Skeletal Muscle Relaxants

Question 1

what are neuromuscular blockades

Answer 1

• depolarizing blocker: succinylcholine

- non depolarizing blocker: benzylisoquinolines and ammonio steroids

Question 2

what are the benzylisoquinolines and the ammonio steroids

Answer 2

Benzylisoquinolines: Cisatracurium, Atracurium, Mivacurium, Tubocurarine

Ammonio Steroids (curoniums) - Pancuronium, Vecuronium, Rocuronium

Question 3

mechanism of action of non depolarizing blockers

Answer 3

• competitive antagonist of nicotonic receptors
• large doses, enter the pores of ion channels for a more intense motor blockade
• block prejunctional Na channels –> reducing release of acetylcholine

Question 4

how can non depolarizing blockade be reversed

Answer 4

using acetylcholinesterase inhibitors – neostigmine and edrophonium –> increase amount of acetylcholine in the cleft

Question 5

what is the phase I block or depolarization block of succinylcholine

Answer 5

bind to nicotinic receptors –> depolarize as acetylcholine would –> not metabolized effectively –> muscle unresponsive to additional impulses –> flaccid paralysis

Question 6

what hydrolyzes succinylcholine/ reverses phase I or depolarization block of succinylcholine

Answer 6

plasma butyrylcholinesterase aka pseudocholinesterase

Question 7

what is the phase II block or desensitization block of succinylcholine

Answer 7

single large dose, repeated doses, or prolonged infusion of succinylcholine repolarizes the membrane –> membrane can’t become depolarized because it is desensitized –> channel act like in prolonged closed state

Question 8

what can reverse phase II block or desensitization block of succinylcholine

Answer 8

acetylcholinesterase inhibitors – neostigmine and edrophonium

Question 9

which of the non depolarizing blocker has a metabolite that can cause hypotension and seizures

Answer 9

Atracurium –> metabolite is Laudanosime –> transient hypotension and seizures (if higher doses)

Question 10

how is Atracurium inactivated

Answer 10

non specific plasma esterases and by spontaneous reaction called Hoffman elimination –> hence duration not altered by absence of renal function

Cisatracurium (stereoisomer)

Question 11

only non depolarizing blocker classified as short acting and its significance

Answer 11

Mivacurium –> hydrolyzed by butyrylcholinesterase –> not dependent on liver or kidney for elimination

Question 12

most rapid onset among all the non depolarizing blocker and can replace succinylcholine

Answer 12

Rocuronium

Question 13

AE of non depolarizing blockers

Answer 13

Histamine Release (Tubocurarine)
Ganglion blockade (Tubocurarine) --> hypotension and tachycardia
Cardiac Muscarinic Receptor blocker (Pancuronium) --> moderate tachycardia

Question 14

AE of depolarizing blocker

Answer 14

-succinylcholine stimulates nicotinic receptors in sympathetic and parasympathetic and muscarinic in heart

Malignant Hyperthermia (esp with halogenated hydrocarbons anesthetics)
Bradycardia
Histamine Release
Muscle pain
Hyperkalemia (loss of tissue K during depolarization)
Increased intraocular pressure
Increased intragastric pressure

Question 15

how do you treat malignant hyperthermia

Answer 15

dantrolene - prevents release of Ca from sarcoplasmic reticulum

Question 16

signs of histamine release

Answer 16

erythema of face and upper chest
transient hypotension
increased HR

Question 17

how can tetracyclines produce neuromuscular blockade

Answer 17

chelating calcium so no calcium release for action potential

Question 18

how can antibiotic aminoglycoside cause neuromuscular blockade

Answer 18

inhibiting ACh release from preganglionic terminal by competing with calcium

Question 19

types of patients that are resistant to non depolarizing muscle relaxants and require additional non depolarizing relaxants

Answer 19

severe burn and UMN disease

Question 20

what disease increases neuromuscular blockade caused by non depolarizing muscle relaxants

Answer 20

Myasthenia Gravis

Question 21

contraindication of succinylcholine

Answer 21

• family or personal history of Malignant Hyperthermia, Skeletal Muscle Myopathies, and Hypersensitivity to drug
• major burns, multiple trauma, extensive denervation of skeletal muscle, UMN injury because succinylcholine can cause hyperkalemia and this results in cardiac arrest in these patients

Question 22

muscarinic antagonist used post surgery and why

Answer 22

Atropine or Glycopyrrolate –> used together with neostigmine and edrophonium (used to reverse the non depolarizing blockade) –> prevent stimulation of muscarinic receptors and avoid bradycardia

Question 23

what is succinylcholine mainly use for

Answer 23

endotracheal intubation

ECT

Question 24

Spasmolytics that work in the CNS

Answer 24

Diazepam
Baclofen
Tizanidine

Question 25

when is diazepam used as a spasmolytic

Answer 25

muscle spasm of any origin --> produces sedation in most patients in doses required to reduce muscle tone

Question 26

mechanism of Baclofen

Answer 26

GABA agonist --> hyperpolarization due to increased K conductance

Question 27

when is Balcofen used

Answer 27

spasticity in Multiple Sclerosis | Spinal cord injuries and diseases

Question 28

mechanism and use of Tizanidine

Answer 28

alpha 2 agonist in the CNS --> MS and spinal cord injury

Question 29

spasmolytics that work on skeletal muscle

Answer 29

Dantrolene | Botulinum Toxin

Question 30

when is dantrolene used

Answer 30

Malignant Hyperthermia

Question 31

when is Botulinum Toxin used

Answer 31

Blepharospasm - persistent and disabling eyelid spasm Local muscle spasm Cerebral Palsy

Question 32

spasmolytics used for acute local spasm

Answer 32

Cyclobenzaprine

Question 33

what is cyclobenzaprine used for

Answer 33

acute, painful, musculoskeletal conditions

Question 34

AE of cyclobenzaprine

Answer 34

sedation, confusion, and transient visual hallucinations