NDNMB reversals

Question 1

2 parts of the CNS

Answer 1

-brain-spinal cord

Question 2

2 parts of the PNS

Answer 2

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

Question 3

Which system conveys information from receptors to the CNS

Answer 3

Afferent system

Question 4

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

Answer 4

Efferent system

Question 5

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

Answer 5

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

Question 6

what does the somatic nervous system (SNS) do

Answer 6

conveys informatin from the CNS to the skeletal muscles

Question 7

what does the ANS do

Answer 7

conveys information from the CNS to smooth musclecardiac muscleand glands

Question 8

diagram of CNS and PNS

Answer 8

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

Question 9

2 parts of the ANS

Answer 9

Sypathetic nervous system and the parasympathetic nervous system

Question 10

ACh is stored where at the synaptic cleft

Answer 10

in vesicles at motor end plate

Question 11

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

Answer 11

5

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

Question 12

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

Answer 12

(both) 2

Question 13

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

Answer 13

1

Question 14

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

Answer 14

both (2)

Question 15

how is reversal of NMB (neuro muscular blockade) achieved?

Answer 15

by competitive antagonism–competition b/t NMBA and ACh for the motoer end plate receptor at the NMJ- whichever is the greatest wins

Question 16

what is RECURARIZATION?

Answer 16

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

Question 17

what is ENCAPSULATION reversal

Answer 17

cyclodextrin surrounds and bonds NMBA in plasma -the concenration gradient reversed drawing NMBAs off receptors into plasma and then quickly bound

Question 18

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

Answer 18

• derived from Calabar beanused in West africa as a poison precursor for organphosphates
• insecticides
• nerve gas

Question 19

what class of drugs are reversal agents

Answer 19

cholinesterase inhibitors

Question 20

basic way cholinesterase inhibitors work for reversals

Answer 20

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

Question 21

Name 4 cholinesterase inhibitors

Answer 21

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

Question 22

what is the most rapid acting cholinesterase inhibitor?

Answer 22

edrophonium

Question 23

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

Answer 23

edrophonium

Question 24

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

Answer 24

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

Question 25

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

Answer 25

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

Question 26

does edrophonium require attenuation of muscarinic response to ACh accumulation?

Answer 26

yes

Question 27

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

Answer 27

simple alcohol with quaternary ammonium group

Question 28

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?

Answer 28

Quaternary ammonium compound

Question 29

Does Neostigmine (Prostigmine) cross the BBB

Answer 29

No

Question 30

What kind of bond does Neostigmine (Prostigmine) make?

Answer 30

IRREVERSABLE enzymatic deactivation (covalent)

Question 31

lipid solubility of Neostigmine: good or poor?

Answer 31

poor

Question 32

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

Answer 32

you bet your ass it does

Question 33

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

Answer 33

pyridostigmine

Question 34

is pyridostigmine a long acting or short acting cholinesterase inhibitor ?

Answer 34

long

Question 35

is pyridostigmine used in anesthesia

Answer 35

no (remember myasthenia gravis)

Question 36

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

Answer 36

physostigmine (antilerium)

Question 37

****seems important b/c it is totally different****what is special about physostigmine (antilerium)

Answer 37

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

Question 38

what is physostigmine (antilerium) used for??

Answer 38

counteract delerium caused by benzos and barbs hint: physostigmine (antiLERIUM)=deLERIUM

Question 39

all cholinesterase inhibitors are eliminated where?

Answer 39

renal: endophonium 70%, Neostigmine 50%

Question 40

Side effects of cholinesterase inhibitors?

Answer 40

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)

Question 41

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

Answer 41

dose: 0.04 - 0.07 mg/kg max dose: 5 mg onset: 5 - 10 minutes peak: 10 minutes duration: 1 hour Renal excretion: 50%

Question 42

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

Answer 42

dose: 0.5 - 1 mg/kg max dose: 40 mg onset: 30 - 60 seconds peak: 1 minute duration: 45 minutes Renal excretion: 70%

Question 43

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

Answer 43

endrophonium

Question 44

whats another name for cholinesterase inhibitor "antidotes"?

Answer 44

anticholinergic agents or parasympatholytics

Question 45

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

Answer 45

atropine-tertiary amine scopolamine- tertiary amine gylcopyrrolate- quaternary amine

Question 46

should you give cholinesterase inhibitors without an anticholinergic?

Answer 46

no

Question 47

why is scopalamine rarely used

Answer 47

b/c of its significant central effects

Question 48

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

Answer 48

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)

Question 49

What is the general dosage recommendation for atropine?

Answer 49

7-15 mcg/kg, given with endrophonium. | typical dose is 1 - 2 mg

Question 50

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

Answer 50

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

Question 51

side effects of anti-cholinergic drugs

Answer 51

``` tachycardia dry mouth mydriasis (dilated pupils) vision disturbance **CONFUSION*** ``` (opposite of cholinesterase inhibitors)

Question 52

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

Answer 52

-cyclodextrin structure -not used in the US-causes encapsulation

Question 53

How is neostigmine (Prostigmine) metabolized?

Answer 53

50% renal, 50% hepatic

Question 54

How is edrophonium (Enlon) metabolized?

Answer 54

75% renal, 25% hepatic

Question 55

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

Answer 55

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

Question 56

Glycopyrrolate (Robinul) mechanism of action.

Answer 56

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

Question 57

How is glycopyrrolate (Robinul) metabolized?

Answer 57

hepatic metabolism renal elimination

Question 58

Does glycopyrrolate (Robinul) cross the blood brain barrier?

Answer 58

no

Question 59

Scopalomine dose, onset, peak, duration?

Answer 59

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

Question 60

Scopalomine mechanism of action.

Answer 60

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

Question 61

Does scopalomine cross the blood brain barrier?

Answer 61

yes

Question 62

How is scopalomine metabolized?

Answer 62

hepatic metabolism renal elimination

Question 63

Pulmonary, cardiac, and neuro effects of scopalomine?

Answer 63

pulmonary - bronchodilation cardiac - increases CO neuro - decreases motion-induced nausea; the best at decreasing secretions, increasing amnesia, and increasing sedation

Question 64

What is contraindicated with scopalomine use?

Answer 64

closed-angle glaucoma

Question 65

Atropine dose, onset, peak, duration?

Answer 65

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

Question 66

Atropine mechanism of action.

Answer 66

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

Question 67

How is atropine metabolized?

Answer 67

hepatic metabolism renal elimination

Question 68

Pulmonary and cardiac effects of atropine?

Answer 68

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

Question 69

Why is atropine given with edrophonium?

Answer 69

d/t its similar rapid onset