Muscle Relaxants

Question 1

*what do muscle relaxants function as?

Answer 1

paralysis NOT anesthesia; they do not cause unconsciousness, amnesia or analgesia

Question 2

*where is the NM junction located?

Answer 2

synaptic cleft between the motor neuron and the muscle cell

Question 3

*how do stored vesicles get released by nerve terminals?

Answer 3

influx of calcium into nerve terminal

Question 4

*what NT is released at the NM junction?

Answer 4

ACh

Question 5

*what receptors bind ACh at the motor end plate?

Answer 5

nicotinic cholinergic receptors

Question 6

*how is the end plate potential generated?

Answer 6

sodium and calcium influx; potassium efflux upon ACh binding

Question 7

*enzyme that hydrolyzes ACh/ location?

Answer 7

acetylcholine esterase; motor end plate membrane near ACh receptors

Question 8

*the structure of nicotinic ACh receptor; what subunits bind ACh molecules?

Answer 8

5 subunits: two a, 1 B, 1 d, 1 e

only the two alpha subunits bind ACh molecules

Question 9

solubility of muscle relaxants

Answer 9

water soluble; poor lipid solubility

Question 10

examples of depolarizing muscle relaxants and non-depolarizing

Answer 10

depolarizing: succinylcholine

non-depolarizing: rocuronium, cis-atracurium

Question 11

**mechanism of action of depolarizing NM blockers e.g. succinylcholine

Answer 11

rapidly bind to ACh receptor, generate AP, not metabolized by AChE, therefore PROLONGED DEPOLARIZATION OF MUSCLE END PLATE

Question 12

*difference between phase 1 block and phase 2 block

Answer 12

1- prolonged end plate depolarization causing muscle relaxation do to time limited closure of sodium channel (succinylcholine)

phase 2: further prolonged depolarization causes conformational change in ACh receptors

Question 13

*mechanism of action of non-depolarizing NM blockers

Answer 13

competitive antagonists: bind to ACh receptors but don’t produce conformational changes for AP; compete with existing levels of ACh for the receptor

Question 14

*metabolism of succinylcholine (enzyme and product)

Answer 14

pseudocholinesterase: succinylmonocholine

enzyme only present in blood, not NM junction

Question 15

*succinylcholine and the percent inhibition of pseudocholinesterases

Answer 15

inhibits 80% of normal pseudocholinesterase

inhibits 20% of homozygous atypical pseudocholinesterase

inhibits 40-60% of heterozygous atypical pseudocholinesterase

Question 16

**why is succinylcholine avoided in pediatrics?

Answer 16

high incidence of undiagnosed myopathies, which would result in severe HYPERKALEMIA and complications

Question 17

*how does succinylcholine cause hyperkalemia?

Answer 17

massive proliferation of immature ACh receptors (UPREGULATION) causing massive potassium release

Question 18

**how are muscarinic side effects avoided?

Answer 18

using specific muscarinic ACh receptor blockers such as atropine, glycopyrrolate*

Question 19

*what drug class can cause muscarinic side effects? what is their function overall?

Answer 19

cholinesterase inhibitors (to reverse NM blockade)

Question 20

rocuronium: non-depolarizing or depolarizing? what subtype?

Answer 20

non-depolarizing, steroidal

Question 21

vecuronium: non-depolarizing or depolarizing? clinical implications?

Answer 21

non-depolarizing; hepatic clearance, renal clearance

Question 22

pancuronium: non-depolarizing or depolarizing? clinical implications?

Answer 22

non-depolarizing; hepatic clearance, renal clerance

Question 23

neostigmine w/ glycopyrollate is used as a

Answer 23

reversal agent

Question 24

cis-atracuronium: non-depolarizing or depolarizing? what suptype? clinical implications? where is it degraded? how?

Answer 24

non-depolarizing, benzylisoquinolines; histamine release

degraded in plasma by Hoffman elimination (non-enzymatic)