Reversal Agents - Quiz 8 Flashcards

1
Q

What happens to the Heart with SNS Stimulation?

A

↑HR

↑Conduction Velocity

↑Automaticity

↑Contractility

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2
Q

What happens to the Heart with PNS Stimulation?

A

↓HR

↓Conduction Velocity

↓Contractility (Slight)

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3
Q

What happens to Bronchial Smooth Muscles with SNS Stimulation and PNS Stimulation?

A

SNS: Relaxation

PNS: Contraction

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4
Q

What happens to Sphincters w/ SNS & PNS Stimulation?

A

SNS: Contraction

PNS: Relaxation

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5
Q

What happens to the Uterus & Ureters w/ SNS & PNS Stimulation?

A

SNS: Contraction

PNS: Relaxation

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6
Q

How does SNS Stimulation affect the Liver?

A

Glycogenolysis & Gluconeogenesis

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7
Q

How does PNS Stimulation affect the Liver?

A

Glycogen Synthesis

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8
Q

What happens to the Pancreas w/ SNS & PNS Stimulation?

A

SNS: ↓B-Cell Secretion

PNS: ↑B-Cell Secretion

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9
Q

How are the Salivary & Sweat Glands affected by SNS & PNS Stimulation?

A

↑Secretions

(More Salivary Secretions w/ PNS)

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10
Q

How are all Arterioles affected by SNS & PNS Stimulation?

A

SNS: Constriction

PNS: Relaxation

(Beta SNS Stimulation of Coronary Arterioles = Relaxation)

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11
Q

Which Anticholinesterase Drug is classified as a Tertiary Amine?

A

Physostigmine

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12
Q

Which Anticholinesterase Drugs are classified as Quaternary Ammoniums?

A

Edrophonium

Neostigmine

Pyridostigmine

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13
Q

How does SNS & PNS Stimulation affect the Eyes?

A

SNS: Mydriasis

PNS: Miosis

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14
Q

How does Neostigmine, Pyridostigmine, & Physostigmine increase ACh Availability?

A

They get hydrolyzed by acetylcholinesterase, which then carbamylates and blocks the enzyme’s ability to hydrolyze ACh

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15
Q

Which Reversal Agent forms magnetic/electrostatic bond that reversibly causes Acetylcholinesterase Inhibition?

A

Edrophonium

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16
Q

What happens if you give Reversal Agents without there being any NMBs?

A

Overflow of ACh = fasciculations/muscle twitches

Can look like a Phase I NMB Block

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17
Q

What is the Onset of Action for Edrophonium?

A

1-2 minutes

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18
Q

How does Neostigmine compare to Edrophonium?

A

More Profound & Potent than Edrophonium

Slower Onset: 7-11 Min

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19
Q

What is the Duration of Action for all of the Reversal Agents?

A

1-2 Hrs

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20
Q

What determines the Potency of Reversal Agents?

A
  • The NMB being reversed
  • Speed of Spont. Recovery
  • Depth of Block when Reversal given
  • End Point
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21
Q

Once anticholinergic enzymes are completely blocked by the reversal agent, how does re-dosing effect patient’s recovery?

A

No benefits = keep patient sedated & intubated until spont recovery

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22
Q

What factors can slow down NMB Reversal?

A

Hypothermia

ABX

Acidosis

Hypokalemia

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23
Q

What are the Muscuranic Side effects of having Increased ACh from Reversal Agents?

A

Bradycardia

Salivation

Bronchoconstriction

Miosis

Hyperperistalsis

PONV

24
Q

Which Reversal Agents have Marked & Prolonged Inhibition of Plasma Cholinesterase?

A

Neostigmine & Pyridostigmine

25
Q

What can be mixed w/ Reversal Agents to minimize Muscuranic Side effects?

A

Anticholinergic Drugs w/ faster onset than Anticholinesterase

26
Q

Which class of Anticholinesterase Drugs can cross the Blood Brain Barrier?

A

Tertiary Amines - Physostigmine

27
Q

What can Physostigmine be used for as a Reversal other than for NMBs?

A

Central Anticholinergic Syndrome

Restlessness/Confusion

Opioids

Benzos

Ketamine

Antidepressants

28
Q

What are some uses for Antiacetylcholinesterases outside of the OR?

A

Myasthenia Gravis

Glaucoma

Post-Op Pain/Shivering

Alzheimer’s - Aricept, Razadyne, Exelon

Chronic Fatigue

29
Q

What are treatments for Reversal Agent Overdose?

A

Atropine

Pralidoxime - Acetylcholinesterase Reactivator

Supportive Measures

30
Q

What are the naturally occuring anticholingergic that are tertiary amines?

A

Atropine & Scopolamine

31
Q

What is the quarternary ammonium anticholinergic?

A

Glycopyrrolate

32
Q

What is the Mechanism of Action for Anticholinergics?

A

Competitively Binds @ Muscuranic Receptor and Blocks ACh from binding there

33
Q

Where are the M1 Muscarinic Receptors?

A

CNS & Stomach

34
Q

Where are the M2 Muscarinic Receptors?

A

Lungs & Heart

35
Q

Where are the M3 Muscarinic Receptors?

A

CNS

Airway

Smooth Muscle

Glandular Tissue

36
Q

Where are the M4 Muscarinic Receptors?

A

CNS & Heart

37
Q

Where are the M5 Muscarinic Receptors?

A

CNS

38
Q

What are the effects at the Odd # Muscarinic Receptors (M1, M3, M5)?

A

Stimulatory

↑Calcium

↑MAP

39
Q

What are the effects at the Even # Muscarinic Receptors (M2, M4)?

A

Inhibitory

↓MAP

↓Calcium

↓Adenylyl Cyclase

40
Q

B/t Atropine & Glycopyrrolate, which has a faster onset and longer duration?

A

Atropine is Faster - 1 Min

Glycopyrrolate - 2-3 Min

Both Lasts 30-60 min

41
Q

What are some Pre-Op uses for Anticholinergics?

A

Sedation

Saliva Reduction

Prevent Vagal Reflexes

Bronchodilation

Prevent Nausea

42
Q

Which Anticholinergic would be most potent for Sedation?

A

Scopolamine

100x more potent than Atropine

Amnesic

43
Q

Why is Neostigmine + Glycopyrrolate preferred over Neostigmime + Atropine?

A

CNS effects of Atropine along w/ Neostigmine cause delayed arousal for first 30 min after cessation of anesthesia

44
Q

What are the effects of using Anticholinergics on the Elderly?

A

Restlessness

Delayed Awakening

Increased IOP

45
Q

How does Scopolamine & Glycopyrrolate compare to Atropine when used to reduce Salivary Effects?

A

Scopolamine 3X more potent

Glycopyrrolate 2x more potent & longer duration

46
Q

Which drug is commonly used to prevent Vagal Reflexes and to treat IntraOp Bradycardia?

A

Atropine

47
Q

Which drug is commonly used to Prevent Motion Sickness?

A

Transdermal Scopolamine

One Pupil might be bigger

48
Q

What are symptoms of Anticholinergic Overdose?

A

Restlessness to Unconsciousness

Dried Out

Blurred Vision

Tachycardia

Increased Temp

Orthostatic Hypotension

Can Be Fatal

49
Q

What should be used to treat Anticholinergic Overdose?

A

Physostigmine 15-60 mcg/kg

50
Q

What were the results of the RECITE study?

A

Rocuronium + Neostigmine = more than half had residual block

51
Q

What chemical structure does Suggamadex have?

A

Used for Vecuronium & Rocuronium

Hydrophobic Center & Hydrophillic Exterior

Able to Reduce Deep Blocks

52
Q

What are the Adverse Effects of Suggamadex?

A

Bradycardia

Bleeding

N/V

Hypotension

Headache

Not Recommended for Renal Patients

53
Q

How is Suggamdex Eliminated?

A

Kidneys

t1/2 = 2hrs

54
Q

How does Suggamadex compare to Neostigmine for Rocuronium & Vecuronium Reversal?

A

Suggamadex is 6x faster & 17x faster for a deep block

Safer

Less Residual Block

55
Q

How does Suggamadex compare to Neostigmine + Glycopyrrolate for reversal after abdominal surgery?

A

Neostigmine + Glygopyrrolate: 43% residual Block

Suggamadex: 0% residual block

56
Q

If someone on Birth Control receives Sugammadex, how long should they use a backup method for Birth Control?

A

For 7 Days after receiving Sugammadex