce the postsynaptic action
It enhances it postsynaptic action
Are neuromuscular relaxants ionized?
Yes, 100% ionized
2 N.M.B.s that are primarily eliminated via biliary excretion
vecuronium - 55%
rocuronium - 80%
most of the rest are eliminated via metabolism
How are atracurium and cisatracurium metabolized
atracurium = esterase hydolysis and Hofmann elimination (pH and temp dependent degradation)
cisatracurium = Hofmann elimination only
what N.M.B.s elicit the release of histamine
succs and atracurium
what N.M.B.s produce bradycardia
succs as it mimics Ach at the muscarinic receptors of the S.A. node
what N.M.B.s produce tachycardia
atracurium and pancuronium
what N.M.B.s produce significant hypotension
what N.M.B.s produce hypertension
succs may cause plasma potassium concentrations to increase by ______ in normal patients and ________ in burn/trauma/head injury patients
by 0.5 m.E.q. in normal patients and by 5 to 10 m.E.q. in burn, trauma, or head injury patients
Up regulation of extra junctional receptors on the hemiplegic side causes an _______ response to nerve muscle stimulators
an increased response
explain the defect that occurs with malignant hyperthermia
a mutation of the ryanodine receptor (RyR1) which is embedded in the sarcoplasmic reticulum of skeletal muscles. The sarcoplasmic reticulum releases calcium continuously leading to sustained contractions
Where does dantrolene act.
On the sarcoplasmic reticulum to decrease the release of calcium
Describe what happens when 95, 90 and 75 % of receptors are blocked
95% blocked = diaphragm moves but no T.O.4 twitch
90% = abdominal relaxation adequate for lap, 1 weak twitch
75% = tidal volume normal (>5ml/kg), 1 strong twitch
Do you get fade with succs
No, no fade
Do you get post tetanic potentiation with succs
No, only with N.D.M.B.s
Is it possible to get a phase 2 block with succs
Yes, with large / repeated doses
A patient has just experienced masseter muscle rigidity from succinylcholine. What lab value may confirm the diagnosis of malignant hyperthermia?
Elevation in creatine phosphokinase (CPK >20,000).
What is the therapeutic blood level for dantrolene?
The therapeutic blood level for dantrolene is 2.5 mcg/mL.
You have successfully treated an acute episode of malignant hyperthermia with dantrolene sodium. Dantrolene should be readministered at what intervals for how long?
Dantrolene should probably be repeated every 10 to 15 hours (this is the half-life of dantrolene) for three days.
What are the clinical manifestations of myotonic dystrophy (Steinert's disease)?
Myotonia dystrophy (Steinert's disease. myotonic atrophica) is a multisystem disease that usually manifests as facial weakness (expressionless facies). wasting and weakness of the sternocleidomastoid muscles. ptosis, dysarthria, dys phagia, and inability to relax the hand grip (myotonia).
Frontal balding, cataracts and testicular atrophy in males form a frequently recog nized triad of characteristics
Should succinylcholine be used in the anesthetic management of the patient with myotonic dystrophy?
Myasthenia gravis is characterized by what symptoms? What is the cause of these symptoms? (Usually ocular symptoms at first)
Myasthenia gravis is characterized by weakness and easy fatigability of skeletal muscles. The weakness can be asymmetric, confined to one group of muscles, or generalized. Easy fatigability of skeletal muscle in myasthenia gravis is caused by autoimmune destruction of nicotinic acetylcholine receptors at the neuromuscular junction
Identify the anesthetic concerns for the patient with scoliosis due to muscular dystrophy.
malignant hyperthermia, cardiac dysrhythmias, and untoward effects of succinylcholine
Is there an active metabolite of succinylcholine?
Yes. Succinylmonocholine is a much weaker metabolite of succinylcholine, but succinylmonocholine is metabolized much more slowly to succinic acid and choline
Which two nondepolarizing neuromuscular relaxants have active metabolites? Compare the activity of the metabolites to the parent compound.
Vecuronium and pancuronium have active metabolites. specifically the 3- hydroxy (3-0H) metabolites (3-desacetylvecuronium and 3- desacetylpancuronium). The 3-desacetlyvecuronium metabolite is about 50-70% as potent as vecuronium. whereas 3-desacetylpancuronium has
about 50% potency of pancuronium at the neuromuscular junction
What effects may carbamazepine have on nondepolarizing muscle relaxants?
Nondepolarizing muscle relaxants may have a shorter duration than expected in the patient receiving chronic carbamazepine therapy.
What is the appropriate premedication dose of atropine for the adult with severe bradycardia?
atropine is administered intravenously or intramuscularly
in a range of 0.01-0.02 mg/kg up to the usual adult dose of 0.4-0.6 mglkg. Larger intravenous doses up to 2 mg may be required to completely block the cardiac vagal nerves in treating severe bradycardia
Identify the incidence of heterozygous atypical plasma cholinesterase (EuEa) in the general population. Identify the incidence of homozygous atypical plasma cholinesterase
(EaEa) in the general population.
The incidence of heterozygous atypical plasma cholinesterase (EuEa) in the general population is about 1 :25, or 4%. The incidence of homozygous atypical plasma cholinesterase (EaEa) in the general population is about
1:2800, or 0.04%. Two comments: (1) the incidence varies by text reference- 496 and 0.04% represent reasonable averages
Which of the 4 common anticholinesterase agents is not a quaternary ammonium?
Physostigmine is a tertiary amine. Edrophoniurn, neostigmine, and pyridostigrnine are all quaternary amines. Remember: physostigmine is not used to reverse neuromuscular blockade because the dose required to
achieve this effect is excessive
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