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Top Shelf Drugs > NDNMB reversals > Flashcards

NDNMB reversals Flashcards

1
Q

2 parts of the CNS

A

-brain-spinal cord

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2
Q

2 parts of the PNS

A

somatic nervous system (SNS)Autonomic nervous system (ANS)

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3
Q

Which system conveys information from receptors to the CNS

A

Afferent system

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4
Q

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

A

Efferent system

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5
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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6
Q

what does the somatic nervous system (SNS) do

A

conveys informatin from the CNS to the skeletal muscles

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7
Q

what does the ANS do

A

conveys information from the CNS to smooth musclecardiac muscleand glands

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8
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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9
Q

2 parts of the ANS

A

Sypathetic nervous system and the parasympathetic nervous system

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10
Q

ACh is stored where at the synaptic cleft

A

in vesicles at motor end plate

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11
Q

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

A

5

2 alpha, 1 beta, 1 delta, and 2 gamma (epsilon)

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12
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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13
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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14
Q

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

A

both (2)

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15
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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16
Q

what is RECURARIZATION?

A

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

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17
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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18
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 beanused in West africa as a poison precursor for organphosphates
  • insecticides
  • nerve gas
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19
Q

what class of drugs are reversal agents

A

cholinesterase inhibitors

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20
Q

basic way cholinesterase inhibitors work for reversals

A

competitive antagonism - inhibits acetylcholinesterase (and other chilinesterases), so it increases the concentration of ACh at the NMJ

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21
Q

Name 4 cholinesterase inhibitors

A

edrophonium (enlon)
neostigmine (prostigmin)
pyridostigmine
physostigmine (antilerium)

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22
Q

what is the most rapid acting cholinesterase inhibitor?

A

edrophonium

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23
Q

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

A

edrophonium

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24
Q

why is the duration of binding short with edrophonium (Enlon)?

A

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

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25
Q

Why is edrophonium (Enlon) not recommended for deep blocks?

A

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

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26
Q

does edrophonium require attenuation of muscarinic response to ACh accumulation?

A

yes

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27
Q

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

A

simple alcohol with quaternary ammonium group

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28
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

29
Q

Does Neostigmine (Prostigmine) cross the BBB

A

No

30
Q

What kind of bond does Neostigmine (Prostigmine) make?

A

IRREVERSABLE enzymatic deactivation (covalent)

31
Q

lipid solubility of Neostigmine: good or poor?

A

poor

32
Q

Does Neostigmine (Prostigmine) require attenuation of muscarinic response to ACh accumulation?

A

you bet your ass it does

33
Q

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

A

pyridostigmine

34
Q

is pyridostigmine a long acting or short acting cholinesterase inhibitor ?

A

long

35
Q

is pyridostigmine used in anesthesia

A

no (remember myasthenia gravis)

36
Q

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

A

physostigmine (antilerium)

37
Q

seems important b/c it is totally differentwhat is special about physostigmine (antilerium)

A

it crosses the BBB increasing the ACh in the brain causing:confusionlethargyweaknessCHOLINERGIC CRISIS*

38
Q

what is physostigmine (antilerium) used for??

A

counteract delerium caused by benzos and barbs

hint: physostigmine (antiLERIUM)=deLERIUM

39
Q

all cholinesterase inhibitors are eliminated where?

A

renal: endophonium 70%, Neostigmine 50%

40
Q

Side effects of cholinesterase inhibitors?

A

Bradycardia, bronchospasm, 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)

41
Q

Neostigmine (Prostigmine) dose, max dose, onset, peak, duration, Renal excretion %?

A

dose: 0.04 - 0.07 mg/kg

max dose: 5 mg

onset: 5 - 10 minutes
peak: 10 minutes
duration: 1 hour

Renal excretion: 50%

42
Q

Endrophonium (Enlon) dose, max dose, onset, peak, duration, Renal excretion %?

A

dose: 0.5 - 1 mg/kg

max dose: 40 mg

onset: 30 - 60 seconds
peak: 1 minute
duration: 45 minutes

Renal excretion: 70%

43
Q

If you had to get your patient reversed as quick as possible what would you give???

A

endrophonium

44
Q

whats another name for cholinesterase inhibitor “antidotes”?

A

anticholinergic agents or parasympatholytics

45
Q

what are 3 main anticholinergic agents, and there basic chemical compound?

A

atropine-tertiary amine

scopolamine- tertiary amine

gylcopyrrolate- quaternary amine

46
Q

should you give cholinesterase inhibitors without an anticholinergic?

A

no

47
Q

why is scopalamine rarely used

A

b/c of its significant central effects

48
Q

What is the general dosage recommendation for gylcopyrrolate (Robinul)?

A

Glyco 0.2mg for each 1mg of Neostigmine given.

(glycopyrrolate- 7mcg/kg–general rule of thumb neo and glyco are equal proportions 1cc to 1cc, because glyco is packaged as 0.2mg/cc and neo is packaged as 1mg/cc)

49
Q

What is the general dosage recommendation for atropine?

A

7-15 mcg/kg, given with endrophonium.

typical dose is 1 - 2 mg

50
Q

How do you reverse children, or anyone for that matter?

A

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

51
Q

side effects of anti-cholinergic drugs

A 
tachycardia
dry mouth
mydriasis (dilated pupils)
vision disturbance
**CONFUSION***

(opposite of cholinesterase inhibitors)

52
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

53
Q

How is neostigmine (Prostigmine) metabolized?

A

50% renal, 50% hepatic

54
Q

How is edrophonium (Enlon) metabolized?

A

75% renal, 25% hepatic

55
Q

Glycopyrrolate (Robinul) dose, onset, peak, duration?

A

dose: 0.2 mg / 1 mg Neostigmine given
onset: 4 minutes
peak: 5 minutes
duration: 2 - 7 hours

56
Q

Glycopyrrolate (Robinul) mechanism of action.

A

muscarinic receptor antagonist - competitively antagonizes muscarinic acetylcholine receptors, displacing acetylcholine, and preventing parasympathetic stimulation by acetylcholine

57
Q

How is glycopyrrolate (Robinul) metabolized?

A

hepatic metabolism

renal elimination

58
Q

Does glycopyrrolate (Robinul) cross the blood brain barrier?

A

no

59
Q

Scopalomine dose, onset, peak, duration?

A

dose: 0.2 - 1 mg (usually given IM)
onset: 5 - 10 minutes
peak: 20 - 60 minutes
duration: 2 hours

60
Q

Scopalomine mechanism of action.

A

muscarinic receptor antagonist - competitively antagonizes muscarinic acetylcholine receptors, displacing acetylcholine, and preventing parasympathetic stimulation by acetylcholine

61
Q

Does scopalomine cross the blood brain barrier?

A

yes

62
Q

How is scopalomine metabolized?

A

hepatic metabolism

renal elimination

63
Q

Pulmonary, cardiac, and neuro effects of scopalomine?

A

pulmonary - bronchodilation

cardiac - increases CO

neuro - decreases motion-induced nausea; the best at decreasing secretions, increasing amnesia, and increasing sedation

64
Q

What is contraindicated with scopalomine use?

A

closed-angle glaucoma

65
Q

Atropine dose, onset, peak, duration?

A

dose: 0.01 mg/kg
onset: 1 minute
peak: 2 minutes
duration: 1 - 4 hours

66
Q

Atropine mechanism of action.

A

muscarinic receptor antagonist - competitively antagonizes muscarinic acetylcholine receptors, displacing acetylcholine, and preventing parasympathetic stimulation by acetylcholine

67
Q

How is atropine metabolized?

A

hepatic metabolism

renal elimination

68
Q

Pulmonary and cardiac effects of atropine?

A

pulmonary - bronchodilation

cardiac - increased HR (d/t vagal inhibition of SA / AV node conduction)

69
Q

Why is atropine given with edrophonium?

A

d/t its similar rapid onset

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