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Pharmacology - Autonomics > Neuromuscular and ganglionic blockers > Flashcards

Neuromuscular and ganglionic blockers Flashcards

1
Q

Definition of Ganglionic Blockers (GBs)?

A

nicotinic receptor antagonists

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2
Q

What do GBs do?

A

block reflexes- baroreceptor, pupillary

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3
Q

Examples of GBs…

A

Trimethaphan-hypotension for surgery

Mecamylamine-in severe hypertension, smoking cessation, Tourette’s Syndrome

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4
Q

Natural state of vascular smooth muscle tone in body

A

Sympathetic > Parasympathetic

blockade=vasodilation

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5
Q

Natural state of all other ANS function

A

Parasympathetic > Sympathetic

blockade=tachycardia

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6
Q

What are the two ways to block Ach transmission?

A

pre-synaptic: decrease Ach formation or release, increase metabolism
post-synaptic: block cholinergic receptors

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7
Q

Which one is the clinical use?

A

block cholinergic receptors

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8
Q

limitation of neuromuscular blockers?

A

quarternary ammonium->only peripheral use

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9
Q

What is the function of neuromuscular blockers?

A

to relax skeletal muscles needed in:

surgery, orthopedic procedures, bronchoscopy, artificial respiration/intubation

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10
Q

First clinically used neuromuscular blockers?

A

curare: D-tubocurarine is the major active alkaloid in it

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11
Q

What is the purpose of neuromuscular blockers?

A

allow for using different classes of drugs for muscle relaxation and anesthesia

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12
Q

Train of Four (TOF)?

A

used to monitor the strength of neuromuscular blockage

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13
Q

TOF ratio can be used for…

A

determine at the end of procedure if the patient can be extubated

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14
Q

When extubation can occur?

A

TOF ration >0.7

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15
Q

What is non-depolarizing blocking agent?

A

competitively blocking the binding of ACh to its receptors

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16
Q

What is depolarizing blocking agent?

A

depolarizing the sarcolemma of the skeletal muscle fiber-> persistent depolarization makes the muscle fiber resistant to further stimulation by ACh

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17
Q

Non-depolarizing vs. depolarizing agent

A

“Fade” vs. no “Fade” until TOF ratio

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18
Q

What determines if the patient’s muscles are sufficiently blocked?

A

the number of twitches: procedures are performed when patient responds with 1-2 twitches
under this condition, blockade can be quickly reversed

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19
Q

Sequence of muscle paralysis under neuromuscular blockers?

A

muscles of eye, speech, then fingers, toes, limbs, lastly intercostals and diaphragm

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20
Q

Sequence of muscle paralysis mimics…

A

Guillain-Barre syndrome

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21
Q

Example of depolarizing agent (nicotinic Ach receptor agonist)

A

Succinylcholine

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22
Q

Characteristics of Succinylcholine

A

short duration=5-10mins

metabolized by butyrylcholinesterase to choline, which incases BP

23
Q

Benefits of using Succinylcholine

A

fast onset, short duration of action

24
Q

When do you use Succinylcholine?

A

trauma care, INTUBATION, electro-convulsant therapy

25
When not to use Succinylcholine?
patients with HYPERKALEMIA -cause cardiac arrest
26
Examples of non-depolarizing agents (curare-like, nicotinic Ach receptor antagonist)
Pancuronium (180mins) Vecuronium, Atracurium (30-40mins) Trimethaphan (short) all easily reversible->widely used
27
mechanism of Succinylcholine?
nicotinic Ach receptor agonist->persistant opening of Na+ channel->prevent repolarization->no further action potentials occurs
28
What is Rocuronium?
non-depolarizing neuromuscular blocker (muscle relaxant)
29
There are two ways to reverse Rocuronium actions.
use AchE inhibitor like Neostigmine | use Sugammadex- sequester Rocuronium by directly binding to it
30
The function of AchE inhibitors is like...
a cholinergic agonist its function relies on the presence of Ach-> so little effect on function of M3 receptors in blood vessels as no Ach in blood stream anyway
31
Two types of cholineesterases
AchE in synapses w/. high affinity for Ach | BuchE in plasma, metabolize Succinylcholine and procaine
32
3 classes of AchE inhibitors
Carbamates Organophosphates Quaternary ammonium alcohols
33
How Carbamates work?
temporarily covalent bound to AchE | reversible, dissociate in 0.5-8hrs
34
1st example of Carbamates
Physostigmine: tertiary amine, enters CNS for atropine overdose Clinical: glaucoma, Alzheimer's Disease
35
2nd and 3rd examples of Carbamates
Neostigmine and Pyridostygmine quartanary amine, peripherally restricted reveal of NMB, post-operative ileus, bladder distention Pyrido=less side effect, longer duration Clinical: Myasthenia gravis
36
How Organophosphates work?
irreversibly covalent bound to AchE -> long duration of action Clinical: glaucoma- not commonly used
37
What other uses of Organophosphates?
as insecticides and nerve gas (sarin)
38
What is Pralindoxime?
antidote for pesticide or never gas (AchE inhibitors) poisoning
39
When to give Pralindoxime?
it is only effective within a few hours of exposure to insecticides
40
What is Organophosphate Aging?
once organophosphate covalently bound to AchE, the bond will be hydrolyzed and this step is IRREVERSIBLE, called aging.
41
Mnemonics for symptoms of AchE inhibitor poisoning is...
``` D=diarrhea(M3) U=urination(M3) M=miosis(M3) B=bronchospasm(M3) B=bradycardia(M2) E=excitation of skeletal muscles and CNS(Nm) L=lacrimation(M3) S=sweating(M3) S=salivation(M3) ```
42
The trigger word for AchE inhibitor poisoning is...
farmer
43
How quaternary ammonium alcohol work?
binds non-covalently, reversible
44
Example of quaternary ammonium alcohol
Edrophonium: short action(5-10mins) Clinical: used for diagnosis of Myasthenia Gravis(MG) and to distinguish it from Lambert Eaton MG
45
Clinical effect of Edrophonium in MG
MG patient exercise-> worsen muscle strength-> give Edrophonium-> improves muscle strength
46
What is Lamber Eaton MG?
Abs against calcium channels rather than Abs against Nm in MG
47
Clinical effect of Edrophonium in Lamber Eaton MG
Lamber Eaton MG patient exercise-> improves muscle strength-> give Edrophonium-> no effect
48
What is cholinergic crisis?
overdose of AchE inhibitors-> overstimulation-> paralysis-> weak muscles
49
How to distinguish MG from cholinergic crisis?
Edrophonium-> no effect in CC | -> improves muscle strength in MG
50
Contraindications to use of parasympathomimetic drugs:
``` Asthma and COPD Coronary deficiency Peptic ulcer->increase acid secretion Obstruction of urinary or GI tract Epilepsy ```
51
Cholinergic and adrenergic centers in CNS
brain stem and nucleus basal is of Meynert ->Ach | locus coeruleus -> NE
52
Alzheimer Disease
loss of cholinergic neurons in brain due to improper processing of beta-amyloid proteins->toxicity->apoptosis of neurons
53
AchE inhibitors in Alzheimer disease
Donepezil, Rivastigmine (carbmate), Galanthamine (from daffodil): reversible binding to AchE enhance cognitive ability lose effect as Ach decreases due to Ach-producing neurons die DO NOT slow progression of AD
54
How to increase Galanthamine bioavailability?
give inhibitors of CYP3A4, CYP2D6

Pharmacology - Autonomics (2 decks)

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