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Spring '20/ L. PHARM TEST 2 - opioids, anticholinergics, cholinesterase > Neuromuscular Blocking Drugs & Reversal Agents > Flashcards

Neuromuscular Blocking Drugs & Reversal Agents Flashcards

(121 cards)

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1
Q

Name the first successful administration of curare to produce relaxation in 1912

A

Arthur Lawen

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2
Q

How does Succs work?

A

Succ produces a prolonged depolarization of the endplate region that results in desensitization of nicotinic acetylcholine receptors; inactivation of voltage gated sodium channels at the neuromuscular junction and increase in potassium permeability in the surrounding membrane. Thus producing the failure of the action potential generation due to membrane hyperpolarization and a block ensues

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3
Q

where is Acetylcholinesterase found?

what is it responsible for?

what are the two end products?

A

(“true” cholinesterase) is present at the neuromuscular junction

responsible for the rapid hydrolysis of released acetylcholine to

ACETIC ACID & CHOLINE

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4
Q

Butyrylcholinesterase

where is it synthesized?

what does it do and where?

A

(plasma cholinesterase or pseudocholinesterase) is synthesized in the liver.

It catalyzes (causes or accelerates) the hydrolysis of succinylcholine

which occurs mainly in the plasma.

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5
Q

Structure of neuromuscular blockers

2 points

what is the exception?

A

All neuromuscular blockers are quaternary ammonium compounds and are structurally related to acetylcholine.

Majority of NMBD are synthetic alkaloids

Exception is tubocurarine which is extracted from and Amazonian vine. It is cheaper to isolate from this plant than to synthesized.

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6
Q

Steroidal: presence of acetyl ester (Ach like) is thought to facilitate what?

A

thought to facilitate interactions of steroidal compounds with nicotinic acetylcholine receptors at the at the postsynaptic muscle membrane.

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7
Q

Tubocurarine:

who is it not suitable for

A

Monoquarternary, long acting
No active metabolism
Excreted unchanged in urine; liver is secondary
Not suitable for renal or liver failure patients
Onset slow
Duration is long
Recovery slow

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8
Q

Tubocurarine: intubating and maintenance

A

Intubating dose 0.5 – 0.6 mg/kg

Maintenance dose are 0.1 – 0.2 mg/kg

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9
Q

Atracurium

A

Racemic mixture of 10 stereoisomers
Isomers are separated into 3 geometrical isomer groups that are designated cis-cis, cis-trans, and trans-trans
Designed to undergo spontaneous degradation at physiologic temp and pH by Hofmann elimination yielding a laudanosine (tertiary amine) and a monoquaternary acrylate metabolite
Can undergo ester hydrolysis
Hoffmann elimination fragments atricurium to laudanosine and a monoquaternary acrylate
Laudanosine depends on the liver for clearance with ~70% excreted in bile with remainder in the urine

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10
Q

Atracurium (continued)

laudanosine does what?

A

Hepatic cirrhosis in humans does not alter clearance of laudanosine (metabolite)
Excretion of this metabolite is impaired in patients with biliary obstruction
Laudanosine easily crosses the BBB and has CNS stimulating properties
No evidence that shows normal or impaired renal function is likely to result in concentrations of laudanosine capable to produce convulsions.
Elimination of laudanosine is similar with normal or impaired renal function

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11
Q

Cisatracurium

Hoffman accounts for how much

how potent?

laudanosine?

A

Isomer of atracurium
Hoffman elimination to laudanosine and a monoquaternary alcohol metabolie
No ester hydrolysis of parent molecule
Hoffman is ~ 77% of clearance
23% is cleared by other organs with 16% being renal
4-5 times as potent as atricurium
5 times less laudanosine is produced and is thought to be of no clinical consequence
Does not cause histamine release like atracurium if given in clinical dose range

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12
Q

Mivacurium

A

Only currently available short acting NMBD
Discontinued in US (not because of safety reasons)
Mixture of 3 stereoisomers
Metabolized by butylcholinesterase at about 70-88% the rate of Sch to a monoester
May produce histamine release especially if given rapidly

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13
Q

Pancuronium

duration?

inhibiting properties?

shelf life?

name the metabolite that increases duration

A

Potent long acting
Vagolytic and butyrylcholinesterase inhibiting properties
~40-60% eliminated by kidneys and 11% in bile
15-20% metabolized by deacetylation in liver
3-OH, 17-OH, and 3,7-di-OH are less potent metabolites and excreted in urine
Accumulation of 3-OH metabolite is responsible for prolongation of the duration of Pancuronium
At room temperature remains stable for 6 months- good for military overseas stuff

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14
Q

Vecuronium

tell me about vagolytic properties

elimination?

what metabolite creates prolonged administration?

A

Monoquarternary with intermediate duration of action
Has a minor molecular difference from pancuronium characterized by:
Slight decrease in potency
Loss of vagolytic properties
Molecular instability in solution explaining shorter duration
Increased in lipid solubility resulting in greater biliary elimination of Vecuronium than pancuronium
Principle elimination is liver with renal accounting for about 30%
30-40% cleared in bile
Duration relies on liver function more so than renal function
Metabolized to 3-OH, 17-OH, 3,17-di-OH
3-OH has 80% the neuromuscular blocking potency of Vecuronium and with prolonged administration this metabolite may contribute to prolonged neuromuscular blockade

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15
Q

Rocuronium

A

Intermediately acting monoquaternary neuromuscular blocker with fast onset
6 times less potent than Vecuronium
Primarily eliminated by liver and excreted in bile
Carried to liver by carrier-mediated active transport system
30% excreted unchanged in urine
Remains stable for 60 days at room temperature

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16
Q

what effects your roc?

A

DES affects your ROC!!!!!

Someone always misses that questions
DES > SEVO > ISO > Halothane > Nitrous Oxide, barbiturate, or propofol

Expressed in terms of dose response relationship
50% depression of twitch height ED50 and 95% would be ED95

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17
Q

Mechanisms for potentiation:

potency of nmbd

A

Mechanisms for potentiation:
Central effect on alpha motoneurons and interneruonal synapses
Inhibition of postsynaptic nicotinic acetylcholine receptors
Augmentation of antagonist’s affinity at the receptor site

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18
Q

Antibiotics can potentiate neuromuscular blockade:

A

Aminoglycoside
Polymyxins
Lincomycine
Clindamycin
All inhibit the prejunctional release of acetylcholine and also depress postjunctional nicotinic acetylcholine receptor sensitivity to acetylcholine
Tetracycline exhibit post junctional activity only

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19
Q

what does Hypothermia or Magnesium Sulfate do to the blockers?

A

Hypothermia or Magnesium Sulfate potentiates blockade of NMBD
High magnesium concentrations inhibit calcium channels at the presynaptic nerve terminals that trigger the release of acetylcholine

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20
Q

Local Anesthetics do what for NMBD

A

LA given in large doses potentiate but in smaller doses not clinically significant

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21
Q

what does Antidysrhythmics such as quinidine do to NMDB

A

also potentiate NMBD

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22
Q

Factors decreasing potency of NMBD

Chronic use of anticonvulsant therapy:

A

thus need for increase doses to achieve block: can be attributed to increased clearance, increased binding of the neuromuscular blockers to alpha 1 acid glycoproteins and/or upregulation of neuromuscular acetylcholine receptors (and street therapy)

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23
Q

factors that decrease potency of NMDB in hyperparathyroidism hypercalcemia and NMBD

A

In hyperparathyroidism, hypercalcemia is associated with decreased sensitivity to atracurium and thus a short duration of neuromuscular blockade.
Muscle-nerve models have shown hypercalcemia to decrease sensitivity to tubocurarine and pancuronium

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24
Q

When is the ion channel of the Ach receptor closed?

A

during the resting state

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25
how does the acetylcholine ion receptor channel open?
it opens by the simultaneous binding of 2 Ach molecules to the Alpha subunits initiates conformational changes that open the channel
26
what happens when binding of a single molecule of a non depolarizing neuromuscular blocker (a competitive antagonist) to one alpha subunit?
it is sufficient to produce a neuromuscular block
27
steroidal compounds 3 drugs
pancuronium, vecuronium, rocuronium
28
steroidal compound Long duration of action >50min
pancuronium
29
steroidal compounds intermediate duration of action 20-50minutes
vecuronium | rocuronium
30
benzlisoquinolinium compounds name 4
tubocurarine atracurium cisatracurium mivacurium
31
benzlisoquinolinium compounds long duration of action >50min
tubocurarine
32
benzlisoquinolinium compounds intermediate duration of action 20-50 minutes
atracurium | cisatracurium
33
benzlisoquinolinium compounds short acting 10-20 minutes
mivacurium
34
long acting tubocurarine pancuronium intubating dose
tubocurarine 0.6mg/kg | pancuronium 0.08mg/kg
35
long acting tubocurarine pancuronium time to maximum block
tubocurarine 5.7min | pancuronium 2.9min
36
long acting tubocurarine pancuronium duration of response
tubocurarine 81min | pancuronium 86min
37
``` intermediate acting rocuronium vecuronium atracurium cisatracurium intubating dose ```
roc- 0.6mg/kg vec- 0.1mg/kg atrac- 0.5mg/kg cistracurium- 0.1mg/kg
38
``` intermediate acting rocuronium vecuronium atracurium cisatracurium time to maximum block ```
roc- 1.7min vec- 2.4min atracurium- 3.2min cisatracurium- 5.2min
39
``` intermediate acting rocuronium vecuronium atracurium cisatracurium clinical duration of response ```
roc- 36min vec- 44min atracurium- 46min cisatracurium 45min
40
low potency=?
rapid onset
41
high potency=?
slow onset
42
Onset of action is ________ proportional to potency of NMBD
inversely
43
Molar potency is highly predictive of a dugs time to onset of effect. Atracurium is the exception to this rule
The rationale for expressing potency in moles per kilogram is…[because] ultimately, we have a variable number of molecules chasing a fixed number of nicotinic receptors. The fewer molecules it takes (per kilogram of body weight) to achieve a given degree of receptor occupancy, the greater the affinity the drug has for the receptor. This is best expressed in micromoles per kilogram rather than in milligrams per kilogram.
44
buffered diffusion
diffusion of a drug is impeded because of its high potency and binding and unbinding to the receptors at the NMJ. Does not occur with low potency drugs. buffered diffusion causes repetitive binding to and unbinding from
45
NMBD interacts which receptors?
nicotinic and muscarinic cholinergic receptors within the SNS and PNS and at the nicotinic receptors of the neuromuscular junction
46
Tubocurarine is associated with marked ganglion blockade which results in?
hypotension; histamine manifestations(hypotension, reflex tachy, bronchospasm) in susceptible patients.
47
pancuronium and its direct vagolytic effect?
Pancuronium has a direct vagolytic effect. Can block muscarinic receptors on sympathetic postganglionic nerve terminals resulting in inhibition of a negative feedback mechanism whereby excessive catecholamine release is modulated or prevented Can also stimulate catecholamine release from adrenergic nerve terminals.
48
Histamine Release:
Seen with benzyllisoquinoliniums: Skin flushing Hypotension Decreased SVR Increases in pulse rate In typical doses, steroidal NMBD are not associated with histamine release Clinical effects of histamine seen with plasma concentrations increase to 200-300% of baseline values (such as seen with rapid administrations) Effect is ~1-5 minutes, is dose related, and clinically insignificant in healthy patients
49
Those patients who may be hemodynamically compromised name 3 considerations
Selecting a drug with less or no histamine release (steroidal compound) Slow administration over 60 seconds of a bynzylisoquinolinium Prophylactic use of the combined histamine H1 and H2 receptor antagonists
50
Benzylisoquinoliniums release histamine which can cause increase airway resistance and bronchospasm in patients with hyperactive airway disease which benzylisoquinolinium does not release histamine
cistatracurium
51
what is concerning about benzylisoquinoliniums
Benzylisoquinoliniums release histamine which can cause increase airway resistance and bronchospasm in patients with hyperactive airway disease
52
how are anaphylactic reactions mediated though?
Anaphylactic reactions are mediated through immune responses involving immunoglobulin E antibodies fixed to mast cells
53
Steroidal compounds have no histamine release however in a study from France NMBD analphylaxis:
43. 1% Rocuronium | 22. 6% Succinylcholine
54
Anaphylactoid reactions are not immune mediated and represent exaggerated pharmacologic responses in very sensitive individuals who represent a very small portion of the population
Anaphylactoid reactions are not immune mediated and represent exaggerated pharmacologic responses in very sensitive individuals who represent a very small portion of the population
55
Treatment of Analyphylaxis
100% O2-GAS OFF, 02 UP ALWAYS- FIRST THING YOU DO!- TELL SURGEON, IV Epinephrine 10-20 micrograms/kg- SUBQ Consider early tracheal intubation if angioedema develops Administer Fluids (crystalloids, and/or colloids) Norepinephrine or a sympathomimetic (phenylephrine) may be needed until fluid status is restored Treat dysrhythmias Antihistamines and Steroids is controversial but will still see in use
56
epi if you don't have an IV?
IF YOU’VE GOT AN IV FINE OTHERWISE GIVE SUB Q
57
SUCCINYLCHOLINE drug class dose what does it mimic?
SCh MIMICS THE ACTION OF ACh AND PRODUCES A SUSTAINED DEPOLARIZATION OF THE POSTJUNCTIONAL MEMBRANE ONLY DEPOLARIZING MUSCLE BLOCKER WE USE 1.0 – 1.5 MG/KG IS COMMONLY USED
58
SUCCINYLCHOLINE half life?
Half-Life: 47 seconds | Follows First-Order Kinetics
59
SIDE EFFECTS OF SCh
Sinus brady, junctional rhythm and sinus arrest may follow administration of Sch. This reflects actions of Sch at cardiac muscarinic cholinergic receptors where it mimics the physiologic effects of acetylcholine Most likely to occur when two doses are given with in 5 minutes Sinus brady from stimulation of cardiac muscarinic receptors is frequently seen in children and adults after repeated dosing Atropine is effective in treating and preventing brady
60
side effects of SCh at the autonomic ganglia
increases in HR and systemic blood pressure | resembles the effect of AcH at these sites.
61
what is attributed to ventricular dysrhythmias after Sch administration
is attributed to autonomic stimuli associated with laryngoscopy and tracheal intubation
62
how much does potassium increase after succs administration
0.5mEq/l -usually well tolerated and generally will not cause dysrhythmias.
63
which type of patient can't tolerated increase in k in succs
caution in renal patients- they usually get dialyzed the day before surgery.
64
name the conditions of hyperkalemia when up regulation of the exntrajunctional acetylcholine receptors occurs
hemiplegia or paraplegia muscular dystrophies, gullian barre burns
65
name some conditions that succs has been associated with severe hyperkalmia
abdominal infections severe metabolic acidosis closed head injury
66
why is succs not widely accepted in open eye cases?
it increases IOP with peak in 2-4 minutes and duration of 6 minutes
67
why is succs not recommended for use in children except for emergency tracheal intubation
risk fo massive rhabdomyolysis, hyperkalmia, and death in children with undiagnosed muscle disease
68
why can myoglobinuria occur in succs
it is unlikely and caused by the fasciculations caused by succs
69
findings in MH or muscular dystrophy after succs
myoglobinuria and rhabdomyolysis
70
what does succs do to the gut?
increases in intragastric and lower esophageal sphincter pressures related to intensity of fasciculations of abomdinal muscles. or a direct increase in vagal tone
71
does succs predispose a patient to regurgitation
no, an intact lower esophageal sphincter because pressure does not exceed the barrier pressure
72
how do we prevent succs and ICP?
pretreatment with a non depolarizing neuromuscular blocker can attenuate this increase in pressure
73
succs and myalgia?
prominent in neck back and abdomen. especially young patients with early ambulation happens more with ambulatory surgery than bedridden patients wide variation o incidence of post succs administration muscle pain of 0.2-89% may be due to muscle damage by fasciculations (despite fasciculation dose)
74
masseter spasm
sch is a trigger agent for MH. may be an earlier indicator of MH not always associated. also suggested that the high incidence of master spasms in children may be due to inadequate succs dosage
75
succs phase 1
SKELETAL MUSCLE PARALYSIS OCCURS BECAUSE A DEPOLARIZED POST JUNCTIONAL MEMBRANE AND INACTIVATED NA+ CHANNELS CANNOT RESPOND TO SUBSEQUENT RELEASE OF ACh. HENCE THE DESIGNATION DEPOLARIZING NEURO-MUSCULAR BLOCKADE THIS DEPOLARIZING NEURO-MUSCULAR BLOCKADE IS ALSO KNOWN AS PHASE I ABSENCE OF FADE AND TETANIC TO TOF
76
SUCCINYLCHOLINE (SCh)PHASE II
PHASE II BLOCKADE IS PRESENT WHEN THE POST JUNCTIONAL MEMBRANE HAS BECOME REPOLARIZED BUT STILL DOES NOT RESPOND NORMALLY TO ACh (DESENSITIZATION NEUROMUSCULAR BLOCKADE) MECHANISM OF PHASE II IS UNKNOWN MAY REFLECT THE DEVELOPMENT OF NONEXCITABLE AREAS AROUND THE ENDPLATES THAT BECOME REPOLARIZED BUT STILL PREVENT THE SPREAD OF IMPULSES INITIATED BY THE ACTION OF ACh AS TACHYPHYLAXIS (ACUTE RAPID DECREASE IN RESPONSE TO A DRUG AFTER ADMINISTRATION) DEVELOPS PHASE I (DEPOLARIZING) CHANGES TO PHASE II PHASE II HAS MORE CHARACTERISTICS OF NDMB AND FADE IS SEEN IN RESPONSE TO TOF
77
tell me about FASCICULATIONS
SUSTAINED DEPOLARIZATION PRODUCED BY THE INITIAL ADMINISTRATION OF SCh IS INITIALLY MANIFESTED AS TRANSIENT GENERALIZED SKELETAL MUSCLE CONTRACTIONS KNOWN AS FASCICULATIONS SUSTAINED OPENING OF SODIUM CHANNELS PRODUCED BY SCh IS ASSOCIATED WITH LEAKAGE OF POTASSIUM FROM THE INTERIOR OF CELLS
78
succs metabolism
BRIEF ACTION IS DUE TO RAPID HYDROLOYSIS OF PLASMA CHOLINESTERASE (PSEUDOCHOLINESTERASE) INTO SUCCINYLMONOCHOLINE WHICH HAS 1/20 TO 1/80 THE ACTIVITY OF SCh AT THE NEUROMUSCULAR JUNCTION PLASMA CHOLINESTERASE (PSEUDOCHOLINESTERASE) IS NOT PRESENT IN THE NMJ BUT RAPIDLY HYDROLYZES AND DECREASES THE AMOUNT OF SCh IN EXTRACELLULAR FLUID BEFORE REACHING THE NMJ.
79
SCh SHOULD NOT BE GIVEN TO PATIENTS 24-72 HOURS AFTER: | 3 things
MAJOR BURNS TRAUMA EXTENSIVE DENERVATION OF SKELETAL MUSCLES
80
why is succs contraindicated after trauma burns and extensive denervation of skeletal muscles
THIS IS BECAUSE IT MAY RESULT IN ACUTE HYPERKALEMIA AND CARDIAC ARREST
81
succs give to apparently health young boys
undiagnosed Muscular dystrophy have resulted in acute hyperkalmia and cardia arrest
82
dart
2cc succs- 40mg | 1cc atropine 0.4mg
83
when are dysrhythmias most likely to be seen with succs
most likely to occur when a second iv dose of Succs is administered 5 min after 1st dose.
84
what can we give 1-3 minutes before succs to decrease the likelihood of bradycardia
atropine 1-3 minutes prior
85
is the atropine IM reliable?
ATROPINE IM DOSE NOT RELIABLY PROTECT AGAINST SCh INDUCED BRADYCARDIAS.
86
FDA warning about succs
THE FDA ISSUED A WARNING AGAINST THE USE OF SCh IN CHILDREN, EXCEPT FOR EMERGENCY CONTROL OF THE AIRWAY.
87
0
WITH DRUG = 100% RECEPTORS BLOCKED
88
1
WITH DRUG = 99% OR LESS RECEPTORS BLOCKED
89
2
WITH DRUG = 95% OR LESS RECEPTORS BLOCKED
90
3
WITH DRUG = 85% OR LESS RECEPTORS BLOCKED
91
4 also 4=nodrug
WITH DRUG = 75% OR LESS RECEPTORS BLOCKED
92
ACETYLCHOLINESTERASE
Highly concentrated at the neuromuscular junction and is present in a lower concentration throughout the length of muscle fibers.
93
enzyme responsible for rapid hydrolysis of release acetylcholine at the NMJ
acetylcholinesterase
94
what percent is hydrolyzed during its diffusion across the synaptic cleft before it reaches the nicotinic ACH receptors
50%
95
how fast is acetylcholinesterase at hydrolyzing ach
4,000 molecules of ach are hydrolyzed per active site per second which is nearly the rate of diffusion
96
name 3 acetylcholinesterase inhibitors
Neostigmine (common) Edrophonium Phridostigmine (less common)
97
acetylcholinesterase inhibitors MOA
The acetylcholine that accumulates at the neuromuscular junction after administration of neostigmine competes with the residual molecules of neuromuscular blocking drug for the available unoccupied nicotinic acetylcholine receptors a the neuromuscular junction. Once the inhibition of acetylcholinesterease is complete, administering additional doses of neostigmine serves no purpose.
98
how many twitches do you need before giving neostigmine? if you get a 4th twitch after administration?
must have one twitch prior to neostigmine if you get return of all 4 then you know neostigmine has done its job
99
antagonism of non depolarizing neuromuscular blockade by AchE inhibitors depend on
Depth of blockade when reversal is attempted Anticholinesterase chosen Dose administered Rate of spontaneous clearing of neuromuscular blocker from the plasma Choice and depth of anesthetic agents administered
100
max dose of neostigmine
5mg
101
Neostigmine: Maximum effective dose range
60-80mcg/kg
102
Edrophonium dose
1.0-1.5 mg/kg range
103
Renal excretion neostigmine edrophonium & pyridostigmine
50% for neostigmine | 75% for edrophonium and pyridostigmine
104
pharmokinetics
Renal failure decreases the plasma clearance of all three as much as or more than that of the longer acting NMBD Elimination half life of edrophonium and neostigmine are similar Elimination half life of pyridostigmine is ~ longer
105
where does inhibition of acetylcholinesterase occur?
Inhibition of acetylcholinesterase increases acetylcholine in all synapses over the body that use acetylcholine as a transmitter.
106
how do you minimize muscarinic cardiovascular side effects?
To minimize the muscarinic cardiovascular side effects of acetylcholinesterase inhibitors and anticholinergic is co-administered
107
atropine plus edrophonium
Atropine 7-10 mcg/kg and edrophonium 0.5 – 1.0 mg/kg both are rapid
108
glycopyrollate plus neostigmine glycopyrolate and pyridostigmine
Glycopyrrolate 7-15 mcg/kg and neostigmine 60-80 mcg/kg both are slower Glycopyrrolate also pairs with pyridostigmine
109
preexisting cardiac disease and acetylcholinerase Inhibitors
Glycopyrrolate over Atropine may be desired
110
how fast do you give acetylcholinesterase inhibitor and anticholinergics?
slowly!! 2-5 minutes
111
anticholinergics side effects
``` hot dry blind red mad CANT SEE CANT SPIT CANT PEE CANT SH*T ```
112
cholinergic mnemonic
DUMBBELLS
113
sugammadex dosing for weight
actual body weight
114
sugammadex cardiovascular effects?
NO CARDIOVASCULAR EFFECT (NO ROBINUL OR ATROPINE)
115
sugammadex and renal impairment
Effectiveness of dialysis removing Sugammadex and Rocuronium has not been proven consistently. Thus sugammadex should be avoided in patients with a creatinine clearance of < 30 mL/min Clearance of sugammadex-Rocuronium complex is decreased in patients with substantial renal impairment.
116
neostigmine
ANTICHOLINESTERASE DRUG ACCELERATES THE ALREADY ESTABLISHED PATTERN OF SPONTANEOUS RECOVERY OF THE NMJ BY INHIBITING ACTIVITY OF ACETYCHOLINESTERASE WHICH LEADS TO ACCUMULATION OF ACh AT THE NICOTINIC AND MUSCARINIC NEUROMUSCULAR SITESALLOWS 2 ACh MOLECULES TO BIND WITH ALPHA SUBUNITS OF THE NICOTINIC CHOLINERGIC RECEPTORS.  THIS ACTION ALTERS THE BALANCE OF THE COMPETITION BETWEEN ACh AND NONDEPOLARIZING MUSCLE BLOCKERSTHIS COMPETITION ALLOWS INCREASE IN ACh AND RESTORES NEUROMUSCULAR TRANSMISSION QUATERNARY AMMONIUM STRUCTURE LIMITS ENTRANCE INTO CNS ALLOWING ANTAGONISM OF NMB AT NMJ TO OCCUR THE PERIPHERAL CARDIAC MUSCARNIC EFFECTS (BRADY) ARE PREVENTED BY ATROPINE OR GLYCOPYRROLATE (ROBINUL MOST COMMON USED). M&P SAY NEOSTIGMINE MAX 60-70 MCG/KG. YOU MAY SEE 40- 70 MCG/KG AS WELL. 5 MG SHOULD BE THE MAX. GLYCOPYRROLATE: 7-15 MCG/KG IS A GOOD DOSE.
117
what percent of sugammadex is excreted within 6 hours?
70%
118
what percent of sugammadex is excreted in 24hrs
>90%
119
can you give sugammadex if no twitch is detected?
yes
120
atracurium tell me its mixture and isomers
racemic mixture of 10 stereoisomers
121
atracurium and laudanosine
depends on the liver for clearance 70% excreted in the bile. biliary obstruction impairs excretion. laudanosine crosses BBB and has CNS stimulating properties.

Spring '20/ L. PHARM TEST 2 - opioids, anticholinergics, cholinesterase (8 decks)

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