Fleming's NMB's Flash Cards

 
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Name a “central” muscle relaxant or spasmolytic Diazepam, Baclofen, Dantrolene
Diazepam - facilitates the effects of GABA in a non-selective fashion and in this case will increase pre-synaptic inhibition of the motor neuron. Baclofen was originally developed as an oral GABA-mimetic drug. It is now
used most frequently in intrathecal pumps where direct administration limits its side effects.
Dantolene vs malignant hyperthermia
0 Tanknurse1 Tue, 19 Aug 2008 01:35:54 GMT view revision history
A patient with burns should NOT be given depolarizing or non-depolarizing agents? succinylcholine (depolarizing)
Severe burns are classically associated with an acute denervation of the muscle tissues and an increased synthesis of extra-junctional cholinergic receptors.
Administration of succinylcholine to these patients depolarizes the receptors and the
PHA 400B-Principles of Pharmacology Instructor: Neal Fleming MD, PhD
Neuromuscular Blockers Lecture # 3
consequent massive efflux of potassium can produce cardiac arrest. A similar change in the neuromuscular junction is induced by immobilization of a muscle such as occurs during casting or prolonged bed rest.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:54 GMT view revision history
Lambert-Eaton myasthenic syndrom is associated with what type of cancer? Lambert-Eaton Myasthenic syndrome is frequently seen in association with
bronchogenic carcinoma
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
A patient with Lambert-Eaton myasthenic syndrome will be more or less sensitive to non-depolarizing agents? To succinylcholine? In contrast, patients with
Lambert-Eaton Myasthenic syndrome have an antibody to the pre-synaptic calcium channel that results in a decreased release of acetylcholine. These patients will demonstrate a
resistance to the effects of non-depolarizing relaxants and sensitivity to succinylcholine.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
A patient with myasthenia gravis will be more or less sensitive to non-depolarizing agents? To succinylcholine? Patients with myasthenia gravis develop autoantibodies to the acetylcholine receptor. The result is a decrease in the number of
post-synaptic receptors and a remarkable sensitivity to non-depolarizing relaxants. In
addition, they will be resistant to the effects of succinylcholine.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What agent is used to reverse paralysis caused by a depolarizing agent? Trick question: succinylcholine is irreversible. Cholinesterase inhibitors would not effectively antagonize paralysis due to succinylcholine. In some settings the administration of recombinant butrylcholinesterase may be indicated to facilitate the metabolism of succinylcholine. 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What must be given concurrently with reversal of a non-depolarizing agent by a cholinesterase inhibitor? Because these are non-selective
inhibitors, an anti-muscarininc drug must be given concurrently (atropine,
glycopyrrolate).
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What agent is used to reverse paralysis caused by a non-depolarizing agent? cholinesterase inhibitors
(neostigmine, pyridostigmine, edrophonium).
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Which of the benzylisoquinolinium's is no longer available for clinical use but, because of its unique short duration of action due to rapid metabolism by plasma cholinesterase, will likely live on in lectures and exams for some time? Mivacurium
Like curare, it is also no longer available for clinical use, but because it is unique with respect to its short
duration of action due to rapid metabolism by plasma cholinesterase, it too will likely live on in lectures and exams for some time.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What is the 'vecuronium' of the benzylisoquinolinium group? Cisatracurium is the vecuronium equivalent from this group i.e. it has a slightly faster onset and intermediate duration of
action. It is devoid of cardiovascular side effects. It is prepared by separation from the racemic preparation of atracurium because of its increased potency and improved side effect profile. Metabolism and spontaneous degradation of cisatracurium results in the
formation of laudanosine, which has been associated with CNS excitation and seizures in animal studies.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What is the prototype benzylisoquinolinium? Curare is the prototype. It is no longer available for clinical use, but as a classic pharmacological agent, it will live on in lectures and exams for an indeterminate period of time. It is a relatively long acting drug. It has a side effect profile that is characterized by tachycardia and hypotension. This is the result of ganglionic blockade and histamine
release with subsequent vasodilatation and bronchospasm. It is eliminated primarily by
renal excretion and has no active metabolites.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Where is Rocuronium metabolized? It is rapidly eliminated via hepatic and biliary routes. 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Which of the aminosteroid relaxants is the least potent, with a rapid onset and a short duration of action? Rocuronium is the 3rd compound in this group. It is less potent, has a rapid onset and
a short duration of action. It has detectable cardiovascular side effects, but much less
so than pancuronium. It is rapidly eliminated via hepatic and biliary routes.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Where is Vecuronium metabolized? It is also metabolized by
the liver with a more prominent degree of biliary secretion and has an active metabolite.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Which of the aminosteroid relaxants is devoid of cardiovascular side effects? Vecuronium is slightly less potent with a slightly faster onset and an intermediate
duration of action. It is devoid of cardiovascular side effects. It is also metabolized by
the liver with a more prominent degree of biliary secretion and has an active metabolite.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Which of the aminosteroid relaxants has a slightly faster onset and an intermediate duration of action? Vecuronium is slightly less potent with a slightly faster onset and an intermediate
duration of action. It is devoid of cardiovascular side effects. It is also metabolized by
the liver with a more prominent degree of biliary secretion and has an active metabolite.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Where is Panuronium metabolized? It is metabolized by the liver with some biliary excretion and has an active metabolite. 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Which of the aminosteroid relaxants is notable for cardiovascular side effect, predominantly tachycardia? Pancuronium is the
prototype. It has an intermediate onset and a long duration of action. Its side effect
profile is notable for cardiovascular effects, predominantly tachycardia. This is the
result of both ganglionic blockade and an inhibition of the reuptake of catecholamines.
It is metabolized by the liver with some biliary excretion and has an active metabolite.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Which of the aminosteroid relaxants has an intermediate onset and a long duration of action? Pancuronium is the
prototype. It has an intermediate onset and a long duration of action. Its side effect
profile is notable for cardiovascular effects, predominantly tachycardia. This is the
result of both ganglionic blockade and an inhibition of the reuptake of catecholamines.
It is metabolized by the liver with some biliary excretion and has an active metabolite.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Name 1 aminosteroid relaxant Pancuronium, Vecuronium, Rocuronium
The aminosteroid relaxants include 3 drugs in current clinical use. Pancuronium is the prototype. It has an intermediate onset and a long duration of action. Its side effect
profile is notable for cardiovascular effects, predominantly tachycardia. This is the result of both ganglionic blockade and an inhibition of the reuptake of catecholamines.
It is metabolized by the liver with some biliary excretion and has an active metabolite.
Vecuronium is slightly less potent with a slightly faster onset and an intermediate duration of action. It is devoid of cardiovascular side effects. It is also metabolized by the liver with a more prominent degree of biliary secretion and has an active metabolite.
Rocuronium is the 3rd compound in this group. It is less potent, has a rapid onset and a short duration of action. It has detectable cardiovascular side effects, but much less so than pancuronium. It is rapidly eliminated via hepatic and biliary routes.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Do non-depolarizing agents increase post-tetanic potentiation? Yes 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Do non-depolarizing agents exhibit tetanic fade? Yes 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Do non-depolarizing agents exhibit train-of-four fade? Yes 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
How are non-depolarizing agents different from succinylcholine? These drugs are competitive antagonists of acetylcholine at the neuromuscular junction. The competitive nature of the paralysis can be distinguished from succinylcholine by the presence of
both tetanic fade and post-tetanic potentiation. Distinctions between drugs in this group are based on their rate of onset, their duration of action and their side effect profile.
Drugs within a chemical class tend to share clinical features with respect to metabolism and side effects.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Membrane depolarization from which type of NMB can
trigger malignant hyperthermia in susceptible individuals?
Succinylcholine 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What type of cholinergic receptor stimulation causes bradycardia? Ganglionic cholinergic receptor stimulation produces bradycardia. 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What are 1-2 of the undesirable side-effects of succinylcholine? Succinylcholine is also associated with a number of undesirable
clinical effects including fasiculations (due to presynaptic depolarization of the motor units) and consequent myalgia, increased intra-ocular pressure, increased intra-gastric
pressure and hyperkalemia.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
How is succinylcholine metabolized? It is quickly metabolized by plasma cholinesterase.There are hereditary dysfunctional isoforms of this cholinesterase enzyme that can be characterized by their decreased
dibucaine number.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Describe succinylcholine's onset and duration of action. Succinylcholine has a number of
desirable clinical characteristics including a rapid onset and a short duration of action. It
is quickly metabolized by plasma cholinesterase.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Does succinylcholine increase post-tetanic potentiation? No 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Does succinylcholine exhibit tetanic fade? No 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Does succinylcholine exhibit train-of-four fade? No 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Is succinylcholine a competetive or non-competitive paralytic? non-competitive paralysis 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
How is succinylcholine different from acetylcholine? Succinylcholine binds to the α sub-units of nicotinic
cholinergic receptors and activates the receptor. However, it does not disassociate rapidly like acetylcholine and thus produces a persistent, non-competitive depolarization
of the post-synaptic membrane.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Name a depolarizing relaxant Depolarizing Relaxants:
Succinylcholine
Decamethonium
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Name 2 non-depolarizing relaxants Non-Depolarizing Relaxants:
Aminosteroids
Pancuronium, vecuronium, rocuronium
Benzylisoquinoliniums
Curare, cisatracurium, mivacurium
Bis-tetrahydroisoquinoliniums
AV430A
Tropinyl-diesters
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
The NMB's in current use can be split into two corresponding groups, based on their mechanism of action, called what and what? The drugs in current use can be split into two corresponding groups
based upon their mechanism of action (non-depolarizing and depolarizing).
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Using specific stimulation patterns, what two types of blockades can be characterized? Using specific stimulation
patterns it is possible to characterize two distinct types of blockade, competitive and
non-competitive.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
The clinical effects of NMB drugs are easily and routinely monitored with what systems? A peripheral nerve is stimulated and the
consequent mechanical or electrical response is recorded.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What type of receptors does acetylcholine bind to, if it is able to diffuse across the synaptic cleft, without being metabolized? Post-synaptic nicotinic cholinergic receptors 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
What is the prototypic nicotinic cholinergic blocking drug, originally isolated from potions concocted by South American witch doctors? Curare 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Presynaptic vesicles contain which type of neurotrasmitter? Acetylcholine
ATP and calcitonin gene related peptide (CGRP) are two commonly mentioned
co-transmitters.
0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Depolarization of the motor neuron
results in the influx of _______ into the nerve terminal ultimately triggering the release of acetylcholine into the synaptic cleft.
Calcium 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Repolarization of the motor nerve terminal is secondary to an efflux of ________ that terminates the release
of acetylcholine.
Potassium 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Pre-synaptic voltage operated calcium channels (are/are not) significantly inhibited by magnesium in a clinically significant fashion. ARE 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history
Pre-synaptic voltage operated calcium channels (are/are not) significantly inhibited by the classic calcium channel blocking drugs Are NOT 0 Tanknurse1 Tue, 19 Aug 2008 01:35:53 GMT view revision history

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