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Anesthesia Drug Test Quick Facts > Acetylcholinesterase Inhibitors > Flashcards

Acetylcholinesterase Inhibitors Flashcards

1
Q

brand name of neostigmine

A

Bloxiverz

prostigmin

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2
Q

how is neostigmine supplied?

A

1mg/mL

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3
Q

classification of neostigmine

A

quaternary ammonium anticholinesterase

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4
Q

MOA of neostigmine

A

reversible inhibition of the enzyme acetylcholinesterase
Hydrolyzed by Achesterase and in the process the ach esterase gets carbamylated (forms a drug enzyme complex) and becomes inefficient at hydrolyzing acetylcholine until the drug enzyme bond dissociates.
This inhibition of the hydrolysis of acetylcholine results in greater availability of Ach at its sites of action, which include preganglionic sympathetic and parasympathetic nerve endings and the NMJ.
Primary effect at post synaptic

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5
Q

use of neostigmine

A

antagonie effects of NDNMB
tx of atony in urinary bladder
off-label for dx and tx of MG in children

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6
Q

dose of reversal of non depolarizing NMB of neostigmine

A

IV 0.03-0.07 mg/kg

*glycopyrolate 0.01mg/kg or atropine 0.02 mg/kg must be given prior to or in conjunction with neostigmine to prevent bradycardia

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7
Q

what determines initial and subsequent doses of neostigmine?

A

TOF

Drug used as paralytic

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8
Q

dose of neostigmine with Roc typically

A

0.03 mg/kg

shorter half life NMBA

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9
Q

dose of neostigmine with NMBA with longer halflives

A 
ved
panc
0.07 mg/kg
or first twitch response is relatively weak
rapid recovery is needed
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10
Q

how is neostigmine dosed with renal patients

A

reduction of dose

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11
Q

how does neostigmine affect elderly pt?

A

prolonged duration

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12
Q

how does neostigmine affect infants?

A

dose can be reduced

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13
Q

dose of neostigmine for post op renal retention

A

IM Sub Q

0.25 mg

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14
Q

onset of neostigmine

A

IV 7-11 minues

intermediate

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15
Q

peak of neostigmine

A

5-10 minues

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16
Q

duration of neostigmine

A

54 minues

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17
Q

half life of neostigmine

A

77 minutes

doubles’ in renal pt

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18
Q

metabolism of neostigmine

A

hepatic metabolist 50%
without renal function
metabolite active 1/10th activity of neostigmine

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19
Q

elimination of neostigmine

A

50% renal unchanged drug

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20
Q

adverse effects of neostigmine

A

CV: BRADYCARDIA, hypotension, decreased SVR, increase is CAD arrhythmias, ACS, or MG or BB pts

Syncope, tachycardia, sinus arrest & brady not stopped post transplant even with glycol

CNS: convulsions, dizzy, drowsy, dysphonia, HA, LOC

Derm, rash, thrombophlebitis, urticarial,

GI: diarrhea, dysphagia, flatulence, hyperperistalsis, Nausea, salivation, cramps vomit, PONV

GU: urgency

NM: arthralgieas fasciculation, crams, spasm, weak

Ocular, small pupils (miosis) can not accomidate near vision

Resp: bronch constrict dyspnea, secretions, laryngospasm, resp arrest, resp depression, resp muscle paralysis

Allergic, analphylaxis, diaphoresis

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21
Q

contraindications of neostigmine

A

cholinergic crisis

hx of rxn with bromides

*crisis= overdose of cholinergic- brady cardia- atropine must be ready all muscarinic symptoms listed – bradycardia and resp muscle paralysis may be fatal

marked and prolonged inhibition of plasma cholinesterase: leaks to prolonged effect of SUCC

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22
Q

how does volatile agent affect neostigmine?

A

delay reversal

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23
Q

what is best for reversing atracurium

A

edrophonium

not neostigmine

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24
Q

typical dose of neostigmine

A

1 mg
glycopyrolate - onset matches onset of neostigmine better than atropine- would see initial tackycardia with atropine/neo and brady cardia as atropine is faster off

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25
Q

brand name of edrophonium

A

Tensilon

Enlon

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26
Q

how is edrophonium supplied

A

10mg/mL

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27
Q

classification of edrophonium

A

quaternary ammonium anticholinesterase

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28
Q

MOA of edrphonium

A

Forms a reversible electrostatic attachment to the acetylcholinesterase enzyme in order to inhibit its activity. Normally it rapidly hydrolyzes Ach into chiline and acetic acid. More Ach at sites of action!
Reversal Pre-Synaptic affecting Ach release more.
But parasympathetic and NMJ as well.
fasciculate d/t pre-synaptic MOA if no NMNMB on board

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29
Q

what can high doses of edrophonium lead to?

A

excess of Ach at the NMJ and cause desensitization leading to neuromuscular blockade

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30
Q

dose of edrophonium for reversal of NBNMB

A

reversal of non depolarizing neuromuscular blocking agents

IV 0.5 mg/kg
MUST give with atropine 7mcg/kg upto 10-15 mcg/kg) 1 mg/kg if twitch is

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31
Q

onset of edrophonium

A

IV 30-60 seconds SHORT ONSET

32
Q

duration of edrophonium

A

60 minutes

33
Q

peak of edrophonium

A

5-10 minutes reach peak

34
Q

half life of edrophonium

A

110 mins (doubles when anephric)

35
Q

elimination of edrophonium

A

67% renal

36
Q

metabolism of edrophonium

A

Without renal function, hepatic metabolism is 30% conjugation

37
Q

adverse reactions with edrophonium

A

Mild b/c short act
CV: BRADYCARDIA, hypotension, av block, nodal rhythm changes

Syncope, tachycardia

CNS: convulsions, dizzy, drowsy, dysphonia, HA, LOC

Derm, rash, thrombophlebitis, urticarial,

GI: diarrhea, dysphagia, flatulence, hyperperistalsis, Nausea, salivation, cramps vomit

GU: urgency

NM: arthralgieas fasciculation, crams, spasm, weak

Ocular, small pupils (miosis) can not accomidate near vision

Resp: bronch constrict dyspnea, secretions, laryngospasm, resp arrest, resp depression, resp muscle paralysis

Allergic, analphylaxis, diaphoresis

38
Q

contraindications with edrophonium

A

Hypersensitivity to this, sulfites, GI/GU obstruction, with MG risk of cholinergic crisis if they have also received NDNMB

39
Q

predominate site of edrophonium’s action?

A

pre-synaptic Ach release

40
Q

predominate site of neostigmine’s action?

A

post-synaptic

41
Q

which anticholineric has the most similar onset to edrophonium?

A

atropine
rapid onset for both
preferred with edrophonim

42
Q

can edrophonium be used to reverse a phase II block fro Sch?

A

yes

as long as the pt does not have atypical plasma cholinesterase

43
Q

what are the desired effects of NMB reversal?

A

want nicotinic cholinergic effects
= reverse weakness

want to minimize muscarinic cholinergic effects (give anti-cholinergic)

44
Q

brand name of physostigmine

A

physostigmine

no brand name

45
Q

how is physostigmine supplied?

A

1 mg/mL

46
Q

classification of physostigmine?

A

lipid soluble tertiary amine

carbamate

47
Q

MOA of physostigmine

A

inhibits the enzyme of acetylcholinesterase and prolongs the central and peripheral effects of acetylcholine

48
Q

property of physostigmine

A

tertiary amine
lipid soluble
crosses BBB easily
increases concentration of Ach in the brain

49
Q

uses of physostigmine

A

antagonism of central anticholinergic effects
reversal of toxic life-threatening delirium
from pure anticholinergic agents (atropine, diphenhydramine, dimenhydrinate, Atropa belladonna, jimson weed)
*treats somnolent effects of opiods and may reverse the depression of the ventilator response to C02 but no analygesia of morphine
*post of shivering

50
Q

dose of physostigmine for reversal of toxic anticholinergic effect

A

15-60 mcg/kg initial, 0.5-2 mg repeat q 10-30 minutes until response
NO faster than 1mg/min

51
Q

peak of physostigmine

A

no peak

52
Q

onset of physostigmine

A

several minutes *

53
Q

duration of physostigmine

A

45-60 minutes

*shorter than the anticholinergics and MAY require redosing

54
Q

adverse reactions with physostigmine

A

CV: Asystole, bradycardia, palpitation

CNS: hallucinations, nervousness, restlessness, seizure

GI: defication, diarrhea, nausea, salivation, stomach pain, vomiting

GU: frequency

NMS: twitching

Ocular: lacrimation, miosis

Respiratory: bronchospasm, dyspnea, pulmonary edema, respiratory distress, respiratory paralysis

Msc. Diaphoresis, hypersensitivity

  • augments secretions of glands innervated by postganglionic cholinergic fibers: bronchial, lacrimal, sweat, salivary, gastric, intestinal, acini pancreatic
55
Q

metabolism of physostigmine

A

hydrolysis of cholinesterases

56
Q

elimination of physostigmine

A

?

57
Q

contraindications of physostigmine

A

Bromide tox possible

NO w/asthma, gangrene, DM, CV disease, obstruction of intestine or GU tract, vagotonic state, pt on choline esters, DNMBA (succs)

*contains sodium bisulfite- allergic rxn

58
Q

how does volatile anesthetic administration influence the effects of neostigmine and pyridostigmine

A

delays reversal

59
Q

what conditions can inhibit reversal?

A

hypothermia
hypokalemia
acidosis
some antibiotics

60
Q

properties of pyridostigmine and neostigmine

A

quaternary ammonium group = POORLY lipid soluble

does not cross GI or BBB

61
Q

brand name of pyridostigmine

A

mestinon

regonol

62
Q

how is pyridostigmine supplied

A

5mg/mL

63
Q

classification of pyridostigmine

A

quaternary ammonium anticholinesterase

64
Q

MOA of Pyridostigmine

A

Reversible inhibition of the enzyme Acetylcholinesterase.

Hydrolyzed by Ach-esterase and in the process the ach esterase gets carbamylated (forms a drug enzyme complex) and becomes inefficient at hydrolyzing acetylcholine until the drug enzyme bond dissociates.

This inhibition of the hydrolysis of acetylcholine results in greater availability of Ach at its sites of action, which include preganglionic sympathetic and parasympathetic nerve endings and the NMJ.

Primary effect at post synaptic

65
Q

where is the primary effect of pyridostigmine?

A

Primary effect at post synaptic

66
Q

dose of pyridostigmine

A

Reversal of NDNMB IV 0.1-0.25 mg/kg
Glyco 10 mcg/kg or Atropine 20 mcg/kg
IV must be given before

Reduce with renal and elderly (d/t delayed plasma clearance)

Push, IM, infusion also

67
Q

MG oral dose of pyridostigmine

A

60-1500 usually 600 mg/day 5-6 dose divided over

68
Q

onset of pyridostigmine

A

as long as 16 minutes

onset is VERY slow expect tachycardia bc the onset of the atropine and glycol will occur before the effect of the drug

69
Q

duration of pyridostigmine

A

IV 2-3 hours

oral upto 6-8 hours

70
Q

what is oral pyridostigmine used to treat?

A

Myasthenia Gravis

71
Q

peak of pyridostigmine

A

plasma concentrations peak in 5-10 minutes

72
Q

half life of pyridostigmine

A

1-2 hours

unto 6 hours in renal failure

73
Q

metabolism of pyridostigmine

A

in absence of renal function

hepatic metabolism is 25%

74
Q

elimination of pyridostigmine

A

75% renal elimination as unchanged drug

75
Q

Adverse effects of pyridostigmine

A

CV: BRADYCARDIA, hypotension, decreased SVR, increase is CAD arrhythmias, ACS, or MG or BB pts

Syncope, tachycardia, sinus arrest & brady not stopped post transplant even with glycol

CNS: convulsions, dizzy, drowsy, dysphonia, HA, LOC

Derm, rash, thrombophlebitis, urticarial,

GI: diarrhea, dysphagia, flatulence, hyperperistalsis, Nausea, salivation, cramps vomit, PONV

GU: urgency

NM: arthralgieas fasciculation, crams, spasm, weak

Ocular, small pupils (miosis) can not accomidate near vision

Resp: bronch constrict dyspnea, secretions, laryngospasm, resp arrest, resp depression, resp muscle paralysis

Allergic, analphylaxis, diaphoresis

76
Q

contraindications with pyridostigmine

A

Bromides rxn history (pills)

GI/GU obstruction

with MG risk of cholinergic crisis if they have also received NDNMB

Anesthesia Drug Test Quick Facts (19 decks)

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