Exam 3 Flashcards
1
Q
Parasympathetic Nervous System (ANS subset)
A
rest and digest
conserve energy
2
Q
Sympathetic Nervous System (ANS subset)
A
fight or flight
(continuously active)
3
Q
ANS has a two neuron system what are the neurons called
A
preganglionic and postganglionic
(synapse combines them together)
4
Q
What molecule has to be produced within a neuron, released when stimulated (ca2+ dependent), inactivated after release, and produce physiological responses
A
neurotransmitters
5
Q
What system has a NT that is ACh -> cholinergic transmission
A
parasympathetic system (rest and digest)
6
Q
In the parasympathetic system what is released at the first synapse and what is released at the second synapse
A
preganglionic: ACh (binds to soma receptors)
postganglionic: ACh (activates receptors in tissue to produce effect)
7
Q
Synapses in pre and postganglionic axons in parasympathetic ganglia are terminal ganglia and intramural ganglia what do they do
A
terminal ganglia: close to target tissue
intramural ganglia: in target tissue
8
Q
What are the two systems in the parasympathetic system (cholinergic system)
A
Parasympathetic system: Contains ganglia
Somatic Nervous System: NOOO ganglia
9
Q
What is the somatic nervous system, what does it activate, how is it activated
A
one neuron pathway
CNS to skeletal muscle (NO ganglia)
Motor neurons are myelinated
NT is ACh
Activates muscle contraction
10
Q
ACh is synthesized in the ________ by acetylation of choline
A
cytoplasm
11
Q
Where is Choline acetyltransferase (ChAT) synthesizes and transported
A
synthesized in soma and transported down axon to nerve terminal (it marks cholinergic neurons)
12
Q
What two things are needed for ACh synthesis
A
AcetylCoA from pyruvate
Choline
13
Q
What are the two places you can get choline
A
diet
liver
(choline is formed from ACh metabolism)
14
Q
Choline is recycled to be resued for ACh synthesis, it is transported inside neurons with what and by what transporter
A
Transported with Na+ by choline transporter (CHT1)
(Rate limiting step in ACh synthesis, high affinity)
15
Q
High choline demand -> _____ affinity choline uptake (LACU) system assists in transporting additional choline into ________
A
low affinity
choline into neurons
16
Q
CHT1 is a symporter, what does it symport
A
Choline and Na+ into cell
(needs Na+ /K+ ATPase antiport)
17
Q
What does hemicholinium (hemicholine) do
A
blocks the transporter of CHT1
-indirect acetylcholine antagonist decreases ACh synthesis
18
Q
ACh is stored in small synaptic vesicles which protect them from what
A
degregation
19
Q
What is vesicular acetylcholine transporter (VAChT)
A
(Used for storage of ACh)
Located in the membrane of vesicles and relies on the H+ pump
20
Q
What is the mechanism of the VAChT (vesicular acetylcholine transporter)
A
Antiporter
transports ACh inside the vesicles in exchange for protons
H+ are provided by the proton pump
21
Q
What do vesamicols do to VAChT
A
They decrease ACh release
Depletion of ACh at synpase
(noncompetitive and reversible inhibitor)
22
Q
How is ACh released from the synaptic vesicles
A
- Axon potential throughout the anion
- Activation of voltage-gated Ca2+ channels
- Exocytosis
23
Q
ACh release is blocked by botulinum and tetanus toxins from __________
A
Clostridium
24
Q
Transient vesicle fusion requires _________ proteins and Ca2+
A
SNARE
(SNARE proteins = soluble NSF attachment protein receptor, NSF = N-ethylmaleimide sensitive fusion proteins)
25
Inhibition of Exocytosis:
Botulinum and tetanus toxins induce what
muscle paralysis
(proteases that hydrolyze some SNARE proteins)
26
Inhibition of Exocytosis:
Toxins are polypeptides that contain two chains what are they
Heavy chain - binding
Light chain - Zn2+ dependent protease
27
What is botulism
-Neurotoxins are absorbed in intestine, pass into bloodstream, travel to synapse in the nervous system
-Flaccid paralysis, preventing release of ACh at NT junctions
28
What is infant boutlism caused by
honey
29
What is tetanus
-Hyperactivity of motor neurons increase muscle activity
-muscle contractions starts in jaw and neck muscles progresses to the rest of the body
30
ACh mechanism
1. ACh is made from choline and acetyl coA
2. In synaptic cleft ACh is rapidly broken down by enzyme acetylcholinesterase
3. Choline is transpored back into the axon terminal and is used to make more ACh
(butytylcholinesterace is a secondary mechanism)
31
AChE (acetylcholinesterase)
localized to postsynaptic membranes in synaptic cleft
inactivation time of ACh -> very fast mechanism
Specific inhibitors for AChE -> used in clinic
32
What are the two catalytic sites in AChE
anionic site that binds ACh
Esteratic site includes a Ser, His, Glu, site for ACh hydrolysis and AChE acetylation
33
AChE mechanism
-binding of ACh to the enzyme
-hydrolysis of ester bond forming acetyl enzyme
-hydrolysis of acetyl enzyme resulting in elimination of acetate originating free enzyme, reactivation of AChE
34
What are the two classes of cholinergic receptors
Muscarinic Receptors: stimulated by muscarine (agonist)
Nicotonic Receptors: stimulated by nicotine (agonist)
35
What are the three cholinergic transmission sites effectors
smooth muscle
cardiac tissue
glands
36
What are the two types of Nicotinic Receptors
Muscle-type (N1) and neuronal-type (N2) receptors
-receptor converts ligand binding (2ACh) into electrical depolarization
37
Nicotinic receptors have ___ subunits arranged around a central pore
5
the alpha and beta subunits are present in many different combinations
38
In nicotinic receptors, the number of ACh binding sites depends on the composition of the ________
receptor (interfaces of alpha-subunits)
39
Nicotinic receptor subtypes are selective primary to _____ and secondary to _____
Na+
Ca2+
40
Muscarinic receptors are ______ onset and _______ duration responses
slow onset long duration
41
M1, M3, M5 receptors
couple to Gq family
phosphotidyl inoaitol -> IP3, DAG -> Excitation
42
M2 and M4 receptors
couple to Gi/o family
adenylyl cylase -> cAMP -> Inhibition
43
ACh activates the postganglionic neuron by binding to receptors in the _____ of the postganglionic neuron releasing ACh at the synapse
soma
44
Postsynaptic membrane in postganglionic nurons effect what
tissues or organs
45
presnaptic receptors regulate the release of what
NTs
46
Nicotinic receptors enhance NT release mainly in the
CNS
47
Muscarinic receptors inhibit _____ release
NT
48
M2 and M4 receptors ______ the effect of ACh
decrease
49
M1 and M3 receptors ________ an effect or response
activate
50
Muscarinic Autoreceptors
presynaptic muscarinic receptors that regulate ACh release -> regulate its own NT
Autoreceptors inhibit NT release -> mechanism or negative feedback
51
Muscarinic Heteroreceptors
-Presynaptic muscarinic receptors that regulate other NTs release
-ACh released from a cholinergic neuron activates M5R present in a dopaminergic neuron
-Activation of M5R increases dopamine release in nucleus accumbens
52
Are blood vessels innervated by the parasympathetic system, but they have muscarinic receptors
No
53
What are the three effect of ACh in the heart (cardiac system): SA, AV node and cardiomyocyte
Pacemaker cells (SA node): Decrease heart rate (negative chronotropic effect)
Pacemaker cells (SA and AV node): Decrease rate of conduction (negative domotropic effect)
Cardiomyocyte cells: Decrease force of cardiac contraction (negatice inotropic effect)
54
Phase 4 of pacemaker cells
Slow depolarization
-slow Na+ channels open (-60)
--I(f) open -> efflux of K+
-T-type (transient) Ca2+ channels open (-55 to -50)
-L-type (long lasting) Ca2+ channels open (-40)
55
Phase 0: Depolarization
Leads to action potential
-Slow inward of Ca2+
-L-type voltage gated Ca2+ channels open
-At threshold = action potential
56
Phase 3: Repolarization
Open of delayed recifier K+ channels (voltage-gated channels)
K+ efflux -> outward current
Inactivation and closing of L-type Ca2+ channels
Membrane potential becomes negative
57
A decrease in phase 4 slope causes what
Increase time to reach threshold increasing heart rate
58
How does ACh effect the SA node
decreases activity of L-type Ca2+ channels (4 and 0)
decrease depolarization of SA node cells decreasing heart rate
Large stimulus can produce bradycardia and SA block
59
ACh effect on potassium channels
-Decrease rate of spontaneous depolarization in SA node
-Activation of ACh-sensitive K+ channels by beta-gamma subunits causing an increase of K+ efflux
-Increase in repolarizing K+ current leading to hyper polarization, decreasing heart rate
60
ACh effects in AV node conduction
Decreases L-type Ca2+ channels
decrease depolarization of AV node cells
decrease rate of conduction increasing refractory period
Large stimulus can produce bradycardia and AV block
61
ACh effect in myocardial cells
parasympathetic innervation is higher in atria than ventricles
Modest reduction in atrial and ventricular contractility
-parasympathetic innervation is lower than sympathetic
62
Cholineric system and blood vessels in parasympathetic
Parasympathetic system does not innervate blood vessels
Postganglionic. neurons do not synapse with blood vessels
63
Blood vessels contains M3 receptors
M3 receptors are present on Endothelium Cells and release nitric oxide
64
Activation of M3 receptors cause vasodilation, how does this occur
If there is high concentration of ACh found in circulation
65
M3 production of cGMP and PKG activation
decreases ca2+ by inhibition of the channel
activation of MLC phosphatase -> MLC dephosphorylation
Relaxation of smooth muscle
66
Constrictor or pupillary muscle
Muscle in the iris
encircles the pupil of the iris
M3R
Miosis
67
Cillary muscle
muscle in the ciliary body that attaches to the ligament that gold the lens
Changes the shape of the lens (round)
M3R
Near vision
68
ACh effects in the respitatory tract
Bronconstriction (M3R in smooth muscle)
increase secretion
M2R in presynaptic causing ACh level decrease
69
ACh effects in the urinary tract
Increase detrusor muscle contraction
relaxation of the sphincter
promotes bladder emptying urination
70
GI tract by ACh
M3R > M2R (more ACh produced)
Increase secretion
Increase muscle contraction
Increase peristalsis and bowel movements
71
What is different about Sweat Glands in the sympathetic system
Postganglioni fiber releases ACh instead of NE
Cholinergic stimulation of muscarinic receptors induces sweating
72
What is the eccrine and apocrine glands
Eccrine: open onto skin surface
Apocrine: open into hair follicle
73
Muscarinic Agonists: ACh related esters
Methacholine (provocholine)
Carbamylcholine (carbahol)
Bethanechol (urecholine)
74
Muscarinic Agonists: natural products
Muscarine
Pilocarpine (salagen, pilocar)
Arecoline
75
Selectivity of muscarinic vs nicotinic receptors in Methacholine, Carbamylcholine, Bethanechol
Methacholine: more specificty for muscarinic receptors
Carbamylcholine: equal activity for muscarinic activity and nicotinic activity
Bethanechol: Muscarinic activity but no nicotinic activity
76
Selectivity of muscarinic vs nicotinic receptors in source of arecoline, muscarine, pilocarpine
Arecoline: nuts, equal muscarinic and nicotinic activity
Muscarine: mushroom, muscarinic activity
Pilocarpine: leaves, muscarinic activity
77
Structure, absorption oral administration, BBB crossing in Methcholine, carbachol, bethanechol, muscarine
Quaternary amine
Poorly absorbed
Limited BBB crossing
78
Structure, absorption oral administration, BBB crossing in Arecoline, Pilocarpine
Tertiary amine
Readily absorbed
can cross BBB
79
Bathanechol gastrointestinal disorders
Bethanechol (urecholine) useful in stimulating GI motility
Largely replaced by compounds with combined cholinergic agonist and dopamine antagonist properties -> GI motility and antimetic effect
80
Bathanechol urinary bladder disorders
Useful in treating urinary retention and inasequate bladder emptying
-postoperative or postpartum urinary retention
-enhances contraction of the bladder detrusor muscle -> avoids catheterizations
81
Xerostomia
Sjogren's syndrome
-Autoimmune disorder
-decrease seretions from salivary and lacrimal glands
-Head and neck chemotherapy and radiation therapy, trauma, and drugs
82
Treatment to promote salivation pilocarpine (salagen) and cavimeline (evoxac)
pilocarpine (salagen): adverse effects include profuse sweating
cavimeline (evoxac): newer with fewer side effects, preferentially activate M1R and M3R
83
Opthalmolgical use of pilocarpine
-In glaucoma (increased intraocular pressure)
-Pilocrine a mitotic agent decreases intraocular pressure by increasing the drainage of intraocular fluid
-Ocular insert allows for release of 20mg of pilocarpine per hour over 7 days
84
Clinical uses of carbachol
eye drops (miostat)
treats open-angle glaucoma by increasing fluid outflow
85
Bronchial challenger test- bronchial hyperreactivity
use of methacholine (by inhalation) to assist in diagnosis of asthma
-provokes broncoconstriction or narrowing of the airways
-asthmatics will react to lower doses of drug -> spirometry to check degree of narrowing
86
Agonists common adverse effects
Sweating
Diarrhea
Bladder tightness
Hypotension
Limited administration
87
ACh has virtually no therapeutic application because it has ______ inactivation
rapid inactivation (causing no pills to be able to be administered)
88
Drugs that inhibit AChE are referred to as what two things
Cholinesterase inhibitors
Anticholinesterase
89
Acetylcholinesterase inhibitors cause what at the synapse and increase of what receptors
Increase of ACh levels at the synapse
Increase activation of muscarinic and nicotinic receptors
90
What are the three types of acetylcholinesterase inhibitors
Noncolvalent inhibitors
Reversible carbamate inhibitors
Organophosphorus inhibitors
91
acetylcholinesterase inhibitors: Noncolvalent inhibitors
Reversible binding and inhibition
Edrophonium and donepezil
92
acetylcholinesterase inhibitors: reversible inhibitors
Physostigmine and neostigmite
93
acetylcholinesterase inhibitors: Organophosphorus inhibitors
Hemisubstrates
Diisopropyl fluorophosphate (DFP)
94
Edrophonium (tensilon): structure, administration, bioavailability, CNS penetration, half life, elimination, therapeutic use
structure: Quaternary Amine
administration: IV, IM, SubQ
bioavailability: N/A
CNS penetration: PNS
half life: short
elimination: Urine
therapeutic use: Diagnosis of myastenia gravis
95
Donepezil (Aricept): structure, administration, bioavailability, CNS penetration, half life, elimination, therapeutic use
structure: Tertiary Amine
administration: Oral
bioavailability: 100%
CNS penetration: Yes
half life: long
elimination: Urine & Feces
therapeutic use: Alzheimer's
96
Reversible inhibitors mechanism
Rapid onset of action and shortest duration of any AChE inhibors
No covalent attachments to AChE
No enzyme intermediate
97
Carbamate Inhibitors
Neostigmine (prostigmin)
Physostigmine
Pyridostigmine (mestinon)
Rivastigmine (exelon)
98
Neostigmine: structure, administration, absorption , onset action, CNS penetration, metabolism, half life, elimination, therapeutic use
structure: Quaternary Amine
administration: IV, IM, oral
absorption: Poor
onset action: very short
CNS penetration: No
metabolism: Plasma and liver esterases
half life: shorter
elimination: Urine
therapeutic use: Myasthenia Gravis
99
Pyridostigmine: structure, administration, absorption , onset action, CNS penetration, metabolism, half life, elimination, therapeutic use
structure: Quaternary Amine
administration: IV, IM, oral
absorption: Poor
onset action: very short
CNS penetration: Yes
metabolism: plasma and liver esterases
half life: shorter
elimination: Urine
therapeutic use: Myasthenia Gravis
100
Physostigmine: structure, administration, absorption , onset action, CNS penetration, metabolism, half life, elimination, therapeutic use
structure: Tertiary Amine
administration: IV, IM
absorption: Readily
onset action: 5 minutes
CNS penetration: Yes
metabolism: plasma and liver esterases
half life: shortest
elimination: Urine
therapeutic use: Reverse toxic anticholinergic effects
101
Rivastigmine: structure, administration, absorption , onset action, CNS penetration, metabolism, half life, elimination, therapeutic use
structure: Tertiary Amine
administration: Oral, patch
absorption: Readily
onset action: n/a
CNS penetration: Yes
metabolism: plasma and liver esterases
half life: short
elimination: Urine, feces
therapeutic use: Alzehimer's, Parkinson's
102
Carbamate Inhibitors: mechanism
Inhibitors are substrates of AChE
Hydrolyzed by AChE but slowly
Form Carbamoylated AChE intermediate
-prolonged inhibition of AChE
103
Organophosphorus Inhibitors
Therapeutics: Echothiophate (phospholine), treat glaucoma
Toxic nerve gas: Sarin, Soman, Tabun
Pesticides: Parathion, Diazinon, Chlorpyrifos, Malathion
104
Absorption properties of organophosphorus inhibitors
Rapid onset of action
Highly lipid soluble liquids
Dispersed as aerosols or particles
(excreted in urine)
105
Organophosphorus Inhibitors mechanism
Formation of phosphorylated AChE intermediate
Enzyme regeneration is very slow
106
Aging process of phosphorylated enzyme intermediate
Stability of the phosphorylated enzyme is enhanced through aging
Conformational change of AChE-organophosphorus complex
Again results from lost of alkyl group with time
AChE after aging is virtually impossible to regenerate
107
Regeneration of AChE by Pralidoxine
Regenerated by hydrolysis of the phosphorylated ester
Pralidoxmine exerts a nucleophile attack and can't cross BBB
High dose inhibit AChE
108
Reactivation of AChE
Reactivating action of oximes in vivo is most marketed at the skeletal neuromusculat junction
Less effect at autonomic effect site -> quaternary ammonium group restricts entry into CNS
109
What are the effect of AChE inhibitors (DUMBBELLS)
D: diarrhea
U: urination
M: miosis
B: bronchospasm
B: bradycardia
E: emesis
L: lacrimation
L: sweating
S: salivation
110
Neuromuscular Junction
Released ACh binds to nicotinic receptors
Depolarization of the muscle cells
Activation of muscle contraction
111
Actions of AChE inhibitors at neuromuscular junction
Increase ACh levels, producing excitation and muscle fasciculation
-High concentrations of ACh, depolarization predominated following by blockage due to extended depolarization
Paralysis of muscles specially respiratory muscles
112
CNS effects from Action of AChE inhibitors at Neuromuscular junction
Confusion, ataxia, slurred speech, loss of reflexes, altered respiration, convulsions, coma, respiratory paralysis
113
Toxic effects mechanism
-Excessive stimulation of the cholinergic system
-Accidental intoxication
-AChE inhibitors also used for suicidal and homicidal purposes
-Duration of toxicity depends on properties of compound
114
Toxic effects: Inhalation
ocular and respitory effects appear first
-miosis, blurred vision, rhinorrhea, difficulty breathing
115
Toxic effects: Ingestion
GI symptoms occur earlier
-nausea and vomiting, abdominal cramps and diarrhea
116
Toxic effects: Percutaneous absorption
Sweating and muscle fasciculation
117
Toxic nicotinic effects
Include muscle fatigue and weakness involuntary twitching or fasciculations, and paralysis
-Paralysis of the respiratory muscles is most serious consequence
118
Toxic CNS effects
Confusion, ataxia, slurred speech, loss of reflexes, altered respiration, convulsions, coma and respiratory paralysis
-Time of death may range from 5 to 24 hr depending on the dose, route, agent (respiratory failure is the main cause)
119
Myasthenia Gravis: What does it do and how does AChE impact it
Autoimmune disease -> antibodies against nicotinic receptor
AChE inhibitors increase ACh which increases channel opening and muscle stimulation
120
How to diagnose and treat Myasthenia Gravis
Diagnose: Edrophonium (tensilon)
Treatment: Pyridostigmine, neostigmine, ambenonium (mytelase)
121
Common adverse effects of AChE inhibitors
GI track problems, dizziness, headache, bradycardia, AV block
122
AChE inhibitors drug interactions
Drugs affecting AChE inhibitors:
Cholinergic agents -> additive effects
Anticholinergic agents -> decrease effects
AChE inhibitors affect other drugs
Beta-blocker increase bradycardia
Nondepolarizing neuromuscular blocking agents exaggerated muscle relaxation
123
Muscarinic Receptor effector organs
Eye
Heart
Lungs
Stomach
Kidneys
Bladder
124
Muscarinic Antagonists compounds derived from natural sources
Solanaceae family
Alkaloids
Atropine
Scopolamine
125
Muscarinic Antagonists synthetic analogs
Quaternary amines used by inhalation -> effects on respiratory tract
126
Analog of Atropine and analog of atropine's analog
Ipratropium (tiotropium): analog of atropine, 4-6 hrs
Tiotropium (Spiriva): analog of ipratropium, last 24 hrs
127
Mydriasis and cycloplegia
mydriasis: pupil dilation
cycloplegia: paralysis of accommodation and ciliary muscle
128
Antagonist drugs used in the eye
Homatropine (Isopto homatropine)
Ophthalmic drops (tertiary amines)
-Cyclopentolate hydrochloride (cyclogyl)
-Tropicamide (mydriacyl)
129
Antagonist effects in the respiratory tract
Brocodilation
Decrease mucus secretion
130
Muscarinic antagonist Ipratropium (atrovent): Route, onset, duration, metabolism
route: inhalation
onset: quick
duration: short
metabolism: non-enzymatic ester cleavage to tropic acid and tropane
131
Muscarinic antagonist Tiotropium (Spiriva): Route, onset, duration, metabolism
route: inhalation
onset: quick
duration: day
metabolism: non-enzymatic ester cleavage to tropic acid and tropane
132
Muscarinic antagonist Aclidinium Bromide (Tudorza Pressair) and Glycopyrrolate (Seebri Neohaler): Route, onset, duration, metabolism
Route: inhalation and oral
Onset: fast
Duration: day
Metabolism: Hydrolysis by esterases for aclidinium, Hepatic for glycopyrrolate
133
Muscarinic antagonist Umeclidinium Bromide (Incruse Ellipta): Route, onset, duration, metabolism
route: inhalation
onset: quick
duration: day
metabolism: Hepatic via CYP2D6
134
Muscarinic Antagonist effects in respiratory disorders
Bronchodilators -> dry mouth side effect
Treatment: Asthma, COPD
135
Side effects of muscarinic antagonists
Dry mouth (M3R, M1R)
blurred vision (M3R)
Urinary Retention (M3R)
136
Antagonist effects in heart
Block M2 Receptors: increase heart rate and AV conduction causing tachycardia
137
Antagonist effects in urinary tract
Decrease detrusor muscle contraction, decrease normal tone, promoting urinary retention
138
Drugs used in urinary disorders
Solifenacin (Vesicare)
Tolterodine (Detrol)
Trospium (Sanctura)
Fesoterodine (Toviaz)
139
Adverse effects in the urinary system
Dry mouth and dry eyes: affinity for M3R
CNS drowsiness, dizziness, confusion
140
Effects of antagonists on GI
Decrease movement of GI tract
Use dicyclomine
141
Antagonist effects in exocrine gland
Use glycopyrrolate
Reduces secretions (treats hyperhidrosis)
Side effect is dry mouth
142
Scopolamine
CNS: Drowsiness, fatigue
Toxic: Hallucinations, coma
Help with motion sickness or vomiting
143
Skeletal muscle is inner aged by motor neurons that release ____
ACh
144
Neuromuscular transmission
Ligand gated ion channel activated by ACh influx of sodium
Have multiple subunits
145
Two classes of antagonists based on the selectivity for nicotinic receptors what are they
Neuromuscular blocking drugs
Ganglionic blocking drugs
146
Neuromuscular blocking drugs
Inhibit ACh action
Do not have CNS effect
Administration by IV
Muscle relaxing drugs
147
Isoquinoline derivatives
Tubicurarine
Metocurine
Atracurium
Cistracurium
Doxacurium
Mivacurium
148
Ammonia steroid derivatives
Pancuronium
Pipecuronium
Rocuronium
Vecuronium
149
Non depolarizing blockers
Competitive antagonists
Compete with ACh for receptors
Block ACh, block neuromuscular transmission
Prevent opening of channel
150
Effects of nondepolarizing blockers
Motor weakness and then flaccid muscle paralysis
Hypotension and bronospasm
151
Reversal of nondepolarizing blockage
Increase in ACh displaces drug from receptors
AChE inhibitors: neostigmine, phridostigmine, edrophonium
152
Succinylcholine is a depolarizing drug what does it do in phase 1 block
Drug binds a long time
Long lasting depolarization and prolong activation of receptor
Repetitive excitation
Muscle twitching
153
Phase 2 block of succinylcholine
Channels remain blocked and in a close state
Flaccid paralysis
154
Succinylcholine is metabolized by what
Butyrylcholinesterase
155
Clinical uses of neuromuscular blocking drugs
Short term muscle relaxation in anesthesia and intensive care
Rapid on set drugs (used in surgery with intubation)
