Nsp Week 5: Neuromuscular Blocking Agents (Garrett)

Front 1

List 4 therapeutic uses for neuromuscular blocking agents

Back 1

1. Muscle relaxation during surgery
2. Intubation of trachea
3. Control of ventilation
4. Treatment of convulsions

Front 2

What is the site of action of NMBs?

Back 2

Neuromuscular nicotinic cholinergic receptors

Front 3

Are any of the NMBs metabolized by acetylchonine esterase?

Back 3

NO

Front 4

Describe which muscles are affected first by NMBs and the order of recovery

Back 4

Small, rapidly acting muscles are affected first (eyes, jaw, larynx), followed by larger muscles in the trunk and limbs.
*The diaphragm is one of the last muscles to be affected

Recovery occurs in the opposite order, beginning with the diaphragm and ending with the small muscles

Front 5

Which drugs tend to release histamine, causing bronchospasm, skin flushing, and hypotension due to vasodilation?

Back 5

1. Atracurium
2.. Mivacurium
3. D-tubocurarine

Front 6

What is an advantage of cisatracurium over atracurium?

Back 6

Cisatracurium does NOT release histamine, therefore it has no cardiovascular or autonomic effects

Front 7

How is mivacurium distinguished from atracurium and cisatracurium based on duration of action?

Back 7

Mivacurium has a SHORT duration of action (12 - 18 minutes), while atracurium and cisatracurium have INTERMEDIATE durations of action.

Front 8

What is unique about the metabolism of mivacurium?

Back 8

Metabolized by plasma and liver butyrylcholine esterase

Front 9

What was the first NMB drug?

Back 9

D-tubocurare

Front 10

Which benzylisoquinoline derivative does NOT release histamine?

Back 10

Cisatracurium

Front 11

What is the onset of action and duration of atracurium?

Back 11

Moderate onset of action (2-3 min)
Intermediate duration of action

*Releases histamine

Front 12

What is the onset of action and duration of cisatracurium?

Back 12

Moderate onset of action (2-3 min)
Intermediate duration of action

*Same as atracurium, but does NOT release histamine

Front 13

What is the onset of action and duration of mivacurium?

Back 13

Moderately rapid onset (2-4 min)
SHORT DURATION (12 - 18 min)

*Releases histamine

Front 14

What is the onset of action and duration of D-tubocurarine?

Back 14

Medium onset and LONG duration

*Releases histamine

Front 15

What are the adverse side effects of D-tubocurarine?

Back 15

Produces hypotension and tachycardia (histamine release)
Causes blockade of autonomic ganglia

Front 16

Which NMB has a long duration of action (1 - 2 hours), and is especially suitable for long surgical procedures?

Back 16

Pancuronium

Front 17

What are the adverse side effects of pancurium?

Back 17

Blocks cardiac muscarinic receptors and stimulates the sympathetic nervous system--> HYPERTENSION and increased risk for ARRHYTHMIAS

Front 18

Which drug is the only non-depolarizing NMB with rapid onset?

Back 18

Rocuronium

Front 19

What is the onset of action and duration of pancuronium?

Back 19

Moderately rapid onset (2-3 min)
LONG DURATION (1 - 2 hours)

Front 20

What is the onset of action and duration of rocuronium?

Back 20

RAPID ONSET (1 - 2 min)
Long duration of action

Front 21

What is the onset of action and duration of vercuronium?

Back 21

Moderately rapid onset (2-3 min)
Intermediate duration

Front 22

What is the mechanism of action of the depolarizing NMBs?

Back 22

Agonist at nicotinic cholinergic receptors
*Prolonged depolarization causes voltage-gated Na+ channels to stay in the inactive conformation

Front 23

Which depolarizing NMB has a rapid onset and short duration of action, and is used when rapid intubation is required?

Back 23

Succinylcholine

Front 24

Which depolarizing NMB is metabolized by butyrylcholine esterase in the plasma?

Back 24

Succinylcholine

Front 25

Which two drugs are metabolized by butyrylcholine esterase in the plasma?

Back 25

1. Mivacurium
2. Succinylcholine

Front 26

List 6 side effects of succinylcholine

Back 26

1. Hyperkalemia
2. Stimulation of autonomic ganglia
3. Intraocular pressure
4. Malignant hyperthermia
5. Histmaine release
6. Muscle pain

Front 27

Which 2 non-depolarizing NMBs are long acting?

Back 27

1. Pancuronium
2. D-tubocurare

Front 28

List 4 Intermediate acting non-depolarizing NMBs

Back 28

1. Atracurium
2. Cisatracurium
3. Rocuronium
4. Vercuronium

Front 29

At the end of surgery, which drugs are administered to increase the synaptic levels of ACh and reverse paralysis caused by NMBs?

Back 29

Acetylcholine esterase inhibitors
(neostigmine, edrophonium)

Front 30

Which muscle relaxant is a GABA-B receptor agonist?

Back 30

Baclofen

Front 31

What is the MOA of Baclofen?

Back 31

1. Inhibits glutamate release from the nerve terminals of corticospinal neurons by blocking Ca2+ channels
2. Hyperpolarizes alpha-motor neurons by stimulating K+ channels

Front 32

How is baclofen administered?

Back 32

1. Orally
2. Intrathecal route suing pumps (spinal cord injury and MS patients)

Front 33

What are the adverse side effects of baclofen?

Back 33

1. Sedation
2. Drowsiness
3. Fatigue

Front 34

Why must the discontinuation of baclofen therapy be done slowly?

Back 34

To avoid withdrawal symptoms

Front 35

Which muscle relaxant is an alpha-2-adrenergic receptor agonist?

Back 35

Tizanidine

Front 36

Does tizanidine result in presynaptic or postsynaptic inhibition?

Back 36

BOTH

Front 37

Which muscle relaxant inhibits Ca2+ release from the sarcoplasmic reticulum?

Back 37

Dantrolene

*Binds to RyR1 receptor

Front 38

What are the 3 major side effects produced by dantrolene?

Back 38

1. Muscle weakness
2. Sedation
3. Occasional hepatitis

Front 39

Which drug is used to treat malignant hyperthermia which can be caused by general anesthetics during surgery?

Back 39

Dantrolene

Front 40

What is the MOA of botulinum toxin?
Which proteins are digested?

Back 40

Inhibits release of ACh from alpha motor neurons
*Digests SNARE proteins involved with fusion and exocytosis of synaptic vesicles