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Pharmacology 1, 680 > Anticholinesterases and Anticholinergics, NMB Reversal > Flashcards

Anticholinesterases and Anticholinergics, NMB Reversal Flashcards

1
Q

Acetycholinesterase AChE

A

enzyme that hydrolyzes acetylcholine

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2
Q

inhibition of AChE allows for more ___ which facilitates?

A

ACh
- depolarization and muscle contraction

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3
Q

Mechanisms of Action for Anticholinesterases

A

inhibit AChE – by being hydrolyzed by the AChE, causing carbamylation of AChE or by attaching to the enzyme

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4
Q

Mechanisms of Action for Anticholinesterases

A

Presynaptic effects – cause increased availability of ACh, cause spontaneous contractions in the absence of NMB

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5
Q

Mechanisms of Action of Anticholinesterases

A

Direct effect on NMJ – too much ACh at the NMJ causes decreased sensitivity resulting in blockade effect

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6
Q

Neostigmine and pyridiostigmine _____ with Ach to be hydrolyzed by the AChE, then cause the enzyme to be _______and decrease its ability to hydrolyze Ach

A

compete
-carbamylated

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7
Q

Edrophonium is not broken down by the _____, but attaches to it electrostatically to decrease its ability to _____ ACh

A

-AChE
- hydrolyze

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8
Q

Carbamylated AChE is a ____ inhibition

A

reversible- 1/2 life of 15-30 min

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9
Q

which drugs are hydrolyzed by AChE, cause chemical change in the enzyme and reversibly inhibit its ability to hydrolyze ACh.

A

Neostigmine, Pyridostigmine and Physostigmine

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10
Q

What type of attachment is performed by edrophonium and is reversible

A

electrostatic bound/attachment

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11
Q

Edrophonium forms a reversible ______ attachment to AChE to inhibit its ability to hydrolyze ACh (it competes with ACh for the bonding site with AChE).

A

-electrostatic
-Edrophonium is not broken down by AChE, but attaches to it electrostatically to decrease its ability to hydrolyze ACh

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12
Q

____ forms an irreversible complex that must be replaced with generation of new enzyme.

A

Organophosphate anticholinesterase

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13
Q

examples of organophosphate anticholinesterases

A

Echothiophate – eye gtts
Insecticides
Nerve gases – tabum, saran, soman

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14
Q

Quaternary ammonium are ionized, _____ soluble and ____ insoluble

A

-water
- lipid

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15
Q

examples of drugs that are quaternary ammonium

A

Neostigmine, pyridostigmine, edrophonium
-Poor lipid solubility (cant cross blood brain barrier), water soluble

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16
Q

Tertiary amine properties:

A

-not ionized
- lipid soluble

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17
Q

which drug is a tertiary amine

A

physostigmine

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18
Q

Neostigmine (Prostigmine) dose , onset and elimination

A

0.06
-7-11 min
- 50% renal, 50% plasma esterases and hepatic metabolism

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19
Q

Edrophonium (Enlon) dose, onset, and elimination

A

Dose 0.5-1 mg/kg

Onset 30-60 seconds (presynaptic effect)

Elimination 75% renal

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20
Q

Pyridostigmine (Mestinon) onset, dose, and elimination

A

Dose 0.3 mg/kg

Onset 10 – 20 minutes

Elimination 75% renal

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21
Q

Physostigmine (Antilirium) dose, onset, elimination

A

Dose 0.5 – 2 mg (0.01-0.03 mg/kg) – give slowly(projectile vomiting) (1 mg/min)

Onset about 5 minutes

Elimination hepatic and hydrolysis by cholinesterases

Used to treat CNS effects of anticholinergic agents, anesthetics, and reduces shivering

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22
Q

Deep NMB reversed better with what drug?

A

Neostigmine

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23
Q

Endrophonium works better with

A

atracurium

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24
Q

Neostigmine works better with

A

Vecuronium

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25
Q

Ceiling effect:

A

Once AChE is maximally inhibited, giving more anticholinesterase will not reverse a NM block.

Max dose Neostigmine 0.07 mg/kg

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26
Q

Reversal of NMB affected by:

A

ANtibiotics, hypothermia, respiratory acidosis(PaCO2 > 50 mmHG) and hypokalemia- metabolic acidosis

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27
Q

Nicotinic receptors (cholinergic) all located within

A

ANS ganglion and at NMJ

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28
Q

Muscarinic receptors M1=

A

CNS, stomach

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29
Q

M2

A

principally in the heart, also airway smooth muscles

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30
Q

M3=

A

airway smooth muscles and salivary glands, contraction and secretion

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31
Q

Effects of Anticholinesterases: Cardiovascular

A

Cardiovascular
Bradycardia, junctional rhythm, PVCs, ventricular rhythm, asystole
Slowing of conduction – AV node

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32
Q

GI/GU effects

A

Increased secretions
Increased motility (treatment for paralytic ileus)
PONV- postoperative n/v

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33
Q

Pulmonary effects

A

Bronchoconstriction
Increased secretions

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34
Q

Opthalmic

A

Miosis – pupil constriction
Constriction of ciliary muscle (far-sighted)
Decreased intraocular pressure

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35
Q

Muscular:

A

Contractions, fasciculations (similar to SCh)
Myotonia, muscular dystrophies, spinal cord transection, and burns (use with caution)

36
Q

Anticholinesterase Overdose: Nicotinic

A

weakness ranging to paralysis

37
Q

muscarinic

A

miosis, inability to focus near vision, salivation, bronchoconstriction, bradycardia, abdominal craples, loss of control of bowel and bladder

38
Q

CNS effects:

A

confusion, ataxia, seizures, coma, respiratory depression

39
Q

Anticholinesterase Overdose treatment

A

Atropine – anti-muscarinic
Pralidoxime – antidote
Need to give within minutes of exposure
Ventilatory support
Control of seizures

40
Q

Prevention of Muscarinic Effects

A

Pretreat with an anticholinergic drug- block receptors so ACH excess wnt cause all those side effects on previous slide before last
Atropine
Glycopyrrolate (Robinul)
Scopolamine

41
Q

Anticholinergic Agents- compete with ACh for all muscarinic receptros and ____ ____ with receptors

A
  • bind reversibly
    ex. belladonna plants- atropine and scopolamine
42
Q

ATropine, dose, onset, and elimination & classification

A

Dose 0.03 mg/kg

Onset 1 minute (use with edrophonium)

Elimination by both liver metabolism, and renal

Tertiary ammonium – lipid soluble, crosses blood-brain barrier

43
Q

Glycopyrrolate (Robinul) dose, onset, elimination, and classification

A

Dose 0.015 mg/kg

Onset 2-3 minutes (use with neostigmine)

Excreted unchanged by renal

Quaternary ammonium – lipid insoluble, minimal or no CNS effect

44
Q

Scopolamine dose, onset, elimination, and classification

A

Dose 0.4 mg IM/IV

Onset IV 10 minutes; IM 30-60 minutes

Elimination hepatic

Tertiary amine – crosses the blood-brain barrier; sedation, amnesia, treat PONV

45
Q

Scopolamine is a good alternative to

A

Versed- amnestic

46
Q

Scopolamine ____ the sedative effects of opioids and benzodiazepines

A

enhances

47
Q

Antisialagogue effect:

A

dries up oral secretion: scopolamine>glycopyrrolate>atropine

48
Q

Pre-op med for sedation:

A

scopolamine>atropine

49
Q

Prophylactic for vagal response

A

atropine>glycopyrrolate>scopolamine

50
Q

Be aware: glaucoma-mydriatic effect and maternal-cross placenta membrane

A
  • can lower HR of fetus
    -blocks muscarinic receptors in the circular muscle of the iris, causing mydriasis, which narrows the anterior angle and may reduce aqueous drainage in angle-closure glaucoma.
51
Q

Treatment of bradycardia

A

block the effect of ACh on the SA node which shortens the P-R interval

52
Q

best anticholinergic for treating bradyarrhythmias

A

atropine due to its potent effects on the heart and bronchial smooth muscle

53
Q

which type of patients should you avoid atropine?

A

CAD- atropine creates increased myocardial oxygen demand and decreased oxygen supply associated with the tachycardia

54
Q

atropine dosage

A

0.015-0.070 mg/kg IV
-atropine has faster onset than glycopyrrolate (Robinol)

55
Q

Combine anticholinergics with anticholinesterases determine the ___ of onset

A

speed of onset of the anticholinergic
- ex. Atropine with endrophonium
Glycopyrrolate with neostigmine

56
Q

Anticholinergics Clinical Use: Bronchodilation

A

-atropine 1-2 mg in 3-5 ml of NS
-Ipratropium- aerosol

57
Q

mydriasis- effect of anticholinergics

A

dilation of pupil

58
Q

cycloplegia- anticholinergics

A

paralysis of muscles that are responsible for accommodation to focus on nearby objects

59
Q

antispasmotic

A

biliary and ureteral

60
Q

Anticholinergics can be used for motion sickness and ____

A

PONV

61
Q

Central Anticholinergic Syndrome

A

-CNS effects from scopolamine and atropine
-restlessness and hallucinations to somnolence and unconsciousness
–Dry mouth, blurred vision, tachycardia, dilation of cutaneous vessels, increased temperature, sensitivity to light

62
Q

Central Anticholinergic Syndrome

A

Physostigmine - 0.015-0.060 mg/kg

63
Q

Increased risk of _____ associated with anticholinergics

A

-aspiration- lower esophageal sphincter is relaxed by both atropine and glycopyrrolate ( can last 60 min)

64
Q

Sugammadex (Bridion) MOA

A
  • encapsulates the steroid NMB (ROC) and forms a stable complex, prevents NMB action on NMJ- no action at the NMJ
65
Q

Sugammadex (Bridion) has no _____ effects and doesn’t have side effects of ____ or create a lot of ACH,doesnt require antichlinergic- no muscarinic side effects

A

cardiovascular
-anticholinesterase

66
Q

Sugammadex classified as a

A

-selective relaxant binding agent
- cyclodextrin compound-byproduct of starch degradation

67
Q

Cyclodextrins have a ____ surface which allows them to ____ in water and

A

hydrophilic surface
-dissolve

68
Q

Cyclodextrins are used as ____ agents for highly insoluble agents

A
  • solubilizing
    -also used for delayed or prolonged drug release
69
Q

Sugammadex was produced specifically for

A

Rocuronium

70
Q

Sugammadex resembles a

A

-hollow truncated cone or doughnut
-with a hydrophobic cavity and a hydrophilic exterior. Hydrophobic interactions trap the drug (eg, rocuronium) in the cyclodextrin cavity (doughnut hole), resulting in tight formation of a water-soluble guest–host complex in a 1:1 ratio. This terminates the neuromuscular blocking action and restrains the drug in extracellular fluid where it cannot interact with nicotinic acetylcholine receptors. Sugammadex is essentially eliminated unchanged via the kidneys. Sugammadex does not require coadministration of an antimuscarinic agent

71
Q

Hydrogen bonds also know as ____ forces create tight complex

A
  • intermolecular forces
72
Q

Reduces effects of progesterone(can encapsulate birth control pills) (BCPs) so females must

A

use additional contraception for 1 week following sugammadex

73
Q

Sugammadex may cause possible anaphylaxis because cyclodextrin is used in the food industry as

A

as carriers and stabilizers of flavors, colors, fat-soluble vitamins, and polyunsaturated fatty acids

74
Q

Possible increased ____ with Sugammadex but fewer _____ and _____ adverse events than glycopyrrolate/neostigmine

A

bleeding
- cardiovascular and respiratory adverse events

75
Q

Compared to Neostigmine, Sugammadex is better at preventing residual ___, faster at reversing ___, more reliable, and ____

A
  • NMB,NMB, safer
76
Q

Reversal of deep block early with Rocuronium: can reverse within ___ mins of roc admin -1.2 mg/kg with 16 mg/kg suggammadex

A
  • 3 minutes, onset 1-3 minutes
  • Increase amount of rocuronium excreted unchanged renally; sugammadex was also excreted unchanged renally.
77
Q

Dose for rocuronium and vecuronium

A

4 mg/kg is recommended if spontaneous recovery of the twitch response has reached 1 to 2 post-tetanic counts (PTC) and there are no twitch responses to train-of-four (TOF) stimulation

78
Q

Dose for rocuronium and vecuronium

A

2 mg/kg is recommended if spontaneous recovery has reached the reappearance of the second twitch in response to TOF stimulation.

79
Q

drugs that sugammadex is incompatible with

A

verapamil, ondansetron, and ranitidine

80
Q

If having to redose with Roc after giving sugammadex and it has been 4 minutes the new dose of Roc would be ____ and the onset of NMB may be delayed up to ___ minutes and the duration by be shortened by ____ minutes

A

1.2 mg/kg, 4 minutes, 15 minutes

81
Q

If it has been 4 hours since administration of Sugammadex then redose of roc would be ____ mg/kg or ____ mg/kg with vecuronium

A

0.6 and 0.1 mg/kg

82
Q

The recommended waiting time in patients with mild or moderate renal impairment for re-use of 0.6 mg/kg
rocuronium or 0.1 mg/kg vecuronium after reversal with up to 4 mg/kg BRIDION should be

A

24 hours

83
Q

If a shorter waiting time is required, the rocuronium dose for a new neuromuscular blockade should be

A
  1. 2 mg/kg
84
Q

For re-administration of rocuronium or administration of vecuronium after reversal of rocuronium with
16 mg/kg BRIDION, a waiting time of ____ hours is suggested.

A

24 hours

85
Q

If neuromuscular blockade is required before the recommended waiting time has elapsed, use a
______ neuromuscular blocking agent

A

nonsteroidal

86
Q

The onset of a depolarizing neuromuscular blocking agent might be ______ than expected, because a substantial fraction of postjunctional nicotinic receptors can still be occupied by the neuromuscular blocking agent.

A

slower

Pharmacology 1, 680 (3 decks)

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