Apex- NMB reversal agents Flashcards

1
Q

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

A. Electrostatic

B. Hydrogen

C. Covalent

d. Ester

A

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.
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2
Q

Explain how NMB are reversed

A

so acetylcholinesterase usually breaks down ACH

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

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3
Q

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

A
  1. Edrophonium
  2. Neostigmine
  3. Pyridostigmine
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4
Q

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

A

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

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5
Q

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

A

False- edrophonium does NOT inhibit pseudocholinesterase , just acetylcholinesterase

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6
Q

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

A
  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
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7
Q

How many binding sites does AchE have for ACH?

A

Two

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8
Q

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

A

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

Hydrogen bond @ the esteratic site

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9
Q

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

A

Neostigmine

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10
Q

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

A
  1. echothiopate
  2. organophosphates
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11
Q

T/F- pyridostigmine is more potent than neostigmine

A

FALSE - neostigmine is more potent than the pyramids

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12
Q

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

A

True

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13
Q

T/F- combining AchE inhibitors produces a synergistic effect

A

False - additive

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14
Q

_____% of Neostigmine is metabolized in the liver.

A

50%

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15
Q

Which anticholinergic is best paired with pyridostigmine

A

glyco (pyramids and neo)

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16
Q

Atropine is best paired with which AchE inhibior?

A

Edrophonium

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17
Q

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

A

true

18
Q

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

A

bc it can cause paradoxical muscle weakness (interesting)

19
Q

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

A

< 0.9

20
Q

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

A

75% RENAL

25% liver.

21
Q

Does renal failure prolong the DOA of AchE inhibitors?

A

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.

22
Q

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

A

true

23
Q

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

A

edrophonium, neostigmine , and pyrimids

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

24
Q

What’s the effect of intrathecal neostigmine?

A

it produces analgesia (50-100mcg)

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

25
Q

Which AchE inhibitor reduces the insidence of postop shivering?

A

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.

26
Q

Neostigmine onset and duration

A

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

27
Q

which AchE inhibitor has the fastest onset of action?

A

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)

28
Q

What 4 drugs reduce the incidence of shivering in the PACU

A
  1. Meperidine
  2. Precedex
  3. Clonidine
  4. Physostigmine
29
Q

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

A

true -dry mouth

30
Q

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

A

glyco- ionized (doesnt cross BBB)

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

31
Q

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

A

false- scopalamine is

32
Q

how can a small dose of atropine cause paradoxical bradycardia?

A
  • 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
33
Q

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

A

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

34
Q

T/F- glyco has antiemetic effects

A

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

35
Q

T/F- sugammadex has the greatest affinity for rocuronium

A

True

36
Q

Roc is primarily excreted by the bilary system

Sugammadex and Sugammadex-roc complex are excreted by the

A

Roc- biliary system

Suga - unchanged by the kidneys

37
Q

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

A

8

38
Q
A
39
Q

What if the patient needs to be reparalyzed after suggamadex?

  1. If 16mg/kg was given
  2. If 4mg/kg or less were given
A

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
40
Q

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 ?

A

5 mins

41
Q

Sugammadex reduces the effectiveness of hormonal contraceptives for up to ___days.

A

7 days

42
Q

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

A

Ester bond