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Pharmacology Pt. 2 > Neuromuscular Blockers > Flashcards

Neuromuscular Blockers Flashcards

1
Q

Which chemical do all NMBs resemble?

A

acetylcholine

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2
Q

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

A

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

succynylcholine are mirror images of acetylcholine

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3
Q

Which type of NMB competes with Ach for the receptor?

A

Non-depolarizing NMBs are competitive.

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4
Q

What are the two types of non-depolarizing NMBs?

A

Amino steroid derivatives and benzylisoquinoline derivatives

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5
Q

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

A

Amino steroids: pancuronium, rocuronium, vecuronium.

Benzylisoquinoline derivatives: atracurium, cistracurium.

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6
Q

NMBs work on ________ Ach receptors.

A

nicotinic

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7
Q

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

A

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

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8
Q

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

A

70%

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9
Q

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

A

spastic during phase 1 and flaccid during phase 2

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10
Q

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

A

For intubation because they are fast acting and wear off fast

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11
Q

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

Is succinylcholine metabolized in an organ independent manner?

A

Atracurium and cistracurium are metabolized organ-independently.

Succinylcholine is organ-independent, too.

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12
Q

Describe the sequence of paralysis for NMBs.

A

Small muscles first, large muscles last

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13
Q

What type of NMBs are often used during hypothermia protocol?

A

Non-depolarizing NMBs

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14
Q

Which NMB is the longest acting?

A

Pancuronium

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15
Q

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

A

Liver, kidneys

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16
Q

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

A

Benzylisoquinoline derivatives

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17
Q

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.

A

Depolarizing NMB

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18
Q

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

A

Succinylcholine

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19
Q

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

A

Steroids

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20
Q

Name four drugs that increase (potentiate) NMB blockade.

A
  1. General (inhaled) anesthetics
  2. Antibiotics
  3. Calcium channel blockers
  4. Local anesthetics
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21
Q

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

A

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

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22
Q

How are non-depolarizing NMBs reversed clinically?

How are depolarizing NMBs reversed clinically?

A

Acetylcholinesterase inhibitors are given for non-depolarizing NMBs.

Depolarizing NMBs cannot be reversed clinically right now.

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23
Q

Name an AE that pancuronium and some rocuroniums may cause.

A

Tachycardia, which leads to hypertension.

24
Q

Name two AEs that atracurium might cause.

A
  1. Histamine release and all the garbo that comes along with that.
  2. Tachycardia and seizure-like activity from the metabolite laudanosine.
25
Q

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

A

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

26
Q

Which non-depolarizing NMB has the fastest onset?

A

Rocuronium.

27
Q

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

A

NMBs

28
Q

old paralyzing agent

A

curare

29
Q

curare can be used in

A

tetanus and spastic disorder

30
Q

first neuromascular drug

A

tubocurarine - no longer used

31
Q

succinylcholine is metabolized by

A

butyrylcholinesterase

32
Q

succinylcholine produces a

A

prolonged refractory period

33
Q

block pre-junctional nonBMB is associated with the

A

fade phenomenon

34
Q

there is a reduction in twitch height with successive stimuli

A

fade phenomenon

35
Q

sequence of paralysis?

A

largest muscles take the longest standing to reason that the diaphragm is the last

same order in onset and offset

36
Q

Facilitation of endotracheal intubation

A
  1. succinylcholine

less important is rocuronium

37
Q

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

A

non-depolarizing NMBs

38
Q

Facilitation or maintenance of synchrony in mechanically ventilated patients

A

non-depolarizing NMBs

39
Q

Anti-shivering during hypothermia protocol

A

non-depolarizing NMBs

40
Q

What do NMBs not do?

A

have no effect on consciousness or pain

41
Q

does NMBs cross the BBB?

A

No, so no CNS effect

42
Q

NonDB

A

pancorium
rocuronium
vecuronium

43
Q

Benzylisoquinoline

A

atracurium
cistracurium
mivacurium

44
Q

Prolonges in end stage in liver and kidney.

A

Mivacurium

45
Q

which drug in addition to succinylcholine is also metabolized by butyrylcholinesterase

A

mivacurium

46
Q

NMB side effects with Tachycardia and hypertension

A
  1. pancuronium
  2. rocuronium some
  3. mivacurium acute
47
Q

NMB histamine release leading to hypotension and reflex tachycardia

A
  1. atracurium- CNS stimulant

2. mivacurium

48
Q

NMB prolonged paralysis with pseudocholinesterase def.

A

mivacarium

49
Q

what is greater for steorid use

A

post residual weakness leading to acute quadriplegic myopathy syndrome

50
Q

Depolarizing NMBs adverse effect

A 
Hyperkalemia
Bradycardia
Masseter muscle rigidity
Malignant hyperthermia
Delayed muscle pain
Prolonged paralysis (pseudocholinesterase deficiency)
Anaphylaxis
51
Q

acetocholyne is a trigger for

A

malignant hyperthermia

52
Q

drugs that potentiate NMB blockade (3)

A
  1. inhlation anesthetics
  2. antibiotics
  3. calcium channel blockers and local anesthetics
53
Q

train-of- four TOF

A

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

54
Q

NMB reversal agent for non-dNMBs

A

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

55
Q

Sugammadex

A

NMB reversal but selectively binds to rocuronium and thus not effective for benzylisoquinoline

has minima lside effects

Pharmacology Pt. 2 (7 decks)

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