Apex- NMB reversal agents

Question 1

What kind of bond is formed when edrophonium binds to the anionic site on acetylcholinesterase?

A. Electrostatic

B. Hydrogen

C. Covalent

d. Ester

Answer 1

A. Electrostatic

• achE hydrolyzes ACH into choline and acetate
• this enzyme can be inhibited at the anionic site and/or the esteratic site
• the type of bond that is formed at these sites determines the drugs DOA
• Edrophonium forms an electrostiatic bond at the anionic site & a hydrogen bond at the esteratic site (wonderful)
• these are weak bonds which explain its short DOA
• Neostigmine, pyridostigmine and physostigmine from a carbamyl ester at the esteratic site. These are stronger bonds, which explain why these drugs have a longer DOA.

Question 2

Explain how NMB are reversed

Answer 2

so acetylcholinesterase usually breaks down ACH

-by inhibiting acetylcholinesterase, more ACH is available at the NMJ to compete and overtake the blocking agent

Question 3

AchE inhibitors used to reverse the effects of non-depolarizers (3)

Answer 3

1. Edrophonium
2. Neostigmine
3. Pyridostigmine

Question 4

What would happen if you reverse your patient with neostigmine and then they need an RSI and you need to give sux

Answer 4

The duration of sux wil lbe prolonged and neostigmine (as well as pyridostigmine) inhibit pseudocholinesterase which is needed to break down sux.

Question 5

T/F- neostigimine, pyridostigmine, and edrophonium all inhibit acetylcholinesterase and pseudocholinesterase

Answer 5

False- edrophonium does NOT inhibit pseudocholinesterase , just acetylcholinesterase

Question 6

Two ways bey which AchE inhibitors increase the concnetration of Ach at the nicotinic receptor

Answer 6

1. Enzyme inhibition
2. Presynaptic effects
   - AchE inhibitors are thought to stimulate the presynaptic recpetor and cause it to release additional Ach directly + indirectly by increasing concentrations of Ach in the NMJ

Question 7

How many binding sites does AchE have for ACH?

Answer 7

Two

Question 8

Edrophonium creates at (electrostatic,hydrogen) bond at the (anionic/esteratic) site on the acetylcholinesterase enzyme

Answer 8

Electrostatic @ Anion site (think anion = a negatively charged ion, so you need electricity to blance it)

Hydrogen bond @ the esteratic site

Question 9

Which NMB reversal agent works by creating a carbamyl ester complex at the esteratic site of AchE ?

Answer 9

Neostigmine

Question 10

Which drug non-competitively inhibits ACH by phosphorlation (2)

Answer 10

1. echothiopate
2. organophosphates

Question 11

T/F- pyridostigmine is more potent than neostigmine

Answer 11

FALSE - neostigmine is more potent than the pyramids

Question 12

T/F- the primary mechanism of edrophonium is most likely presynaptic

Answer 12

True

Question 13

T/F- combining AchE inhibitors produces a synergistic effect

Answer 13

False - additive

Question 14

_____% of Neostigmine is metabolized in the liver.

Answer 14

50%

Question 15

Which anticholinergic is best paired with pyridostigmine

Answer 15

glyco (pyramids and neo)

Question 16

Atropine is best paired with which AchE inhibior?

Answer 16

Edrophonium

Question 17

T/f- the deeper the degree of neuromuscular blockade, the longer the onset time of the AchE inhibitor

Answer 17

true

Question 18

Why shouldn’t you give more than what is required of neostigmine (or any AchE inhibitor)

Answer 18

bc it can cause paradoxical muscle weakness (interesting)

Question 19

A TOF < _____ increases the risk of airway obstruction, hypoxemic events, and postop pulm complications.

Answer 19

< 0.9

Question 20

Edrophonium and Pyridostigmine are metabolized 75% by the (kidneys/liver) and 25% by the (kidneys/liver)

Answer 20

75% RENAL

25% liver.

Question 21

Does renal failure prolong the DOA of AchE inhibitors?

Answer 21

Yes but it also prolongs the DOA of NMBs-

-so since both drugs wil lremain in the body for a longer time, there is no need to adjust the dose of the AchE inhibitor or to re-dose it.

Question 22

T/F- compared to adults, antagonism with neostigmine is faster in infants and children

Answer 22

true

Question 23

Which AchE’s are quaternary amines and what does that mean

Answer 23

edrophonium, neostigmine , and pyrimids

-quaternary amines do not pass thru the BBB or placenta - they are ionized, hydrophillic, lipophobic

Question 24

What’s the effect of intrathecal neostigmine?

Answer 24

it produces analgesia (50-100mcg)

S/E = NV, pruritis, and prolonged sensory and motor block

Question 25

Which AchE inhibitor reduces the insidence of postop shivering?

Answer 25

Physostigmine (40mcg/kg) -remember that's the wone that can cross the BBB and exert it's effects centrally and shivering is a CNS mechanism.

Question 26

Neostigmine onset and duration

Answer 26

onset: 5-15 mins duration: 45-90 mins

Question 27

which AchE inhibitor has the fastest onset of action?

Answer 27

Edrophonium 1-2 mins -I think this is becaue it's the least potent, meaning it requires a higher dosage to exert it's effect , and since there are a higher amount of molecules going to the receptor, the onset is quicker (like with a roc induction dose)

Question 28

What 4 drugs reduce the incidence of shivering in the PACU

Answer 28

1. Meperidine 2. Precedex 3. Clonidine 4. Physostigmine

Question 29

T/F- comapred to atropine, glyco is more likely to cause xerostomia

Answer 29

true -dry mouth

Question 30

Which anticholinergics are ionized vs nonionized (glyco, atropipne, scop)

Answer 30

glyco- ionized (doesnt cross BBB) atropine and scop - non-ionized ( do cross BBB and cause central effects such as sedation and mydrasis)

Question 31

T/F- glycopyrrolate is the anticholinergic with teh strongest antisialagogue properties

Answer 31

false- scopalamine is

Question 32

how can a small dose of atropine cause paradoxical bradycardia?

Answer 32

- prob due to the inhibition of **presynaptic M1 on the vagal nerve endings** - the job of this receptor is to reduce ACH release via a negative feedback loop - blocking it, turns off the negative feedback and allows for continued AcH release and bradycardia

Question 33

T/F- pt's with a denervated heart (heart transplant) don't need an anticholinergic with an AchE inhibitor

Answer 33

False- even though the anticholinergic won't effect the heart rate bc of denervation, the rest of the body will experience cholinergic effects

Question 34

T/F- glyco has antiemetic effects

Answer 34

False - bc it doesnt cross BBB (atropine and scop might though)

Question 35

T/F- sugammadex has the greatest affinity for rocuronium

Answer 35

True

Question 36

Roc is primarily excreted by the bilary system Sugammadex and Sugammadex-roc complex are excreted by the

Answer 36

Roc- biliary system Suga - unchanged by the kidneys

Question 37

Sugammadex is a gamma-cyclodextrin made of ___ (#) sugars, assembled in a ring.

Answer 37

8

Question 39

What if the patient needs to be reparalyzed after suggamadex? 1. If 16mg/kg was given 2. If 4mg/kg or less were given

Answer 39

_if 16mg/kg given within 24 hours_ * use a paralytic outside of the aminosteroid class * (you can do this regardless of dose given, but with 16mg/kg it's your only option) _if 4mg/kg of suga given:_ * **\<4 hours:** Give Roc at full 1.2mg/kg dose * **\>4 hours:** Can give Roc at 0.6mg/kg or vec at 0.1mg/kg

Question 40

If you gave 4mg/kg of suga to reverse a patient, what's the minimum amount of time you must wait if you need to reparalyze and want to use full dose roc ?

Answer 40

5 mins

Question 41

Sugammadex reduces the effectiveness of hormonal contraceptives for up to \_\_\_days.

Answer 41

7 days

Question 42

What kind of bond is formed when neostigmine binds to acetylcholinesterase?

Answer 42

Ester bond