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

Pharmacology of Neuromuscular and Ganglionic Blockers Flashcards

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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
Molecular activity of succinylcholine?
Agonist to nicotine acetylcholinergic receptors Influx of Sodium Ions, Stuck Open Prevents repolarization and thus preventing more action potentials.
26
Why does acetylcholine have a short duration?
Quick degradation by acetylcholinesterase
27
First use of Sux will do what?
Muscle Twitch
28
Non-depolarizing neuromuscular blockers are frequently used why?
Easily Reversible with a Long Duration of Action
29
Non-depolarizing neuromuscular blockers are antagonists of ____ receptors
Nm
30
What it trimethaphan?
A ganglionic blocker used as short acting non-depolarizing neuromuscular blocker
31
What is Pancuronium?
An antagonist nicotinic acetylcholine with a long duration
32
Endogenous acetylcholine binds to _______
An agonist to nicotine acetylcholinergic receptors | Allows a sodium influx
33
Rocuronium is what kind of drug?
A non-depolarizing muscle relaxant and antagonist of NAchR (blocking acetylcholine induced activation and nerve transmission)
34
How do you reverse Rocuronium?
``` AchE inhibitor (neostigmine) Sugammedex (binds and sequesters rocuronium) ```
35
Two types of cholinesterases?
Acetylcholinesterase in synapses, high affinity | Butyrylcholinesterase in plasma
36
Acetylcholinesterase of Butrylcholinesterase -- who breaks down Sux and other anesthetics?
BuchE
37
Three classes of AchE inhibitors
Carbamates Organophosphates Quaternary ammonium alcohols
38
How to carbamates interact with AchE? What is important to remember about this interaction?
Temporarily create a covalent modification to AChE | Rapid and Reversible
39
Three important types of carbamate AchE inhibitors?
Physostigmine Neostigmine Pyridostigmine
40
Physostigmine is an _______ amine.
Tertiary
41
Physostigmine can act where in the body?
Can get into CNS
42
Indications for use of Physostigmine?
Atropine Overdose | Glaucoma, Alzheimer's Disease
43
Neostigmine and Pyridostigmine are _____ amines
Quaternary
44
Neostigmine and Pyridostigmine can act where in the body?
Only peripherally
45
Indications for use of Neostigmine and Pyridostigmine?
Myasthenia gravis Reversal of NM blockers Post Operative Ileus
46
Neostigmine and Pyridostigmine. Which one has fewer side effects and a longer duration?
Pyrido
47
How to organophosphate acetylcholinesterase inhibitors work?
They bind covalently, irreversibly to AchE | Makes for a very long duration of action (over a week)
48
Why care about organophosphate acetylcholinesterases?
Historically used in glaucoma treatment, but not anymore. | They show up now in the context of nerve gas or insecticide poisoning.
49
Especially famous organophosphate nerve gases
Sarin and Soman
50
Poisoning with organophosphates can be reversed if....
Antidote (Pralidoxime Chloride-2PAM) must be given within a few hours of exposure
51
Symptomatic treatment for organophosphate poisoning?
Atropine (a competitive agonist of muscarinic)
52
Why can't you just use 2-pam to reverse organophosphate poisoning whenever?
After the organophosphate and AchE covalently bind, the AchE will be further hydrolyzed, forming a permanent bond that can't be rescued.
53
Symptoms of Acetylcholinesterase Inhibitor Poisoning
``` Diarrhea Urination Miosis Branchospasms Bradycardia Excitation of skeletal muscle and CNS (perm in diaphragm = fatal) Lacrimation Sweating Salivation ```
54
Who is most likely to get acetylcholinesterase inhibitor poisoning?
Farmers
55
Describe the chemical structure of Edrophonium
Quaterenary Ammonium Alcohol
56
What is Edrophonium used for?
Diagnosis of Myasthenia Gravis
57
Two things Edrophonium can be used to distinguish?
MG from Lambert Eaton induced MG | Myasthenic Crisis from a Cholinergic Crosis
58
What is Lambert Eaton MG?
Antibodies against vg Calcium Channels
59
Edrophonium influence on a patient in cholinergic crisis?
None, maybe a small decrease in muscle strength
60
Edrophonium influence on MG
Improves overall muscle strength
61
Contraindications for the use of PS drugs
``` Asthma and COPD Coronary deficiency Peptic ulcer Obstruction of urinary or GI tract Epilepsy ```
62
CNS Norepinephrine is produced by...
locus ceruleus
63
Ach is produced where in the CNS
Brain Stem and Nucelus Basalis of Meynert
64
Degeneration of cholinergic cells in the nucleus basalis occurs in what disease processes? How are these diseases identified?
Dementia and PD | Lewy Bodies
65
Reversible AchE inhibitors that are used to manage symptoms of Alz. Disease
Donepezil, Rivastigmine, and Glanthamine
66
Locus ceruleus plays a role in....
Stress, panic, and emotional pain
67
Important details for Donepezil (Aricept)
Bind to anionic site and block ACh binding Reversible Enhances cognitive ability
68
Important details for Rivastigmine?
Reversible AChE inhibitor Increased cholinergic function --> increased cognitive ability Nausea, Vomiting, Weight-loss
69
Important details for Galanthamine?
Reversible AChE inhibitor | use with inhibitors of p450 to increase half life/bioavailability

Pharmacology -- Test #3 (13 decks)

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