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Pharmacology -- Test #3 > Pharmacology of Neuromuscular and Ganglionic Blockers > Flashcards

Pharmacology of Neuromuscular and Ganglionic Blockers Flashcards

1
Q

Why are nicotinic receptor blockers not commonly used?

A

Nn receptors are in the ganglia, thus blocking the entire ANS.

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2
Q

What are nicotinic receptor blockers also called?

A

Ganglionic blockers

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3
Q

Examples of reflexes blocked by ganglionic blockers?

A

Baroreceptors

Pupillary

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4
Q

Name the two important ganglionic blockers used.

A

Mecamylamine and Trimethaphan

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5
Q

Mecamylamine is a treatment for….

A

Tourette’s
Smoking Cessation
Severe hypertension

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6
Q

At rest, which system (SANS or PANS) has the largest role in vascular smooth muscle tone?

A

SANS

The endogenous tone is mild vasoconstriction

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7
Q

An autonomic blockade of the vascular smooth muscle will cause…

A

vasodilation

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8
Q

At rest, which system (SANS or PANS) has the largest role in non-vascular functions.

A

PANS

The endogenous tone is mild bradycardia

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9
Q

An autonomic blockade of the heart will trigger…

A

Tachycardia

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10
Q

Neuromuscular blockers work by (general)….

A

blocking local nicotinic receptors on skeletal muscle in the somatic nervous system

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11
Q

More specifically, how does acetylcholine blockage happen pre- and post-synaptically?

A

Pre – Decreased Ach formation/release or increased metab.

Post – Block cholinergic receptors (Nm->Clinical Use)

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12
Q

What is unique about the structure of nicotinic receptor blockers used for skeletal muscle?

A

Drugs have a quaternary amonium

This restricts them peripherally

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13
Q

When would you used a neuromuscular blocker?

A

Surgery
Orthopedic Procedures
Bronchoscopy
Intubation

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14
Q

The first clinically used nicotinic receptor neuromuscular blocker?

A

Curare

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15
Q

How does one monitor a neuromuscular blockade?

A

Train of Four electrical stimulation test

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16
Q

What is a train of Four electrical stimulation test?

A

Electrode on wrist and nerves in the hand
Without blockade, you see 4 twitches with stimulation
Look for 75% block (patient responds to 1-2)

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17
Q

Problem with knocking a person down to having no twitches?

A

No way to monitor anymore

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18
Q

Sequence of muscle paralysis in a neuromuscular block?

A

Eye Muscles, Speech Control First

Intercostals and Diaphragm last

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19
Q

The order of muscle loss folowing curare/neuromoscular blocker od looks a lot like what disease?

A

Guillain Barre Syndrome

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20
Q

Two types of neuromuscular blockers?

A

Depolarizing and Non-depolarizing

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21
Q

The depolarizing agonist you need to know?

A

Succinylcholine

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22
Q

What is so great about succinylcholine (Sux)?

A

Short Acting

Rapidly metabolised by BeChE

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23
Q

When would you use Succinylcholine?

A

Trauma care

Reduce muscle stress from anti-convulsant therapy

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24
Q

Who should you never use a depolarizing agent on?

A

Patients with hyperkalemia

Extra potassium release from the agent can cause cardiac arrest

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25
Q

Molecular activity of succinylcholine?

A

Agonist to nicotine acetylcholinergic receptors
Influx of Sodium Ions, Stuck Open
Prevents repolarization and thus preventing more action potentials.

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26
Q

Why does acetylcholine have a short duration?

A

Quick degradation by acetylcholinesterase

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27
Q

First use of Sux will do what?

A

Muscle Twitch

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28
Q

Non-depolarizing neuromuscular blockers are frequently used why?

A

Easily Reversible with a Long Duration of Action

29
Q

Non-depolarizing neuromuscular blockers are antagonists of ____ receptors

A

Nm

30
Q

What it trimethaphan?

A

A ganglionic blocker used as short acting non-depolarizing neuromuscular blocker

31
Q

What is Pancuronium?

A

An antagonist nicotinic acetylcholine with a long duration

32
Q

Endogenous acetylcholine binds to _______

A

An agonist to nicotine acetylcholinergic receptors

Allows a sodium influx

33
Q

Rocuronium is what kind of drug?

A

A non-depolarizing muscle relaxant and antagonist of NAchR (blocking acetylcholine induced activation and nerve transmission)

34
Q

How do you reverse Rocuronium?

A 
AchE inhibitor (neostigmine)
Sugammedex (binds and sequesters rocuronium)
35
Q

Two types of cholinesterases?

A

Acetylcholinesterase in synapses, high affinity

Butyrylcholinesterase in plasma

36
Q

Acetylcholinesterase of Butrylcholinesterase – who breaks down Sux and other anesthetics?

A

BuchE

37
Q

Three classes of AchE inhibitors

A

Carbamates
Organophosphates
Quaternary ammonium alcohols

38
Q

How to carbamates interact with AchE? What is important to remember about this interaction?

A

Temporarily create a covalent modification to AChE

Rapid and Reversible

39
Q

Three important types of carbamate AchE inhibitors?

A

Physostigmine
Neostigmine
Pyridostigmine

40
Q

Physostigmine is an _______ amine.

A

Tertiary

41
Q

Physostigmine can act where in the body?

A

Can get into CNS

42
Q

Indications for use of Physostigmine?

A

Atropine Overdose

Glaucoma, Alzheimer’s Disease

43
Q

Neostigmine and Pyridostigmine are _____ amines

A

Quaternary

44
Q

Neostigmine and Pyridostigmine can act where in the body?

A

Only peripherally

45
Q

Indications for use of Neostigmine and Pyridostigmine?

A

Myasthenia gravis
Reversal of NM blockers
Post Operative Ileus

46
Q

Neostigmine and Pyridostigmine. Which one has fewer side effects and a longer duration?

A

Pyrido

47
Q

How to organophosphate acetylcholinesterase inhibitors work?

A

They bind covalently, irreversibly to AchE

Makes for a very long duration of action (over a week)

48
Q

Why care about organophosphate acetylcholinesterases?

A

Historically used in glaucoma treatment, but not anymore.

They show up now in the context of nerve gas or insecticide poisoning.

49
Q

Especially famous organophosphate nerve gases

A

Sarin and Soman

50
Q

Poisoning with organophosphates can be reversed if….

A

Antidote (Pralidoxime Chloride-2PAM) must be given within a few hours of exposure

51
Q

Symptomatic treatment for organophosphate poisoning?

A

Atropine (a competitive agonist of muscarinic)

52
Q

Why can’t you just use 2-pam to reverse organophosphate poisoning whenever?

A

After the organophosphate and AchE covalently bind, the AchE will be further hydrolyzed, forming a permanent bond that can’t be rescued.

53
Q

Symptoms of Acetylcholinesterase Inhibitor Poisoning

A 
Diarrhea
Urination
Miosis
Branchospasms
Bradycardia
Excitation of skeletal muscle and CNS (perm in diaphragm = fatal)
Lacrimation
Sweating
Salivation
54
Q

Who is most likely to get acetylcholinesterase inhibitor poisoning?

A

Farmers

55
Q

Describe the chemical structure of Edrophonium

A

Quaterenary Ammonium Alcohol

56
Q

What is Edrophonium used for?

A

Diagnosis of Myasthenia Gravis

57
Q

Two things Edrophonium can be used to distinguish?

A

MG from Lambert Eaton induced MG

Myasthenic Crisis from a Cholinergic Crosis

58
Q

What is Lambert Eaton MG?

A

Antibodies against vg Calcium Channels

59
Q

Edrophonium influence on a patient in cholinergic crisis?

A

None, maybe a small decrease in muscle strength

60
Q

Edrophonium influence on MG

A

Improves overall muscle strength

61
Q

Contraindications for the use of PS drugs

A 
Asthma and COPD
Coronary deficiency
Peptic ulcer
Obstruction of urinary or GI tract
Epilepsy
62
Q

CNS Norepinephrine is produced by…

A

locus ceruleus

63
Q

Ach is produced where in the CNS

A

Brain Stem and Nucelus Basalis of Meynert

64
Q

Degeneration of cholinergic cells in the nucleus basalis occurs in what disease processes? How are these diseases identified?

A

Dementia and PD

Lewy Bodies

65
Q

Reversible AchE inhibitors that are used to manage symptoms of Alz. Disease

A

Donepezil, Rivastigmine, and Glanthamine

66
Q

Locus ceruleus plays a role in….

A

Stress, panic, and emotional pain

67
Q

Important details for Donepezil (Aricept)

A

Bind to anionic site and block ACh binding
Reversible
Enhances cognitive ability

68
Q

Important details for Rivastigmine?

A

Reversible AChE inhibitor
Increased cholinergic function –> increased cognitive ability
Nausea, Vomiting, Weight-loss

69
Q

Important details for Galanthamine?

A

Reversible AChE inhibitor

use with inhibitors of p450 to increase half life/bioavailability

Pharmacology -- Test #3 (13 decks)

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