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Mo and Mik > m and m 12 Cholinesterase Inhibitors & Other Pharmacologic Antagonists > Flashcards

m and m 12 Cholinesterase Inhibitors & Other Pharmacologic Antagonists Flashcards

1
Q

Where his acetylcholine made? What his name the enzyme in order the 2 moieties used to make acetylcholine?

A

Acetylcholine is made in the nerve terminal
Components are acetylcoA and choline
Enzyme is choline-acetyltransferase

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2
Q

What enzyme metabolizes acetylcholine? What are the breakdown products?

A

Acetylcholine esterase

Choline and acetate

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3
Q

What parts of the sympathetic NS use acetylcholine as a neurotransmitter?

A

Adrenal medulla
Sweat glands
Sympathetic ganglions

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4
Q

Where are muscarinic receptors found (3)? What about nicotinic?

A

Muscarinic - bronchial smooth muscle, sinoatrial node, salivary glands
Nicotinic - skeletal muscle

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5
Q

What receptors to bethanechol, methacholine and carbachol target?

A

Methacholine and bethanechol target muscarinic receptors, carbachol targets both muscarinic and nicotinic receptors

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6
Q

Name a specific use of methacholine, bethanechol and carbachol (1 each)?

A

Methacholine - asthma provocation test
Bethanechol - bladder atony
Carbachol - topically for wide angle glaucoma

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7
Q

true/false - primary goal in reversing neuromuscular blockade is maximizing muscarinic transmission while minimizing nicotinic transmission.

A

False - other way around

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8
Q

What are the 4 mechanisms / components of “spontaneous reversal” of non-depolarizing neuromuscular block? What is the other means of reversal?

A 
Gradual Diffusion 
Redistribution 
Metabolism 
Excretion 
Pharmacological reversal
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9
Q

Cholinesterase inhibitors block acetylcholine by binding reversibly. What types of bonds do edrophonium, pyridostigmine and neostigmine form?

A

Edrophonium - electrostatic bonds, short lived

Pyridostigmine and neostigmine - covalent bonds, longer lived bonds

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10
Q

What differentiates organophosphates from edrophonium, pyridostigmine and neostigmine with regards to the types of binds formed with cholinesterase?

A

Organophosphates form stable irreversible bonds

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11
Q

Beyond acetylcholinesterase inhibition, some cholinesterase blockers may reverse neuromuscular blockade in other ways. Edrophonium for example does what?

A

Edrophonium may enhance the release of acetylcholine

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12
Q

Beyond acetylcholinesterase inhibition, some cholinesterase blockers may reverse neuromuscular blockade in other ways. Neostigmine for example does what?

A

Neostigmine may have weak agonist effects at nicotinic receptors

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13
Q

What is the effect of excess acetylcholinesterase inhibitors?

A
  • Paradoxically potentiate a non-depolarizing neuromuscular block
  • Prolong depolarization blockade by succinylcholine
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14
Q

Edrophonium, pyridostigmine and neostigmine. Which one(s) blocks pseudocholinesterase at higher doses?

A

Pyridostigmine and neostigmine.

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15
Q

True or false - large doses of neostigmine can cause weak depolarizing neuromuscular blockade?

A

True

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16
Q

What is the effect of increased cholinergic transmission on the CV system?

A

Increased bradycardia that can become sinus arrest

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17
Q

What is the effect of increased cholinergic transmission on the Respiratory system?

A

Will cause bronchospasm and increased secretions

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18
Q

What acetylcholinesterase inhibitor will cross the blood brain barrier? What might be seen on EEG? Mechanism? Significance for anesthetics?

A
  • Physostigmine
  • Diffuse activation of the EEG by stimulating muscarinic and nicotinic receptors in the CNS
  • General anesthetics may work by blocking nicotinic acetylcholine receptors in the CNS. If used (it is not), physostigmine may alter the effects of general anesthetics
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19
Q

What is the effect of increased cholinergic transmission on the GI system?

A

Increases peristalsis

Increases glandular secretions

20
Q

It is hard/impossible to immediately reverse a block so intense that there is no response to tetanic peripheral nerve stimulation. What should be seen before reversal is attempted?

A

At least the first twitch of the train of four.

21
Q

The post tetanic count (number of palpable twitches after tetanus) correlates with _.

A

The time of return of the first twitch of the train of four, which signifies the ability to reverse intense paralysis

22
Q

Arrange in order of sensitivity for adequacy of reversal. Tidal volume, sustained head lift, inspiratory force, vital capacity

A

Sustain head lift > inspiratory force > vital capacity > tidal volume

23
Q

What are the 2 moieties that make up neostigmine?

A

Carbamate group and a quaternary ammonium (latter makes lipid insoluble, can’t cross BBB)

24
Q

What is the ratio of glycopyrrolate used for each mg of neostigmine?

A

0.2 mg glyco for each 1 mg of neostigmine

25
Q

In what group of patients is duration of action prolonged for neostigmine?

A

Geriatric patients

26
Q

Which anticholinergic agent is associated with more tachycardia, atropine or glycopyrrolate?

A

Atropine is assoc with more tachycardia

27
Q

True of false, neostigmine can be used to treat myasthenia gravis, paralytic ileus and bladder atony.

A

True

28
Q

What is the difference structurally between neostigmine and pyridostigmine?

A

Quaternary group of pyridostigmine is incorporated into the phenol ring.

29
Q

How strong is pyridostigmine relative to neostigmine?

A

Pyridostigmine is only 20% as strong as neostigmine

30
Q

How do the onset of action and duration of action of neostigmine and pyridostigmine compare?

A 
Neostigmine onset (5 mins), duration (1 hour) 
Pyridostigmine onset (10-15 minutes), duration (2 hr)
31
Q

What is the preferred anticholinergic for pyridostigmine and why?

A

Glycopyrolate - because its slower onset matches that of pyridostigmine (compared to atropine)

32
Q

What is the reason, structurally, that edrophonium doesn’t bind covalently to acetylcholinesterase?

A

It lacks a carbamate group

33
Q

What is the potency of edrophonium relative to neostigmine?

A

It is less than 10% as potent as neostigmine

34
Q

How does onset of action of edrophonium compare to neostigmine? How can you prolong the duration of action of edrophonium?

A

Edrophonium onset is 1-2 mins, compared to 5 for neostigmine. Can get longer duration of action for edrophonium by using higher doses

35
Q

What is the preferred anticholinergic for Edrophonium and why?

A

Atropine, because it has the same fast onset of action

36
Q

What make physostigmine structurally different from the other cholinesterase inhibitors?

A

Has carbamate like the rest but no quaternary amine, making it able to cross the BBB

37
Q

Why is physostigmine not useful for reversing neusomuscular blockade? What is it used for instead?

A

It will cross BBB
Used instead for the treatment of central anticholinergic toxicity from atropine or scopolamine, can also reverse CNS depression and delirium from benzos and volatile anesthetics

38
Q

Which acetylcholinesterase blocker can be used for post-op shivering? What is the mechanism of this agent being able to block morphine induce respiratory depression?

A

Physostigmine
Blocks morphine induced respiratory depression as presumed mechanism is morphine reduces acetylcholine signaling in the brain

39
Q

What is the mechanism of inactivation of physostigmine?

A

Almost completely metabolized by plasma esterases, making renal excretion unimportant (unlike the other acetylcholinesterase blockers)

40
Q

You want to reverse CNS effects of physostigmine. Glycopyrrolate or atropine and why?

A

Atropine, because glycopyrrolate doesn’t cross the BBB

41
Q

What electrolyte disturbances potentiate neuromuscular blockade?

A

Hypermagnesemia
Hypocalcemia
Hypokalemia
Respiratory acidosis

42
Q

Which potentiates neuromuscular block, hyperthermia or hypothermia?

A

Hypothermia

43
Q

What are the class of neuromuscular blockers that can be reversed by sugammadex? What are 3 examples?

A

Aminosteroids

Rocuronium, pancuronium, vecuronium

44
Q

What is the structural basis for sugammadex reversal of neuromuscular blockers?

A

Traps the aminosteroid in the hydrophobic cavity in a 1:1 ratio, restraining its ability to interact with receptors

45
Q

What is the time line of recovery of a rocuronium block by sugammadex?

A

Can reverse a rocuronium block to 0.9 TOF ratio in 2 minutes

46
Q

L-cysteine is able to reverse neuromuscular block by what class of neuromuscular blockers? What is the mechanism?

A

Reverses block by fumarates (e.g. gantacurium)

Mechanism is it binds and forms less active degradation products (adducts)

Mo and Mik (9 decks)

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