Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anesthesia MM/TL > Nmba > Flashcards

Nmba Flashcards

1
Q

What is the structure of succinylcholine?

A

2 joined Ach molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the dosage of succinylcholine ?

A

1-1.5 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the intubating dose of suc if you use a defasciculating dose of roc?

A

1.5-2 mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the defasciculating dose of roc?

A

0.03mg/kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is succinylcholine metabolized?

A

By pseudocholinesterases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How long can paralysis last in someone homozygous for pseudocholinesterase deficiency?

A

3-8 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How can you tell if they have pseudocholinesterase deficiency?

A

Dibucaine inhibits normal pseudocholinesterase by 80% but only 20% in abnormal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What drug prolongs neuromuscular blockade?

A 
Cyclosporine (has solvent polyethoxylated castor oil) 
Aminoglycosides
Tetracyclines
Polymixin
Clindamycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What drug prolongs the action of succinylcholine?

A

Echothiophate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does Echothiophate prolong succinylcholine ?

A

By inhibiting pseudocholinesterase

Can cause 95% decrease in plasma butyrylcholinesterase for 4-6 weeks after stopping the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Echothiophate?

A

A topical eye medication for glaucoma- an acetylcholinesterase inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do all neuromuscular blocking agents work?

A

They are quaternary ammonium compounds with a positively charged nitrogen that has an affinity for the nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a phase I block?

A

When a depolarizing muscle blocker is bound to Ach receptors the perijunctional voltage gated Na channels close after a certain amount of time so you get the initial excitation (propagation of signal via the sodium channels and then release of calcium from the sarcoplasmic reticulum) and then the sodium channel closes again. The endplate cannot repolarize while the muscle blocker is bound to the Ach receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do nondepolarizing muscle relaxants work?

A

Competitive antagonism

They do not produce a conformational change for ion channel opening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the two subunits on the neuromuscular Ach receptors that bind acetylcholine?

A

Two identical alpha subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How many binding sites have to be occupied by acetylcholine to elicit a conformational change?

A

The 2 alpha subunits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the difference in the fetal form of Ach receptor?

A

It has a gamma unit instead of epsilon

Low channel conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What happens in conditions of chronically decreased acetylcholine release?

A

More expression of the extrajudicial all Ach receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why do states with more extrajunctional receptors have prolonged blockade with depolarizing muscle relaxants?

A

Because there are more receptors being depolarized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the sensitivity of neuromuscular blockade in myasthenia gravis.

A

A resistance to depolarizing relaxants (because there are fewer receptors)
Increased sensitivity to nondepolarizing relaxants (only takes one subunit to bind to cause muscle relaxation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are other ways of causing neuromuscular blockade?

A

Channel blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What drugs may cause channel blockade?

A

Neostigmine
Antibiotics
Cocaine
Quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is sugammadex

A

A cyclodextrin that binds tightly in a 1:1 ratio with steroidal nondepolarizing agents (roc, vec)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How much current should a peripheral nerve monitor be able to create for muscle contraction?

A

50 mA across 1000 ohm load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How long is the stimulus of a peripheral nerve monitor?

A

200 nanoseconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the train of four stimulation?

A

Four successive 200 nanosecond stimuli in 2 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens to the train of four as the block increases?

A

Train of four decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How much block do you after disappearance of the fourth twitch (3)?

A

75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How much block do you have after disappearance of the third twitch? (Two twitches)

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How much block do you have with disappearance of the second twitch?

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How much block does clinical relaxation require?

A

75-95% so 1-3 twitches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is tetany a test of?

A

Neuromuscular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is double burst more sensitive than?

A

More sensitive than train of four for fade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does 5 second tetany indicate?

A

Adequate but not full reversal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What muscles recover faster than adductor pollicis?

A

Diaphragm
Rectus abdominis
Laryngeal adductors
Orbicularis ocular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is tetany

A

A sustained stimulus 50-100 Hz usually lasting 5 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is fade indicative of?

A

A nondepolarizing block (phase 2 block)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What does the absence of fade indicate?

A

Adequate clinical recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is fade due to?

A

Prejunctional effect of NMBs that reduces the amount of acetylcholine available for release (the higher the calcium influx, the more quanta of Ach released - nondepolarizing agents don’t allow for influx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is posttetanic potentiation?

A

The ability of theta if stimulation to increase the evoked response to a subsequent twitch during a partial nondepolarizing block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Why is post-tetanic potentiation possible?

A

Transient increase in Ach mobilization due to tetany

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the lipid solubility of succinylcholine

A

Low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How does succinylcholine stop working?

A

It diffuses away from the membrane and gets broken done by pseudocholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does hypothermia due to succinylcholine metabolism?

A

Decreases the rate of its hydrolysis so prolongs its action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

In what conditions are there reduced levels of pseudocholinesterase?

A

Pregnancy
Liver disease
Renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is dibucaine

A

A local anesthetic that inhibits normal pseudocholinesterase by 80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Why is dibucaine used to test for pseudocholinesterase deficiency?

A

Because abnormal pseudocholinesterase is only inhibited 20% by dibucaine as opposed to normal which is 80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is a normal dibucaine number?

A

80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How long will a heterozygote of pseudocholinesterase deficiency have a block from succinylcholine

A

20-30 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How long will a homozygous of pseudocholinesterase deficiency have a block from succinylcholine

A

4-8 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How do acetylcholinesterase inhibitors prolong depolarizing blockade?

A
  1. Inhibit acetylcholinesterase so that more acetylcholine is in the junction causing more polarization
  2. Reduce hydrolysis of succinylcholine by inhibiting pseudocholinesterase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How do nondepolarizing agents antagonize a phase 1 block?

A

They occupy some acetylcholine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Why do children require higher doses of succinylcholine?

A

Because they have a larger extra cellular space than adults and succinylcholine is not lipid soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Why isn’t succinylcholine used in children?

A

May cause a systole in children with undiagnosed myopathies or prolonged paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Where does succinylcholine work?

A

At ALL acetylcholine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the CV effects of succinylcholine in children?

A

Profound bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the CV effects of low dose succinylcholine in an adult?

A

Negative chronograph and inotropy due to stimulation of parasympathetic ganglia to SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the CV effects of high dose succinylcholine in an adult?

A

Increased heart rate and contractility
Increased catecholamines

Due to SNS stimulation in Heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What may happen to heart rate in an adult after second dose of succinylcholine?

A

Bradycardia due to succinylmonocholine (hydrolyzed succinylcholine) sensitization of muscarinic cholinergic receptors in the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How long after a spinal cord or burn injury can you use succinylcholine before it becomes unsafe?

A

24 hours

61
Q

Why is using succinylcholine unsafe in burn or spinal cord patients?

A

Because of hyperkalemia cardiac arrest refractory to treatment

62
Q

When is the risk of hyperkalemia the highest after injury?

A

7-10 days

63
Q

How do you prevent myalgia from succinylcholine?

A

Pretreatment with 0.06 mg/kg - 0.1 mg/kg of or uranium

64
Q

How do you treat myalgias

A

NSAID

65
Q

How does succinylcholine increase intraocular pressure?

A

Extra ocular muscles have more motor end-plates on each cell

66
Q

What is a premonitory sign of malignant hyperthermia?

A

Increased tone of the masseter muscle preventing malignant hyperthermia

67
Q

Can you give succinylcholine to someone with NMS

A

Yes

68
Q

What does succinylcholine do to CBF?

A

Increases it

69
Q

What does succinylcholine do to ICP?

A

Increases it

70
Q

Is succinylcholine contraindicated in patients with hig ICP?

A

No

71
Q

How can increased ICP with succinylcholine be avoided?

A

Pretreatment with rocuronium and lidocaine

Hyperventilating

72
Q

Which nondepolarizing muscle relaxant is vagolytic?

A

Pancuronium

73
Q

What kind of nondepolarizing agents cause histamine release ?

A

Benzylisoquinolones (atracurium, gantacurium)

74
Q

What is the purpose of a priming dose?

A

To produce intubating conditions within 60-90 seconds

75
Q

What is the dose of a priming dose?

A

10-15% of the usual intubating dose

76
Q

How much do volatile agents decrease nondepolarizing dosage requirements?

A

By at least 15%

77
Q

Do the newer nondepolarizing agents affect the autonomic systems?

A

No

78
Q

Which nondepolarizing agents are metabolized significantly by the liver?

A

Pancuronium and vecuronium

79
Q

Which 2 nondepolarizing agents are excreted via the biliary system?

A

Roc and vec

80
Q

Which 2 nondepolarizing agents have prolonged effect in liver failure?

A

Pancuronium and rocuronium

81
Q

Which nondepolarizing agents are excreted by the kidney?

A

Pancuronium
Vecuronium
Doxacurium
Pipecurium

82
Q

How does hypothermia prolong blockade?

A

By decreasing metabolism and excretion

83
Q

How does respiratory acidosis affect nondepolarizing blockade?

A

Prolongs it and antagonizes its reversal

84
Q

How does hypermagnesemia affect nondepolarizing blockade?

A

Prolongs it because mg competes with calcium at the motor end plate

85
Q

How does hypokalemia and hypocalcemia affect nondepolarizing blockade?

A

Increases the block

86
Q

What is special about vec in the pediatric population?

A

Longer acting in neonate X

87
Q

Which nondepolarizing agent is not prolonged in the elderly?

A

Cisatracurium

88
Q

What do you have to do to the dosage of nondepolarizing agents in the obese population?

A

Increase by 20% of lean body weight

89
Q

What kind of nondepolarizing agent is atracurium?

A

Benzylisoquinolone

90
Q

How is atracurium metabolized?

A

Ester hydrolysis and spontaneous chemical breakdown (Hoffman elimination)

91
Q

What is the intubating dose of atracurium?

A

0.5mg/kg

92
Q

What are the side effects of atracurium?

A

Bronchospasm
Transient drop in SVR and increase in CO
Seizure (laudanosine toxicity)
Anaphylaxis (acrylate immune activation)

93
Q

What is laudanosine toxicity?

A

It is a tertiary amine that is a breakdown product of atracurium which causes CNS excitation

94
Q

What happens to atracurium if you run it with lidocaine or thiopental?

A

It will precipitate as a free acid because those are bases

95
Q

What is acrylate?

A

Metabolite of atracurium that can cause anaphylaxis

96
Q

What is cisatracurium?

A

A stereoisomers of atracurium that is 4 times more potent

97
Q

How is cisatracurium metabolized?

A

Hoffman elimination only

98
Q

What is the intubating dose of cisatracurium?

A

0.1-0.15 mg/kg within 2 minutes

99
Q

What does pancuronium look like?

A

Steroid ring with two modified Ach molecules

It resembles Ach enough to bind the nicotinic receptor but not activate it

100
Q

How is pancuronium metabolized?

A

By the liver

101
Q

How is pancuronium excreted?

A

Renally

102
Q

What is the induction dose of pancuronium?

A

.08-.12 mg/kg

103
Q

What are the side effects of pancuronium?

A

Vagolytic - tachycardia
SNS stimulation - HTN
Arrhythmias due increased catecholamines and decreased uptake

104
Q

What drugs should pancuronium not be used with and why?

A

Halothane and TCAs because of ventricular arrhythmias

105
Q

What allergy should you avoid using pancuronium with?

A

Bromide

106
Q

How long does pancuronium last?

A

60-120 minutes

107
Q

How is vecuronium metabolized?

A

Liver a little

But then excreted in biliary and renal systems

108
Q

What is vecuronium linked to in ICU?

A

Polyneuropathy from prolonged blockade

109
Q

What is the intubating dose of vecuronium?

A

0.08-0.12 mg/kg

110
Q

What is interesting about women and men with vecuronium?

A

Women are 30% more sensitive than men (greater and longer blockade) same with roc and pan

111
Q

What changes about the dosage of vec in the anhepatic phase of liver transplantation?

A

They are reduced

112
Q

How is rocuronium metabolized?

A

It’s not

113
Q

How is roc eliminate?

A

Primarily by liver through the biliary system

114
Q

What conditions prolong roc?

A

Liver disease

Pregnancy

115
Q

What kind of nondepolarizing agents are pan, roc, and vec?

A

Steroids

116
Q

What is the intubating dose of rocuronium?

A

0.6-1.2 mg/kg

117
Q

What is gantacurium?

A

A nondepolarizing agent that has a ultra short duration of action and comes in a powder

118
Q

How is gantacurium metabolized?

A

Ester hydrolysis

Cysteine adduction

119
Q

What ion is responsible for neuron depolarization?

A

Sodium influx

120
Q

What does sodium influx into a neuron lead to in the nerve terminal?

A

Calcium influx in the nerve terminal

121
Q

What does influx of calcium do at the nerve terminal?

A

Facilitates the release of Ach molecules out of the presynaptic nerve into the NMJ

122
Q

What do the Ach molecules in the NMJ do?

A

Bind nicotinic Ach receptors on the motor end plate which depolarizers the muscle

123
Q

What is the titanic fade due to?

A

Blockade of pre-junctional receptors

Due to blocking of the positive feedback system (normally release more acetylcholine in response to stimulation, but cannot when blocked by NMB)

124
Q

How should succinylcholine be dosed?

A

Using TBW

125
Q

How should NMBs be dosed?

A

IBW or LBW

126
Q

How much reversal should be given for a phase II block from succinylcholine?

A

0.03 mg/kg

127
Q

Why must the minimum amount of neostigmine be used to reverse a patient with pseudocholinesterase deficiency?

A

Because neostigmine inhibits pseudocholinesterase as well and at higher doses will do this which will prolong blockade cause by succinylcholine and acetylcholinesterase inhibition

128
Q

What does phenytoin do to NMBs?

A

Enhances the blockade if acute

Chronically reduces duration of blockade action

129
Q

What does a phase II block mean?

A

Means the postjunctional membrane has become repolarized, but it is desensitized to acetylcholine

130
Q

How would you reverse succinylcholine apnea in a patient with abnormal pseudocholinesterase?

A

Low dose neostigmine after phase II blocks occurs
- low dose because neostigmine preferentially inhibits acetylcholinesterase, but higher dose inhibits pseudocholinesterase which would impair metabolism of sux even further

131
Q

What is the dosage of sugammadex for routine reversal?

A

2 mg/kg of actual body weight

132
Q

How much sugammadex for no twitches?

A

4 mg/kg

133
Q

What is the dosage of sugammadex for immediate reversal aft RSI dose of roc?

A

16 mg/kg

134
Q

What is the advantage of double burst stimulation of train of four?

A

It allows better tactile and visual assessment of neuromuscular blockade

135
Q

What are the clinical signs of a TOF ratio greater than 0.7?

A 
Head lift greater than 5 seconds
Leg lift
Hand grip
Tidal volume of 15-20ml/kg
Effective cough
Negative inspiratory pressure of -25 cmH2O
136
Q

What side effect of succinylcholine cannot be blunted with a defasciculating dose of roc?

A

Increased IOP

137
Q

How much does IOP increase with succinylcholine?

A

5-15 mm Hg

138
Q

What does carbamazepine do to P450?

A

Induces it so it may cause decrease NMB by vec, roc

139
Q

How do amino glycosides prolong the NMB?

A

Inhibit the release of acetylcholine from alpha motor neurons

140
Q

How does clindamycin prolong NMB?

A

Prevents prejunctionsl release of Ach and decreases postjunctional nicotinic Ach receptors to Ach

141
Q

How do tetracyclines prolong NMB?

A

Postjunctional inhibitor

142
Q

How does cyclophosphamide affect NMB?

A

It is a pseudocholinesterase inhibitor so causes prolonged apnea after succinylcholine administration

143
Q

How long do the anti-pseudocholinesterase activities of cyclophosphamide last?

A

3-4 weeks after administration

144
Q

Which volatile augments NMB the most?

A

Desflurane

145
Q

What drugs potentiate NMBs?

A 
Aminoglycosides
Tetracyclines
Clindamycin
Lincomycin
Polymixin
Volatile
Lithium
Anticonvulsant
146
Q

Which volatile potentiates NMB the most?

A

Desflurane

147
Q

How is gantacurium metabolized?

A

Ester hydrolysis

148
Q

How is gantacurium inactivated?

A

By L-cysteine which replaces a chlorine atom

149
Q

Which NMB has an active metabolite?

A

Vecuronium

Metabolite = 3-desacetyl and has 80% activity, can accumulate in renal disease

Anesthesia MM/TL (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions