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Anesthesia Pharm I > Neuromuscular blocking agent reversal (13) > Flashcards

Neuromuscular blocking agent reversal (13) Flashcards

to reverse the effects of those badass blockers when we fuck up and gave too much (opps). Just make sure you have at least 1 twitch (it helps)

1
Q

What do you call a CRNA who graduates school in last place and has the lowest passing scores on the boards????

A

A CRNA (bitch)!!!!!!!!!!

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2
Q

2 parts of the CNS

A
  • brain

- spinal cord

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3
Q

2 parts of the PNS

A

somatic nervous system (SNS)

Autonomic nervous system (ANS)

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4
Q

Which system conveys information from receptors to the CNS

A

Afferent system

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5
Q

which system conveys information from the CNS to the muscles and glands

A

Efferent system

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6
Q

what are the 2 main areas the efferent system sends information to?

A

the somatic nervous system (SNS)

and Autonomic nervous system (ANS)

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7
Q

what does the somatic nervous system (SNS) do

A

conveys informatin from the CNS to the skeletal muscles

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8
Q

what does the ANS do

A

conveys information from the CNS to smooth muscle
cardiac muscle
and glands

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9
Q

diagram of CNS and PNS

A

C Brain Spinal Cord
N ^ v
S Afferent Efferent
V V
P Somatic Autonomic
N Nervous Nervous
S System System
V V
SNS PNS

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10
Q

2 parts of the ANS

A

Sypathetic nervous sytem

parasympathetic nervous system

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11
Q

ACh is stored where at the synaptic cleft

A

in vessicles at motor end plate

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12
Q

the nicotinic ACh receptor consist of how many gycoproteiin subunits to form an ion channel? what are the named?

A

5

  • 2 alpha
  • 1 beta
  • 1 delta
  • 2 gamma (epsilon)
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13
Q

how many alpha glycoprotein subunits on the nicotinic receptor need to bound to for ACh to open the channel

A

(both) 2

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14
Q

how many alpha glycoprotein subunits on the nicotinic receptor need to bound to for NDMBs to block the channel

A

1

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15
Q

how many alpha glycoprotein subunits on the nicotinic receptor need to bound by Sux’s to cause a block

A

both (2)

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16
Q

how is reversal of NMB (neuro muscular blockade) achieved

A

by competitive antagonism

  • -competition b/t NMBA and ACh for the motoer end plate receptor at the NMJ
  • whichever is the greatest wins
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17
Q

what is RECURARIZATION?

A

was a problem with long acting NMBAs whose effects outlasted the reversal agents

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18
Q

what is ENCAPSULATION reversal

A

cyclodextrin surrounds and bonds NMBA in plasma

-the concenration gradient reversed drawing NMBAs off receptors into plasma and then quickly bound

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19
Q

side notes about cholinesterase inhibitors
what were they derived from?
what were they used for?
precursor of what (give ex)

A 
derived from Calabar bean
used in West africa as a poison
precursor for organphosphates
-insecticides 
-nerve gas
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20
Q

what class of drugs are reversal agents

A

cholinesterase inhibitors

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21
Q

basic way cholinesterase inhibitors work for reversals

A

competitive antagonism

  • inhibits acethlcholinesterase (and other chilinesterases)
  • so it increases the concentration of ACh at NMJ
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22
Q

Name 4 cholinesterase inhibitors

A

Edrophonium (Enlon)
Neostigmine (prostigmin)
pyridostigmine
Physostigmine (antilerium)

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23
Q

what is the most rapid acting cholinesterase inhibitor

A

edrophonium

24
Q

which cholinesterase inhibitor binds REVERSIBLY to the negative charged enzyme site (cholinesterase enzyme)

A

edrophonium

25
Q

wy is the duration of binding short with edrophonium

A

b/c once it binds it is liberated finds another site to bind to, and so on

26
Q

why is edrophonium not recommended for deep blocks

A

b/c of the type of bonds it makes (reversable it’s not a covalent bond)

27
Q

does edrophonium require attenuation of muscarinic response to ACh accumulation?

A

yes

28
Q

just b/c shores may ask what is the basic chemical make up of edrophonium

A

simple alcohol with quaternary ammonium group

29
Q

just b/c shores may ask (b/c he is jealous that jake is a fucking wizard) what is the basic chemical make up of Neostigmine

A

Quaternary ammonium compound

30
Q

does Neostigmine cross the BBB

A

No way

31
Q

what kind of bond does Neostigmine make

A

IRREVERSABLE enzymatic deactivation (covalent)

32
Q

lipid solubility of Neostigmine

A

poor

33
Q

onset and duration of Neostigmine

A

onset 4-8 minutes

duration 1 hour (can last up to 4)

34
Q

does Neostigmine require attenuation of muscarinic response to ACh accumulation

A

you bet your ass it does

35
Q

which Cholinesterase inhibitor is used for myasthenia gravis??? Hmmmmm

A

pyridostigmine

36
Q

is pyridostigmine a long acting or short acting cholinesterase inhibitor

A

long

37
Q

is pyridostigmine used in anesthesia

A

no (remember myasthenia gravis)

38
Q

what is a cholinesterase that is a precusor of neostigmine and is a teriary amine

A

physostigmine (antilerium)

39
Q

seems important b/c it is totally different

what is special about physostigmine (antilerium)

A 
it crosses the BBB increasing the ACh in the brain causing:
confusion
lethargy
weakness
***CHOLINERGIC CRISIS****
40
Q

what is physostigmine (antilerium) used for??

A

counteract delerium caused by benzos and barbs

hint: physostigmine (antiLERIUM)=deLERIUM

41
Q

all cholinesterase inhibitors are eliminated where

A

renal
endophonium 70%
Neostigmine 50%

42
Q

Side effects of cholinesterase inhibitors

A

Bradycardia
bronckospasm
increased airway secretions
nausea
vomiting
abd cramping
miosis (constriction of pupil)
vision disturbance
micturation (voiding, peeing, weeing, pissing, etc)
so basically you go into a cholinergic chrisis
SLUDGE (too much ACh at postsynaptic cleft thus extreme PNS activation)

43
Q

**so with doses he said he only expects us to know neostigmine I am going to include endophonium also for KNOWLEDGE b/c that is in out top drawer as well. all others are not in our immediate use

A

( ``````````````````````|)

UU`````````````````

44
Q 
*******Neostigmine********
dose (mg/kg)
MAX DOSE
onset (min)
duration
Renal exretion
gycopyrrolate(mcg/kg)
atropine (usually not needed)
A 
dose--0.035-0.07 mg/kg 
MAX DOSE-- 5mg 
onset (min)- 7 min 
duration-- 55-75min (1hr-1hr 15 min)
Renal exretion- 50%
gycopyrrolate-- 7 mcg/kg
atropine- 15-30 mcg/kg
(hint: know the max dose almost every pt will always get the max dose the only exception is the old lady with a hip fracture
for example a 70 kg pt X 0.07= 4.9mg so anyone who is over 70 kg will just get the MAX amount.
45
Q 
just look at this and see the differences no need to memorize
endrophonium
dose (mg/kg)
MAX DOSE
onset (min)
duration
Renal exretion
gycopyrrolate(mcg/kg)
atropine
A 
dose 0.5-1 mg/kg
MAX DOSE 40 mg
onset (min) 1 min
duration 40-65min
Renal exretion 70%
gycopyrrolate ( do not use )
atropine (7-10mcg/kg)
ok so what to get out of it
--compared to neostigmine endrophonium is:
dose is twice as much
more rapid onset
shorter duration
and don't use glyco
46
Q

So here is a question!!! if you had to get your pt reversed as quick as possible what would you give???
(he specifically asked this in his lecture)

A

endrophonium

47
Q

whats another name for cholinesterase inhibitor “antidotes”

A

anticholinergic agents

or parasympatholytics

48
Q

what are 3 main anticholinergic agents, and there basic chemical coumpoud

A

atropine-tertiary Amine
scopolamine- tertiary Amine
gylcopyrolate- quaternary amine

49
Q

should you give cholinesterase inhibitors without an anticholinergic

A

no

50
Q

why is scopalamine rarely used

A

b/c of its significant central effects

51
Q

****what are the general dosage recommendations for anti-cholinergics
gylcopyrrolate

A

glycopyrrolate- 7mcg/kg

–general rule of thumb neo and glyco are equal proportions 1cc to 1cc

52
Q

what are the general dosage recommendations for anti-cholinergics
atropine

A

7-15 mcg/kg

given with endrophonium

53
Q

how do you reverse children

A

you always give your anti-cholinergic, wait for an increased HR, then give the cholinesterase inhibitor

54
Q

side effects of anti-cholinergic drugs

A

-tachycardia
-dry mouth
-mydriasis (dilated pupils)
-vision disturbance
-CONFUSION*
(opposite of cholinesterase inhibotors)

55
Q

**what shores whats us to know about sugammadex ( he stated in his lecture just know this)

A
  • cyclodextrin structure
  • not used in the US
  • causes encapsulation

Anesthesia Pharm I (9 decks)

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