Neuromuscular Blockers

Question 1

Which chemical do all NMBs resemble?

Answer 1

acetylcholine

Question 2

Name the only depolarizing NMB on the market. What enzyme degrades it? Is this enzyme found in the synaptic cleft?

Answer 2

Succinylcholine. Degraded by pseudocholinesterase aka butyrylcholinesterase. Not found in the cleft in high amounts.

succynylcholine are mirror images of acetylcholine

Question 3

Which type of NMB competes with Ach for the receptor?

Answer 3

Non-depolarizing NMBs are competitive.

Question 4

What are the two types of non-depolarizing NMBs?

Answer 4

Amino steroid derivatives and benzylisoquinoline derivatives

Question 5

Name the three amino steroid derivatives and the two benzylisoquinoline derivatives.

Answer 5

Amino steroids: pancuronium, rocuronium, vecuronium.

Benzylisoquinoline derivatives: atracurium, cistracurium.

Question 6

NMBs work on ________ Ach receptors.

Answer 6

nicotinic

Question 7

Briefly describe the mechanism of action of non-depolarizing NMBs.

Answer 7

They competitively block nicotinic Ach receptors to prevent Ach from binding, causing flaccid paralysis.

Question 8

___% blockage of Ach nicotinic receptors is needed for paralysis from non-depolarizing NMBs.

Answer 8

70%

Question 9

Depolarizing NMBs cause _______ paralysis during phase 1 and _______ paralysis during phase 2.

Answer 9

spastic during phase 1 and flaccid during phase 2

Question 10

What is the primary clinical use for depolarizing NMBs? Why?

Answer 10

For intubation because they are fast acting and wear off fast

Question 11

Which two non-depolarizing NMBs are cleared organ-independently?

Is succinylcholine metabolized in an organ independent manner?

Answer 11

Atracurium and cistracurium are metabolized organ-independently.

Succinylcholine is organ-independent, too.

Question 12

Describe the sequence of paralysis for NMBs.

Answer 12

Small muscles first, large muscles last

Question 13

What type of NMBs are often used during hypothermia protocol?

Answer 13

Non-depolarizing NMBs

Question 14

Which NMB is the longest acting?

Answer 14

Pancuronium

Question 15

Amino-steroid derivative NMBs are dependent on these two organs for metabolism.

Answer 15

Liver, kidneys

Question 16

Which NMBs are deactivated via spontaneous Hofmann elimination reactions in vivo?

Answer 16

Benzylisoquinoline derivatives

Question 17

What type of NMBs have the following AEs: Bradycardia, Masseter muscle rigidity, hyperkalemia, malignant hyperthermia, muscle pain, anaphylaxis, increased intragastric pressure, increased intra-ocular pressure.

Answer 17

Depolarizing NMB

Question 18

Butyrylcholinesterase deficiency would be a contraindication to using which specific NMB?

Answer 18

Succinylcholine

Question 19

Name the medication, when taken concomitantly, increases risk for acute quadriplegic myopathy syndrome.

Answer 19

Steroids

Question 20

Name four drugs that increase (potentiate) NMB blockade.

Answer 20

1. General (inhaled) anesthetics
2. Antibiotics
3. Calcium channel blockers
4. Local anesthetics

Question 21

What train-of-four values are “ideal” for surgical procedures and what percentage of receptors blocked correspond to each value?

Answer 21

2/4 twitches = 85% blocked
1/4 twitches = 90% blocked
this is ideal

Question 22

How are non-depolarizing NMBs reversed clinically?

How are depolarizing NMBs reversed clinically?

Answer 22

Acetylcholinesterase inhibitors are given for non-depolarizing NMBs.

Depolarizing NMBs cannot be reversed clinically right now.

Question 23

Name an AE that pancuronium and some rocuroniums may cause.

Answer 23

Tachycardia, which leads to hypertension.

Question 24

Name two AEs that atracurium might cause.

Answer 24

1. Histamine release and all the garbo that comes along with that.
2. Tachycardia and seizure-like activity from the metabolite laudanosine.

Question 25

What is Acute Quadriplegic Myopathy Snydrome (AQMS)? What NMBs can cause it? Concomitant use of which drugs increase risk for this?

Answer 25

Residual and prolonged paralysis from the NMB lasting days to weeks. Non-depolarizing NMBs can cause it. Higher risk with concomitant steroid use.

Question 26

Which non-depolarizing NMB has the fastest onset?

Answer 26

Rocuronium.

Question 27

drugs that block transmission at the NMJ causing paralysis of the affected skeletal muscle

Answer 27

NMBs

Question 28

old paralyzing agent

Answer 28

curare

Question 29

curare can be used in

Answer 29

tetanus and spastic disorder

Question 30

first neuromascular drug

Answer 30

tubocurarine - no longer used

Question 31

succinylcholine is metabolized by

Answer 31

butyrylcholinesterase

Question 32

succinylcholine produces a

Answer 32

prolonged refractory period

Question 33

block pre-junctional nonBMB is associated with the

Answer 33

fade phenomenon

Question 34

there is a reduction in twitch height with successive stimuli

Answer 34

fade phenomenon

Question 35

sequence of paralysis?

Answer 35

largest muscles take the longest standing to reason that the diaphragm is the last same order in onset and offset

Question 36

Facilitation of endotracheal intubation

Answer 36

1. succinylcholine | less important is rocuronium

Question 37

Facilitation of skeletal muscle relaxation for surgical procedures or as an adjuvant to anesthesia

Answer 37

non-depolarizing NMBs

Question 38

Facilitation or maintenance of synchrony in mechanically ventilated patients

Answer 38

non-depolarizing NMBs

Question 39

Anti-shivering during hypothermia protocol

Answer 39

non-depolarizing NMBs

Question 40

What do NMBs not do?

Answer 40

have no effect on consciousness or pain

Question 41

does NMBs cross the BBB?

Answer 41

No, so no CNS effect

Question 42

NonDB

Answer 42

pancorium rocuronium vecuronium

Question 43

Benzylisoquinoline

Answer 43

atracurium cistracurium mivacurium

Question 44

Prolonges in end stage in liver and kidney.

Answer 44

Mivacurium

Question 45

which drug in addition to succinylcholine is also metabolized by butyrylcholinesterase

Answer 45

mivacurium

Question 46

NMB side effects with Tachycardia and hypertension

Answer 46

1. pancuronium 2. rocuronium some 3. mivacurium acute

Question 47

NMB histamine release leading to hypotension and reflex tachycardia

Answer 47

1. atracurium- CNS stimulant | 2. mivacurium

Question 48

NMB prolonged paralysis with pseudocholinesterase def.

Answer 48

mivacarium

Question 49

what is greater for steorid use

Answer 49

post residual weakness leading to acute quadriplegic myopathy syndrome

Question 50

Depolarizing NMBs adverse effect

Answer 50

``` Hyperkalemia Bradycardia Masseter muscle rigidity Malignant hyperthermia Delayed muscle pain Prolonged paralysis (pseudocholinesterase deficiency) Anaphylaxis ```

Question 51

acetocholyne is a trigger for

Answer 51

malignant hyperthermia

Question 52

drugs that potentiate NMB blockade (3)

Answer 52

1. inhlation anesthetics 2. antibiotics 3. calcium channel blockers and local anesthetics

Question 53

train-of- four TOF

Answer 53

monitor NMBs by eyebrow twitch (4/4- not blocked and 0/4 is 100% blocked) we shoot for 1-2/4

Question 54

NMB reversal agent for non-dNMBs

Answer 54

decrease breakdown of Ach and reverse NMB block but dont worh that well

Question 55

Sugammadex

Answer 55

NMB reversal but selectively binds to rocuronium and thus not effective for benzylisoquinoline has minima lside effects