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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
Chemical Structure of Physostigmine
Tertiary amine (crosses the blood brain barrier)
26
What is an effective treatment of cholinergic syndrome?
Atropine
27
What can cause anticholinergic syndrome? How is it treated?
can be caused by the antimuscarinics: atropine and scopolamine **physostigmine** is an effective treatment for anticholinergic syndrome
28
Onset and DOA of Edrophonium
Onset: 1 minute DOA: 5-10 minutes •Due to similar distribution profile, edrophonium is paired with atropine during neuromuscular blockade reversal
29
What patient population is more at risk for cholinergic syndrome?
**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
Symptoms of cholinergic syndrome
**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
Treatment of cholinergic syndrome
**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
Class and Absorption of Sugammadex
Class: Selective Relaxant Binding Agent Absorption: IV
33
Mechanism of Action of Sugammadex
Irreversibly encapsulates steroidal neuromuscular blocking agents
34
Dosing & Onset of Sugammadex
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
Metabolism and Excretion of Sugammadex
Metabolism: Not metabolized Excretion: Eliminated by the kidneys
36
Special Considerations with Sugammadex
* 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
Name four antimuscarinic agents
Atropine Glycopyrrolate Scopolamine Ipratropium
38
MOA and Site of Action of Antimuscarinics
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
With antimuscarinics, the blockade of postsynaptic muscarinic receptors leads to \_\_\_\_\_.
**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
Class & Absorption of Atropine
Class: Antimuscarinic (tertiary amine) Absorption: IV, IM, PO
41
Dosing, Onset and DOA of Atropine
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
Metabolism and Excretion of Atropine
Metabolism: Metabolized by the liver Excreted: Renally and hepatically eliminated
43
Atropine can cause \_\_\_\_
Tachycardia, sedation, anticholinergic syndrome
44
Which patient conditions would make you avoid giving atropine, scopolomine and glycopyrolate?
CAD, pheochromocytoma, hyperthyroidism, myasthenia gravis
45
Class and Absorption of Glycopyrrolate
Class: Antimuscarinic (quaternary ammonium) Absorption: IV, IM, PO
46
Dosing of glycopyrrolate
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
Onset and DOA of glycopyrrolate
Onset: **2 minutes** DOA: **2**-4 **hours**
48
Metabolism & Excretion of Glycopyrrolate
Metabolism: A portion is metabolized by the liver Excretion: A larger portion renally eliminated unchanged
49
Glycopyrrolate can cause a side effect of \_\_\_\_
tachycardia
50
Class, Use and Absorption of Scopolamine
**Class**: Antimuscarinic (tertiary amine) **Clinical use**: Antiemetic **Absorption**: Transdermal, IV
51
Transdermal dosing of Scopolamine
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
Onset & DOA of Scopolamine
Onset: **4 hours** DOA: **24 hours** **Crosses the blood brain barrier**
53
Metabolism and Excretion of Scopolamine
Metabolized by the liver Renally and hepatically eliminated
54
Side Effects of Scopolamine
Tachycardia, sedation, anticholinergic syndrome
55
Anticholinergic syndrome may develop in response to \_\_\_\_\_\_.
high doses of atropine or scopolamine.
56
Central and peripheral symptoms of Scopolamine
**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
Treatment of Anticholinergic syndrome
the cholinesterase inhibitor, physostigmine (Antilirium).
58
Bronchial smooth muscle tone is under the influence of \_\_\_\_.
beta-2 receptors, nitric oxide, muscarinic-3 receptors.
59
Explain the mechanism of action of Ipratropium
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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