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Anesthesia Pharm I > anticholinesterases and anticholinergics > Flashcards

anticholinesterases and anticholinergics Flashcards

1
Q

what is AChE?

A

enzyme that hydrolyzes 300,000 ACh molecules per minute

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2
Q

what dos the inhibition of AChE allow?

A

allows for more ACh to be available to facilitate action at the NMJ (depolarization and contraction)

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3
Q

what are the mechanisms of action of anticholinesterases?

A
  • enzymatic inhibition: inhibit AChE by being hydrolyzed by the AChE, causing carbamylation of AChE or by attaching to the enzyme (ties up or distracts the enzyme)
  • presynaptic effects: cause increased availability of ACh, causing spontaneous contractions in the absence of NMB
  • avoid in myotonia dystrophica
  • direct effect on the NMJ: too much ACh at the NMJ causes decreased sensitivity resulting in blockade effect
  • opposite effect of what we want
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4
Q

describe carbamylation of AChE.

A
  • reversible inhibition
  • neostigmine, pyridostigmine, and physostigmine are hydrolyzed by AChE, causing chemical change in the enzyme and reversibly inhibiting its ability to hydrolyze ACh
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5
Q

describe electrostatic binding of AChE.

A
  • truly reversible inhibition
  • edrophonium forms a reversible electrostatic attachment to AChE to inhibit its ability to hydrolyze ACh
  • competes with ACh for the bonding site on AChE
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6
Q

describe organophosphate anticholinesterase agents.

A
  • form an irreversible complex that must be replaced with generation of new enzyme
  • echothiophate: eye gtts
  • insecticides
  • nerve gases: tabum, saran, soman
  • there is a massive amount of ACh released hitting muscarinic and nicotinic receptors
  • side effects take longer to subside
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7
Q

what are the chemical properties of anticholinesterases?

A

-quaternary ammoniums
*neostigmine, pyridostigmine, edrophonium
*poor lipid solubility, water soluble
-tertiary amine
*physostigmine
*lipid soluble- crosses the BBB
*not usually used for reversal, but more for post op
delirium

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8
Q

describe neostigmine (Prostigmine) elimination

A

50% renal, other 50% plasma esterases and hepatic metabolism

*doesn’t matter about renal failure since we want reversal

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9
Q

what is the dose and max dose of neostigmine?

A

dose: 0.06 mg/kg
max: 5 mg
* if not reversed with max dose, may use about 10 mg of edrophonium

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10
Q

what is the onset of neostigmine?

A

7-11 minutes

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11
Q

describe edrophonium (Enlon) elimination.

A

75% renal

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12
Q

what is the dose of edrophonium?

A

0.5-1 mg/kg (weaker than neostigmine)

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13
Q

what is the onset of edrophonium?

A

30-60 seconds (presynaptic effect)

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14
Q

describe pyridostigmine (Mestinon) elimination.

A

75% renal

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15
Q

what is the dose of pyridostigmine?

A

dose: 0.3 mg/kg

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16
Q

what is the onset of pyridostigmine?

A

onset: 10-20 minutes

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17
Q

describe physostigmine (Antilirium).

A
  • elimination hepatic and hydrolysis by cholinesterases
  • used to treat CNS effects of anticholinergic agents, anesthetics, and reduces shivering
  • tx for post op delirium
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18
Q

what is the dose of physostigmine?

A

dose: 0.5-2 mg/kg (0.01-0.03 mg/kg)
* give slowly, 1 mg/min
* if pushed rapidly, pt. will projectile vomit

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19
Q

what is the onset of physostigmine?

A

about 5 minutes

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20
Q

what are some considerations when selecting which reversal to use?

A
  • Deep NMB is reversed better with neostigmine
  • infusions of atracurium, vecuronium, and pancuronium
  • edrophonium better with atracurium
  • neostigmine better with vecuronium
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21
Q

what is the ceiling effect of reversal agents?

A

-once AChE is maximally inhibited, giving more anticholinesterase will not reverse a NMB

22
Q

what can affect the reversal of NMB?

A
  • antibiotics
  • hypothermia
  • respiratory acidosis (PaCO2 > 50 mmHg)
  • hypokalemia and metabolic acidosis
  • hyperventilation causes K+ to move into the cell
23
Q

when AChE is inhibited, what receptors does ACh affect?

A

-cholinergic (nicotinic)
*receptors within ANS ganglion and at NMJ
-muscarinic
*M1: CNS, stomach
-post op N/V (neostigmine enhances)
-if at risk, goal is to not use reversal
*M2: mainly heart, also airway smooth muscle
*M3: airway smooth muscles and salivary, contraction
and secretion
*side effects: significant secretions, relaxation of
gut/bladder, relaxation of bronchial smooth muscles,
bradycardia, dysrhythmias

24
Q

what are some cardiac side effects of anticholinesterases?

A
  • bradycardia
  • junctional rhythm
  • PVCs
  • ventricular rhythm
  • asystole
  • slowing of conduction- AV node
25
Q

what are some GI and GU effects of anticholinesterases?

A
  • increased secretions
  • increased motility
  • sometimes used in treatment of paralytic ileus
  • post of N/V
26
Q

what are some pulmonary effects of anticholinesterases?

A
  • bronchoconstriction

- increased secretions

27
Q

what are some ophthalmic effects of anticholinesterases?

A
  • miosis (pupil constriction)
  • constriction of ciliary muscle (far-sighted)
  • decreased intraocular pressure
28
Q

what are some muscular effects of anticholinesterases?

A
  • contractions, fasciculations similar to SCh

* use with caution with myotonia, muscular dystrophies, spinal cord transection, and burns

29
Q

how can you prevent the muscarinic effects of anticholinesterases?

A
  • pretreat with an anticholinergic drug
  • atropine
  • glycopyrrolate (Robinul)
  • scopolamine
30
Q

what are the symptoms of anticholinesterase overdose?

A

*side effects are amplified
-nicotinic: weakness ranging to paralysis
-muscarinic: miosis, inability to focus vision near,
salivation, bronchoconstriction, bradycardia, abdominal
cramps, loss of bladder/bowel control
-CNS: confusion, ataxia, seizures, coma, respiratory
depression

31
Q

what is the treatment for anticholinesterase OD?

A
  • atropine: muscarinic blocker
  • pralidoxime: needs to be given within minutes of exposure
  • ventilatory support
  • control of seizures
32
Q

what is the mechanism of action for anticholinergic agents?

A
  • compete with ACh for all MUSCARINIC receptors
  • bind reversibly with receptors
  • belladonna plants- atropine, scopolamine
33
Q

describe atropine.

A

-tertiary ammonium
*lipid soluble, crosses the BBB
-elimination by both liver metabolism and renal
*always want to see an increase in HR before giving
anticholinesterase, especially in infants
*used with edrophonium

34
Q

what is the dose of atropine?

A

0.03 mg/kg

35
Q

what is the onset of atropine?

A

1 minute

36
Q

describe Robinul.

A
  • quaternary ammonium
  • lipid insoluble, no CNS effect
  • excreted unchanged by renal
  • want to start seeing an increasing HR before giving anticholinesterase
  • used with neostigmine
37
Q

what is the dose of Robinul?

A

0.015 mg/kg

38
Q

what is the onset of Robinul?

A

2-3 minutes

39
Q

describe scopolamine.

A
  • tertiary amine
  • crosses BBB
  • causes sedation, amnesia
  • treats post of N/V
  • elimination hepatic
  • no hemodynamic effect, no significant change in HR, may be used as an amnestic
40
Q

what is the dose of scopolamine?

A

0.4 mg IM/IV

41
Q

what is the onset of scopolamine?

A

onset IV: 10 minutes

onset IM: 30-60 minutes

42
Q

describe anticholinergic pre op clinical use?

A
  • antisialagogue effect (drying effect of secretions)
  • scopolamine > glycopyrrolate > atropine
  • sedation
  • scopolamine > atropine
  • prophylactic for vagal response
  • atropine > glycopyrrolate > scopolamine
  • *be aware glaucoma pts. may have problems and if the drug crosses the BBB, it crosses the placental membrane and may increase fetal HR
43
Q

describe anticholinergic clinical use to treat bradycardia.

A

-block the effect of ACh on the SA node (shortens the P-R interval
*underlying vagal tone determines response
higher vagal tones (like athletes) have a better effect
*atropine has a greater onset than glycopyrrolate
*dose of atropine for bradycardia 0.015-0.070 mg/kg IV
*with CAD, you want a slower onset, so use Robinul
**if you under dose, enhances bradycardia

44
Q

describe anticholinergic clinical use for bronchodilation.

A

-atropine dose 1-2 mg in 3-5 ml of NS

ipratropium- aerosol

45
Q

what are other clinical uses of anticholinergics?

A
  • antispasmotic: biliary and ureteral
  • mydriasis and cycloplegia
  • prophylaxis for PONV and motion sickness
46
Q

describe central anticholinergic syndrome.

A
  • CNS effects from scopolamine and atropine
  • restlessness and hallucinations, to somnolence and unconsciousness
  • treatment: physostigmine 0.015-0.060 mg/kg
47
Q

what causes an increased for aspiration with anticholinergics?

A
  • lower esophageal sphincter is relaxed by both atropine (can last 40 min) and glycopyrrolate (can last 60 min)
  • not sure of clinical significance
  • at small doses, there is no bronchodilation effect
48
Q

describe Org 25969 (sugammadex)

A
  • encapsulates the steroid NMB and forms a stable (wont break down) complex, preventing NMB action on the NMJ- excreted unchanged with NMB renally
  • no action at the NMJ
  • not an anticholinesterase, does not require an anticholinergic
  • reversal of deep block early (rocuronium)
  • don’t need twitches to reverse
  • helped stop anaphylaxis with rocuronium
  • *affects the immune system
49
Q

what is the dose of sugammadex?

A

dose: 2-4 mg/kg when given with 2/4 on TOF

50
Q

what is the onset of sugammadex?

A

onset: 1-3 minutes

Anesthesia Pharm I (28 decks)

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