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Anesthesia-phar > Anticholinergics Week 5 > Flashcards

Anticholinergics Week 5 Flashcards

1
Q

The parasympathetic outflow is also called the _____.

A

craniosacral outflow

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2
Q

The parasympathetic, or craniosacral, outflow arises from _____.

A

cranial nerves III, VII, IX, and X and sacral segments S2, S3, and S4

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3
Q

Cranial nerve III arises from _____

A

the midbrain, cranial nerve VII arises in the pons, and cranial nerves IX and X arise from the medulla.

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4
Q

The parasympathetic nervous system functions primarily to ____.

A

conserve energy and maintain organ function (resting and digest)

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5
Q

The PNS is anatomically and functionally more _____

A

selective and localized in its effects when compared to the SNS

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6
Q

A massive parasympathetic response would lead to ____.

A

salivation, wheezing, weeping, vomiting, urinating, defecating, and seizing.

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7
Q

Effects of stimulation of the parasynpathetic NS on organs

A

Eye - The pupil constricts (miosis)

Heart - Decreased heart rate

Secretions - Increased salivary and bronchial secretions

Smooth Muscle - Bronchoconstriction, gall bladder contraction, increased motility and tone of the stomach and intestines and contraction of the bladder (detrusor muscle)

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8
Q

Name five Anticholinesterase agents

A

Neostigmine

Edrophonium

Pyridostigmine

Physostigmine

Echothopate

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9
Q

Mechanism of Action of Cholinesterase Inhibitors

A

Cholinesterase inhibitors antagonize postsynaptic acetylcholinesterase at the neuromuscular junction, while increasing the concentration of acetylcholine in the synaptic cleft, and excess acetylcholine displaces nondepolarizing neuromuscular blocking agents and binds to nicotinic receptors.

Of note, the excess acetylcholine from cholinesterase inhibitors will also bind to muscarinic receptors throughout the body.

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10
Q

Mechanism of Action of Cholinesterase Inhibitors at nicotinic sites

A

Stimulation of autonomic ganglia

Stimulation of neuromuscular junction

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11
Q

Mechanism of Action of Cholinesterase Inhibitors at Muscarinic receptor sites

A

Miosis (inability to focus for near vision)

Bradycardia

Salivation

Enhanced gastric secretion

Bronchoconstriction

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12
Q

Uses of cholinesterase inhibitors

A

Reversal of non-depolarizing neuromuscular blockade

Produce parasympathetic effect to treat

1.glaucoma (echothiophate 2.paralytic ileus 3.atonic bladder

Treat myasthenia gravis (neostigmine, pyridostigmine)

Treat anticholinergic syndrome (physostigmine)

Alzheimer’s disease (tacrine, donepezil, rivastigmine, galantamine)

Postoperative analgesia (neostigmine, intrathecal or epidural)

Postoperative shivering (physostigmine, 40 mg/kg IV)

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13
Q

What is the stimulating neurotransmitter for all cholinergic receptors?

A

Acetylcholine (ACh)

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14
Q

What are two major subtypes of cholinergic receptors?

A

muscarinic and nicotinic

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15
Q

Where are muscarinic receptors found?

A

centrally and peripherally in tissues innervated by parasympathetic postganglionic neurons

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16
Q

Where are nicotinic receptors found?

A

peripherally in the motor end-plate of skeletal muscle and in cell bodies of both sympathetic and parasympathetic postganglionic neurons

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17
Q

Describe how ACh works to terminate neurotransmitter action

A
  1. Acetylcholinesterase (AChE), also known as “true” cholinesterase, breaks down acetylcholine to choline and acetate.
  2. As ACh is metabolized, the motor end-plate repolarizes and the muscle cell becomes ready for another squirt of ACh from the nerve terminal.
  3. The choline is transported back into the nerve terminal where it is used to re-synthesize ACh
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18
Q

Class and Route of Admin of Neostigmine

A

Class: Anticholinesterase

Absorption: IV, PO, epidural

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19
Q

Dosing of Neostigmine

A

0 twitches = WAIT 1 twitch = WAIT

2-3 twitches = 50mcg/kg

4 twitches with fade = 40mcg/kg

4 twitches without fade = 15-25mcg/kg

5 mg maximum

Administered with an antimuscarinic (eg glycopyrrolate)

Ex: I mg of neostigmine with 0.2 mg of glycopyrrolate

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20
Q

Neostigmine Onset and DOA

A

Onset: 5 – 15 minutes

DOA: 45 – 90 minutes

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21
Q

Metabolism and Elimination of Neostigmine

A

Metabolism: Psuedocholinesterases (50%)

Excretion: Eliminated by the kidneys (50% unchanged)

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22
Q

Neostigmine may cause ____

A

miosis, bradycardia, salivation, bronchoconstriction, peristalsis

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23
Q

Caution use of Neostigmine in patients with ___.

A

brady arrythmias and certain respiratory pathologies

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24
Q

If given alone, anticholinesterases can cause _____.

A

bradycardia and arrythmias, bronchoconstriction and salivation due a build-up of systemic acetylcholine

These symptoms are increasing problematic if they occur during emergence of anesthesia

Therefor, antimuscarinics: glycopyrrolate and atropine, are used in combination with neostigmine and edrophonium to prevent the side effects of anticholinesterase drugs

25
Q

Chemical Structure of Physostigmine

A

Tertiary amine (crosses the blood brain barrier)

26
Q

What is an effective treatment of cholinergic syndrome?

A

Atropine

27
Q

What can cause anticholinergic syndrome? How is it treated?

A

can be caused by the antimuscarinics: atropine and scopolamine

physostigmine is an effective treatment for anticholinergic syndrome

28
Q

Onset and DOA of Edrophonium

A

Onset: 1 minute

DOA: 5-10 minutes

•Due to similar distribution profile, edrophonium is paired with atropine during neuromuscular blockade reversal

29
Q

What patient population is more at risk for cholinergic syndrome?

A

Farmers

Organic insecticides (cholinesterase inhibitors) can produce signs and symptoms of excessive acetylcholine peripherally and centrally, thus farmers may fall victim to cholinergic syndrome

30
Q

Symptoms of cholinergic syndrome

A

Muscarinic: miosis, difficulty focusing, salivation, bronchoconstriction, bradycardia, abdominal cramps

Nicotinic: weakness (ranging from mild weakness to paralysis).

Central nervous system: dysphoria, confusion, ataxia, seizures, coma.

31
Q

Treatment of cholinergic syndrome

A

Atropine, boluses every 3 to 10 minutes until muscarinic symptoms disappear.

Pralidoxime boluses every 20 minutes until skeletal muscle weakness is reversed (pralidoxime reactivates acetylcholinesterase).

Diazepam (for seizures)

32
Q

Class and Absorption of Sugammadex

A

Class: Selective Relaxant Binding Agent

Absorption: IV

33
Q

Mechanism of Action of Sugammadex

A

Irreversibly encapsulates steroidal neuromuscular blocking agents

34
Q

Dosing & Onset of Sugammadex

A

If TOF 2 twitches or more = 2mg/kg

If TOF 1 twitch = 4mg/kg

If TOF = 0, do a post tetanic count.

If Post tetanic count < 2: give 16 mg/kg

If Post tetanic count > 2: give 4 mg/kg

Onset: 3 minutes

35
Q

Metabolism and Excretion of Sugammadex

A

Metabolism: Not metabolized

Excretion: Eliminated by the kidneys

36
Q

Special Considerations with Sugammadex

A
  • Patients with ESRD
  • Anaphylaxis (Potentially more common in Japan)
  • Patients using hormonal contraceptives must use an additional, nonhormonal method of contraception for the next 7 days
  • If paralysis is desired after sugammadex administration, succinylcholine or a bezylisoquinoline must be used
37
Q

Name four antimuscarinic agents

A

Atropine

Glycopyrrolate

Scopolamine

Ipratropium

38
Q

MOA and Site of Action of Antimuscarinics

A

Mechanism of Action: Antimuscarinics are competitive antagonists of acetylcholine at muscarinic receptors

Site of Action

  • Antimuscarinics act at peripheral tissues innervated parasympathetic postganglionic nerves
  • Of note, atropine and scopolamine are tertiary amines and can cross the blood-brain barrier, therefor they have actions at sites of cholinergic transmission in the central nervous system
39
Q

With antimuscarinics, the blockade of postsynaptic muscarinic receptors leads to _____.

A

an action opposite those seen with parasympathetic nervous system stimulation

  • pupillary dilatation (mydriasis) •bronchodilation
  • failure of accommodation (blurred vision) •tachycardia
  • increased speed of conduction through AV node
  • decreased salivary and pharyngeal secretions
  • decreased bronchial secretions •decreased bladder tone (urinary retention possible)
  • decreased tone and motility (“weakening”) of lower esophageal sphincter
40
Q

Class & Absorption of Atropine

A

Class: Antimuscarinic (tertiary amine)

Absorption: IV, IM, PO

41
Q

Dosing, Onset and DOA of Atropine

A

Dosing (IV): With edrophonium: 7 mcg/kg

  • Non-symptomatic bradycardia: titrate to effect with small incremental doses
  • Symptomatic bradycardia in ACLS: 1 mg bolus, 3 mg maximum

Onset: 1-2 minutes

DOA: 1-2 hours

•Crosses the blood brain barrier

42
Q

Metabolism and Excretion of Atropine

A

Metabolism: Metabolized by the liver

Excreted: Renally and hepatically eliminated

43
Q

Atropine can cause ____

A

Tachycardia, sedation, anticholinergic syndrome

44
Q

Which patient conditions would make you avoid giving atropine, scopolomine and glycopyrolate?

A

CAD, pheochromocytoma, hyperthyroidism, myasthenia gravis

45
Q

Class and Absorption of Glycopyrrolate

A

Class: Antimuscarinic (quaternary ammonium)

Absorption: IV, IM, PO

46
Q

Dosing of glycopyrrolate

A

With neostigmine: 0.2 mg of glycopyrrolate for every 1 mg of neostigmine

Glycopyrrolate concentration: 0.2 mg/mL

Neostigmine concentration: 1 mg/mL

Therefore: 1 mL of glycopyrrolate per 1 mL of neostigmine

Non-symptomatic bradycardia: titrate to effect with small incremental doses of 0.1-0.2 mg

47
Q

Onset and DOA of glycopyrrolate

A

Onset: 2 minutes

DOA: 2-4 hours

48
Q

Metabolism & Excretion of Glycopyrrolate

A

Metabolism: A portion is metabolized by the liver

Excretion: A larger portion renally eliminated unchanged

49
Q

Glycopyrrolate can cause a side effect of ____

A

tachycardia

50
Q

Class, Use and Absorption of Scopolamine

A

Class: Antimuscarinic (tertiary amine)

Clinical use: Antiemetic

Absorption: Transdermal, IV

51
Q

Transdermal dosing of Scopolamine

A

A scopolamine patch contains a total dose of 1.5 mg is usually applied behind the ear

Most effective when placed 4 hours before induction of anesthesia

Patient should be informed that the patch can cause dry mouth, blurred vision, dilated pupils, stay on for 24 hours, and hands should be washed after removal without touching eyes

52
Q

Onset & DOA of Scopolamine

A

Onset: 4 hours

DOA: 24 hours

Crosses the blood brain barrier

53
Q

Metabolism and Excretion of Scopolamine

A

Metabolized by the liver

Renally and hepatically eliminated

54
Q

Side Effects of Scopolamine

A

Tachycardia, sedation, anticholinergic syndrome

55
Q

Anticholinergic syndrome may develop in response to ______.

A

high doses of atropine or scopolamine.

56
Q

Central and peripheral symptoms of Scopolamine

A

Central: behaviors such as restlessness, shivering, mania, hallucinations, delirium, drowsiness, coma, excitation, agitation, disorientation, short-term memory loss, emotional instability, and motor incoordination. These signs and symptoms are due to excessive antagonism of muscarinic receptors in the brain.

Peripheral manifestations: blurred vision, dry mouth, tachycardia, dry and flushed skin, rash over face, neck and upper chest, and hypotension.

57
Q

Treatment of Anticholinergic syndrome

A

the cholinesterase inhibitor, physostigmine (Antilirium).

58
Q

Bronchial smooth muscle tone is under the influence of ____.

A

beta-2 receptors, nitric oxide, muscarinic-3 receptors.

59
Q

Explain the mechanism of action of Ipratropium

A
  1. Activation of M3 receptors leads to the conversion of PIP to IP3 by phospholipase C
  2. IP3 stimulates the release of Ca++ from intracellular storage sites
  3. Ca++ activates the contractile mechanism, which promotes bronchoconstriction

The inhaled antimuscarinic agent, ipratropium (Atrovent), can produce bronchodilation because it competitively inhibit muscarinic-3 receptors

Anesthesia-phar (18 decks)

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